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Page 1: Vet•Med•Lab IDEXXcms2.netnews.cz/files/attachments/67030/16695-Manual-English.pdf · Directory of Services Directory of Services IDEXX Vet•Med•Lab IDEXX Vet•Med•Lab INT-001-0707

www.idexx.com

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Directory of ServicesIDEXX Vet•Med•Lab

IDE

XX V

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Me

d•L

ab

INT-001-0707

19 mm

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IIDDEEXXXX VVeett••MMeedd••LLaabb, July 2007

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Content

11 IInnddeexx

22 GGeenneerraall IInnffoorrmmaattiioonn 11

2.1 General Advice on Blood Sampling ............................................................................42.2 General Advice on Molecularbiological Tests ..........................................................82.3 General Advice on Histopathology Examinations ...................................................102.4 Reference ranges .......................................................................................................12

2.4.1 Conventional Units ...............................................................................................122.4.2 SI Units ..................................................................................................................18

2.5 Conversion Table ........................................................................................................24

33 SSccrreeeenniinngg PPrrooffiilleess 2266

3.1 General Screening Profiles .......................................................................................263.2 Special Screening Profiles ........................................................................................293.3 Species Specific Profiles ...........................................................................................40

3.3.1 Feline .....................................................................................................................403.3.2 Equine ....................................................................................................................413.3.3 Avian, Reptile, Rabbit ..........................................................................................453.3.4 Bovine ...................................................................................................................463.3.5 Porcine ..................................................................................................................49

44 HHaaeemmaattoollooggyy 5500

4.1 Haematology ...............................................................................................................504.1.1 Domestic Animals ................................................................................................504.1.2 Avian, Reptile .......................................................................................................51

4.2 Coagulation Parameters ............................................................................................524.3 Blood Groups ...............................................................................................................544.4 Blood Parasites and Haemotrophic Bacteria ..........................................................55

55 BBiioocchheemmiissttrryy 6600

66 TTooxxiiccoollooggyy aanndd DDrruuggss 9922

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77 GGaassttrrooiinntteessttiinnaall DDiisseeaasseess,, LLiivveerr aanndd PPaannccrreeaass 9933

7.1 Gastrointestinal Diseases ..........................................................................................937.2 Liver Diseases ...........................................................................................................1027.3 Exocrine Pancreatic Diseases ................................................................................105

88 UUrriinnaarryy TTrraacctt DDiisseeaasseess 110088

8.1 Blood Tests ................................................................................................................1088.2 Urine Tests .................................................................................................................110

99 MMuussccllee,, SSkkeelleettoonn aanndd JJooiinnttss 111144

9.1 Muscle Diseases ......................................................................................................1149.1.1 Infectious ............................................................................................................1149.1.2 Non infectious ....................................................................................................116

9.2 Skeletal Diseases .....................................................................................................1199.3 Joint Diseases ...........................................................................................................121

9.3.1 Infectious ............................................................................................................1219.3.2 Non infectious ....................................................................................................123

1100 CCeennttrraall NNeerrvvoouuss SSyysstteemm 112244

10.1 Infectious ...................................................................................................................12410.2 Non infectious ...........................................................................................................128

1111 SSkkiinn DDiisseeaasseess 112299

11.1 Allergic / Infectious Skin Diseases .........................................................................12911.2 Non infectious Skin Diseases ..................................................................................13311.3 Histological Skin Examination .................................................................................134

1122 EEnnddooccrriinnoollooggyy 113355

12.1 Adrenal Gland ...........................................................................................................13512.1.1 Hyperadrenocorticism .......................................................................................13512.1.2 Hypoadrenocorticism ........................................................................................145

12.2 Thyroid Gland ............................................................................................................14712.2.1 Individual Parameters .......................................................................................14712.2.2 Hypothyroidism ...................................................................................................15012.2.3 Hyperthyroidism .................................................................................................151

12.3 Sex hormones/Pregnancy ........................................................................................15312.4 Other Hormones ........................................................................................................156

Content

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1133 IInnffeeccttiioouuss DDiisseeaasseess 115588

1144 IImmmmuunnoollooggyy aanndd AAlllleerrggyy 220033

14.1 Autoimmune Diseases ..............................................................................................20314.2 Allergy Diagnostics ..................................................................................................208

1155 MMoolleeccuullaarrggeenneettiiccaall TTeessttss 221133

15.1 General Information on PCR ....................................................................................21315.2 Pathogen Detection using PCR ...............................................................................21615.3 Hereditary Diseases .................................................................................................23015.4 Avian Sex Identification ...........................................................................................24415.5 Parentage Verification .............................................................................................245

1166 MMiiccrroobbiioollooggyy 224477

16.1 General Bacteriology ...............................................................................................24716.2 Faecal Examinations .................................................................................................25016.3 Mycology ...................................................................................................................25416.4 Autovaccines .............................................................................................................25716.5 Hygiene Control .........................................................................................................258

1177 PPaarraassiittoollooggyy 225599

17.1 Faecal Examination for Parasites ...........................................................................25917.2 Ectoparasites ............................................................................................................26117.3 Blood Parasites .........................................................................................................262

1188 HHiissttooppaatthhoollooggyy 226644

18.1 Histopathological Examinations ..............................................................................26418.2 Biological Fluids ........................................................................................................266

Content

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AA

α1-Globulins . . . . . . . . . . . . . . . . . . . . . 34α2-Globulins . . . . . . . . . . . . . . . . . . . . . 34α-Amylase . . . . . . . . . . . . . . . . . . . . . . . 64α-HBDH (LDH1-Isoenzyme) . . . . . . . . . 77Acetylcholine Receptor Antibodies . 118ACTH . . . . . . . . . . . . . . . . . . . . . . . . . . 138ACTH stimulation test . . . . . . . . . . . . 137Addison's Disease . . . . . . . . . . . . . . . 145Adenovirus Antibodies (dog) . . . . . . . 186ADH (Vasopressin) . . . . . . . . . . . . . . . 156Albumin . . . . . . . . . . . . . . . . . . . . . . . . . 60Aldosterone . . . . . . . . . . . . . . . . . . . . . 146Allergy Diagnostics . . . . . . . . . . . . . . 208Allergy test Allercept™

Screening Test . . . . . . . . . . . . . . . . . 209Allergy test Allercept™

LARGE Panel . . . . . . . . . . . . . . . . . . 210Allergy test Allercept™

SMALL Panel . . . . . . . . . . . . . . . . . . 211Allergy test Equine Insects . . . . . . . . 211Alkaline Phosphatase . . . . . . . . . . . . . . 61Alkaline Phosphatase (heat stable) . . 64ALT (GPT) . . . . . . . . . . . . . . . . . . . . . . . . 62Ammonia . . . . . . . . . . . . . . . . . . . . . . . . 63Ammonia tolerance test . . . . . . . . . . . . 63Amylase, α- . . . . . . . . . . . . . . . . . . . . . . 64Anaemia, Autoimmune Haemolytic . . 207Anaemia, Equine Infectious . . . . . . . . 185Anaemia Profile . . . . . . . . . . . . . . . . . . 29Anaplasma (Ehrlichia) . . . . . . . . . . . . 173Anti-epileptic drugs, therapeutic

monitoring . . . . . . . . . . . . . . . . . . . . 128Anti-inflammatory Screening . . . . . . . 44Antinuclear Antibodies (ANA test) . . 123AP . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61AP (heat stable) . . . . . . . . . . . . . . . . . . 64Arsenic . . . . . . . . . . . . . . . . . . . . . . . . . . 92Arteritis, Equine Viral . . . . . . . . . . . . . 202Aspirate Profile I . . . . . . . . . . . . . . . . . . 29Aspirate Profile II . . . . . . . . . . . . . . . . . 29AST (GOT) . . . . . . . . . . . . . . . . . . . . . . . 64Autoimmune Haemolytic Anaemia . . 207Autovaccine Against Viral or Bacterial

Pathogens. . . . . . . . . . . . . . . . . . . . . 257

Autovaccine, E. coli . . . . . . . . . . . . . . 257Autovaccine, Equine sarcoid . . . . . . . 257Autovaccine, Papilloma . . . . . . . . . . . 257Autovaccine, Pseudomonas

aeruginosa . . . . . . . . . . . . . . . . . . . . 257Autovaccine, Staphylococcus . . . . . . 257Avian Screening . . . . . . . . . . . . . . . . . . 45Avian Sex Identification . . . . . . . . . . . 244

BB

β-Carotene . . . . . . . . . . . . . . . . . . . . . . 68β-Globulins . . . . . . . . . . . . . . . . . . . . . . . 35β-Hydroxybutyrate . . . . . . . . . . . . . . . . 77Babesia CFT . . . . . . . . . . . . . . . . . . . . . 160Babesia Direct Detection . . . . . . . . . . 159Babesia IFT . . . . . . . . . . . . . . . . . . . . . 160Babesia spp. PCR . . . . . . . . . . . . . . . . 216Babesiosis (canine) . . . . . . . . . . . . . . 159Babesiosis (equine) . . . . . . . . . . . . . . 159Baermann method

(larval migration test) . . . . . . . . . . . 260Bacteriology, aerobic . . . . . . . . . . . . . 248Bacteriology, anaerobic . . . . . . . . . . . 249Bacteriology, faecal . . . . . . . . . . . . . . 251Bacteriology, urine . . . . . . . . . . . . . . . 112Bartonella henselae PCR . . . . . . . . . . 216Basic Check-up . . . . . . . . . . . . . . . . . . . 27Benzodiazepine . . . . . . . . . . . . . . . . . . . 92BHV I Antibodies . . . . . . . . . . . . . . . . . 183BHV I field/marker virus . . . . . . . . . . . 183Bile Acids . . . . . . . . . . . . . . . . . . . . . . . 65Bile Acid Stimulation Test . . . . . . . . . . 66Bilirubin (direct) . . . . . . . . . . . . . . . . . . 66Bilirubin (total) . . . . . . . . . . . . . . . . . . . 66Biotin (Vit. H) . . . . . . . . . . . . . . . . . . . . . 91BLAD . . . . . . . . . . . . . . . . . . . . . . . . . . 231Blood, Occult . . . . . . . . . . . . . . . . . . . . 253Blood Count, Differential . . . . . . . . . . . 50Blood Count, Differential (Avian) . . . . 51Blood Count, Large . . . . . . . . . . . . . . . . 50Blood Count, Large (Avian) . . . . . . . . . 51Blood Count, Large (Reptile) . . . . . . . . 51Blood Count, Small . . . . . . . . . . . . . . . . 50Blood Count, Small (Avian) . . . . . . . . . 51

1 Index

I

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Blood Culture . . . . . . . . . . . . . . . . . . . . 249Blood Groups (dog, cat) . . . . . . . . . . . . 54Blood Parasites, Comprehensive . . . . 55BLV Antibodies . . . . . . . . . . . . . . . . . . 190Border Disease . . . . . . . . . . . . . . . . . . 160Border Disease Antibodies . . . . . . . . 161Borna Disease . . . . . . . . . . . . . . . . . . . 161Borna Antibodies . . . . . . . . . . . . . . . . 161Borrelia C6 Antibodies EIA . . . . . . . . 164Borrelia Antibodies ELISA . . . . . . . . . 163Borrelia Antibodies Immunoblot . . . . 163Borrelia burgdorferi PCR . . . . . . . . . . 217Borreliosis . . . . . . . . . . . . . . . . . . . . . . 162Bovine Herpesvirus I . . . . . . . . . . . . . 182Bovine Profile . . . . . . . . . . . . . . . . . . . . 47Bovine Profile, Large . . . . . . . . . . . . . . 46Bovine Leukocyte Adhesion

Deficiency (BLAD) . . . . . . . . . . . . . 231Bovine Leukosis Virus (BLV)

Antibodies . . . . . . . . . . . . . . . . . . . . 190Bovine Respiratory Syncytial

virus Antibodies . . . . . . . . . . . . . . . 166Bovine Viral Diarrhoea (BVD) . . . . . . 165Bromide . . . . . . . . . . . . . . . . . . . . . . . . . 92BRSV Antibodies . . . . . . . . . . . . . . . . . 166Brucella abortus Antibodies . . . . . . . 166Brucella canis Antibodies . . . . . . . . . 167Brucella suis Antibodies . . . . . . . . . . 167Brucellosis . . . . . . . . . . . . . . . . . . . . . . 166Burkholderia (Pseudomonas)

mallei Antibodies . . . . . . . . . . . . . . 181BVD Antibodies . . . . . . . . . . . . . . . . . . 165BVD Antigen . . . . . . . . . . . . . . . . . . . . 165

CC

CAE Antibodies . . . . . . . . . . . . . . . . . . 168Caffeine . . . . . . . . . . . . . . . . . . . . . . . . . 44Calcium . . . . . . . . . . . . . . . . . . . . . . . . . 67Calicivirus Antibodies . . . . . . . . . . . . . 167Calicivirus PCR . . . . . . . . . . . . . . . . . . 217Canine Coronavirus PCR . . . . . . . . . . 217Canine faecal elastase-1 . . . . . . . . . . 250Canine Hepatitis, Infectious (ICH) . . . 186Canine Herpesvirus I Antibodies . . . 183

Canine Herpesvirus I PCR . . . . . . . . . 218Canine Leukocyte Adhesion

Deficiency (CLAD) . . . . . . . . . . . . . . 233Canine Malignant Hyperthermia . . . . 232Canine Pancreas Specific Lipase . . . . 79Canine TSH . . . . . . . . . . . . . . . . . . . . . 148Caprine Arthritis Encephalitis . . . . . . 168Carotene, β- . . . . . . . . . . . . . . . . . . . . . 68Cat scratch disease . . . . . . . . . . . . . . 216CEM (Taylorella equigenitalis) . . . . . . 247Central Nervous System . . . . . . . . . . 124Cervical swab (equine) . . . . . . . . . . . 247Check-up . . . . . . . . . . . . . . . . . . . . . . . . 26Check-up, Basic . . . . . . . . . . . . . . . . . . 27Check-up, Large . . . . . . . . . . . . . . . . . . 26Chestnut Colour Gene . . . . . . . . . . . . 232CLAD . . . . . . . . . . . . . . . . . . . . . . . . . . . 233Chlamydia (Chlamydophila)

Antibodies . . . . . . . . . . . . . . . . . . . . 169Chlamydia (Chlamydophila)

felis PCR . . . . . . . . . . . . . . . . . . . . . . 218Chlamydia (Chlamydophila)

psittaci PCR . . . . . . . . . . . . . . . . . . . 219Chloride . . . . . . . . . . . . . . . . . . . . . . . . . 68Cholesterol . . . . . . . . . . . . . . . . . . . . . . 69Cholinesterase . . . . . . . . . . . . . . . . . . . 70CHV I Antibodies . . . . . . . . . . . . . . . . . 183CHV I PCR . . . . . . . . . . . . . . . . . . . . . . 218Cimetidine . . . . . . . . . . . . . . . . . . . . . . . 44CK (CPK) . . . . . . . . . . . . . . . . . . . . . . . . . 70Clenbuterol . . . . . . . . . . . . . . . . . . . . . . 92Clostridium, quantitatively in faeces 250Clostridium perfringens enterotoxin . 250Coagulation Parameters, Comprehensive . . . . . . . . . . . . . . . . . . . 53Cobalamin (Vit. B12) . . . . . . . . . . . . . . . 89Coggins test . . . . . . . . . . . . . . . . . . . . . 185Conversion table

(conventional/SI units) . . . . . . . . . . . 24Coombs Test, direct . . . . . . . . . . . . . . 207Copper . . . . . . . . . . . . . . . . . . . . . . . . . . 71Copper Storage Hepatopathy . . . . . . 233Coronavirus, Canine PCR . . . . . . . . . . 217Coronavirus, Feline Antibodies . . . . . 176Coronavirus, Feline PCR . . . . . . . . . . . 223Cortisol . . . . . . . . . . . . . . . . . . . . . . . . . 135

1 Index

II

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Cortisol/Creatinine Ratio . . . . . . . . . . 136Coxiella burnetii (Q Fever) . . . . . . . . . 196CPK (CK) . . . . . . . . . . . . . . . . . . . . . . . . . 70C-Reactive Protein (CRP) . . . . . . . . . . . 72Creatinine . . . . . . . . . . . . . . . . . . . . . . . 72Creatinine clearance,

modified exogenous . . . . . . . . . . . . 108Cryptosporidia antigen . . . . . . . . . . . . 259CSF Profile I . . . . . . . . . . . . . . . . . . . . . . 29CSF Profile II . . . . . . . . . . . . . . . . . . . . . 29Cumarin . . . . . . . . . . . . . . . . . . . . . . . . . 92Cushing Monitoring Profile . . . . . . . . . 30Cushing's Syndrome . . . . . . . . . . . . . . 135Cushing's Syndrome, treatment . . . . 143Cystatin C . . . . . . . . . . . . . . . . . . . . . . . 108Cystine . . . . . . . . . . . . . . . . . . . . . . . . . . 73Cystinuria (Newfoundland dog) . . . . . 233Cytological examination . . . . . . . . . . . 265

DD

Dermatophytes . . . . . . . . . . . . . . . . . . 255Dexamethasone . . . . . . . . . . . . . . . . . . 92Dexamethasone High-Dose Test . . . . 139Dexamethasone Low-Dose Test . . . . 140Diarrhoea Profile B (dog, cat) . . . . . . . 30Diarrhoea Profile C . . . . . . . . . . . . . . . . 31Diarrhoea Profile E (dog) . . . . . . . . . . . 31Differential Blood Count . . . . . . . . . . . . 50Differential Blood Count (Avian) . . . . . 51Digestion test, faecal . . . . . . . . . . . . . 105Digoxin . . . . . . . . . . . . . . . . . . . . . . . . . . 92Direct Coombs test . . . . . . . . . . . . . . . 207Dirofilariasis . . . . . . . . . . . . . . . . . . . . 170Distemper . . . . . . . . . . . . . . . . . . . . . . 171Distempervirus Antibodies . . . . . . . . . 171Distempervirus PCR . . . . . . . . . . . . . . 219Dourine (Tryp. equiperdum) . . . . . . . . 201Downer Cow Profile . . . . . . . . . . . . . . . 47Drugs, and Toxicology . . . . . . . . . . . . . 92Drug screening (equine) . . . . . . . . . . . 42

EE

Ear swab . . . . . . . . . . . . . . . . . . . . . . . 247E. coli autovaccine . . . . . . . . . . . . . . . 257Ectoparasites, biopsy . . . . . . . . . . . . . 261Ectoparasites, scraping . . . . . . . . . . . 261Ehrlichia/Anaplasma spp. PCR . . . . . 220Ehrlichia canis Antibodies . . . . . . . . . 173Ehrlichia canis PCR . . . . . . . . . . . . . . 220Ehrlichia Direct Detection . . . . . . . . . 173Ehrlichia (Anaplasma)

phagocytophilum Antibodies . . . . . 173Ehrlichiosis . . . . . . . . . . . . . . . . . . . . . 172EHV 1, 4 Antibodies . . . . . . . . . . . . . . . 184EHV 1, 4 Antigen PCR . . . . . . . . . . . . . 221EHV 2, 5 Antigen PCR . . . . . . . . . . . . . 222EIA Antibodies . . . . . . . . . . . . . . . . . . . 185Elastase-1, Faecal (dog) . . . . . . . . . . . 105Electrolyte Profile . . . . . . . . . . . . . . . . . 32Electrophoresis, Serum Protein . . . . . 33Electrophoresis, Urine Protein . . . . . 111Encephalitozoon cuniculi . . . . . . . . . . 175Endocrinology . . . . . . . . . . . . . . . . . . . 135Endoparasites . . . . . . . . . . . . . . . . . . . 259Equine Geriatric Profile. . . . . . . . . . . . . 42Equine Herpesvirus . . . . . . . . . . . . . . . 184Equine Herpesvirus PCR . . . . . . . . . . 221Equine Infectious Anaemia . . . . . . . . 185Equine Influenza . . . . . . . . . . . . . . . . . 186Equine Profile . . . . . . . . . . . . . . . . . . . . 41Equine Profile, Large . . . . . . . . . . . . . . 41Equine Purchase Profile . . . . . . . . . . . 42Equine sarcoid autovaccine . . . . . . . 257Equine Viral Arteritis (EVA)

Antibodies . . . . . . . . . . . . . . . . . . . . 202Equine Viral Arteritis (EVA) PCR . . . . 222EVA Antibodies . . . . . . . . . . . . . . . . . . 202EVA PCR . . . . . . . . . . . . . . . . . . . . . . . . 222Exogenous creatinine clearance,

modified . . . . . . . . . . . . . . . . . . . . . . 108

FF

Factor VIII . . . . . . . . . . . . . . . . . . . . . . . 52Faecal bacteriology . . . . . . . . . . . . . . 251Faecal digestion test . . . . . . . . . . . . . 105

1 Index

III

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Faecal virology (electron microscopy) . . . . . . . . . . 252

FCoV Antibodies . . . . . . . . . . . . . . . . . 177Feline Coronavirus Antibodies . . . . . 177Feline Coronavirus PCR . . . . . . . . . . . 223Feline Herpesvirus Antibodies . . . . . 185Feline Herpesvirus PCR . . . . . . . . . . . 223Feline Immunodeficiency Virus

FIV Antibodies . . . . . . . . . . . . . . . . . 180Feline Immunodeficiency

Virus FIV PCR . . . . . . . . . . . . . . . . . 224Feline Leukaemia Virus FeLV . . . . . . . 178FeLV Antigen ELISA/IFA . . . . . . . . . . . 179FeLV Progenome PCR . . . . . . . . . . . . . 224FeLV/FIV + FIP Screening . . . . . . . . . . 40Fertility Profile 1 . . . . . . . . . . . . . . . . . . 48Fertility Profile 2 . . . . . . . . . . . . . . . . . . 48Fertility Profile 3 . . . . . . . . . . . . . . . . . . 48Fibrinogen . . . . . . . . . . . . . . . . . . . . . . . 52Fine Needle Aspirate . . . . . . . . . . . . . 265Fingerprint, genetic . . . . . . . . . . . . . . 246FHV Antibodies . . . . . . . . . . . . . . . . . . 185FIP Antibodies . . . . . . . . . . . . . . . . . . . 177FIP Infection . . . . . . . . . . . . . . . . . . . . 176FIP Screening . . . . . . . . . . . . . . . . . . . . 40FIV Antibodies ELISA/Blot . . . . . . 180, 181FIV Progenome PCR. . . . . . . . . . . . . . . 224Foal Profile . . . . . . . . . . . . . . . . . . . . . . . 43Folic acid . . . . . . . . . . . . . . . . . . . . . . . . 73Fructosamine . . . . . . . . . . . . . . . . . . . . . 74FT3 (Triiodothyronine) . . . . . . . . . . . . . 148FT4 (Thyroxine) . . . . . . . . . . . . . . . . . . 147FT4 (Thyroxine),

Equilibrium Dialysis . . . . . . . . . . . . 147FT4/Cholesterol Ratio (dog) . . . . . . . . 149Fucosidosis . . . . . . . . . . . . . . . . . . . . . 234Fungal Skin Disease . . . . . . . . . . . . . . 255Furosemide . . . . . . . . . . . . . . . . . . . . . . 44

GG

γ-Globulins . . . . . . . . . . . . . . . . . . . . . . . 35Galactomannan test . . . . . . . . . . . . . . 158Gangliosidosis (Korat cat) . . . . . . . . . 234Gastrointestinal Diseases . . . . . . . . . . 93

Genetic Fingerprint . . . . . . . . . . . . . . . 246Genetic Identity Determination . . . . . 246Geriatric Profile . . . . . . . . . . . . . . . . . . 28Geriatric Profile

without blood count . . . . . . . . . . . . . 28Geriatric Profile, Equine . . . . . . . . . . . . 42GGT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74Giardia Antigen . . . . . . . . . . . . . . . . . . 259Glanders . . . . . . . . . . . . . . . . . . . . . . . . 181Glanders Antibodies . . . . . . . . . . . . . . 181GLDH . . . . . . . . . . . . . . . . . . . . . . . . . . . 75Globoid Cell Leukodystrophy . . . . . . . 235Glucocorticoid Screening . . . . . . . . . . 43Glucose . . . . . . . . . . . . . . . . . . . . . . . . . 76GOT (AST) . . . . . . . . . . . . . . . . . . . . . . . 64GPT (ALT) . . . . . . . . . . . . . . . . . . . . . . . . 62

HH

Haemobartonellosis . . . . . . . . . . . . . . 192Haemolytic Anaemia, Autoimmune . . 207HBDH, α- (LDH1-Isoenzyme) . . . . . . . . 77HCG Stimulation Test . . . . . . . . . . . . . 154Heartworm (Dirofilaria immitis) . . . . . 170Helicobacter . . . . . . . . . . . . . . . . . . . . 182Helicobacter spp. PCR . . . . . . . . . . . . 225Hepatic Encephalopathy Syndrome . 128Hepatozoa Direct Detection . . . . . . . . . 56Hereditary Diseases . . . . . . . . . . . . . . 230Herpesvirus, Bovine . . . . . . . . . . . . . . 182Herpesvirus, Canine . . . . . . . . . . . . . . 183Herpesvirus, Canine PCR . . . . . . . . . . 218Herpesvirus, Equine (1,4) Antibodies 184Herpesvirus, Equine (1,2,4,5) PCR . . . 221Herpesvirus, Feline . . . . . . . . . . . . . . . 184Herpesvirus, Feline Antibodies . . . . . 185Herpesvirus, Feline PCR . . . . . . . . . . . 223Histopathology . . . . . . . . . . . . . . . . . . 264Hydroxybutyrate, β- . . . . . . . . . . . . . . . 77Hyperadrenocorticism . . . . . . . . . . . . 135Hyperkalaemic Periodic Paralysis

(HYPP) . . . . . . . . . . . . . . . . . . . . . . . 235Hyperthermia, Canine Malignant . . . 232Hyperthermia, Porcine Malignant . . . 236Hyperthyroidism . . . . . . . . . . . . . . . . . 151

1 Index

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Hypoadrenocorticism . . . . . . . . . . . . . 135Hyposensitisation Solution . . . . . . . . 212HYPP . . . . . . . . . . . . . . . . . . . . . . . . . . . 235

II

IBR/IPV (Bovine Herpesvirus) . . . . . . 182ICH (Infectious Canine Hepatitis)

Antibodies . . . . . . . . . . . . . . . . . . . . 186Identity Determination, Genetic . . . . 246IGF I (Somatomedine) . . . . . . . . . . . . . 157Immunodeficiency Virus, Feline . . . . 180Immunodeficiency Virus,

Feline Antibodies . . . . . . . . . . 180, 181Immunodeficiency Virus, Feline PCR 224Immunology . . . . . . . . . . . . . . . . . . . . . 204Infectious Anaemia, Equine . . . . . . . . 185Infectious Canine Hepatitis . . . . . . . . 186Influenza, Equine . . . . . . . . . . . . . . . . . 186Insect Allergy Test, Equine . . . . . . . . 211Insulin . . . . . . . . . . . . . . . . . . . . . . . . . . 156Iron . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77

KK

Kidney Profile . . . . . . . . . . . . . . . . . . . . 32

LL

Lactate . . . . . . . . . . . . . . . . . . . . . . . . . . 78Large Blood Count . . . . . . . . . . . . . . . . 50Large Blood Count (Avian) . . . . . . . . . . 51Large Blood Count (Reptile) . . . . . . . . 51Large Bovine Profile . . . . . . . . . . . . . . . 46Large Check-up . . . . . . . . . . . . . . . . . . . 26Large Equine Profile . . . . . . . . . . . . . . . 41Large Feline Profile . . . . . . . . . . . . . . . 40Large Porcine Profile . . . . . . . . . . . . . . 49Large Reptile Profile . . . . . . . . . . . . . . . 45Large Screening . . . . . . . . . . . . . . . . . . 27Larval migration test

(Baermann method) . . . . . . . . . . . . 260LDH . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78

Lead . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92Leishmania Antibodies (dog) . . . . . . . 187Leishmania Direct Detection . . . . . . . 188Leishmaniasis . . . . . . . . . . . . . . . . . . . 187Leishmania spp. PCR . . . . . . . . . . . . . 225Leptospira Antibodies . . . . . . . . . . . . 189Leptospira spp. PCR . . . . . . . . . . . . . . 225Leptospirosis . . . . . . . . . . . . . . . . . . . . 189Leukaemia Virus Infection, Feline . . . 178Leukodystrophy, Globoid Cell . . . . . . 235Leukosis Virus, Bovine . . . . . . . . . . . . 190Lipase . . . . . . . . . . . . . . . . . . . . . . . . . . . 79Lipase, canine pancreas specific . . . . 79Listeria moncytogenes PCR . . . . . . . . 226Liver Diseases . . . . . . . . . . . . . . . . . . . 102Liver Profile I . . . . . . . . . . . . . . . . . . . . . 32Liver Profile II . . . . . . . . . . . . . . . . . . . . . 32Lupus Erythematosus, Systemic . . . . 123

MM

Macrofilaria Antigen (D. immitis) . . . 170MDR 1 . . . . . . . . . . . . . . . . . . . . . . . . . . 235Maedi/Visna Antibodies . . . . . . . . . . . 191Magnesium . . . . . . . . . . . . . . . . . . . . . . 80Malignant Hyperthermia, Canine . . . 232Malignant Hyperthermia Syndrome,

Porcine . . . . . . . . . . . . . . . . . . . . . . . 236Manganese . . . . . . . . . . . . . . . . . . . . . . 80Mercury . . . . . . . . . . . . . . . . . . . . . . . . . 92Metamizole . . . . . . . . . . . . . . . . . . . . . . 92Microbiology . . . . . . . . . . . . . . . . . . . . 130Microfilaria Antigen . . . . . . . . . . . . . . 170Microfilaria Direct Detection . . . . . . 170Milk sample . . . . . . . . . . . . . . . . . . . . . 247Modified exogenous creatinine

clearance . . . . . . . . . . . . . . . . . . . . . 108Moleculargenetical Tests . . . . . . . . . 213Mucopolysaccharidosis VII . . . . . . . . 237Muscle Profile . . . . . . . . . . . . . . . . . . . . 33Myasthenia gravis . . . . . . . . . . . . . . . 117Mycology . . . . . . . . . . . . . . . . . . . . . . . 254Mycoplasma (Haemobartonella) . . . . 192Mycoplasma Direct Detection . . . . . . 193

1 Index

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Mycoplasma haemofelis + Cand. M. haemominutum PCR . . . . 226

Myotonia congenita. . . . . . . . . . . . . . . 237

NN

Nandrolone . . . . . . . . . . . . . . . . . . . . . . 44Neospora caninum Antibodies . . . . . 194Night Blindness (Briard dog) . . . . . . . 237Nosematosis . . . . . . . . . . . . . . . . . . . . 175Nt-proBNP . . . . . . . . . . . . . . . . . . . . . . . 80NSAID Screening . . . . . . . . . . . . . . . . . 44

OO

Occult Blood . . . . . . . . . . . . . . . . . . . . 253Oestradiol, 17 β- . . . . . . . . . . . . . . . . . 153Oestrone Sulphate . . . . . . . . . . . . . . . 154OLWS . . . . . . . . . . . . . . . . . . . . . . . . . . 238Osmolality (urine) . . . . . . . . . . . . . . . . 112Overo Lethal White Syndrome

(OLWS) . . . . . . . . . . . . . . . . . . . . . . . 238

PP

Pancreas Diseases . . . . . . . . . . . . . . . 105Panleukopenia . . . . . . . . . . . . . . . . . . . 195Papilloma Autovaccine . . . . . . . . . . . 257Paracetamol . . . . . . . . . . . . . . . . . . . . . 92Parasitology . . . . . . . . . . . . . . . . . . . . . 259Paratuberculosis

Antibodies (bovine) . . . . . . . . . . . . . 194Parentage Verification . . . . . . . . . . . . 245Parvovirus Antibodies (dog, cat) . . . . 195Parvovirus Direct Detection . . . . . . . 195Parvovirus PCR (dog, cat) . . . . . . . . . 227PBFD Virus PCR . . . . . . . . . . . . . . . . . . 227PCR Tests . . . . . . . . . . . . . . . . . . . . . . . 213Phenobarbitone . . . . . . . . . . . . . . . . . . . 92Phenylbutazone . . . . . . . . . . . . . . . . . . . 92Phenytoin . . . . . . . . . . . . . . . . . . . . . . . . 92Phosphate . . . . . . . . . . . . . . . . . . . . . . . 81Phosphofructokinase Deficiency . . . 238

PKD . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239PMSG . . . . . . . . . . . . . . . . . . . . . . . . . . 155Polyarthritis, Rheumatoid . . . . . . . . . . 122Polyomavirus PCR . . . . . . . . . . . . . . . . 228Porcine Malignant Hyperthermia

Syndrome . . . . . . . . . . . . . . . . . . . . . 236Porcine Profile, Large . . . . . . . . . . . . . . 49Porcine Reproductive and

Respiratory Syndrome . . . . . . . . . . 196Potassium . . . . . . . . . . . . . . . . . . . . . . . 82PRA . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239Pregnancy/Sex hormones . . . . . . . . . 153Primidone . . . . . . . . . . . . . . . . . . . . . . . . 92Profile S . . . . . . . . . . . . . . . . . . . . . . . . . 43Progesterone . . . . . . . . . . . . . . . . . . . . 153Progressive Retinal Atrophy (PRA) . . 239Protein/Creatinine Ratio (urine) . . . . 110Protein Electrophoresis, Serum . . . . . 33Protein Electrophoresis, Urine . . . . . 111Protein, Total . . . . . . . . . . . . . . . . . . . . . 84Prothrombin Time (PT) . . . . . . . . . . . . . 52PRRS Antibodies . . . . . . . . . . . . . . . . . 196Pseudomonas aeruginosa

Autovaccine . . . . . . . . . . . . . . . . . . 257Psittacine Beak and Feather

Disease PCR . . . . . . . . . . . . . . . . . . 227PT (Prothrombin time) . . . . . . . . . . . . . 52PTT (Partial Thromboplastin Time) . . . 52PU/PD Profile . . . . . . . . . . . . . . . . . . . . 108Pyridoxine (Vit. B6) . . . . . . . . . . . . . . . . 89Pyruvate Kinase Deficiency

(Basenji dog) . . . . . . . . . . . . . . . . . . 240Pyruvate Kinase Deficiency

(West Highland White Terrier + Cairn T.) . . . . . . . . . . . . . . . . . . . . . 241

QQ

Q Fever Antibodies . . . . . . . . . . . . . . . 196

RR

Rabbit Profile . . . . . . . . . . . . . . . . . . . . . 45Rabies Antibody (IFT) . . . . . . . . . . . . . 197

1 Index

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Reference ranges - conventional units . . . . . . . . . . . . . . 12

Reference ranges - SI units . . . . . . . . 18Reproductive and Respiratory

Syndrome, Porcine . . . . . . . . . . . . . 196Reptile Profile . . . . . . . . . . . . . . . . . . . . 45Reptile Profile, Large. . . . . . . . . . . . . . . 45Reticulocytes . . . . . . . . . . . . . . . . . . . . . 50Rheumatoid Arthritis Factor

(Waaler-Rose test) . . . . . . . . . . . . . 122Rheumatoid Polyarthritis . . . . . . . . . . 122Riboflavin (Vit. B2) . . . . . . . . . . . . . . . . . 89Rotavirus Antigen . . . . . . . . . . . . . . . . 101

SS

Salmonella (faeces) . . . . . . . . . . . . . . 253Sarcoptes Antibodies (dog) . . . . . . . . 198SCID . . . . . . . . . . . . . . . . . . . . . . . . . . . 241Scrapie . . . . . . . . . . . . . . . . . . . . . . . . . 242Screening, Large . . . . . . . . . . . . . . . . . . 27Screening, Small . . . . . . . . . . . . . . . . . . 28Sedative/Tranquiliser Screening . . . . . 44Sedimentation Method . . . . . . . . . . . . 260Selected Drugs . . . . . . . . . . . . . . . . . . . 44Selenium . . . . . . . . . . . . . . . . . . . . . . . . 83Serum Protein Electrophoresis . . . . . . 33Severe Combined

Immunodeficiency (SCID) . . . . . . . 241Severe Combined Immunodeficiency,

X-linked (X-SCID) . . . . . . . . . . . . . . 243Sex Hormones/Pregnancy . . . . . . . . . 153Sex Identification, Avian . . . . . . . . . . 244Skin Diseases . . . . . . . . . . . . . . . . . . . 130Skin Profile 1 . . . . . . . . . . . . . . . . . . . . . 36Skin Profile 2 . . . . . . . . . . . . . . . . . . . . . 36Skin Profile 3 . . . . . . . . . . . . . . . . . . . . . 36Skin Profile 4 (dog only) . . . . . . . . . . . . 36Skin Profile 5 (horse only) . . . . . . . . . . 36Skin Profile 6 (dog, cattle) . . . . . . . . . . 36Skin Profile 7 (dog, cat) . . . . . . . . . . . . 37Small Blood Count . . . . . . . . . . . . . . . . 50Small Blood Count (Avian) . . . . . . . . . . 51Small Screening . . . . . . . . . . . . . . . . . . 28Sodium . . . . . . . . . . . . . . . . . . . . . . . . . . 83

Somatomedine (IGF I) . . . . . . . . . . . . . 157Spec. cPL®

(canine pancreas specific lipase) . . 79Staphylococcus Autovaccine . . . . . . 257Stone Analysis (urinary) . . . . . . . . . . . 112Synovial fluid profile I . . . . . . . . . . . . . . 37Synovial fluid profile II . . . . . . . . . . . . . 37Synovial fluid profile III . . . . . . . . . . . . . 37Systemic Lupus Erythematosus . . . . 123

TT

T3, Free . . . . . . . . . . . . . . . . . . . . . . . . . 148T3, Total . . . . . . . . . . . . . . . . . . . . . . . . 148T3, Suppression Test (cat) . . . . . . . . . 151T4, Free . . . . . . . . . . . . . . . . . . . . . . . . . 147T4, Free, by Equilibrium Dialysis . . . . 147T4, Total . . . . . . . . . . . . . . . . . . . . . . . . 147Taylorella equigenitalis (CEM) . . . . . . 247T-cell Carcinoma Screening (dog) . . 113Testosterone . . . . . . . . . . . . . . . . . . . . 154Thallium . . . . . . . . . . . . . . . . . . . . . . . . . 92Thiamine (Vit. B1) . . . . . . . . . . . . . . . . . 88Thrombin Time . . . . . . . . . . . . . . . . . . . . 52Thromboplastin Time, Partial (PTT) . . 52Thyroglobulin Antibodies (TAB) . . . . . 149Thyroid Profile I . . . . . . . . . . . . . . . . . . 38Thyroid Profile II (dog only) . . . . . . . . . 38Thyroxine (T4), Total . . . . . . . . . . . . . . 147Thyroxine (T4), Free . . . . . . . . . . . . . . 147Thyroxine (T4), Free, by

Equilibrium Dialysis . . . . . . . . . . . . 147Tickborne Encephalitis Antibodies . . 199Tickborne Encephalitis Virus PCR . . . 228TLI (dog, cat) . . . . . . . . . . . . . . . . . . . . . 84Tocopherol (Vit. E) . . . . . . . . . . . . . . . . . 91Total Protein . . . . . . . . . . . . . . . . . . . . . 84Toxicology and Drugs . . . . . . . . . . . . . . 92Toxoplasma . . . . . . . . . . . . . . . . . . . . . 199Toxoplasma Antibodies . . . . . . . . . . . 200Toxoplasma Direct Detection . . . . . . 201Toxoplasma gondii PCR . . . . . . . . . . . 229Travel Disease Profile I (dog only) . . . 38Travel Disease Profile II (dog only) . . 39TRH Stimulation Test (dog) . . . . . . . . 150

1 Index

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Triiodothyronine (T3), Total . . . . . . . . . 148Triiodothyronine (T3), Free . . . . . . . . . 148Triglycerides . . . . . . . . . . . . . . . . . . . . . 85Troponin I . . . . . . . . . . . . . . . . . . . . . . . . 86Trypanosoma Direct Detection . . . . . 202Trypanosoma equiperdum

Antibodies . . . . . . . . . . . . . . . . . . . . 201TSH, canine . . . . . . . . . . . . . . . . . . . . . 148

UU

Urea (BUN) . . . . . . . . . . . . . . . . . . . . . . 86Uric Acid . . . . . . . . . . . . . . . . . . . . . . . . 87Urinary Stone Analysis . . . . . . . . . . . . 112Urinary Tract Diseases . . . . . . . . . . . . 108Urine Analysis . . . . . . . . . . . . . . . . . . . 110Urine Bacteriology . . . . . . . . . . . . . . . 112Urine Protein/Creatinine Ratio . . . . . 110Urine Protein Electrophoresis . . . . . . 111Urine Screening Profile (bovine) . . . . . 48Urine Sediment . . . . . . . . . . . . . . . . . . 110

VV

Vasopressin (ADH) . . . . . . . . . . . . . . . 156Virology, Faecal

(electron microscopy) . . . . . . . . . . 252Visna/Maedi . . . . . . . . . . . . . . . . . . . . 191Vitamin A . . . . . . . . . . . . . . . . . . . . . . . . 88Vitamin B1 (Thiamine) . . . . . . . . . . . . . . 88Vitamin B2 (Riboflavin) . . . . . . . . . . . . . 89Vitamin B6 (Pyridoxine) . . . . . . . . . . . . 89Vitamin B12 (Cobalamin) . . . . . . . . . . . . 89Vitamin D3 (1,25-di-OH) . . . . . . . . . . . . . 90Vitamin D3 (25-OH) . . . . . . . . . . . . . . . . 90Vitamin E (Tocopherol) . . . . . . . . . . . . . 91Vitamin H (Biotin) . . . . . . . . . . . . . . . . . 91Viral Arteritis, Equine . . . . . . . . . . . . . 202Viral Diarrhoea, Bovine . . . . . . . . . . . 165von Willebrand's Disease . . . . . . . . . 242Vomitus Profile . . . . . . . . . . . . . . . . . . . . 39von Willebrand's Factor . . . . . . . . . . . . 53

WW

Waaler-Rose test (Rheumatoid Arthritis Factor) . . . . 122

Willebrand's Disease, von . . . . . . . . . 242Willebrand's Factor, von . . . . . . . . . . . 53

XX

X-SCID . . . . . . . . . . . . . . . . . . . . . . . . . 243

YY

Yeasts and Moulds . . . . . . . . . . . . . . . 256Yeasts in faeces . . . . . . . . . . . . . . . . . 256

ZZ

Zinc . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91

1 Index

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22 GGeenneerraall IInnffoorrmmaattiioonn

SSaammppllee aanndd MMaaiilliinngg MMaatteerriiaall

We will be glad to provide all our sample tubes, including protective mailing containers,submission forms, barcode labels, cooling containers, as well as dispatch bags/boxes free-of-charge. Please contact your Regional Manager.

Protective containers as well as boxes are designed to be recycled.

SSuubbmmiissssiioonn ffoorrmmss

For easier recognition there are different submission forms:

1. Submission form I (green) for Small Animals: Clinical chemistry which includesspecific profiles, haematology, serology, endocrinology, allergy testing, PCR tests etc.

2. Submission form II (blue) for Large Animals: Clinical chemistry which includes specificprofiles, haematology, serology, endocrinology, allergy testing, PCR tests etc.

3. Submission form III (beige) for microbiology.

4. Submission form IV (white) for histopathology.

5. Submission form for PCR/genetic testing.

6. Submission form for rabies.

Please fill out the submission form completely:

- veterinary surgeon (stamp), owner’s name, animal species, sex and age of the animal(we provide reference ranges depending on age).

- mark off on the form how you would like to receive the test results(for example via fax, e-mail and post).

- mark off all the testing that you wish to have performed. Should you require a specifictest which you have not found on the form, please contact us directly or contact yourRegional Manager.

2 General Information

1

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22 GGeenneerraall IInnffoorrmmaattiioonn

SSaammppllee iiddeennttiiffiiccaattiioonn aanndd ppaacckkaaggiinngg

The safest way to identify your sample is to use the barcode which we will provide. The barcode contains your address, therefore should you forget to include your stamp on the submission form we can assign your sample to your practice.

Each row of barcodes consists of a column of seven stickers all with the same number.Please give each patient a new number.

For safe identification and packaging of your samples please follow the guidelinesmentioned below:

- always use a barcode on the submission form - number towards the top.

- include one barcode in your patient file.

- place one barcode on every sample tube - please do not place a sticker on theprotective outer. Use the small barcodes for small sample tubes and slides.

- make sure that the barcode on the submission form is the same one as on all thesamples you are submitting of that particular patient.

- make sure you have closed the sample tubes carefully and place them in theprotective outer.

- use only our red dispatch bag/courier boxes. Other envelopes may get lost in the post more easily. Close the dispatch bag/box carefully, even if you are using a courier collection service.

- if you are sending the dispatch bag via post please make sure you apply sufficient postage.

CCoouurriieerr ccoolllleeccttiioonn sseerrvviiccee

Courier services allow for a quick and efficient transport of your samples to the lab. Please contact your Regional Manager. He/she will be able to tell you if this service is available in your area.

2 General Information

2

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22 GGeenneerraall IInnffoorrmmaattiioonn

TTrraannssmmiissssiioonn ooff yyoouurr tteesstt rreessuullttss

You can receive your test results:

1. By post.

2. By fax. Final results are sent out several times a day. Provisional results are sent outonce in the late afternoon.

3. By E-mail. Final results are sent out every 10 minutes. Validated provisional resultsare sent out every 30 minutes.

4. By direct data transfer.

For information on electronic data transfer please contact your Regional Manager.

The means by which you wish to receive your results is noted on our computer systemtogether with your practice data. Should you wish to change this please notify us by fax, or clearly mark your request as a change in practice details on the submission form.

AAddddiittiioonnaall tteesstt rreeqquueessttss ((oonn bblloooodd ssaammpplleess))

This is possible during a time frame of 77 ddaayyss, depending on the parameter requested. Allblood samples are kept refrigerated until they are disposed of.

PPaayymmeenntt

Your practice will be charged directly. You can receive an invoice either weekly or monthly. On extra request you may receive a provisional invoice with every single result.Please note that discounts are not taken into account on the provisional invoice.

In certain countries it is possible to arrange for the invoices to be sent directly to the owners. Please contact your RReeggiioonnaall MMaannaaggeerr.

Current prices are listed on our price list.

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22..11 GGeenneerraall AAddvviiccee oonn BBlloooodd SSaammpplliinngg

SSaammpplliinngg ffoorr llaabboorraattoorryy aannaallyyssiiss

11.. PPrreeppaarriinngg tthhee ppaattiieenntt

Satisfactory blood results depend on good preparation of the patient. If possible, the patient should be starved 10-12 hours prior to blood sampling. Otherwise many parameters can be inaccurate:

Cholesterol, triglycerides, glucose, TLI, and also α-amylase, ALT (GPT), AST, bilirubin, bile acids and calcium.

The patient should not have been physically worked immediately prior to sampling and theprocedure should be carried out quickly and calmly. Agitation and exertion could lead toincreased CK, LDH, lactate and cortisol levels as well as a rise in circulating lymphocytes.Especially in cats, but also in dogs, stress leads to raised blood glucose levels.

22.. BBlloooodd ssaammpplliinngg tteecchhnniiqquuee

To avoid haemolysis blood should be taken immediately after the vein has been raised.‘Pumping’ blood from the vein can impair results.

Avoid high negative pressure in the syringe or erythrocytes will fracture. Do not squirt the blood forcefully into the tube. Instead, let it run down the tube wall. Do not try to get the last remaining blood drops that are left in the needle.

When using a tube with an anticoagulant, do not shake but gently turn upside down several times after sampling is completed.

Please remember to remove the needle before mailing your sample.

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22..11 GGeenneerraall AAddvviiccee oonn BBlloooodd SSaammpplliinngg

33.. WWhhiicchh ttyyppee ooff bblloooodd ffoorr wwhhiicchh tteesstt??

Our manual quotes for each parameter whether serum or whole blood is required. Generally, most laboratory tests can be carried out with either serum or plasma.Exceptions are mentioned below and the type and amount of material needed is also stated on the submission form.

PPllaassmmaa

Def.: Aqueous part of blood made noncoagulable by means of an anticoagulant.

Easier to obtain than serum, also higher yield and reduced risk of haemolysis.

Please note that the mixing ratio of blood and coagulant must be met or the sample may haemolyse. The sample should not exceed or fall below the required amount ofblood stated on the tube.

Immediately after blood sampling the tube should gently be turned upside down several times to mix the contents. Then centrifuge for 5 - 10 minutes (approx. 3500 r/min).

The most important anticoagulants are EDTA (eethyleneddiaminttetraaacetate), heparin and citrate.

Please note that certain parameters cannot be determined from EDTA-plasma:- potassium, calcium, magnesium, iron, alkaline phosphatase and glucose.

Other parameters require special anticoagulants:- cciittrraatteedd ppllaassmmaa: frozen, to determine coagulation parameters.

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22..11 GGeenneerraall AAddvviiccee oonn BBlloooodd SSaammpplliinngg

SSeerruumm

Def.: Aqueous part of blood freed from fibrin and blood cells by means of coagulation(plasma without fibrin).

Coagulation time varies between individuals and species. The collection of serum ismore time-consuming than the collection of plasma.

To gain serum leave blood standing until coagulation is complete. This procedure canbe shortened by adding a coagulation aid to the tube (e.g. coagulation tube with plastic globules).

Then gently loosen coagulate from the tube wall and centrifuge for 5 minutes (3500 r/min). Immediately transfer serum into serum tube. The yield is approximately 30%.

Please note that it is important to separate the serum and blood clot completely,especially to determine glucose, potassium and LDH.

WWhhoollee bblloooodd

Submitting whole blood is not recommended. Transport often causes haemolysis which impairs various parameters.

Blood glucose breaks down almost completely due to the continuing blood cell metabolism.

EEDDTTAA bblloooodd

The anticoagulant EDTA is used to stabilise blood for blood counts, thrombocyte counts, blood group testing and PCR testing.

BBlloooodd ssmmeeaarr

For differential blood counts it is worthwhile sending an air dried blood film in additionto EDTA blood. It is also required for detection of blood parasites.

Place a small drop of whole blood or EDTA blood on a glass slide (approx. 1 cm fromedge). Grip slide with one hand, take a cover slip (or extra microscope slide) with theother hand and move it towards the drop of blood at an angle of 30-45 degrees until the capillary forces draw the blood and spread it along the edge of the cover slip. Then push cover slip along slide. The blood should be evenly distributed in a mono layer of cells. Allow to dry completely before packing.

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22..11 GGeenneerraall AAddvviiccee oonn BBlloooodd SSaammpplliinngg

44.. SSaammppllee vvoolluummee

Most biochemical parameters require a sample volume of 30 µl. Additionally there is a dead volume of 200 µl.

55.. FFaaccttoorrss tthhaatt ccaann ssppooiill rreessuullttss

HHaaeemmoollyyssiiss: Haemolysed material will spoil the results of the following parameters: PCV, RBC, MCHC, alkal. phos. (AP), AST (GOT), GGT, GLDH, LDH, potassium, Ca, phosphate, iron, cholesterol, glucose and total bilirubin.

LLiippaaeemmiiaa: Total protein, Ca, potassium, phosphate, bilirubin, glucose, α-amylase and triglycerides.

66.. FFrroozzeenn ssaammpplleess

Certain parameters require frozen sample material:

- coagulation factors: - citrated plasma

- ADH, ammonia, ACTH: - EDTA plasma

- Insulin: - serum, plasma

- somatomedin (IGF I): - serum

The sample should be submitted in a special frozen container, available from the laboratoryon request. Both container and sample should be stored (separately) in a freezer overnightbefore mailing the next day. Samples should not be mailed before a weekend.

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22..22 GGeenneerraall AAddvviiccee oonn MMoolleeccuullaarrbbiioollooggiiccaall TTeessttss

SSaammppllee MMaatteerriiaall

Samples used for PCR testing should be those with the highest possible content of theorganism in question. Therefore, before taking a sample, it must be taken into account:

- whether the animal is currently in a viraemic/bacteraemic stage.

- whether the organism has possibly reached its final target organ and if so, where is it likely to be found when considering the clinical symptoms.

- whether there is an organ where the organism likes to hide in the non-acutephase (e.g. EHV-1 in leukocytes).

MMaatteerriiaall rreeqquuiirreedd ffoorr PPCCRR eexxaammiinnaattiioonn::

- SSwwaabbss: Use a sterile, dry swab to wipe the area. Then place it in a sterileplain tube - do not use transport medium!

- BBiioollooggiiccaall FFlluuiiddss: (synovial fluid, cerebrospinal fluid, aspirate, aqueous humor,urine etc): Submit the material in a sterile plain tube. Approx. 400 µl material is usually sufficient, except for urine where 5 ml is required. If you can ensure that your sample will arrive within 48 hours after collection, it is sufficient to store it at +4°C and to submit it unfrozen. Should you expect more time to pass, then you should deep freeze (-20°C) the sample and make sure the tteemmppeerraattuurree ooff ––2200°°CC iiss mmaaiinnttaaiinneedd tthhrroouugghhoouutt ttrraannssppoorrtt. Please mark the dispatch bag/box clearly that it contains a frozen sample. It is important that the sample does not thaw and refreeze.

- BBiiooppssiieess,, oorrggaann ppaarrttss,, aabboorrttiioonn mmaatteerriiaall: Material should be submitted in a plain tube which contains sterile NaCl that should just cover the sample. If the sample may not arrive within 48 hours, do not cover the sample with NaCl but deep freeze it. Again, mark the dispatch bag/box to indicate that it contains a frozen sample. Make sure the cooling chain is maintained throughout transport. Make sure the sample does not thaw and refreeze.

- EEDDTTAA bblloooodd,, cciittrraatteedd bblloooodd: The amount of sample material required varies according to the desired analysis, as well as the stage of the disease. Please never send thesesamples frozen.

PPlleeaassee ddoo nnoott sseenndd hheeppaarriinn bblloooodd!!

- FFaaeecceess: About 2 g of material are required. The faeces should be submitted in a plain sterile tube.

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22..22 GGeenneerraall AAddvviiccee oonn MMoolleeccuullaarrbbiioollooggiiccaall TTeessttss

PPrreeccaauuttiioonnaarryy mmeeaassuurreess rreeqquuiirreedd wwhheenn hhaannddlliinngg ssaammpplleess::

1. PCR is a highly sensitive method. Therefore sterile collection instruments as well as sterile sample tubes are required. Avoid contamination after the collection during handling of the sample (e.g. changing containers, packaging the sample for transport).

2. The sample may be posted without cooling if it will arrive in the lab within 48 hours. Until it is posted, it should be stored at +4°C.

3. If long transport times cannot be avoided the sample should be sent frozen (except EDTA blood or citrated blood). Make sure the freezing temperature is kept constant throughout transport (e.g. use dry ice). If the temperature cannot be maintained, it is better not to freeze the sample. The sample must not thaw and refreeze.

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22..33 GGeenneerraall AAddvviiccee oonn HHiissttooppaatthhoollooggyy EExxaammiinnaattiioonnss

GGeenneerraall IInnffoorrmmaattiioonn oonn HHiissttooppaatthhoollooggyy

Our laboratory performs the following tissue examinations:

- histopathology of neoplasias, skin punches, skin and organ biopsies, fine needle aspirates, as well as from any nonspecific changes found in tissues. Also from tissue or organs or parts of organs collected during surgery or autopsy/post mortem examination.

- cytology of fine needle aspirates collected from body fluids (e.g. joint or pleural fluids, ascites, urine) or from organs (e.g. mammary gland, kidney, liver, thyroid gland or lymph nodes).

In order for your sample to be processed efficiently, please follow this advice:

- clearly fill out the histopathology submission form (white).

- please additionally complete the reverse side of the submission form when submitting dermatological samples.

- all samples should be submitted completely covered in fixative and avoid crushing the sample. Make sure your submission pot is large enough, otherwise your sample may not be entirely covered by fixative. The autolytic processes will then continue.

- use pots with a large opening. The sample hardens due to the action of the fixative. If the opening is too small, artefacts due to crushing can occur when removing the sample from the tube.

FFiinnee NNeeeeddllee BBiiooppssyy

In order to perform a fine needle biopsy you may use a 0.8-2 mm needle of sufficientlength. The use of an aspiration guide is often helpful. This enables you to safely collectseveral aspirates.

Sample collection is completed after a single and short aspiration. If possible, whencollecting several aspirates, use a new needle for each new biopsy. Try not to collect youraspirates by poking the needle around in the tissue. Also, try not to collect your sample bylengthy aspiration of the tissue. This will lead to excessive mixing of blood into the sample.It can also increase the risk of metastasis of neoplastic or purulent infectious processes.

The collected aspirate can be treated like a blood smear and it can be transferred to aglass slide.

Liquid aspirates should be centrifuged at 1500 U/min for 5-10 minutes. Reject thesupernatant fluid and transfer the sediment onto a glass slide. Make a smear and allow to dry naturally, then place in a slide protection box and send to the lab.

Tissue cylinders collected with wide lumen needles can be put directly into formaldehydesolution and mailed. Fixated tissue cylinders have the advantage over aspirates in that tissue morphology is preserved.

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22..33 GGeenneerraall AAddvviiccee oonn HHiissttooppaatthhoollooggyy EExxaammiinnaattiioonnss

PPrriiccee iinnffoorrmmaattiioonn

A higher fee is charged for very large samples, samples containing several tumours or several samples from the same animal, as well as for more than six skin biopsies from a single animal. This is due to the increase in time required for processing the sample, as well as the larger number of sections and possibly diagnoses that have to be made.

IIff yyoouu hhaavvee aannyy ffuurrtthheerr qquueessttiioonnss pplleeaassee ccoonnttaacctt yyoouurr RReeggiioonnaall MMaannaaggeerr..

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22..44 RReeffeerreennccee RRaannggeess22..44..11 RReeffeerreennccee RRaannggeess –– CCoonnvveennttiioonnaall UUnniittss

�� BBiioocchheemmiissttrryy

1 = breed-dependent, 2 = age-dependant, 3 = high-yielding dairy cows

DDoogg CCaatt HHoorrssee CCaattttllee

Albumin 3.2 - 4.7 2.6 - 5.6 2.5 - 4.4 g/dl

Aldolase < 6.5 U/l

ALT (GPT) 5 - 125 < 1751 2 - 15 12.5 - 112.5 U/l

α-Amylase < 3250 < 35101 < 400 < 40 - 161 U/l

Ammonium < 60 < 60 < 40 < 40 µmol/l

AP2 < 81 7.5 - 105 Adult < 450 < 90 U/l

Foal < 650

AST (GOT) 15 - 120 < 120 < 600 15 - 105 U/l

Bile acids < 20 < 20 < 12 µmol/l

Bilirubin (direct) < 0.12 < 0.12 < 1.2 mg/dl

Bilirubin (total) < 0.3 < 0.3 0.5 - 3.5 < 1.0 mg/dl

Calcium 2.0 - 3.0 2.3 - 3.0 2.3 - 3.4 2.4 - 3.0 mmol/l

ß-Carotene >700 µg/l

Chloride 96 - 113 100 - 124 95 - 105 97 - 111 mmol/l

Cholesterol 108 - 300 70 - 150 70 - 180 75 - 175 mg/dl

Cholinesterase 3.75 - 6.0 2.25 - 4.5 > 1.5 0.075 - 0.15 kU/l

CK < 180 < 475 < 260 < 400 U/l

Copper 34 - 94 50 - 150 > 80 µg/dl

Creatinine < 1.4 < 2.0 < 2.0 < 2.0 mg/dl

Folic acid 7 - 17 13 - 38 5 - 17 ng/ml

Fructosamine < 390 < 390 < 280 µmol/l

GGT < 6 < 5 < 30 7 - 27 U/l

GLDH < 9 < 91 < 12 < 10.5 U/l

< 253

Glucose 54 - 100 54 - 100 50 - 94 47 - 75 mg/dl

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22..44..11 RReeffeerreennccee RRaannggeess –– CCoonnvveennttiioonnaall UUnniittss

1 = breed-dependent, 2 = age-dependant, 3 = high-yielding dairy cows

BBiioocchheemmiissttrryy DDoogg CCaatt HHoorrssee CCaattttllee

β-Hydroxybutyrate 0 - 90 mg/l

Iron 84 - 230 70 - 210 80 - 240 100 - 190 µg/dl

Lactate 0.5 - 3.0 < 1.0 0.5 - 2.0 mmol/l

LDH < 100 < 2602 < 400 < 1500 U/l

Lipase < 300 < 250 < 250 10 - 80 U/l

Magnesium 0.6 - 1.3 0.6 - 2.0 0.7 - 0.9 0.8 - 1.3 mmol/l

Manganese > 3 µg/l

Phosphate2 0.7 - 1.6 0.8 - 1.9 Adult 0.7 - 1.5 1.8 - 2.4 mmol/l

Foal 1.3 - 2.5

Potassium 3.6 - 5.8 3.0 - 5.0 2.8 - 4.5 3.5 - 5.0 mmol/l

Selenium 100 - 200 > 50 µg/l

Sodium 140 - 155 146 - 165 125 - 150 132 - 152 mmol/l

TLI 5 - 35 12 - 82 µg/l

Total protein 5.3 - 7.7 5.7 - 9.4 5.5 - 7.5 6.0 - 8.5 g/dl

Triglycerides 50 - 100 50 - 100 < 50 15 - 45 mg/dl

Urea (BUN) 10 - 25 10 - 33 10 - 20 6 - 22 mg/dl

Uric acid 0 - 2 0 - 1 < 1.1 mg/dl

Vitamin A 2.0 - 3.0 0.2 - 1.6 0.2 - 0.7 mg/l

Vitamin B1 46 - 112 20 - 90 24 - 54 µg/l

Vitamin B2 185 - 420 196 - 660 µg/l

Vitamin B6 40 - 270 86 - 350 µg/l

Vitamin B12 225 - 860 200 - 1680 pg/ml

Vitamin E 3 - 24 3 - 11 > 1 > 3 mg/l

Vitamin H (Biotin) 530 - 5000 1000 - 3000 pg/ml

Zinc 400 - 1600 450 - 1600 500 - 1300 > 800 µg/l

Zinc (hair) 124 - 320 124 - 320 124 - 320 124 - 320 mg/kg

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22..44..11 RReeffeerreennccee RRaannggeess –– CCoonnvveennttiioonnaall UUnniittss

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�� DDrruuggss//TTooxxiiccoollooggyy

DDoogg CCaatt HHoorrssee CCaattttllee

DDrruuggss

((tthheerraappeeuuttiicc rraannggee))

Bromide 200 - 300 mg/dl

(100 - 200 as

add-on)

Digoxin 0.7 - 2.0 0.7 - 2.0 µg/l

Phenobarbitone 10 - 40 10 - 40 mg/l

TTooxxiicc lliimmiitt

Digoxin > 2.5 > 2.5 µg/l

Phenobarbitone > 40 mg/l

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22..44..11 RReeffeerreennccee RRaannggeess –– CCoonnvveennttiioonnaall UUnniittss

�� EEnnddooccrriinnoollooggyy

DDoogg CCaatt HHoorrssee CCaattttllee

AAddrreennaall ggllaanndd

ACTH 9 - 67.7 4.5 - 90.2 6.5 - 30.8 pg/ml

(4.9 - 13.6 Pony)

Cortisol 0.36 - 5.8 0.5 - 5.4 3.0 - 6.7 0.72 - 18.0 µg/dl

TThhyyrrooiidd ggllaanndd

FT3 2.5 - 9.8 1.6 - 4.9 ng/l

FT4 0.6 - 3.7 0.5 - 2.6 0.7 - 3.5 ng/dl

FT4/Cholesterol Ratio > 1 > 1

T3 0.2 - 2.0 0.8 - 1.5 0.3 - 0.9 µg/l

T4 1.5 - 4.5 0.8 - 3.9 1.3 - 4.1 µg/dl

TSH < 0.5 ng/ml

SSeexx hhoorrmmoonneess//PPrreeggnnaannccyy

Oestradiol (17β-)

(cycle-dependent) ng/l

Oestrone sulfate > 20 ng/ml

(= pregnant)

PMSG < 20 not pregnant ng/ml

20 - 80 borderline

> 80 pregnant

Progesterone

(cycle-dependent) 0.5 - 4.0 (male) ng/ml

Testosterone (male) 0.3 - 5.8 0.3 - 5.8 < 0.04 (castr.) 0.4 - 3.0 ng/ml

0.1 - 1.3 (cryptorch.)

< 0.02 (female)

OOtthheerr hhoorrmmoonneess

Insulin 4.9 - 27.8 4.9 - 27.8 7 - 51 mU/l

Parathormone 18.9 - 122.6 0 - 37.7 pg/ml

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22..44..11 RReeffeerreennccee RRaannggeess –– CCoonnvveennttiioonnaall UUnniittss

�� HHaaeemmaattoollooggyy

DDoogg CCaatt HHoorrssee CCaattttllee

BBlloooodd ccoouunntt

Erythrocytes 6 - 9 5 - 10 6 - 12 5 - 10 T/l

Haematocrit (PCV) 38 - 55 28 - 45 30 - 50 28 - 38 %

Haemoglobin 15 - 19 9 - 15 11 - 17 9 - 14 g/dl

Leukocytes 6 - 12 6 - 11 5 - 10 5 - 10 G/l

MCH 17 - 23 13 - 17 13 - 19 11 - 17 pg

MCHC 31 - 34 31 - 35 31 - 36 31 - 34 g/dl

MCV 60 - 77 40 - 55 37 - 55 46 - 65 fl

Reticulocytes > 60.000* > 60.000* µmol/l

Thrombocytes 150 - 500 150 - 500 90 - 500 300 - 800 G/l

*starting regeneration

DDiiffffeerreennttiiaall bblloooodd ccoouunntt

Basophilic 0 - 1 0 - 1 0 - 2 0 - 2 %

granulocytes up to 200 up to 200 up to 200 up to 200 /µl

Eosinophilic 0 - 6 0 - 6 0 - 4 1 - 10 %

granulocytes 0 - 600 0 - 600 40 - 350 300 - 1500 /µl

Lymphocytes 12 - 30 15 - 50 20 - 45 45 - 65 %

1000 - 4000 1000 - 6000 1500 - 4000 2500 - 5500 /µl

Monocytes 0 - 4 0 - 4 0 - 5 2 - 6 %

0 - 500 0 - 500 40 - 400 0 - 330 /µl

Neutrophilic

granulocytes

- segmented 55 - 75 50 - 75 45 - 70 25 - 45 %

3000 - 10000 3000 - 12000 3000 - 7000 1000 - 3500 /µl

- band 0 - 3 0 - 3 0 - 6 0 - 3 %

0 - 300 0 - 300 0 - 600 0 - 200 /µ

Atypical cells 0 0 0 0

Anisocytosis neg. neg. neg. neg.

Polychromatia neg. neg. neg. neg.

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22..44..11 RReeffeerreennccee RRaannggeess –– CCoonnvveennttiioonnaall UUnniittss

�� CCooaagguullaattiioonn

�� SSeerruumm PPrrootteeiinn EElleeccttrroopphhoorreessiiss

�� UUrriinnee//FFaaeeccaall EExxaammiinnaattiioonnss,, FFuunnccttiioonn TTeessttss

EEnnddooccrriinnee ffuunnccttiioonn tteessttss See → Endocrinology

DDoogg CCaatt HHoorrssee CCaattttllee

FFaaeeccaall eexxaammiinnaattiioonnss

Canine Elastase-1 > 40 ug/g

faeces

UUrriinnee eexxaammiinnaattiioonnss

Prot./Creatinine Ratio < 0.5 < 0.33

DDoogg CCaatt HHoorrssee CCaattttllee

Albumin 47 - 59 45 - 60 56.2 - 56.4 51 - 59 %

α1-Globulin 4 - 7 4 - 14 2.4 - 3.2 2 - 7 %

α2-Globulin 5 - 12 7 - 12 6.6 - 8.3 3 - 22 %

β1-Globulin 21 - 38 16 - 31 7.8 - 20.6 3 - 22 %

β2-Globulin 10 - 20 %

γ-Globulin 8 - 18 10 - 28 15.2 - 20 8 - 12 %

Total protein 5.5 - 7.5 5.7 - 9.4 5.5 - 7.5 6.0 - 8.5 g/dl

DDoogg CCaatt HHoorrssee CCaattttllee

Fibrinogen 120 - 290 100 - 300 150 - 330 mg/dl

PTT < 13.5 < 13.4 39 - 63 Sec.

PT < 8.8 < 11 10 - 15 Sec.

Thrombin time < 18 21 - 29 Sec.

Factor VIII 70 - 135 %

von Willebrand's factor 55 - 150 %

Factor lX 75 - 150 %

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22..44..22 RReeffeerreennccee RRaannggeess –– SSII UUnniittss

�� BBiioocchheemmiissttrryy

1 = breed-dependent, 2 = age-dependant, 3 = high-yielding dairy cows

DDoogg CCaatt HHoorrssee CCaattttllee

Albumin 32 - 47 26 - 56 25 - 44 35 - 42 g/l

Aldolase < 6.5 U/l

ALT (GPT) 5 - 125 < 1751 2 - 15 12.5 - 112.5 U/l

α-Amylase < 3250 < 35101 < 400 < 40 - 161 U/l

Ammonium < 60 < 60 < 40 < 40 µmol/l

AP2 < 110 < 57 Adult < 450 < 90 U/l

Foal < 650

AST (GOT) 15 - 120 < 120 < 600 15 - 105 U/l

Bile acids < 20 < 20 < 12 µmol/l

Bilirubin (direct) < 2.1 < 2.1 < 20.5 µmol/l

Bilirubin (total) < 5.1 < 5.1 8.6 - 53 < 17.1 µmol/l

Calcium 2.0 - 3.0 2.3 - 3.0 2.3 - 3.4 2.4 - 3.0 mmol/l

β-Carotene > 1.3 µmol/l

Chloride 96 - 113 100 - 124 95 - 105 97 - 111 mmol/l

Cholesterol 2.8 - 7.8 1.8 - 3.9 1.8 - 4.7 2 - 4.6 mmol/l

Cholinesterase 3750 - 6000 2250 - 4500 > 1500 75 - 150 U/l

CK < 180 < 475 < 260 < 400 U/l

Copper 5,4 - 14,8 7.9 - 23.6 14.2 - 18.9 µmol/l

Creatinine < 124 < 177 < 177 < 177 µmol/l

Folic acid 159 - 385 295 - 861 113 - 385 nmol/l

Fructosamine < 390 < 390 < 280 µmol/l

GGT < 6 < 5 < 30 7 - 27 U/l

GLDH < 9 < 91 < 12 < 10.5 U/l

< 253

Glucose 3.0 - 5.6 3.0 - 5.6 2.8 - 5.2 2.6 - 4.2 mmol/l

β-Hydroxybutyrate 0 - 865 µmol/l

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22..44..22 RReeffeerreennccee RRaannggeess –– SSII UUnniittss

1 = breed-dependent, 2 = age-dependant, 3 = high-yielding dairy cows

DDoogg CCaatt HHoorrssee CCaattttllee

Iron 15 - 41 13 - 38 14.3 - 43 18 - 34 µmol/l

Lactate 0.5 - 3.0 < 1.0 0.5 - 2.0 mmol/l

LDH < 100 < 2602 < 400 < 1500 U/l

Lipase < 300 < 250 < 250 10 - 80 U/l

Manganese 0.8 - 1.3 nmol/l

Phosphate2 0.7 - 1.6 0.8 - 1.9 Adult 0.7 - 1.5 1.8 - 2.4 mmol/l

Foal 1.3 - 2.5

Potassium 3.6 - 5.8 3.0 - 5.0 2.8 - 4.5 3.5 - 5.0 mmol/l

Selenium 100 - 200 > 50 µg/l

Sodium 140 - 155 146 - 165 125 - 150 132 - 152 mmol/l

TLI 5 - 35 12 - 82 µg/l

Total protein 53 - 77 57 - 94 55 - 75 60 - 85 g/l

Triglycerides 0.6 - 1.1 0.6 - 1.1 < 0.6 < 0.2 mmol/l

Urea (BUN) 1.7 - 4.2 1.7 - 5.5 1.7 - 3.3 1.0 - 3.7 mmol/l

Uric acid 0 - 119 0 - 60 < 65 µmol/l

Vitamin A 2 - 3 0.2 - 1.6 0.1 - 0.37 0.2 - 0.7 mg/l

Vitamin B1 46 - 112 20 - 90 5 - 23 24 - 54 µg/l

Vitamin B2 185 - 420 196 - 660 110 - 170 µg/l

Vitamin B6 40 - 270 86 - 350 26 - 33 µg/l

Vitamin B12 16.6 - 63.5 14.8 - 124 51.7 - 131.4 µmol/l

Vitamin E 3 - 24 3 - 11 > 1 > 3 mg/l

Vitamin H (Biotin) 530 - 5000 1000 - 3000 310 - 665 pg/ml

Zinc 400 - 1600 450 - 1600 500 - 1300 > 80 µg/l

Zinc (hair) 124 - 320 124 - 320 124 - 320 124 - 320 mg/kg

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22..44..22 RReeffeerreennccee RRaannggeess –– SSII UUnniittss

�� DDrruuggss//TTooxxiiccoollooggyy

DDoogg CCaatt HHoorrssee CCaattttllee

DDrruuggss//TTooxxiiccoollooggyy

((tthheerraappeeuuttiicc rraannggee))

Bromide 200 - 300

(100 - 200 as

add-on) mg/dl

Digoxin 0.7 - 2.0 0.7 - 2.0 0.7 - 2.0 µg/l

Phenobarbitone 10 - 40 10 - 40 µg/ml

TTooxxiicc lliimmiitt

Digoxin > 2.5 > 2.5 > 2.5 µg/l

Phenobarbitone > 40 µg/ml

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22..44..22 RReeffeerreennccee RRaannggeess –– SSII UUnniittss

�� EEnnddooccrriinnoollooggyy

DDoogg CCaatt HHoorrssee CCaattttllee

AAddrreennaall ggllaanndd

ACTH 9 - 67.7 4.5 - 90.2 6.5 - 30.8 pg/ml

4.9 - 13.6 (Pony)

Cortisol 9.9 - 160.1 14 - 150 82.8 - 185 20 - 497 nmol/l

TThhyyrrooiidd ggllaanndd

FT3 3.7 - 9.2 0.8 - 1.4 pmol/l

FT4 7.7 - 47.6 6.4 - 33.5 9 - 45 pmol/l

FT4/Cholesterol ratio > 1 > 1

T3 0.3 - 3.1 1.2 - 2.3 0.46 - 1.4 nmol/l

T4 19 - 58 10 - 50 9 - 48 45 - 103 nmol/l

TSH < 0.5 ng/ml

SSeexx hhoorrmmoonneess//PPrreeggnnaannccyy

Oestradiol (17ß-)

cycle-dependent ng/l

Oestrone sulfate > 20 = pregnant ng/ml

PMSG < 20 not pregnant ng/ml

20 - 80 borderline

> 80 pregnant

Progesterone

cycle-dependent 0.5 - 4.0 male nmol/l

Testosterone (male) 0.3 - 5.8 0.3 - 5.8 < 0.04 (castr.) 0.4 - 3.0 ng/ml

0.1 - 1.3 (cryptorch.)

< 0.02 (female)

OOtthheerr hhoorrmmoonneess

Insulin 34 - 194 34 - 194 7 - 51 pmol/l

Parathormone 18.9 - 122.6 0 - 37.7 ng/l

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22..44..22 RReeffeerreennccee RRaannggeess –– SSII UUnniittss

�� HHaaeemmaattoollooggyy

DDoogg CCaatt HHoorrssee CCaattttllee

BBlloooodd ccoouunntt

Erythrocytes 6 - 9 5 - 10 6 - 12 5 - 10 T/l

Haematocrit (PCV) 38 - 55 28 - 45 30 - 50 28 - 38 %

Haemoglobin 15 - 19 9 - 15 11 - 17 90 - 140 g/dl

Leukocytes 6 - 12 6 - 11 5 - 10 5 - 10 G/l

MCH 17 - 23 13 - 17 13 - 19 11 - 17 pg

MCHC 31 - 34 31 - 35 31 - 36 31 - 34 g/dl

MCV 60 - 77 40 - 55 37 - 55 46 - 65 fl

Reticulocytes > 60.000* > 60.000* /µl

Thrombocytes 150 - 500 150 - 550 90 - 500 300 - 800 x 109/µl

*suggesting regeneration

DDiiffffeerreennttiiaall bblloooodd ccoouunntt

Basophilic 0 - 1 0 - 1 0 - 2 0 - 2 %

granulocytes up to 40 (rare) up to 40 (rare) 0 - 150 0 - 100 /µl

Eosinophilic 0 - 6 0 - 6 0 - 4 1 - 10 %

granulocytes 0 - 600 0 - 600 0 - 350 300 - 1500 /µl

Lymphocytes 12 - 30 15 - 50 20 - 45 45 - 65 %

1000 - 4000 1000 - 6000 1500 - 4000 2500 - 5500 /µl

Monocytes 0 - 4 0 - 4 0 - 5 2 - 6 %

0 - 500 0 - 500 0 - 400 0 - 330 /µl

Neutrophilic

granulocytes

- segmented 55 - 75 50 - 75 45 - 70 25 - 45 %

3000 - 10000 3000 - 11000 3000 - 7000 1000 - 3500 /µl

- band 0 - 3 0 - 4 0 - 6 0 - 3 %

0 - 300 0 - 300 0 - 600 0 - 200 /µ

Atypical 0 0 0 0

Anisocytosis neg. neg. neg. neg.

Polychromatica neg. neg. neg. neg.

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22..44..22 RReeffeerreennccee RRaannggeess –– SSII UUnniittss

�� CCooaagguullaattiioonn

�� SSeerruumm pprrootteeiinn eelleeccttrroopphhoorreessiiss

DDoogg CCaatt HHoorrssee CCaattttllee

Albumin 47 - 59 45 - 60 56.2 - 56.4 51 - 59 %

α1-Globulin 4 - 7 4 - 14 2.4 - 3.2 2 - 7 %

α2-Globulin 5 - 12 7 - 12 6.6 - 8.3 3 - 22 %

β1-Globulin 21 - 38 16 - 31 7.8 - 20.6 3 - 22 %

β2-Globulin 10 - 20 %

γ-Globulin 8 - 18 10 - 28 15.2 - 20 8 - 12 %

Total protein 53 - 77 57 - 94 55 - 75 60 - 85 g/l

DDoogg CCaatt HHoorrssee CCaattttllee

Fibrinogen 3.5 - 8.5 2.9 - 8.8 4.4 - 9.7 µmol/l

PTT < 13.5 < 13.4 39 - 63 Sec.

PT < 8.8 < 11 10 - 15 Sec.

Thrombin time < 18 21 - 29 Sec.

Factor VIII 70 - 135 %

von Willebrand's factor 55 - 150 %

Factor lX 75 -140 %

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22..55 CCoonnvveerrssiioonn TTaabbllee

SI units → conventional units/conventional units → SI units

PPaarraammeetteerr UUnniitt ((ccoonnvv..)) UUnniitt ((SSII)) ccoonnvv.. →→ SSII SSII →→ ccoonnvv..

Acetyl salicylic acid µg/ml mmol/l x 7.25 x 0.138

ACTH ng/l pmol/l x 0.2202 x 4.5410

Adrenalin ng/l pmol/l x 5.4582 x 0.1832

Albumin g/dl g/l x 10 x 0.1

Aldosterone ng/dl pmol/l x 27.743 x 0.03605

Ammonium µg/dl µmol/l x 0.587 x 1.703

Ascorbic acid mg/dl µmol/l x 56.78 x 0.0176

Bilirubin mg/dl µmol/l x 17.104 x 0.0585

Calcitonin g/l mmol/l x 0.292 x 3.42

Calcium mg/dl mmol/l x 0.2495 x 4.008

Chloride mg/dl mmol/l x 0.2821 x 3.5453

Cholesterol mg/dl mmol/l x 0.026 x 38.66

Copper µg/dl µmol/l x 0.1574 x 6.3532

Cortisol µg/dl nmol/l x 27.6 x 0.036

Creatinine mg/dl µmol/l x 88.402 x 0.0113

Digoxin µg/l nmol/l x 1.28 x 0.781

Fibrinogen mg/dl g/l x 0.01 x 100

Folic acid µg/dl nmol/l x 22.655 x 0.0441

Fructose mg/dl mmol/l x 0.0555 x 18.016

FT3 pg/ml pmol/l x 1.536 x 0.651

FT4 ng/dl pmol/l x 12.87 x 0.078

Glucose mg/dl mmol/l x 0.0555 x 18.016

Haemoglobin g/dl mmol/l x 0.6206 x 1.611

Insulin µg/l pmol/l x 172.1 x 0.0058

Iron µg/dl µmol/l x 0.1791 x 5.5847

Lactate mg/dl mmol/l x 0.111 x 9.008

Lead µg/dl µmol/l x 0.0483 x 20.719

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22..55 CCoonnvveerrssiioonn TTaabbllee

SI units → conventional units/conventional units → SI units

PPaarraammeetteerr UUnniitt ((ccoonnvv..)) UUnniitt ((SSII)) ccoonnvv.. →→ SSII SSII →→ ccoonnvv..

Magnesium mg/dl mmol/l x 0.4113 x 2.4312

Noradrenalin µg/dl nmol/l x 0.059109 x 16.95

Oestradiol µg/dl nmol/l x 0.34675 x 0.02884

Phenobarbitone mg/l µmol/l x 4.31 x 0.232

Phosphate mg/dl mmol/l x 0.3229 x 3.0974

Potassium mg/dl mmol/l x 0.2557 x 3.9102

Primidone mg/l µmol/l x 4.58 x 0.218

Progesterone ng/ml nmol/l x 3.18 x 0.314

Sodium mg/dl mmol/l x 0.435 x 2.2989

T3 ng/ml nmol/l x 1.536 x 0.651

T4 µg/dl nmol/l x 12.87 x 0.078

Testosterone ng/ml nmol/l x 3.47 x 0.288

Total protein g/dl g/l x 10 x 0.1

Triglycerides mg/dl mmol/l x 0.0114 x 87.5

Urea mg/dl mmol/l x 0.1665 x 6.006

Urea (BUN) mg/dl mmol/l x 0.3651 x 2.808

Uric acid mg/dl µmol/l x 59.48 x 0.0168

Vitamin A µg/dl µmol/l x 0.0349 x 28.646

Vitamin B12 ng/dl µmol/l x 0.7378 x 1.3554

Vitamin C mg/dl µmol/l x 56.776 x 0.0176

Zinc µg/dl µmol/l x 0.153 x 6.537

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KKiiddnneeyyUrea (BUN), creatinine, sodium, potassium, phosphate

LLiivveerrBilirubin (total), ALT (GPT), AP, GGT, AST (GOT), GLDH, total protein, albumin, globulin, albumin/globulin (not horse)ratio (feline only)

PPaannccrreeaassGlucose, α-amylase (not cat), lipase (not cat, not horse)cholesterol, fructosamine (not horse)

MMuusscclleeCK, LDH, calcium, magnesium

MMeettaabboolliissmmTriglycerides

HHaaeemmaattoollooggyyLarge blood count (Small blood count + Diff. blood count)

Includes all parameters as in ‘Large Check-up’ except the ‘Large blood count’.

CChheecckk--uupp 11 mmll SSeerruumm ((++ NNaaFF bblloooodd))

LLaarrggee CChheecckk--uupp 11 mmll SSeerruumm ++ 00..55 EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr ((++ NNaaFF bblloooodd))

33..11 GGeenneerraall SSccrreeeenniinngg PPrrooffiilleess

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KKiiddnneeyyUrea (BUN), creatinine, total protein, sodium, potassium, phosphate

LLiivveerrBilirubin (total), ALT (GPT), AP, AST (GOT), GLDH

PPaannccrreeaassGlucose, α−amylase (not cat), cholesterol

MMuusscclleeCK, LDH, calcium, magnesium

HHaaeemmaattoollooggyySmall blood count

KKiiddnneeyyUrea (BUN), creatinine, total protein, sodium, potassium, phosphate

LLiivveerrBilirubin (total), ALT (GPT), AP, GGT, AST (GOT), GLDH

PPaannccrreeaassGlucose, α−amylase (not cat), lipase (not cat), cholesterol

MMuusscclleeLDH, calcium

HHaaeemmaattoollooggyyLarge blood count (Small blood count + Diff. blood count)

LLaarrggee SSccrreeeenniinngg 11 mmll SSeerruumm ++ 00..55 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr ((++ NNaaFF bblloooodd))

BBaassiicc CChheecckk--uupp 11 mmll SSeerruumm ++ 00..55 mmll EEDDTTAA bblloooodd ((++ NNaaFF bblloooodd))

33..11 GGeenneerraall SSccrreeeenniinngg PPrrooffiilleess

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Includes all parameters as in ‘Large Screening’ except ‘Large blood count’

Large Check-up + total T4

‘Geriatric Profile’ but without Large blood count

GGeerriiaattrriicc PPrrooffiilleewwiitthhoouutt bblloooodd ccoouunntt

11 mmll SSeerruumm ((++ NNaaFF bblloooodd))

GGeerriiaattrriicc PPrrooffiillee(dog and cat only)

11 mmll SSeerruumm ++ 00..55 mmll EEDDTTAA bblloooodd++ BBlloooodd ssmmeeaarr ((++ NNaaFF bblloooodd))

SSmmaallll SSccrreeeenniinngg 11 mmll SSeerruumm ((++ NNaaFF bblloooodd))

33..11 GGeenneerraall SSccrreeeenniinngg PPrrooffiilleess

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Large blood count (Small blood count + Differential blood count),reticulocyte count, bilirubin (total), total protein, LDH

Cytology, total protein, specific gravity

Please note: As early as four hours after sampling the results may beinfluenced by transport and aging. For cytology it isrecommended to prepare a smear of the sediment(centrifuge at 1500 rpm for 3 to 5 minutes).

Cytology, total protein, specific gravity, bacteriology (aerobic + anaerobic)

See → Aspirate Profile I

Cell count, total protein

Please note: As early as four hours after sampling the results may beinfluenced by transport and aging. For cytology it isrecommended to prepare a smear of the sediment(centrifuge at 1500 rpm for 3 to 5 minutes).

Cell count, total protein, bacteriology (aerobic + anaerobic)

See → CSF Profile I

CCSSFF PPrrooffiillee IIII aapppprrooxx.. 33 mmll CCeerreebbrroossppiinnaall fflluuiidd

CCSSFF PPrrooffiillee II aapppprrooxx.. 33 mmll CCeerreebbrroossppiinnaall fflluuiidd

AAssppiirraattee PPrrooffiillee IIII aapppprrooxx.. 33 mmll AAssppiirraattee

AAssppiirraattee PPrrooffiillee II aapppprrooxx.. 33 mmll AAssppiirraattee

AAnnaaeemmiiaa PPrrooffiillee (dog/cat) 11 mmll SSeerruumm ++ 00..55 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr

33..22 SSppeecciiaall SSccrreeeenniinngg PPrrooffiilleess ((iinn aallpphhaabbeettiiccaall oorrddeerr))

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Urea (BUN), creatinine,

potassium, glucose, ALP, ALT,

ACTH-Stimulation test (2 cortisol values)

TLI, folic acid, vitamin B12: The TTLLII test (trypsin-like immunoreactivity) measures thepancreas-specific enzymes trypsin and trypsinogen in theblood, aiding in the diagnosis of exocrine pancreatic insufficiency or acute pancreatitis. Oral substitution withpancreatic enzymes does not influence the test result.

If the pancreas is inflamed or if the animal has been fedprior to blood sampling, there will be an increase in TLI concentration found in the serum. This will lead to misinterpretation of the results, therefore the animal should be starved for 10-12 hours prior to blood sampling.

FFoolliicc aacciidd aanndd VViittaammiinn BB1122:: The determination of folic acid and vitamin B12 values in the serum aids in the determination of the small intestinalabsorptive performance. Furthermore, small intestinalbacterial overgrowth can be diagnosed.

Folic acid increased: - bacterial overgrowth- exocrine pancreatic insufficiency

Folic acid decreased: - disturbed absorption in the jejunum

- malabsorption syndrome

Vitamin B12 decreased: - disturbed absorption in the ileum- exocrine pancreatic insufficiency- bacterial overgrowth

DDiiaarrrrhhooeeaa PPrrooffiillee BB(dog and cat only)

22 mmll SSeerruumm ((ddoogg))33 mmll SSeerruumm ((ccaatt))

33..22 SSppeecciiaall SSccrreeeenniinngg PPrrooffiilleess ((iinn aallpphhaabbeettiiccaall oorrddeerr))

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CCuusshhiinngg MMoonniittoorriinngg PPrrooffiillee

22xx 00,,55 mmll SSeerruumm

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Bacteriological examination: test for enteropathogenic germs

Mycological examination: (semi-quantitative)

Parasitological examination: detection of cestode eggs, nematode eggs, coccidialoocysts

Additionally in large animals: trematode eggs and lungworm larvae

Giardia antigen: dog and cat only

Examinations as in Diarrhoea Profile C, but includingBacteriological examination Canine Elastase-1.Mycological examinationParasitological examinationGiardia antigenCanine Elastase-1

DDiiaarrrrhhooeeaa PPrrooffiillee EE(dog only)

mmiinniimmuumm 11 ffuullll SSAA ffaaeeccaall ttuubbee

DDiiaarrrrhhooeeaa PPrrooffiillee CC(dog, cat)

SSmmaallll aanniimmaallss:: mmiinniimmuumm 11 ffuullll SSAA ffaaeeccaall ttuubbee

33..22 SSppeecciiaall SSccrreeeenniinngg PPrrooffiilleess ((iinn aallpphhaabbeettiiccaall oorrddeerr))

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Calcium, magnesium, phosphate, sodium, potassium, chloride

Please note: It is important to submit serum that is not haemolysed (do not send EDTA or heparin blood)!

For the early detection of nephropathies we recommend the Urea (BUN), creatinine, determination of the protein/creatinine ratio in urine total protein, as a sensitive method.sodium, potassium, Furthermore, urine protein electrophoresis is a useful method calcium, phosphate to differentiate between tubular and glomerular damage as

well as to determine extra-renal proteinuria.

Bilirubin (total), ALT (GPT), AP, GGT, GLDH, Urea (BUN), bile acids, albumin

Liverprofile I + small blood count, quick test (PT), aPTT, serum protein electrophoresis

LLiivveerr PPrrooffiillee IIII 11 mmll SSeerruumm ++ 00,,55 mmll EEDDTTAA ++ 11 mmll CCiittrrooppllaassmmaa ffrroozzeenn ++ bbllooooddssmmeeaarr

LLiivveerr PPrrooffiillee II 11 mmll SSeerruumm

KKiiddnneeyy PPrrooffiillee 11 mmll SSeerruumm

EElleeccttrroollyyttee PPrrooffiillee 11 mmll SSeerruumm

33..22 SSppeecciiaall SSccrreeeenniinngg PPrrooffiilleess ((iinn aallpphhaabbeettiiccaall oorrddeerr))

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CK, LDH, AST (GOT), calcium

Please note: It is important to submit serum that it is not haemolysed!

Indication: Diagnosis of hyper- or hypoproteinaemia, e.g. diagnosis orevaluation of the course of inflammation/infection,hepatopathies, antibody deficiency, gammopathies, etc.

AAllbbuummiinn//gglloobbuulliinn rraattiioo

Increased: - hypogammaglobulinaemia (e.g. in newborns with insufficient intake of colostrum, rare)

- congenital immunodeficiency- aquired immunodeficiency (e.g. distemper in newborns,

canine parvovirus infection, FeLV, FIV)

Decreased: - see: increased globulins- see: decreased albumin- see: FIP

AAllbbuummiinn

Decreased: - protein deficiency (nutritional)- anorexia- malassimilation- hepatopathies- renal loss (nephrosis, nephrotic syndrome)- protein-losing enteropathy- FIP- burns- blood loss- effusions- hypoadrenocorticism- CNS diseases- relative deficiency due to overhydration- hypergammaglobulinaemia

Increased: - dehydration

SSeerruumm PPrrootteeiinnEElleeccttrroopphhoorreessiiss

00..22 mmll SSeerruumm

MMuussccllee PPrrooffiillee 11 mmll SSeerruumm

33..22 SSppeecciiaall SSccrreeeenniinngg PPrrooffiilleess ((iinn aallpphhaabbeettiiccaall oorrddeerr))

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αα11--GGlloobbuulliinnss

Increased: - acute and subacute inflammation (e.g. acute hepatitis)- fever- tissue damage, postoperatively- malignant neoplasias (e.g. chronic lymphatic leukaemia)- glomerulonephritis, renal amyloidosis- rheumatoid arthritis- infectious diseases (see also albumin)- hyperthyroidism- burns- reticulosis- post infection- cytostatic therapy- lupus erythematosus- bacterial endocarditis- pregnancy- physiological in newborns

Decreased: - exudative enteritis- nephrotic syndrome- severe hepatopathy

αα22--GGlloobbuulliinnss

Increased: - acute inflammation- burns- postoperatively- malignant tumours- lymphatic leukaemias (leukosis)- fatty liver- bile duct obstruction- nephrotic syndrome- (chronic pyelonephritis, interstitial nephritis)- (advanced renal insufficiency)- hyperlipoproteinaemia- lupus erythematosus- pregnancy

Decreased: - (acute viral hepatitis)- chronic active hepatitis- nephrotic syndrome- haemolytic anaemia

33..22 SSppeecciiaall SSccrreeeenniinngg PPrrooffiilleess ((iinn aallpphhaabbeettiiccaall oorrddeerr))

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ββ--GGlloobbuulliinnss

Increased: - acute inflammation- hepatopathy- cholestasis- neoplasia (esp. of the liver)- purulent dermatitis- nephrotic syndrome- lymphosarcoma- lupus erythematosus- pregnancy- chronic blood loss, haemolysis

Decreased: - postoperatively- haemolytic anaemia- coagulopathy, haemophilia- autoimmune diseases

γγ--GGlloobbuulliinnss

Increased: - subacute or chronic inflammation- neoplasia (liver carcinoma, lymphosarcoma)- infectious diseases (FIP, FIV, leishmaniasis, ehrlichiosis)- autoimmune diseases (systemic lupus erythematosus,

rheumatoid arthritis)- glomerulonephritis, renal amyloidosis- purulent dermatitis- burns- myeloid leukaemia- hepatopathy- nephropathy- congestive heart failure (esp. congestion of the liver)- hypothyroidism

Decreased: - nephrosis, nephrotic syndrome- lymphatic leukaemia- hypo- or agammaglobulinaemia- immunosuppression (e.g. long-term corticosteroid therapy,

hyperadrenocorticism)

33..22 SSppeecciiaall SSccrreeeenniinngg PPrrooffiilleess ((iinn aallpphhaabbeettiiccaall oorrddeerr))

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Histopathology, bacteriology (aerobic)

Histopathology, mycology

Histopathology, bacteriology (aerobic), mycology

Histopathology, sarcoptes antibodies

Histopathology, production of an autogenous vaccine (following diagnosis of equine sarcoid)

Please note: Approx. 3-5 g tissue is needed for preparation of the autoge-nous vaccine. Please contact us if vaccine for species otherthan the horse is required.

Histopathology, preparation of an autogenous vaccine (following diagnosis of papilloma)

See also: → Skin Profile 5

SSkkiinn PPrrooffiillee 66(dog, cattle)

TTiissssuuee iinn NNaaCCll ++ TTiissssuuee iinn ffoorrmmaalliinn

SSkkiinn PPrrooffiillee 55(horse only)

TTiissssuuee iinn NNaaCCll ++ TTiissssuuee iinn ffoorrmmaalliinn

SSkkiinn PPrrooffiillee 44(dog only)

TTiissssuuee iinn ffoorrmmaalliinn ++ 11 mmll SSeerruumm

SSkkiinn PPrrooffiillee 33 TTiissssuuee iinn ffoorrmmaalliinn ++ SSkkiinn ssccrraappiinngg ++ SSwwaabb

SSkkiinn PPrrooffiillee 22 TTiissssuuee iinn ffoorrmmaalliinn ++ SSkkiinn ssccrraappiinngg

SSkkiinn PPrrooffiillee 11 TTiissssuuee iinn ffoorrmmaalliinn ++ SSwwaabb

33..22 SSppeecciiaall SSccrreeeenniinngg PPrrooffiilleess ((iinn aallpphhaabbeettiiccaall oorrddeerr))

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Histopathology, allergy test (Allercept™)

Cell count, total protein

profile I + cytology

profile II + bacteriology (aerobe + anaerobe)

The examination of synovial fluid enables you to get an idea about severity of an inflamma-tion, or the existence of metabolic imbalance in the joint. An exact diagnosis is in mostcases not possible.The values of the different parameters can vary from case to case especially in traumaticand infectious arthritis.

SSyynnoovviiaall fflluuiidd pprrooffiillee IIIIII 22 mmll SSeerruumm

SSyynnoovviiaall fflluuiidd pprrooffiillee IIII 22 mmll SSeerruumm

SSyynnoovviiaall fflluuiidd pprrooffiillee II 22 mmll SSeerruumm

SSkkiinn PPrrooffiillee 77(dog and cat only)

TTiissssuuee iinn ffoorrmmaalliinn ++ 11 mmll SSeerruumm

33..22 SSppeecciiaall SSccrreeeenniinngg PPrrooffiilleess ((iinn aallpphhaabbeettiiccaall oorrddeerr))

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For diagnosis of hypo- or hyperthyroidism and to determineDDoogg:: the efficacy of thyroid therapy.

Thyroxine (T4), Please see: → 12 Endocrinology free T4, TSH

CCaatt::Thyroxine (T4), free T4

HHoorrssee::Thyroxine (T4), free T4, T3,

For diagnosis of autoimmune mediated hypothyroidism and asTSH, free T4, a screening test for predisposed breeds. thyroglobulin antibodies Please see: → 12 Endocrinology

- direct detection of blood parasites and haemotrophic bacteria in blood smear

- Leishmania antibodies- Ehrlichia antibodies (E. canis)- Babesia spp. antigen (PCR)

TTrraavveell DDiisseeaassee PPrrooffiillee II(dog only)

00..55 mmll EEDDTTAA bblloooodd ++ 22 mmll SSeerruumm ++ BBlloooodd ssmmeeaarr

TThhyyrrooiidd PPrrooffiillee IIII(dog only)

22 mmll SSeerruumm

TThhyyrrooiidd PPrrooffiillee II 22 mmll SSeerruumm

33..22 SSppeecciiaall SSccrreeeenniinngg PPrrooffiilleess ((iinn aallpphhaabbeettiiccaall oorrddeerr))

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- Dirofilaria immitis antigen- Leishmania antibodies- Ehrlichia antibodies (E. canis)- Babesia spp. antigen (PCR)

KKiiddnneeyy Urea (BUN), creatinine, total protein

LLiivveerrBile acids, AP, ALT, albumin

PPaannccrreeaassssppeecc.. ccPPLL, glucose

EElleeccttrroollyytteessSodium, potassium, calcium

HHaaeemmaattoollooggyy Blood count

VVoommiittuuss PPrrooffiillee (dog) 11 mmll SSeerruumm ++ 00..55 mmll EEDDTTAA bblloooodd

TTrraavveell DDiisseeaassee PPrrooffiillee IIII(dog only)

00..55 mmll EEDDTTAA bblloooodd ++ 22 mmll SSeerruumm

33..22 SSppeecciiaall SSccrreeeenniinngg PPrrooffiilleess ((iinn aallpphhaabbeettiiccaall oorrddeerr))

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KKiiddnneeyyUrea (BUN), creatinine, total protein, sodium, potassium, phosphate

LLiivveerrBilirubin (total), ALT (GPT), AP, AST (GOT), GLDH

PPaannccrreeaassGlucose, cholesterol, fructosamine

MMuusscclleeCK, LDH, calcium, magnesium

MMeettaabboolliissmmTriglycerides

HHaaeemmaattoollooggyyLarge blood count (Small blood count + Diff. blood count)

SSeerroollooggyyFeLV, FIV, FIP/coronavirus antibody titre

SSeerruumm pprrootteeiinn eelleeccttrroopphhoorreessiiss

FIP/coronavirus antibody titre, ALT (GPT), bilirubin, Serum protein electrophoresis, Large blood count (Small blood count + Diff. blood count)

FIP Screening + FeLV + FIV

FFeeLLVV//FFIIVV ++ FFIIPP SSccrreeeenniinngg

11 mmll SSeerruumm ++ 00..55 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr

FFIIPP SSccrreeeenniinngg 11 mmll SSeerruumm ++ 00..55 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr

LLaarrggee FFeelliinnee PPrrooffiillee 22 mmll SSeerruumm ++ 00..55 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr ((++ NNaaFF bblloooodd))

33..33 SSppeecciieess SSppeecciiffiicc PPrrooffiilleess33..33..11 SSppeecciieess SSppeecciiffiicc PPrrooffiilleess --FFeelliinnee

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KKiiddnneeyyUrea (BUN), creatinine, total protein, sodium, potassium, phosphate

LLiivveerrBilirubin (total), bilirubin (direct), AP, GGT, AST (GOT), GLDH, cholinesterase, albumin

PPaannccrreeaassGlucose, α-amylase, cholesterol

MMuusscclleeCK, LDH, calcium, magnesium

MMeettaabboolliissmmTriglycerides

TTrraaccee eelleemmeennttssZinc, copper, selenium

HHaaeemmaattoollooggyyLarge blood count (Small blood count + Diff. blood count)

‘Large Equine Profile’ without ‘Large blood count’

EEqquuiinnee PPrrooffiillee 33 mmll SSeerruumm ++ NNaaFF bblloooodd

LLaarrggee EEqquuiinnee PPrrooffiillee 33 mmll SSeerruumm ++ 11 mmll EEDDTTAA bblloooodd++ BBlloooodd ssmmeeaarr ++ NNaaFF bblloooodd

33..33..22 SSppeecciieess SSppeecciiffiicc PPrrooffiilleess -- EEqquuiinnee

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KKiiddnneeyyUrea (BUN), creatinine, phosphate

LLiivveerrBilirubin (total), g-GT, AST, GLDH

MMeettaabboolliissmmGlucose, Triglycerides

MMuusscclleeCa

TTrraaccee eelleemmeennttssZn, Se

HHaaeemmaattoollooggyyLarge blood count (incl. differential blood count)

SSeerruumm eelleeccttrroopphhoorreessiiss

GGlluuccooccoorrttiiccooiiddssCortisol (endogenous),prednisolone,flumethasone,betamethasone,dexamethasone,triamcinolone

NNSSAAIIDDssPhenylbutazone,flunixin meglumine,meclofenamic acid,ketoprofen,vedaprofen,salicylic acid,flufenamic acid,ixosuprine,theophylline,acepromazine

EEqquuiinnee PPuurrcchhaassee PPrrooffiillee

1155 mmll SSeerruumm

EEqquuiinnee GGeerriiaattrriicc PPrrooffiillee 22 mmll SSeerruumm ++ 00..55 mmll EEDDTTAA BBlloooodd ++ NNaaFF bblloooodd ++ BBlloooodd ssmmeeaarr

33..33..22 SSppeecciieess SSppeecciiffiicc PPrrooffiilleess -- EEqquuiinnee

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KKiiddnneeyyUrea (BUN), creatinine, Na, K, total protein

LLiivveerrBilirubin (total), AP, g-glutamyl transferase, AST (GOT)

MMuusscclleeCK, Ca, Mg

MMeettaabboolliissmmGlucose, triglycerides

TTrraaccee eelleemmeennttssFe

HHaaeemmaattoollooggyyLarge blood count

IIggGG

TTrraaccee eelleemmeennttssZinc, copper, selenium

EElleeccttrroollyytteessSodium, potassium, calcium, magnesium, phosphate, chloride

Cortisol (endogenous), betamethasone, flumethasone, prednisolone, dexamethasone, triamcinolone

GGlluuccooccoorrttiiccooiiddSSccrreeeenniinngg

1100 mmll SSeerruumm

PPrrooffiillee SS 33 mmll SSeerruumm

FFooaall PPrrooffiillee 22 mmll SSeerruumm ++ 00..55 EEDDTTAA BBlloooodd ++ NNaaFF bblloooodd ++ BBlloooodd ssmmeeaarr

33..33..22 SSppeecciieess SSppeecciiffiicc PPrrooffiilleess -- EEqquuiinnee

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Phenylbutazone, flunixin meglumine, meclofenamic acid, ketoprofen, vedaprofen, salicylic acid

Glucocorticoids (see above) + NSAIDs (see above)

Phenothiazine, benzodiazepine, detomidine, romifidine, xylazine

All parameters from the glucocorticoid/NSAID/anti inflammatory/sedatives/tranquilizerscreenings are also available individually.Further parameters are available on request, e.g.:cimetidine, clenbuterol, furosemide, caffeine, nandrolone, theobromine, theophylline,phenobarbitone etc.

Should you suspect that a specific drug has been administered which is not listed above,please contact your Regional Manager or the lab directly.

SSeelleecctteedd DDrruuggss(qualitative)

1100 mmll SSeerruumm//UUrriinnee

SSeeddaattiivveess//TTrraannqquuiilliizzeerrSSccrreeeenniinngg

1100 mmll SSeerruumm//UUrriinnee

AAnnttii IInnffllaammmmaattoorryySSccrreeeenniinngg

1155 mmll SSeerruumm

NNSSAAIIDD SSccrreeeenniinngg 1100 mmll SSeerruumm//UUrriinnee

33..33..22 SSppeecciieess SSppeecciiffiicc PPrrooffiilleess -- EEqquuiinnee

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AST (GOT), bile acids, albumin, cholinesterase, urea (BUN), CK, LDH, phosphate, calcium, potassium, total protein

KKiiddnneeyyUrea (BUN), uric acid, total protein, phosphate

LLiivveerrALT (GPT), AST (GOT), bile acids, glucose

MMeettaabboolliissmmCalcium

HHaaeemmaattoollooggyyLarge blood count (leukocytes, PCV, diff. blood count)

Same as ‘Large Reptile Profile’ but without ‘Large blood count’

KKiiddnneeyyUrea (BUN), creatinine

LLiivveerrTotal protein, albumin, globulin, GGT, AST (GOT), glucose

MMuusscclleeCK, LDH, calcium

MMeettaabboolliissmmTriglycerides

HHaaeemmaattoollooggyyLarge blood count (leukocytes, PCV, diff. blood count)

RRaabbbbiitt PPrrooffiillee 11 mmll SSeerruumm ++ 00..55 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr

RReeppttiillee PPrrooffiillee 00..55 mmll SSeerruumm

LLaarrggee RReeppttiillee PPrrooffiillee 00..55 mmll SSeerruumm ++ 00..55 mmll HHeeppaarriinn bblloooodd ++ BBlloooodd ssmmeeaarr

AAvviiaann SSccrreeeenniinngg 00..55 mmll SSeerruumm

33..33..33 SSppeecciieess SSppeecciiffiicc PPrrooffiilleess –– AAvviiaann,, RReeppttiillee,, RRaabbbbiitt

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KKiiddnneeyyUrea (BUN), creatinine, total protein, sodium, chloride, potassium, phosphate

LLiivveerrBilirubin (total), AP, AST (GOT), bile acids, cholinesterase, GLDH, GGT

PPaannccrreeaassGlucose, fructosamine, cholesterol

MMuusscclleeCK, calcium, magnesium

MMeettaabboolliissmmTriglycerides, β-hydroxybutyrate

TThhyyrrooiidd ggllaannddT4

TTrraaccee eelleemmeennttssZinc (serum, hair), copper, selenium,

manganese (serum, hair), sodium (urine)

VViittaammiinnssBiotin, folic acid, vitamin A, β-carotene, vitamin B1, vitamin B12, vitamin E

LLaarrggee BBoovviinnee PPrrooffiillee 33 mmll SSeerruumm ++ 11 mmll EEDDTTAA bblloooodd++ 1100 mmll UUrriinnee ++ HHaaiirr ((++ NNaaFF bblloooodd))

33..33..44 SSppeecciieess SSppeecciiffiicc PPrrooffiilleess -- BBoovviinnee

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KKiiddnneeyyUrea (BUN), creatinine, total protein, sodium, chloride, potassium, phosphate

LLiivveerrBilirubin (total), AP, AST (GOT), bile acids, cholinesterase, GLDH, GGT

PPaannccrreeaassGlucose, fructosamine, cholesterol

MMuusscclleeCK, calcium, magnesium

MMeettaabboolliissmmβ-Hydroxybutyrate

TTrraaccee eelleemmeennttssZinc, copper, selenium

VViittaammiinnssβ-Carotene

KKiiddnneeyyUrea (BUN), total proteins, phosphate

LLiivveerrAST (GOT), GGT

PPaannccrreeaassGlucose, cholesterol

MMuusscclleeCK, calcium, magnesium

Please note: It is important that the serum is not haemolysed!

DDoowwnneerr CCooww PPrrooffiillee 11 mmll SSeerruumm ((++ NNaaFF bblloooodd))

BBoovviinnee PPrrooffiillee 33 mmll SSeerruumm ((++ NNaaFF bblloooodd))

33..33..44 SSppeecciieess SSppeecciiffiicc PPrrooffiilleess -- BBoovviinnee

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TTrraaccee eelleemmeennttssZinc, copper, selenium

EElleeccttrroollyytteessSodium, potassium, calcium, magnesium, phosphate, chloride

Net acid-base excretion, pH, phosphate, calcium, sodium, potassium

KKiiddnneeyyUrea (BUN), total protein, sodium, potassium, phosphate

LLiivveerrAST(GOT)

MMuusscclleeCalcium, magnesium

Fertility Profile 1 + β-Carotene

Fertility Profile 1 + β-Carotene + Selenium + Vitamin E

Individual profiles can be compiled for the special needs of herd managementprogrammes. Please contact your Regional Manager.

NNoottiiccee oonn HHeerrdd MMaannaaggeemmeenntt

FFeerrttiilliittyy PPrrooffiillee 33 33 mmll SSeerruumm

FFeerrttiilliittyy PPrrooffiillee 22 11 mmll SSeerruumm

FFeerrttiilliittyy PPrrooffiillee 11 11 mmll SSeerruumm

UUrriinnee SSccrreeeenniinngg PPrrooffiillee 1100 mmll UUrriinnee ffrroozzeenn

PPrrooffiillee SS 33 mmll SSeerruumm

33..33..44 SSppeecciieess SSppeecciiffiicc PPrrooffiilleess -- BBoovviinnee

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KKiiddnneeyyUrea (BUN), creatinine, total protein, sodium, chloride, potassium, phosphate

LLiivveerrBilirubin (total), bilirubin (direct), AP, AST (GOT),GLDH, GGT

PPaannccrreeaassα-amylase, lipase, cholesterol

MMuusscclleeCK, calcium, LDH

MMeettaabboolliissmmTriglycerides

TTrraaccee eelleemmeennttssZinc, copper, selenium

HHaaeemmaattoollooggyyLarge blood count (Small blood count + Diff. blood count)

LLaarrggee PPoorrcciinnee PPrrooffiillee 33 mmll SSeerruumm ++ 11 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr

33..33..55 SSppeecciieess SSppeecciiffiicc PPrrooffiilleess -- PPoorrcciinnee

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Leukocytes, erythrocytes, haemoglobin, haematocrit, MCV, HBE, MCHC, thrombocytes

Basophilic granulocytes, eosinophilic granulocytes, segmented neutrophilic granulocytes, nonsegmented neutrophilic granulocytes, lymphocytes, monocytes, atypical cells, anisocytosis, polychromasia

Small blood count + Differential blood count

The reticulocyte count in an anaemic animal measures theregenerative capability of the bone marrow.

See → 3.2 Special Screening Profiles

AAnnaaeemmiiaa PPrrooffiillee 11 mmll SSeerruumm ++ 11 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr

RReettiiccuullooccyytteess 00..55 mmll EEDDTTAA bblloooodd

LLaarrggee BBlloooodd CCoouunntt 00..55 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr

DDiiffffeerreennttiiaallBBlloooodd CCoouunntt

00..55 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr

SSmmaallll BBlloooodd CCoouunntt 00..55 mmll EEDDTTAA bblloooodd

44..11 HHaaeemmaattoollooggyy44..11..11 HHaaeemmaattoollooggyy –– DDoommeessttiicc aanniimmaallss

4 Haematology

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Leukocytes, erythrocytes, haemoglobin, haematocrit

Basophilic granulocytes, eosinophilic granulocytes, heterophilic granulocytes, lymphocytes, monocytes, atypical cells, anisocytosis, polychromasia

Small blood count + Differential blood count

Leukocytes, haematocrit, differential blood count (as in avian)

Please note: Avian and reptile blood have certain special properties. The erythrocytes and thrombocytes contain nucleoli. This isthe reason why cell differentiations are carried out by hand.Furthermore, birds as well as reptiles have heterophiliccells instead of neutrophilic granulocytes. Heterophilic cells are characterised by containing pale, longeosinophilic granules. A left shift in the white cell count inthese species is therefore called heterophilia.

The normal differential blood count in parrots, several ama-zon species and cockatoos is characterised as heterophilic,whereas in parakeets, finches and canaries it ispredominantly lymphocytic.

LLaarrggee BBlloooodd CCoouunntt(Reptile)

00..55 mmll HHeeppaarriinn bblloooodd ++ BBlloooodd ssmmeeaarr

LLaarrggee BBlloooodd CCoouunntt(Avian)

00..55 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr

DDiiffffeerreennttiiaall BBlloooodd CCoouunntt(Avian)

00..55 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr

SSmmaallll BBlloooodd CCoouunntt(Avian)

00..55 mmll EEDDTTAA bblloooodd

44..11..22 HHaaeemmaattoollooggyy –– AAvviiaann,, RReeppttiillee

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(thromboplastin time, prothrombin time, Quick's)

Indication: - a screening test for the extrinsic coagulation pathway - diagnosis and supervision of your patient following

vitamin K antagonist intoxication - a test for hepatic associated haemostatic disorders

(activated partial thromboplastin time)

Indication: - screening test for the intrinsic coagulation pathway - a test for factor VIII, IX, XI, XII deficiencies - supervision of heparin therapy

Indication: - suspected fibrinogen deficiency or disturbance of fibrinogen production

- fibrinolysis therapy control - heparin therapy control

Indication: - diagnosis of consumption coagulopathy or hyperfibrinolysis

- as an acute phase protein marker during inflammation

Indication: - diagnosis of haemophilia A. - in deficiency disorders PTT is prolonged,

while PT is normal

FFaaccttoorr VVIIIIII (dog) 00..55 mmll CCiittrraatteedd ppllaassmmaa ffrroozzeenn

FFiibbrriinnooggeenn 00..55 mmll CCiittrraatteedd ppllaassmmaa ffrroozzeenn

TThhrroommbbiinn TTiimmee 00..55 mmll CCiittrraatteedd ppllaassmmaa ffrroozzeenn

aaPPTTTT 00..55 mmll CCiittrraatteedd ppllaassmmaa ffrroozzeenn

PPTT 00..55 mmll CCiittrraatteedd ppllaassmmaa ffrroozzeenn

44..22 CCooaagguullaattiioonn PPaarraammeetteerrss

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Mediates the adhesion of thrombocytes to the endothelialwall of blood vessels and acts as a carrier protein forFactor VIII. The von Willebrand syndrome has beendescribed in numerous dog breeds. It is mostly found inDobermanns and Scottish Terriers.

Fibrinogen, thrombin time, PT, PTT

Please note: For all test requests concerning coagulation status frozencitrated plasma, diluted 1:10, is required. This is the onlyway to obtain interpretable results. To obtain 1:10 dilutedcitrated blood it is best to use a commercial tube which isfilled with blood up to the mark. It should be gently turnedupside down several times but not shaken. Then centrifugethe tube. The supernatant must be sent frozen (uponrequest the laboratory will provide special frozencontainers).

If commercial citrate tubes are not available it is possible tomix nine parts of blood with one part of sodium citrate solu-tion (0.11 M) to obtain the same result.

Further coagulation parameters on request. Please contact your Regional Manager or the lab directly.

CCoommpprreehheennssiivvee 11 mmll CCiittrraatteedd ppllaassmmaa ffrroozzeenn

vvoonn WWiilllleebbrraanndd´́ss FFaaccttoorr 00..55 mmll CCiittrraatteedd ppllaassmmaa ffrroozzeenn

44..22 CCooaagguullaattiioonn PPaarraammeetteerrss

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DDoogg:: Presently there are 13 blood groups described in dogs.These are marked DEA (dog erythrocyte antigen) 1.1,1.2,etc. Dogs do not have any clinically significant endogenousantibodies towards other blood groups. This is the reasonwhy following the first blood transfusion, haemolysis due toa transfusion reaction is not expected. The blood group DEA1.1 is being tested with our test, since it is the one showingthe strongest antigenic potential.

CCaatt:: In cats the blood groups A, B and AB are found. The mostcommon one is blood group A (96%). Type B varies according to the breed, e.g. there is an increasedprevalence in Devon Rex or British Shorthair cats (20-45%).Blood group AB is extremely rare. Cats have naturallyoccurring antibodies towards other blood groups. Bloodgroup testing reduces the chance of the occurrence ofneonatal erythrolysis when both parents are tested prior to breeding.

BBlloooodd GGrroouuppss 00..55 mmll EEDDTTAA bblloooodd

44..33 BBlloooodd GGrroouuppss

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See → Infectious Diseases

The intra-erythrocytic, pear-shaped trophozoites are foundusing a giemsa stained blood smear. Ideally, the bloodsmear should have been prepared from capillary blood. The first parasitaemia occurs one to two days followinginfection. It lasts approximately 4 days. The second, moreintensive parasitaemia, is found approximately 10-14 dayslater. A chronic infection will alternate between remissionand parasitaemic phases.Therefore there are times when the organism cannot bedirectly detected!

For further information, see: → Infectious Diseases

See → 15 Moleculargenetical Tests

Microscopic detection of babesia, plus (species specific)mycoplasma / hepatozoon / trypanosoma / anaplasma.

Please also note our Travel Disease Profiles (see → 3.2 Special Screening Profiles).

See → 13 Infectious Diseases

EEhhrrlliicchhiiaa AAnnttiibbooddiieess((sseeee CCoommpprreehheennssiivvee))

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

CCoommpprreehheennssiivvee 11 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr

BBaabbeessiiaa sspppp.. PPCCRR 00..55 mmll EEDDTTAA bblloooodd

BBaabbeessiiaa DDiirreeccttDDeetteeccttiioonn ((sseeee CCoommpprreehheennssiivvee))

00..55 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr

BBaabbeessiiaa AAnnttiibbooddiieess(dog and horse only)

11 mmll SSeerruumm

44..44 BBlloooodd PPaarraassiitteess aanndd HHaaeemmoottrroopphhiicc BBaacctteerriiaa

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The direct detection of the pathogenic agent which is foundin the monocyte will only be successful during the acutestage. The parasite is found in a giemsa stained bloodsmear, ideally prepared from capillary blood.

Further information, see → 13 Infectious Diseases

See → 15 Moleculargenetical Tests

Schizonts are found in bone marrow, spleen and liver. Thedetection of gametocytes in monocytes and granulocytes isonly possible after remission of the disease symptoms.

See → 13 Infectious Diseases

The direct detection of leishmania is useful only on lymphnode aspirates, bone marrow aspirates or skin impressionsmears (sensitivity 30 - 50%). The detection of leishmania ina blood smear is usually not successful.A negative direct detection test does not rule out infection!

See → 13 Infectious Diseases

LLeeiisshhmmaanniiaa DDiirreeccttDDeetteeccttiioonn

SSmmeeaarr

LLeeiisshhmmaanniiaa AAnnttiibbooddiieess 11 mmll SSeerruumm

HHeeppaattoozzooaa DDiirreeccttDDeetteeccttiioonn((sseeee CCoommpprreehheennssiivvee))

BBlloooodd ssmmeeaarr ++ EEDDTTAA bblloooodd

EEhhrrlliicchhiiaa PPCCRR 22 mmll EEDDTTAA bblloooodd

EEhhrrlliicchhiiaa DDiirreeccttDDeetteeccttiioonn((sseeee CCoommpprreehheennssiivvee))

BBlloooodd ssmmeeaarr ++ EEDDTTAA bblloooodd

44..44 BBlloooodd PPaarraassiitteess aanndd HHaaeemmoottrroopphhiicc BBaacctteerriiaa

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See → 15 Moleculargenetical Tests

See → 13 Infectious Diseases

Microfilaria detection is performed by microscopicexamination after enrichment (Knott test).Capillary blood is best collected during late afternoon or in the evening.The earliest detection is possible is six months postinfection. The sensitivity of the test is approximately 60%.Therefore the organism cannot always be directly detected!

A negative result may also be seen if the adult parasites areof the same sex.

See → 13 Infectious Diseases

MMiiccrrooffiillaarriiaaDDiirreecctt DDeetteeccttiioonn

11 mmll EEDDTTAA bblloooodd

MMaaccrrooffiillaarriiaa AAnnttiiggeenn 11 mmll SSeerruumm

LLeeiisshhmmaanniiaa sspppp.. PPCCRR

44..44 BBlloooodd PPaarraassiitteess aanndd HHaaeemmoottrroopphhiicc BBaacctteerriiaa

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H. felis has been reclassified as a Mycoplasma and thereare 2 strains - Mycoplasma haemofelis and CandidatusMycoplasma haemominutum. M. haemofelis is generallyconsidered the most pathogenic.

Cand. M. haemominutum in immunocompetent animals doesnot normally cause any clinical symptoms, but in rare casesmild transient febrile conditions are possible. However, con-current infection with FeLV is of importance. In theseanimals, Cand. M. haemominutum can cause similarsymptoms as infection with M. haemofelis.

The detection of the epicellular organism is performed bymicroscopic examination of a giemsa stained blood smear.

A chronic infection will alternate between remission andparasitaemic phases.Therefore there are times when the organism cannot bedirectly detected!

SSyymmppttoommss:: Depending on the pathogenicity of the organism and theimmunological state of the animal the course of disease canbe either acute or latently chronic.

- pyrexia (above 40.0 °C) - autoimmune haemolytic anaemia - jaundice, bilirubinuria- hepatomegaly and splenomegaly- anorexia, lethargy

TTrreeaattmmeenntt:: - tetracycline 5-15 mg/kg orally q 12 h- prednisolone 1-4 mg/kg orally q 24 h

MMyyccooppllaassmmaa((HHaaeemmoobbaarrttoonneellllaa))DDiirreecctt DDeetteeccttiioonn

BBlloooodd ssmmeeaarr ++ EEDDTTAA bblloooodd

44..44 BBlloooodd PPaarraassiitteess aanndd HHaaeemmoottrroopphhiicc BBaacctteerriiaa

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The organism is detected by microscopic examination ofblood smears or genital secretions.

Direct detection is not always possible!

See → 13 Infectious Diseases

See → 13 Infectious Diseases

TTrryyppaannoossoommaa AAnnttiibbooddiieess 11 mmll SSeerruumm

TTrryyppaannoossoommaaDDiirreecctt DDeetteeccttiioonn

BBlloooodd ssmmeeaarr ++ EEDDTTAA bblloooodd

44..44 BBlloooodd PPaarraassiitteess aanndd HHaaeemmoottrroopphhiicc BBaacctteerriiaa

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Indications: hepatopathies, nephropathies, determination of albumin/globulin ratio (FIP diagnostics)

Occurrence: albumin is synthesized in the liver

Decreased: - protein deficiency (nutritional)- anorexia- malassimilation- hepatopathies- renal, glomerular loss (nephritis,

nephrotic syndrome)- protein-losing enteropathy- FIP- burns- blood loss- body cavity effusions- hypoadrenocorticism- CNS disease- relative deficiency due to overhydration- hypergammaglobulinaemia

Increased: - dehydration

AAllbbuummiinn 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indications: hepatopathies, hyperadrenocorticism, osteopathies

Occurrence: alkaline phosphatase is found in the liver (membrane-boundin biliary duct epithelium), small intestinal mucosa, bones,kidneys, placenta, spleen, leukocytes, erythrocytes

Increased: pphhyyssiioollooggiiccaallllyy- growth

lliivveerr ssppeecciiffiicc iinnccrreeaassee- hepatopathies with intra- or extra-hepatic cholestasis

(cats/ruminants show a very slow reaction)- liver neoplasia- hepatotoxicity- pancreatitis

nnoonn--ssppeecciiffiicc iinnccrreeaassee- hyperadrenocorticism (esp. dogs)- hyperthyroidism- diabetes mellitus- hyperparathyroidism- bone healing- osteopathies- neoplasias- pregnancy (esp. cats)- medication (e.g. glucocorticoids, anticonvulsant drugs,

barbiturates, certain antibiotics)

Artefact: haemolysis, EDTA, severe lipaemia and bilirubinaemia

Please note: Young animals show considerably higher alkalinephosphatase values than adults.

AAllkkaalliinnee PPhhoosspphhaattaassee 00..22 mmll SSeerruumm,, HHeeppaarriinn ppllaassmmaa

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Indications: hepatopathies

Occurrence: liver (cytoplasmic) (esp. dogs, cats), kidneys, heart andskeletal muscle (esp. horse, cattle, pig, sheep)

Increased: Especially increased with these hepatopathies: - acute hepatitis- acute phase of chronic hepatitis- hepatic cell degeneration and necrosis

(acute and chronic)- hypoxic damage- hepatic fibrosis or cirrhosis (acute phase) - extrahepatic biliary duct obstruction- cholangitis, cholangiohepatitis- hepatic lipidosis- hepatic amyloidosis- disturbed venous drainage (hepatic congestion)- focal lesions (e.g. tumours, abscesses), often not or

only mildly increased- acute necrosis due to toxins and drugs (rapid drop

after initial increase) - medication (e.g. anticonvulsants, glucocorticoids)- pyrexia (mild increase)

Artefact: haemolysis, severe lipaemia

AALLTT (GPT) 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indications: hepatopathy, hepatic-encephalopathy

Occurrence: (toxic) metabolite from protein metabolism, synthesised in the intestines, further metabolised to urea (BUN) in the liver

Increase: - portosystemic shunt- severe chronic hepatopathies (fibrosis, cirrhosis)- severe acute hepatopathies (acute hepatitis,

acute liver cell necrosis)- uraemia- primary hyperammonaemia (rare)

Please note: For blood collection use pre-cooled collection tubes. Closethe tube immediately after collection and centrifuge. Sendthe plasma frozen! The animal should be starved for 12 hrsprior to collection.

Test principle: Administration of ammonium chloride increases theformation of ammonia in the intestines, which is thenmetabolised to urea in the liver. In cases of liver damagethis mechanism is disturbed and increased ammonia can be detected in the blood.

Testing: 1. First blood sample = starved animal2. Administration of ammonium chloride 100 mg/kg body

weight orally, dissolved in water. The solution should be administered by stomach tube.

3. Second blood sample collected 30 min. after administration of ammonium chloride.

Interpretation: - physiological: no or very little increase above reference range

- borderline: 100 - 120 microgram/dl- pathological: > 120 microgram/dl

Please note: For blood collection use pre-cooled collection tubes. Closethe tube immediately after collection and centrifuge. Sendthe plasma frozen! The animal should be starved for 12 hrsprior to collection.

AAmmmmoonniiaa TToolleerraannccee TTeesstt 22 xx 11 mmll EEDDTTAA ppllaassmmaa ffrroozzeenn

AAmmmmoonniiaa 11 mmll EEDDTTAA ppllaassmmaa ffrroozzeenn

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Indications: disease of the exocrine pancreas

Occurrence: α-amylase is found in the pancreas, liver, small intestine,salivary glands, (dog: kidney)

Increased: - acute pancreatitis- pancreatic necrosis- pancreatic tumour- obstruction of the pancreatic duct- nephropathies- hepatopathies (carcinoma)- ileus, peritonitis, cholecystitis, small intestinal disease- hyperadrenocorticism- medication (e.g. glucocorticoids)

Indications: Cushing's diagnosis: determination of the steroid-induced,heat stable fraction of alkaline phosphatase. Exogenous orendogenous glucocorticoids will mainly induce the heat sta-ble fraction of the enzyme, whereas the bone, liver and kid-ney alkaline phosphatase is heat unstable. The heat stableAP is determined after the serum has been heated to 65 °C.

Artefacts: haemolysis, EDTA, severe lipaemia and bilirubinaemia

Indications: - myopathies: all animal species- hepatopathies: horses, cattle, sheep, goats,

pigs, (dogs, cats)

Occurrence: AST (GOT) is found especially in skeletal muscles and liver(cytoplasmic, mitochondrial)

Increase: - hepatopathies- myopathies (possibly also cardiomyopathies)

(to differentiate also determine CPK/ALT)- medication (e.g. anticonvulsants, oestrogens)- training

Artefact: haemolysis

AASSTT (GOT) 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

AAPP (heat stable) 00..22 mmll SSeerruumm,, HHeeppaarriinn ppllaassmmaa

αα--AAmmyyllaassee 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indications: hepatopathies

Occurrence: bile acids are synthesised in the liver from cholesterol. Theyare responsible for digestion and absorption of lipids in theintestines (bile acids reach the intestines in bile and a smallamount is passed with the faeces. A larger amount isreabsorbed and transported back to the liver).

Hepatopathies lead to disturbances in bile acid secretion.The accumulation of bile acids then leads to functional disorders due to their toxic properties.

Increased: ssppeecciiffiicc iinnccrreeaasseeliver and bile duct disease with intra- or post-hepatic cholestasis, e.g.- hepatitis- chronic hepatitis- portosystemic shunt

nnoonn ssppeecciiffiicc iinnccrreeaassee- normal up to 24 hrs following a fatty meal- hyperthyroidism- hyperadrenocorticism- diabetes mellitus

Please note: Animal must be starved 12 hrs prior to sampling!

BBiillee aacciiddss 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa

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Indications: - testing for liver function disorders- suspected portosystemic shunt

Test principle: under normal conditions blood bile acid concentration will increase following a fatty meal. If the liver function is disturbed, or in the case of a shunt this increase will be abnormally high.

Test method: 1. first blood sample = bile acid basal level (starved)2. stress feeding (small fatty meal or recovery diet)3. second blood sample 2 hrs following the

meal = postprandial level

or

1. first blood sample = bile acid basal level (starved)2. injection of Ceruletid (Takus®, Pharmacia) 0.3 µg/kg i.m.3. second blood sample 20 min. following

injection = stimulation value

Interpretation: - basal level < 20 µmol/l and postprandial level < 40 µmol/l = normal

- basal level > 20 µmol/l and postprandial level 20-40 µmol/l = borderline

- postprandial level > 40 µmol/l = pathological

Indirect (unconjugated) bilirubin can be calculated fromtotal bilirubin and direct (conjugated) bilirubin.

Indications: cholestasis, hepatopathies, anaemia, haemolysis

Occurrence: mainly when haemoglobin is broken down into bilirubin I,(unconjugated bilirubin, indirect bilirubin), conjugation takesplace in the liver (dog: also in the kidneys) to bilirubin II,(conjugated bilirubin, direct bilirubin).

Artefact: haemolysis, daylight

BBiilliirruubbiinn (total) 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

BBiilliirruubbiinn (direct) 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

BBiillee AAcciidd SSttiimmuullaattiioonn TTeesstt

22 xx 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa

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Indication: see below

Occurrence: especially in bones

Increased: - primary/tertiary hyperparathyroidism- hypervitaminosis D- hypoadrenocorticism- acidosis- neoplasia (lymphoma, adenocarcinoma)- osteolytic tumours- osteomyelitis- osteoporosis- nephropathies- hyperalbuminaemia (increase of the protein bound part)- malignant hypercalcaemia

Decreased: - hypoparathyroidism- secondary (renal) hyperparathyroidism- nephropathies- hypoalbuminaemia- hypovitaminosis D- (necrotic) pancreatitis- tetanus- puerperal tetany- milk fever (parturient paresis)- malabsorption- hypercalcitonism- ethylene glycol intoxication (e.g. antifreeze)

Artefact: lipaemia, haemolysis, EDTA

Please note: In the case of abnormal serum protein levels the changedprotein-bound calcium fraction must be taken into account and therefore the total serum calcium level corrected (only dog):corrected calcium level (mg/dl) = serum calcium level(mg/dl) - serum albumin (g/dl) + 3.5.

CCaallcciiuumm 00..22 mmll SSeerruumm,, HHeeppaarriinn ppllaassmmaa

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Indications: - fertility problems in cattle, horses, pigs (silent oestrus, delayed ovulation, frequent failure of fertilization, embryonic death)

- increased susceptibility of infection in neonates

Occurrence: - provitamin A (exception: cats cannot convert β-Carotene into vitamin A)

- main storage organ is the liver

Decreased: - nutritional (e.g. feeding silage that has been stored for a long time)

Indications: electrolyte disturbances

Occurrence: chloride is the most important extracellular anion found.Under normal physiological conditions of acid/base balancethe serum chloride concentration equals the sodiumconcentration.

Increased: - dehydration (fluid loss, reduced fluid intake)- increased intake of sodium chloride- diabetes insipidus- diabetes mellitus (following insulin therapy)- mineralocorticoids (retention of sodium)- nephropathy- acidosis- small intestinal diarrhoea

Decreased: - increased loss of sodium chloride (vomiting, diarrhoea, sweating)

- insufficient intake of sodium chloride- increased intake of water- hypoadrenocorticism- osmotic diuresis (e.g. diabetes mellitus)- congestive heart failure (oedema)- nephropathy- loop diuretics (e.g. furosemide), aldosterone antagonists

(e.g. spironolactone)- reduced colloid osmotic pressure (hypoalbuminaemia)- metabolic alkalosis

CChhlloorriiddee 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

ββ--CCaarrootteennee 22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indications: metabolic disturbances (and endocrinopathies)

Occurrence: - nutritional intake or synthesis in the liver- precursor of steroid hormones and bile acids

Increased: - postprandial- nutritional- hypothyroidism- diabetes mellitus- hyperadrenocorticism- nephrotic syndrome- hepatopathies- extrahepatic cholestasis- hyperlipaemia syndrome (e.g. hereditary in certain

families of Miniature Schnauzer and Beagle dogs)- acute pancreatitis, pancreatic necrosis- idiopathic hypercholesterolaemia in Dobermann and

Rottweiler dogs- pony lipidosis- medication (e.g. glucocorticoids)

Decreased: - malassimilation- reduced liver function (e.g. liver cirrhosis,

portosystemic shunt)- cachexia- exocrine pancreatic insufficiency- protein losing enteropathy- hyperthyroidism

Artefact: haemolysis, lipaemia

Please note: Animal must be starved!

CChhoolleesstteerrooll 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indications: - hepatopathies - organophosphate intoxication- prior to administration of muscle relaxants if there

is evidence of hepatopathy in the case history

Occurrence: brain, nervous tissue, erythrocytes;it is synthesised in the liver

Decreased: - severe hepatopathies- poisoning due to organophosphates and alkylphosphates

(parathion, E-605)- medication with carbamic acid derivates (neostigmine)- severe protein deficiency- cachexia- chronic infection

Increased: - nephropathies- exudative enteropathy

Indications: primary/secondary myopathies

Occurrence: skeletal muscle, heart muscle, brain, urinary bladder (cats)

Increased: - myopathies- myositis (infectious, immune-mediated, endocrine)- i.m. injection- physical exercise- tetanus- exercise myopathy- deficiency myopathy- shock- urinary bladder obstruction (cat)- corticosteroids- halothane anaesthesia- barbiturates

Artefact: haemolysis, bilirubinaemia

Please note: The reference range in dogs varies according to age. CK in newborn puppies may be five times higher than in adult dogs.

CCKK (CPK) 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

CChhoolliinneesstteerraassee 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indication: - especially in cattle: reduced performance, reduced growth rate

- changes in wool quality (sheep)- enzootic ataxia (lambs)- hepatopathies- haemolytic anaemia

Occurrence: - part of many enzymes- important for haematopoiesis- stored in the liver

Increased: - copper storage disease (Bedlington Terrier, West Highland White Terrier, Cocker Spaniel and Dobermann Pinscher); rarely increased! Reliable results with histopathology examination

- bile duct obstruction- nutritional (copper poisoning, esp. in sheep) (not always!)

Decreased: - primary Cu deficiency due to reduced intake- secondary Cu deficiency (disturbed absorption due

to Cu antagonists)

CCooppppeerr 11 mmll SSeerruumm

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Indication: nephropathies

Occurrence: - creatinine is a product of endogenous muscle metabolism (young animals have a lower serum creatinine concentration compared to muscular adult animals)

- excretion takes place mainly via glomerular filtration

Increased: Independent from diet!

ssppeecciiffiicc iinnccrreeaassee::- nephropathies (needs at least 70%

non-functional nephrons)- post-renal azotaemia

nnoonn ssppeecciiffiicc iinnccrreeaassee::- dehydration- electrolyte imbalance- heart/circulation failure- hypoadrenocorticism- hypalbuminaemia- medication (e.g. corticosteroids, tetracycline, cimitidine,

cephalosporin, trimethoprim)- diabetic ketoacidosis- tissue catabolism (pyrexia, muscle trauma, myositis)

Decreased: - emaciation

Artefact: haemolysis

CCrreeaattiinniinnee 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indications: cystinuria, cystine urolithiasis

Occurrence: cystinuria is a hereditary disease involving a dysfunction ofthe reabsorption of cystine (as well as other amino acidssuch as lysine, ornithine and arginine) in the proximal renaltubules. Cystine is insoluble in acidic and neutral urine (pH 5.5-7.0). A raised cystine concentration can thereforelead to precipitation of cystine crystals or to cystinecalculus formation in the kidneys or bladder. Clinicalsymptoms are often only noticed with severe urolithiasis orbacterial urinary tract infection (haematuria, dysuria).

Cystinuria is found in several dog breeds: Boxer, Cairn Terrier, German Shepherd, Great Dane, Irish Terrier, Newfoundland, Scottish Terrier, Mastiff,Bullmastiff, Basenji, Chihuahua, Bichon Frise

See → 15 Moleculargenetical Tests

Indications: - testing small intestinal absorption efficiency- detection of intestinal bacterial overgrowth- blood production disorder - disorder of the immune system

Occurrence: as tetrahydrofolic acid coenzyme for synthesis of purine bodies

Increased: - bacterial disturbance- pancreatic insufficiency

Decreased: - jejunal absorption disorder (malabsorption)- inhibition of microbial folic acid synthesis by sulfonamides

FFoolliicc AAcciidd 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

CCyyssttiinnee 55 mmll UUrriinnee

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Indications: - differentiation of transient and long-term hyperglycaemia- monitoring of diabetes mellitus therapy

Occurrence: Fructosamines are serum proteins glycolysed independentlyof insulin. Their occurrence is in direct proportion to the blood glucose concentration of theprevious one to three weeks

Increased: - diabetes mellitus- persistent hyperglycaemia of other origin- hyperalbuminaemia

Artefact: haemolysis, severe bilirubinaemia

Please note: Hypoalbuminaemia may lead to decreased fructosamine levels.Concurrent hypothyroidism may lead to false highfructosamine values whereas hyperthyroidism may lead to false low fructosamine values.

Indications: hepatopathies, cholestasis (more suitable than AP in horses, cattle, pigs and sheep), colostrum intake in calves

Occurrence: liver (membrane-bound in bile duct epithelium), kidneys, pancreas, small intestine

Increased: ssppeecciiffiicc iinnccrreeaassee- hepatopathies with cholestasis (intra- and extra-hepatic)

non specific increase- pancreatitis/enteritis with liver involvement- colic (horses)- Diabetes mellitus- right heart failure- leukosis

Artefact: haemolysis

Please note: Very slow reaction in cats!

GGGGTT 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

FFrruuccttoossaammiinnee 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indications: hepatopathies

Occurrence: liver (mitochondrial, centrilobular)

Increased: Small increases are not clinically significant. 3-fold increases or more are clinically significant esp. in thefollowing hepatopathies:- cholestasis- hypoxia- acute hepatitis- liver cell necrosis- chronic hepatitis- liver fibrosis, liver cirrhosis- hepatotoxicity- in liver congestion due to congestive cardiomyopathy

Artefact: haemolysis

Please note: In horses moderately increased values may be found without the presence of liver disease.

In cats, GLDH is not necessarily specific for the liver.

GGLLDDHH 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indications: diabetes mellitusInsulinoma

Increased: pprriimmaarryy iinnccrreeaassee- diabetes mellitus

sseeccoonnddaarryy iinnccrreeaassee- postprandial (up to 150 mg/dl - 8.25 mmol/l)- stress (cats up to 400 mg/dl - 22 mmol/l)- hyperadrenocorticism- hyperthyroidism- acromegaly- CNS diseases- convulsions- pancreatitis- severe trauma- medication (e.g. glucose, glucocorticoids, ACTH,

progestagens, morphine, adrenaline, thiazide diuretics)

Decreased: pprriimmaarryy ddeeccrreeaassee- hyperinsulinism, insulinoma

sseeccoonnddaarryy ddeeccrreeaassee- renal glucosuria- hepatopathies- glycogen storage disease- malassimilation- starvation- idiopathic hypoglycaemic syndrome (dwarf breeds)- hypothyroidism- septicaemia- hypoadrenocorticism- severe polycythaemia- neonatal hypoglycaemia- hunting dog hypoglycaemia- paraneoplastic syndrome- medication (e.g. beta-blockers, antihistamines)

Artefact: haemolysis, whole blood

Please note: Use only sodium fluoride (NaF) blood, fluoride oxalate, orblood which is not haemolytic and completely free from erythrocytes. Do not send whole blood.

GGlluuccoossee 00..22 mmll SSeerruumm,, NNaaFF bblloooodd,, HHeeppaarriinn ppllaassmmaa

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Indications: assisting in the diagnosis of heart muscle damage

Occurrence: isoenzyme of LDH which is found in the heart muscle,erythrocytes, skeletal muscle, kidneys, gastro-intestinal tract

Increased: - heart muscle damage- haemolytic diseases

Artefacts: haemolysis

Indications: acetonaemia

Occurrence: β-Hydroxybutyrate is found in body fluids (serum, milk, urine)

Increased: - ketosis- pregnancy toxicosis (sheep)- diabetes mellitus (with ketoacidosis)- pyrexia- starvation

Indications: differential diagnosis for anaemia, deficiency diseases

Occurrence: nutritional intake, haemoglobulin catabolism

Increased: - haemolytic anaemia - hepatopathies- haemochromatosis

Decreased: - massive chronic blood loss- young animals fed on a milk diet only- infections- neoplasias- nephropathies

Artefact: haemolysis

IIrroonn 00..22 mmll SSeerruumm,, HHeeppaarriinn ppllaassmmaa

ββ--HHyyddrrooxxyybbuuttyyrraattee 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

αα--HHBBDDHH (LDH1-Isoenzyme) 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indication: checking the training status (horse), myopathies

Occurrence: lactate is produced in the tissues (muscle) during anaerobic glucose breakdown or it is increasingly produced by intestinal bacteria when feeding acarbohydrate rich diet

Increased: - increased anaerobic glycolysis- disturbed lactate metabolism in the liver

(e.g. due to shock)- burns- leukosis- in new borns in the first 24 hrs- hard physical exercise- intestinal torsion, strangulation or rupture (horse),

postoperative

Artefact: whole blood

Please note: It is useful to use NaF/fluoride oxalate blood, otherwise thelactate value may be falsely high.

Indication: myopathies (hepatopathies)

Occurrence: all tissues especially muscle, liver, erythrocytes

Increased: - myopathies of skeletal muscles and heart muscle- hepatopathies- cell necrosis- haemolysis- (malignant neoplasia)

Artefact: haemolysis, whole blood

LLDDHH 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

LLaaccttaattee 00..22 mmll SSeerruumm,, NNaaFF bblloooodd,, ((HHeeppaarriinn ppllaassmmaa))

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Indication: diseases of the exocrine pancreas

Occurrence: pancreas, gastric mucosa

Increased: - acute pancreatitis- pancreatic necrosis- pancreatic neoplasia- pancreatic duct obstruction- nephropathies- hepatopathies (carcinoma)- (ileus, peritonitis, cholecystitis)- (medication, e.g. glucocorticoids)- hyperadrenocorticism

Artefact: Haemolysis, bilirubinaemia, lipaemia

Please note: Cats with acute pancreatitis may occasionally show normal lipase values.

Indications: Acute/chronic pancreatitis

Occurrence: The acinar cells of the exocrine pancreas secrete enzymes,one of them is lipase. Lipase is responsible for thebreakdown of triglycerides. In case of pancreatitis there isinjury or death of the acinar cells which results in leakageof lipase from these cells. The spec. cPL™ only measuresthe lipase from the pancreas acinar cells.

Increased: = 400 µg/l or above: very likely to be a pancreatitis201-399 µg/l: results in the grey area.

Depending on the development of clinical symptoms and the diseasea retest can be done in couple of weeks.

Please note: Animal must be starved 6-12 hours prior to sampling! Noinfluence from lipemia, haemolysis, corticosteroids orchronic renal failure.

SSppeecc ccPPLL™ (caninepancreas specific lipase)

00,,55 mmll -- 11,,00 mmll SSeerruumm

LLiippaassee 00..22 mmll SSeerruumm,, HHeeppaarriinn ppllaassmmaa

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Indication: electrolyte imbalance

Occurrence: especially in bones, all tissues. Magnesium is important forcellular energy metabolism and neuromuscular impulse generation (decrease leads to convulsion, increase leads to flaccid paralysis)

Increased: - hypoadrenocorticism- renal failure during anuric/oliguric phase

Decreased: - malabsorption- tetany- disturbed renal function- hypoparathyroidism- medication (e.g. aminoglycosides, amphothericin B, insulin)- hypercalcaemia- hyperkalaemia

Artefact: haemolysis, hyperbilirubinaemia, EDTA

Indication: reduced growth, fertility problems, abortion, stillbirths, locomotor disorders

Decreased: nutritional

Indication: early detection of heart disease diagnosis of heart failurescreening of elderly pets and/or predisposed breedspreanaesthetic testing

Increased: heart disease very likely, diagnosis only possible incombination with clinical symptomacy and further investiga-tions (ultrasound, specialist advise)

NNtt--pprrooBBNNPP 00,,55 mmll SSeerruumm

MMaannggaanneessee 11 mmll SSeerruumm,, UUrriinnee

MMaaggnneessiiuumm 00..22 mmll SSeerruumm,, HHeeppaarriinn ppllaassmmaa

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Indication: osteopathies, nephropathies, hypo/hyperparathyroidism, see below

Occurrence: especially in the skeletal system and erythrocytes

Increased: - juveniles- nephropathies (reduced glomerular filtration rate)- primary hypoparathyroidism- hypervitaminosis D- secondary hyperparathyroidism- nutritional- osteolytic tumours- hyperthyroidism (cats)- medication (e.g. anabolics, furosemide)- soft tissue trauma- acidosis- post-renal obstruction

Decreased: - primary hyperparathyroidism- malabsorption- medication (e.g. glucocorticoids, insulin)- malignant hypercalcaemia- hypovitaminosis D- osteomalacia- milk fever (hypocalcaemic parturient paresis)- Fanconi syndrome- hyperadrenocorticism- alkalosis

Artefact: haemolysis, whole blood

Please note: Juvenile animals show much higher phosphate levels thanadults.

PPhhoosspphhaattee 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indications: - electrolyte imbalance- hypokalaemia leads to paralysis of the smooth and

striated muscles (ST decrease in the ECG)- hyperkalaemia leads to neuromuscular symptoms

and myocardial damage

Occurrence: 96 - 98% in the intracellular space

Increased: - decreased potassium excretion- hypoadrenocorticism (a sodium/potassium ratio

< 27:1 is indicative for Addison's Disease)- nephropathies (oliguric/anuric phase)- rupture of the bladder, post-renal obstruction- diabetic ketoacidosis- tissue damage (potassium from within the cells)- hypoxia- haemolysis (esp. in Akita Inu dogs)- acidosis- iatrogenic

Decreased: - low potassium diet- increased potassium excretion (chronic vomiting/diarrhoea)- increased diuresis- chronic hepatopathies- hyperadrenocorticism (low decrease)- medication (e.g. glucocorticoids, diuretics, insulin)- nephropathies (polyuric phase)- alkalosis

Artefact: haemolysis, (lipaemia), EDTA, severe hyperproteinaemia

PPoottaassssiiuumm 00..22 mmll SSeerruumm,, HHeeppaarriinn ppllaassmmaa

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Indication: selenium imbalance, wasting, embryonic death, reduced performance, fertility problems, recurrent illness, reduced immune response

Occurrence: antioxidant, metabolic function in prostaglandin synthesis, steroid and cholesterol metabolism

Decreased: - nutritional- increased requirement (growth, stress, high milk production)- vitamin E deficiency- selenium antagonists (zinc, sulphur)

Indication: electrolyte imbalance

Occurrence: intracellular and extracellular (responsible for extracellular osmolality)

Increased: - dehydration (fluid loss, reduced fluid intake)- increased sodium intake - hyperadrenocorticism- (vomiting, diarrhoea)- fever- diabetes mellitus (following insulin therapy)- diabetes insipidus- mineralocorticoids (sodium retention)- nephropathies, post-renal obstruction

Decreased: - increased sodium chloride loss (vomiting, diarrhoea, perspiration)

- reduced sodium chloride intake- increased water intake- hypoadrenocorticism- osmotic diuresis (e.g. diabetes mellitus)- congestive heart failure (oedema)- nephropathy- loop diuretics (e.g. furosemide), aldosterone antagonists

(e.g. spironolactone)- reduced colloid-osmotic pressure (hypoalbuminaemia)

Artefact: lipaemia, severe hyperproteinaemia

SSooddiiuumm 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

SSeelleenniiuumm 11 mmll SSeerruumm

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The TLI test (trypsin-like immunoreactivity) measures thespecific pancreatic enzymes trypsin and trypsinogen in theblood. Oral substitution of pancreatic enzymes does notinfluence the test result.Inflammation of pancreatic sections or food intake before sampling may lead to an increase in serum TLIconcentration, which can be misleading (therefore it is important to starve the animal before sampling!).

Please note: Exocrine pancreatic insufficiency due to blockage of thepancreatic ducts will not be diagnosed with the TLI test. In this case the test for faecal elastase-1 is recommended(dog only).

Indication: exocrine pancreatic insufficiency, (acute pancreatitis)

Occurrence: pancreas

Increased: - acute pancreatitis (short-term)- acute phase of chronic recurring pancreatitis

Decreased: - exocrine pancreatic insufficiency

Indications: hepatopathies, gastrointestinal disease, nephropathies, FIP, dehydration, overhydration

Occurrence: except for immunoglobulins, total proteins are synthesized in the liver

Increased: especially globulins!- dehydration- chronic infectious diseases (e.g. ehrlichiosis, FIP,

leishmaniasis)- chronic bacterial infections- parasitic diseases (e.g. demodex, dirofilaria, sarcoptes)- neoplasia- multiple myeloma- autoimmune diseases

TToottaall PPrrootteeiinn 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

TTLLII (dog and cat only)

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa ((ddoogg))22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa ((ccaatt))

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- haemolysisDecreased: - malabsorption

- maldigestion- nutritional deficiency (low in protein)- chronic hepatopathies- nephropathies (esp. nephrotic syndrome)- protein-losing enteropathy- blood loss- effusion into body cavities- hypoadrenocorticism- burns- relative decrease due to overhydration

Artefact: haemolysis

Please note: A lower protein concentration in young animals is normal.

Indication: metabolic disorders

Occurrence: triglycerides are taken in with the diet (exogenous lipids) or are produced by the liver cells

Increased: PPrriimmaarryy hhyyppeerrlliippaaeemmiiaa (congenital):- idiopathic hyperlipaemia

(certain families e.g. Dwarf Schnauzer, Beagle)- pony hyperlipaemia- lipomobilisation syndrome (cattle)

SSeeccoonnddaarryy hhyyppeerrlliippaaeemmiiaa (acquired):- postprandial hyperlipaemia: increased levels

possible up to 12 hrs- diabetes mellitus- hypothyroidism- hyperadrenocorticism- administration of glucocorticoids- cholestasis- acute pancreatitis, pancreatic necrosis- exudative enteropathy- nephrotic syndrome- (fasting in obese animals)

Artefact: feeding (starve 12 hrs prior to blood sampling), hard exercise

TTrriiggllyycceerriiddeess 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indication: diagnosing damage to the cardiac muscle

Occurrence: cardiac muscle, (skeletal muscle)

Increased: cardiomyopathies with damage to cardiac muscle cells

UUrreeaa--nniittrrooggeenn ((mmgg//ddll -- mmmmooll//ll)) xx 22..1144 == UUrreeaa ((mmgg//ddll -- mmmmooll//ll))

Indications: nephropathies (hepatopathies)

Occurrence: urea is a metabolic product of protein metabolism in the liver. Excretion occurs mainly via the kidney.

Increased: dependent on diet!

SSppeecciiffiicc iinnccrreeaassee::- nephropathies (minimum of 75% loss of functional

nephrons)- post-renal azotaemia

NNoonn ssppeecciiffiicc iinnccrreeaassee::- following high protein meal- dehydration- heart/circulation failure- gastro-intestinal bleeding- increased metabolism, e.g. pyrexia, infections- muscle trauma, hard physical exercise- medication (e.g. glucocorticoids, tetracycline, thyroxine)- hyperthyroidism- hypoadrenocorticism

Decreased: SSppeecciiffiicc ddeeccrreeaassee::- severe hepatopathies- portosystemic shunt

NNoonn--ssppeecciiffiicc ddeeccrreeaassee::- low protein diet- anabolic steroids- severe polyuria/polydipsia (e.g. hyperadrenocorticism,

diabetes insipidus)

UUrreeaa (BUN) 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

TTrrooppoonniinn II 00..55 mmll SSeerruumm,, HHeeppaarriinn ppllaassmmaa

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Artefact: (haemolysis)

Please note: Compared to other species even a mild increase must beconsidered pathological in the horse.

Indications: - bronzing syndrome in Dalmatian dogs- urinary urate calculi

Occurrence: - Dalmatian dogs: urate level: approx. 2 mg/dlexcretion: 400-600 mg/day urate

- other dogs: in the liver urate is metabolised by the enzyme uricase to allantoin, therefore:urate level: < 1 mg/dl excretion: < 100 mg/day urate

- birds: in birds the measurement of uric acid in the blood is more important than blood urea (BUN) or creatinine levels. In birds uric acid is an indicator of renal function. Damage to kidney epithelium (due to Vitamin A deficiency, infections, water deprivation, etc.) will lead to an increase in uric acid. Especially gout will lead to a marked increase in the uric acid level.

UUrriicc AAcciidd 00..22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indication: metaplastic keratinization of epithelium, increased susceptibility to infection, various ocular symptoms, fertility problems, osteopathies, neuropathies

Occurrence: retinol is the active form, β-carotene is transformed to retinol (except in cats),main storage is in the liver

Decreased: - nutritional- lack of transport proteins- diarrhoea- infections and parasites (increased consumption)- hepatopathies (disturbed storage)- disturbed carotene utilization (high nitrate concentration,

phosphate and vitamin E deficiency)

Increased: - nutritional

Indication: CNS disorder

Occurrence: coenzyme in ketoacid metabolism (transformation of pyruvate into acetyl-CoA)

Decreased: - thiaminase-producing bacteria- nutritional (exclusive feeding of raw fish)- CCN (cortical necrosis in sheep)

Please note: EDTA blood must be sent in a dark container (protected from light).

VViittaammiinn BB11 (Thiamine) 00..55 mmll EEDDTTAA bblloooodd

VViittaammiinn AA 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indication: reduced growth, fertility problems, diseases of the skin and horn, anaemia, reduced immunity, conjunctivitis/keratitis, myopathies

Occurrence: involved in oxidative processes

Decreased: - nutritional

Please note: EDTA blood must be sent in a dark container (protected from light).

Indication: anaemia, severe weight loss (small animals, horses, cattle),convulsions (small animals), growth disturbances, diarrhoea, muscle atrophy (pigs)

Occurrence: coenzyme in amino acid metabolism, cats have an extremely high requirement

Decreased: - medication (e.g. penicillamine)- nutritional (horsetail = Equisetum spp.)

Please note: EDTA blood must be sent in a dark container (protected from light).

Indication: anaemia, leukopenia, growth disturbances (mainly large animals)

Occurrence: breakdown of proprionic acid, resynthesis of methionine

Decreased: - decreased cobalt supply- reduced absorption rate in the ileum

VViittaammiinn BB1122 (Cobalamin) 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

VViittaammiinn BB66 (Pyridoxin) 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

VViittaammiinn BB22 (Riboflavin) 00..55 mmll EEDDTTAA bblloooodd

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Indication: osteopathies

Occurrence: produced in the skin from 7-dehydrocholesterol or absorbedfrom food in the small intestine. Hydroxylated to 25-hydroxycholecalciferol in the liver, then transformed to 1.25-dihydroxy cholecalciferol in the kidneys

Decreased: - hepatopathies- nephropathies- phosphate over-supplementation- rapid growth- lack of UV exposure- chronic diarrhoea

Increased: - iatrogenic (application of 10 times the required dosage)- nutritional

See: → Vitamin D3 (1.25-di-OH)

VViittaammiinn DD33 (25-OH) 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

VViittaammiinn DD33 (1.25-di-OH) 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Indication: myopathies, placental retention, fertility problems, yellow fat disease (horse, cat)

Significance: antioxidant

Decreased: - reduced amount in diet (poor storage or spoilage)- increased amount of unsaturated fatty acids- vitamin A and carotene deficiency- increased requirement (high performance,

stress, hepatopathy)- selenium deficiency

Indications: skin, hair and horn disease, growth problems, fertility problems

Occurrence: involved in numerous carboxylation processes, synthesized in the intestines

Decreased: rare- nutritional

Indication: para- and hyperkeratosis of the skin, disturbed performance, fertility and growth, disturbed wound healing, reduced immune response

Occurrence: needed in protein, lipid, and vitamin A metabolism; immune response

Decreased: - nutritional- zinc antagonists- reduced zinc absorption

ZZiinncc 22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa,, HHaaiirr

VViittaammiinn HH (Biotin) 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

VViittaammiinn EE (Tocopherol) 22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

5 Biochemistry

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DDeexxaammeetthhaassoonnee 22 mmll SSeerruumm

CCuummaarriinn 22 mmll SSeerruumm

CClleennbbuutteerrooll 22 mmll SSeerruumm

CCaaddmmiiuumm 22 mmll EEDDTTAA bblloooodd

BBrroommiiddee 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

BBeennzzooddiiaazzeeppiinnee 22 mmll SSeerruumm,, UUrriinnee

AArrsseenniicc 22 mmll SSeerruumm,, HHaaiirr

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PPaarraacceettaammooll 22 mmll SSeerruumm

MMeettaammiizzoollee 22 mmll SSeerruumm

MMeerrccuurryy 22 mmll SSeerruumm

LLeeaadd 22 mmll EEDDTTAA bblloooodd

EE 660055 22 mmll SSeerruumm

DDiiggooxxiinn 11 mmll SSeerruumm

DDiiggiittooxxiinn 11 mmll SSeerruumm

Please note! Many other special analyses can be performed on request.

TThhaalllliiuumm 22 mmll SSeerruumm,, HHaaiirr,, 55 mmll UUrriinnee

PPrroommiiddoonnee 11 mmll SSeerruumm

PPhheennyyttooiinn 11 mmll SSeerruumm

PPhheennyyllbbuuttaazzoonnee 22 mmll SSeerruumm

PPhheennoobbaarrbbiittoonnee 11 mmll SSeerruumm

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Includes: TLI (RIA), Folic acid, Vitamin B12

TTLLIIThe TLI test (trypsin-like-immunoreactivity) measures thespecific pancreatic enzymes trypsin and trypsinogen in the blood. Oral substitution of pancreatic enzymes does not influence the test result.Inflammation of pancreatic sections or food intake before sampling may lead to an increase in serum TLIconcentration, which can be misleading (therefore it isimportant to starve the animal before sampling!).

Please note that exocrine pancreatic insufficiency due to blockage of the pancreatic ducts will not be diagnosed with the TLI test. In this case the test for faecal elastase-1 is recommended (dog only).

FFoolliicc aacciidd//VViittaammiinn BB1122The determination of folic acid and Vitamin B12 make it possible to judge small intestinal absorption. Furthermore,bacterial overgrowth can be identified.

Folic acid increased: - imbalance of bacterial species in the intestinal flora- pancreatic insufficiency

Folic acid decreased: - disturbance of the absorptive performance in the jejunum (malabsorption)

- inhibition of microbial folic acid synthesis by sulfonamides

Vitamin B12 decreased: - disturbed intestinal absorption- reduced cobalt supply

DDiiaarrrrhhooeeaa PPrrooffiillee BB(dog/cat)

22 mmll SSeerruumm ((ddoogg))33 mmll SSeerruumm ((ccaatt))

77..11 GGaassttrrooiinntteessttiinnaall DDiisseeaasseess

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BBaacctteerriioollooggiiccaall ffaaeeccaall eexxaammiinnaattiioonn- examination for enteropathogenic bacteria

MMyyccoollooggiiccaall ffaaeeccaall eexxaammiinnaattiioonn- (semiquantitatively)

PPaarraassiittoollooggiiccaall ffaaeeccaall eexxaammiinnaattiioonn- detection of cestode eggs, nematode eggs, coccidia oocyts;

additionally in large animals: rumen fluke and liver fluke eggs, lungworm larvae

GGiiaarrddiiaa (dog and cat only)

Diarrhoea Profile E corresponds to 'Diarrhoea Profile C' but also includes canine faecal elastase-1:

Bacteriological faecal examination, mycological faecal examination, parasitological faecal examination, giardia, canine elastase-1

DDiiaarrrrhhooeeaa PPrrooffiillee EE (dog only)

mmiinniimmuumm 11 ffuullll SSAA ffaaeeccaall ttuubbee

DDiiaarrrrhhooeeaa PPrrooffiillee CC(dog/cat)DDiiaarrrrhhooeeaa PPrrooffiillee CC(horse/cattle/pig)

SSmmaallll aanniimmaallss:: mmiinniimmuumm 11 ffuullll SSAA ffaaeeccaall ttuubbeeLLaarrggee aanniimmaallss:: mmiinniimmuumm 11 ffuullll LLAA ffaaeeccaall ttuubbee

77..11 GGaassttrrooiinntteessttiinnaall DDiisseeaasseess

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Faecal samples and rectal swabs are examined for enteropath-ogenic germs using selective media and enrichment methods.

The culture includes: - Salmonella- thermophilic Campylobacter species (Campylobacter

jejuni, Campylobacter coli, Campylobacter lari)- Yersinia enterocolitica- species specific pathogenic and facultative pathogenic

enterobacteriaceae (e.g. Klebsiella spp., haemolytic and mucoid E. coli strains, Proteus spp.)

- coagulase-positive staphylococci (Staphylococcus aureus,Staphylococcus intermedius)

- Pseudomonas aeruginosa- yeasts (semiquantitative detection in case of

excessive growth)

In carnivores the composition of the faecal flora is judgedsemiquantitatively. A quantitative increase in gram positiveor gram negative bacteria could be a sign of imbalance ofthe large intestinal flora.

FFaaeeccaall BBaacctteerriioollooggyy (enteropathogenic germs)

FFaaeecceess,, RReeccttaall sswwaabb

77..11 GGaassttrrooiinntteessttiinnaall DDiisseeaasseess

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Specific faecal examination for Salmonella. Pooled faecalsamples can be used.

By specific dilution of the faecal sample and anaerobic culture on selective media the number of Clostridium pergram of faeces can be determined. A quantitative increasemay indicate dysbiosis.

Clostridium perfringens enterotoxin can cause diarrhoea indogs and cats.

CCrryyppttoossppoorriiddiiaa AAnnttiiggeenn(ELISA)

22 -- 33 gg FFaaeecceess

CClloossttrriiddiiuumm ppeerrffrriinnggeennssEEnntteerroottooxxiinn

00..55 -- 11 SSAA ffaaeeccaall ttuubbee

DDeetteeccttiioonn ooff CClloossttrriiddiiuumm(quantitatively)

00..55 -- 11 SSAA ffaaeeccaall ttuubbee

DDeetteeccttiioonn ooff SSaallmmoonneellllaa FFaaeecceess,, RReeccttaall sswwaabb

77..11 GGaassttrrooiinntteessttiinnaall DDiisseeaasseess

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Flotation method: Detection of cestode eggs, thin and thickwalled nematode eggs, coccidia oocyts (including toxoplas-ma oocysts).

Please note: Collect several small samples from different places in thefaeces.

Including: - native preparation, stained and unstained: protozoa (flagellates, amoeba, ciliates, microsporidia), nematode larvae, trematodes

- flotation method: nematode eggs, cestode eggs, pentastomid eggs, coccidia oocyts

To examine further for lungworms and trematodes, the sedimentation and larval migration methods arerecommended.

Including: - flotation method: cestode eggs, thin and thick walled nematode eggs, coccidia oocysts

- sedimentation method(not horse): rumen and liver fluke eggs

- larval migration method (Baermann method): lungworm larvae

EEnnddooppaarraassiitteess(horse, cattle, pig)

mmiinniimmuumm 11 ffuullll SSAA ffaaeeccaall ttuubbee

EEnnddooppaarraassiitteess (reptile)

mmiinniimmuumm 22 gg ffrreesshh FFaaeecceess

EEnnddooppaarraassiitteess mmiinniimmuumm 00..55 SSAA ffaaeeccaall ttuubbee(dog/cat/bird/rabbit/small pets)

GGiiaarrddiiaa AAnnttiiggeenn (ELISA) 22 -- 33 gg FFaaeecceess

77..11 GGaassttrrooiinntteessttiinnaall DDiisseeaasseess

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Indication: checking absorptive performance of the small intestine,detection of intestinal bacterial overgrowth

Occurrence: as tetrahydrofolic acid coenzyme needed for the synthesisof purine

Increased: - imbalance of bacterial species in the intestinal flora- pancreatic insufficiency

Decreased: - disturbance of the absorptive performance in the jejunum (malabsorption)

- inhibition of microbial folic acid synthesis by sulfonamides

Indication: gastrointestinal diseases

Occurrence: breakdown of propionic acid, resynthesis of methionine

Decreased: - disturbed intestinal absorption- reduced cobalt supply

VViittaammiinn BB1122 (Cobalamin) 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

FFoolliicc AAcciidd 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

77..11 GGaassttrrooiinntteessttiinnaall DDiisseeaasseess

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�� HHeelliiccoobbaacctteerr GGeenneerraall IInnffoorrmmaattiioonn

The pathogenicity of helicobacter infection in animals is difficult to evaluate and the avail-able data is often contradictory. Helicobacter spp. can be isolated from the gastric mucosain dogs and cats with gastritis, chronic vomiting or enteritis. But it can also be isolated inhealthy animals. The prevalence might therefore reach 90-100%. Apart from H. pylori, the following helicobacter species can be found in dogs and cats: H. heilmanni,H. felis, H. canis or H. mustelae. Genome sequencing is the only way to differentiatebetween these. It is being disputed whether pets play a role in the infection of humans.

Symptoms: bearing in mind the above mentioned uncertainties,helicobacter positive animals may show the following symptoms:

- vomiting- diarrhoea- gastric ulcer- gastric carcinoma

See → 15 Moleculargenetical Tests

Please note: To avoid false positive results do not feed meat for threedays prior to sample collection.

OOccccuulltt BBlloooodd FFaaeecceess

HHeelliiccoobbaacctteerr (PCR)

77..11 GGaassttrrooiinntteessttiinnaall DDiisseeaasseess

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�� PPaarrvvoovviirruuss//PPaannlleeuukkooppeenniiaa GGeenneerraall IInnffoorrmmaattiioonn

The pathogens causing canine parvovirus enteritis (CPV) and feline parvovirus enteritis(FPV) are very closely related. New strains of CPV are even able to cause disease in cats.Transmission takes place via the oronasal route after direct contact with faeces orcontaminated objects. The progression of the disease may be clinically inapparent, to peracute, depending on theage and immune status of the animal. Virus replication takes place in all tissues that havea high mitotic rate, especially intestinal mucosa, bone marrow, lymphatic system andmyocardium, additionally in cats in the retina and cerebellum.

Symptoms: puppies/kittens often show the following symptoms:

- pyrexia/hypothermia- anorexia, lethargy- vomiting, diarrhoea (haemorrhagic)- dehydration- leukopenia- dyspnoea, cardiac symptoms- abortion, mummification, cerebellar hypoplasia (cats)

A haemagglutination inhibition test is used to demonstrateparvovirus antibodies in ddooggss and ccaattss 4-6 days after infection. A differentiation between vaccination titer andinfection titer is not possible.A rise in the titer within 10-14 days is proof of parvovirusinfection. If acute infection is suspected, direct virus detection in the faeces is recommended.

In ddooggss and ccaattss, direct detection of parvovirus antigen is possible from a small faecal sample or a rectal swab, usingimmunochromatography. Excretion of the antigen starts 3-4days post infection and lasts approximately 7-10 days, in singlecases much longer. Certain vaccines will lead to excretion ofvirus approx. 3-12 days post vaccination. It is not possible todifferentiate between vaccination virus and field virus.

A negative result in the direct detection does not rule outinfection!

PPaarrvvoovviirruuss DDiirreecctt DDeetteeccttiioonn FFaaeecceess,, RReeccttaall sswwaabb

PPaarrvvoovviirruuss AAnnttiibbooddiieess 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

77..11 GGaassttrrooiinntteessttiinnaall DDiisseeaasseess

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See → 15 Moleculargenetical Tests

�� RRoottaavviirruuss GGeenneerraall IInnffoorrmmaattiioonn

Rotaviruses are found in almost all animal species. The virus has a high affinity to the smallintestinal epithelium. Virus replication leads to massive destruction of the epithelium of thevilli resulting in malabsorption and hypersecretion. This leads to severe diarrhoeaespecially in young animals. The infectious route is oral. Older animals are usually thereservoir for the infection.

Symptoms: clinical symptoms after an incubation period of 1-2 days:

- watery diarrhoea- vomiting- dehydration

The excretion of virus in the faeces lasts approximately 3-10 days. The ELISA test demonstrates a surface antigen. It can be performed in all animal species.

Detection and classification of virus passed with the faeces using an electron microscope.

VViirroollooggiiccaall FFaaeeccaall EExxaammiinnaattiioonn

00..55 -- 11 SSAA ffaaeeccaall ttuubbee

RRoottaavviirruuss AAnnttiiggeenn 11 gg FFaaeecceess

PPaarrvvoovviirruuss PPCCRR FFaaeecceess,, RReeccttaall sswwaabb

77..11 GGaassttrrooiinntteessttiinnaall DDiisseeaasseess

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Bilirubin, ALT (GPT), AP, GGT, GLDH, AST (GOT), bile acids, albumin

�� IInnffeeccttiioouuss CCaanniinnee HHeeppaattiittiiss GGeenneerraall IInnffoorrmmaattiioonn

Infectious Canine Hepatitis (ICH)/Hepatitis contagiosa canis (HCC) in the dog is caused bythe Canine adenovirus I (CAV I). It is closely related to CAV II, which plays a role in kennelcough infection. The virus is shed with any secretion and excretion (e.g. for up to sixmonths in the urine).

Symptoms: after an incubation period of 2-7 days the clinical symptoms vary according to the severity of the cell destruction by the virus:

- pyrexia- anorexia, lethargy- tonsillitis, pharyngitis- hepatomegaly- oedema, ascites- haemorrhagic diathesis- corneal opacity, uveitis

The detection of adenovirus antibodies in the dog isperformed using CFT. The test can be performed at the earli-est 10-14 days after infection. The differentiation betweenCAV I and CAV II antibodies as well as between an infectiontiter and a vaccination titer is not possible. A rise of the titerwithin 10-14 days can substantiate infection.

AAddeennoovviirruuss AAnnttiibbooddiieess(dog)

00..55 mmll SSeerruumm

LLiivveerr PPrrooffiillee 11 mmll SSeerruumm

77..22 LLiivveerr DDiisseeaasseess

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�� LLeeppttoossppiirroossiiss GGeenneerraall IInnffoorrmmaattiioonn

Leptospirosis is caused by the following leptospira serotypes: Leptospira australis(bratislava), L. autumnalis, L. canicola, L. copenhageni (icterohaemorrhagiae), L. grippotyphosa, L. saxkoebing, L. sejroe and L. tarassovi.Transmission occurs by direct contact with shedders (urine) or indirectly via contaminatedwater. The organism is spread haematogenously, especially into the liver and kidneys.

Symptoms (incubation period: 4-12 days): - pyrexia

- anorexia, vomiting, enteritis- polydipsia, polyuria- haemolysis, jaundice- haemorrhagic diathesis- chronic liver and kidney disease- uveitis, retinitis

Please note: Leptospirosis is a zoonosis!

The detection of leptospira antibodies using microagglutina-tion reaction (MAR) is the method of choice to prove a sus-pected infection. The test should be performed at theearliest 14 days after infection.

In dogs eigth different serotypes are tested. In horses only L. grippotyphosa, L. copenhageni (icterohaemorrhagiae), L. pomona, L. australis and L. autumnalis are tested. A limited differentiation between an infection titer and avaccination titer is possible (titer level). Only L. canicola andL. copenhagni (icterohaemorrhagiae) are used in vaccines,but cross reactions with other serotypes are possible.

See → 15 Moleculargenetical Tests

LLeeppttoossppiirraa (PCR)

LLeeppttoossppiirraa AAnnttiibbooddiieess 11 mmll SSeerruumm

77..22 LLiivveerr DDiisseeaasseess

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Includes: TLI, folic acid, vitamin B12

See → 7.1 Gastrointestinal Diseases

See → 7.1 Gastrointestinal Diseases

DDiiaarrrrhhooeeaa PPrrooffiillee EE (dog only)

mmiinniimmuumm 11 ffuullll SSAA ffaaeeccaall ttuubbee

DDiiaarrrrhhooeeaa PPrrooffiillee BB(dog/cat)

22 mmll SSeerruumm ((ddoogg))33 mmll SSeerruumm ((ccaatt))

77..22 LLiivveerr DDiisseeaasseess

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Canine faecal elastase-1 is produced in the pancreas andreleased along with the pancreatic juices into the intestinesduring digestion. It is stable in the intestines and can bedetected unaltered in a faecal sample for some period oftime. To rule out EPI it is usually sufficient to test once forelastase, but borderline results should be re-tested orverified using TLI testing from blood.

Species: dog only

Indication: suspected pancreatic insufficiency

Please note: Enzyme substitution does not have to be discontinuedbefore testing as this does not affect the results. Thedilution effect of liquid faeces may lead to false low values.

Undigested nutritional components are detected in thefaeces: fatty acid crystals, neutral fat, muscle fibers andstarch

Species: only useful in carnivores and omnivores

Indication: suspected maldigestion e.g. due to exocrine pancreaticinsufficiency

Influencing factors: - the faecal digestion test is dependent on the composition of the diet, e.g. if the animal is fed raw meat fatty acid crystals and muscle fibers may be found

- accelerated intestinal passage (diarrhoea) will lead to poor utilisation of the food

FFaaeeccaall DDiiggeessttiioonn TTeesstt 33 gg FFaaeecceess

EEllaassttaassee (dog only) 33 gg FFaaeecceess

77..33 EExxooccrriinnee PPaannccrreeaattiicc DDiisseeaasseess

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The TLI test (trypsin-like-immunoreactivity) measures thespecific pancreatic enzymes trypsin and trypsinogen in theblood. Oral substitution of pancreatic enzymes does notinfluence the test result.Inflammation of pancreatic sections or food intake beforesampling may lead to an increase in serum TLIconcentration, which can be misleading (therefore it isimportant to starve the animal before sampling!).

Please note: The exocrine pancreatic insufficiency due to blockage ofthe pancreatic ducts will not be diagnosed with the TLI test.In this case the test for faecal elastase-1 is recommended(dog only).

Indication: exocrine pancreatic insufficiency, (acute pancreatitis)

Occurrence: pancreas

Increased: - acute pancreatitis (short-term)- acute episode of chronic relapsing pancreatitis

Decreased: - exocrine pancreatic insufficiency

Test method: RIA (radio immuno assay)

See → 7.1 Gastrointestinal Diseases

See → 7.1 Gastrointestinal Diseases

VViittaammiinn BB1122 (Cobalamin) 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

FFoolliicc AAcciidd 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

TTLLII (dog/cat) 11 mmll SSeerruumm ((ddoogg)) // 22 mmll SSeerruumm ((ccaatt)),,EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

77..33 EExxooccrriinnee PPaannccrreeaattiicc DDiisseeaasseess

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Indications: Acute/chronic pancreatitis

Occurrence: The acinar cells of the exocrine pancreas secrete enzymes,one of them is lipase. Lipase is responsible for thebreakdown of triglycerides. In case of pancreatitis there isinjury or death of the acinar cells which results in leakageof lipase from these cells. The Spec cPL™ only measures thelipase from the pancreas acinar cells.

Increased: = 400 µg/l or above: very likely to be a pancreatitis201-399 µg/l: results in the grey area.

Depending on the development of clinical symptoms and the diseasea retest can be done in couple of weeks.

Please note: Animal must be starved 6-12 hours prior to sampling!

KKiiddnneeyy Urea (BUN), creatinine, total protein

LLiivveerrBile acids, AP, ALT, albumin

PPaannccrreeaassSpec cPL™, glucose

EElleeccttrroollyytteessSodium, potassium, calcium

HHaaeemmaattoollooggyy Small blood count

VVoommiittuuss PPrrooffiillee (dog) 11 mmll SSeerruumm ++ 00..55 mmll EEDDTTAA bblloooodd

SSppeecc ccPPLL™ (caninepancreas specific lipase)

00,,55 mmll -- 11,,00 mmll SSeerruumm

77..33 EExxooccrriinnee PPaannccrreeaattiicc DDiisseeaasseess

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88..11 BBlloooodd TTeessttss

Urea (BUN), creatinine, Protein/creatinine ratio in the urine is recommended as a total proteins, sodium, sensitive method to detect early stage nephropathies.potassium, calcium, Urine protein electrophoresis is useful for the differentiationphosphate between tubular and glomerular damage and to rule out

extra-renal proteinuria.

This test aids in the assessment of renal glomerular filtration rate. The calculation is based on the excretion rate of the exogenous marker substance - ccrreeaattiinniinnee in the serum.After blood sampling for a basal creatinine concentration, the marker substance creatinineis injected and within 3-8 hours three further blood samples are taken.

To order the marker substance and for a detailed description of the test please contactyour Regional Manager.

Just like creatinine, Cystatin C is synthesised in every nucleated cell at a constant rate and excreted almost exclusively by glomerular filtration and subsequent tubular resorption,followed by immediate complete decomposition to eliminate it from the circulation. Cystatin C can therefore be used to determine the glomerular filtration rate.

The sensitivity is specified to be 85%, whereas specificity is only 72%.

Large Blood count, creatinine, Ca, Na, K, glucosefructosamine, ALP, ALT, bile acid,albumine, proteine,

urine sediment, urin status, proteine-/creatinine-quotient, cortisol-/creatinine-quotient (dog), T4 (cat)

PPoollyyuurriiaa//PPoollyyddiippssiiaa PPrrooffiillee

11 mmll SSeerruumm ++ 00,,55 mmll EEDDTTAA bblloooodd ++ BBlloooodd SSmmeeaarr ++1100 mmll UUrriinnee

CCyyssttaattiinn CC 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

MMooddiiffiieedd EExxooggeennoouussCCrreeaattiinniinnee CClleeaarraannccee

44 xx 00..55 mmll SSeerruumm

KKiiddnneeyy PPrrooffiillee 11 mmll SSeerruumm

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88..11 BBlloooodd TTeessttss

See → 7.2 Liver Diseases, 13 Infectious Diseases

See → 15 Moleculargenetical Tests

LLeeppttoossppiirraa (PCR) 00..55 mmll EEDDTTAA--bblloooodd,, 00..55 mmll UUrriinnee,, 00,,55 mmll CCSSFF

LLeeppttoossppiirraa AAnnttiibbooddiieess 11 mmll SSeerruumm

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88..22 UUrriinnee TTeessttss

Total proteins, pH, glucose, nitrite, ketone bodies, blood, bilirubin, urobilirubin, specific gravity

Leukocytes, erythrocytes, If nitrite or bacteria are found in the sediment a epithelial cells, crystals, bacteriological examination is recommended.casts Please submit a new sterile urine sample.

Indication: nephropathies, differentiation of proteinuria

The protein/creatinine ratio correlates well with the 24 hourprotein excretion, therefore this test is used to determinethe cause of proteinuria. Its high sensitivity allows earlydetection of glomerulonephropathies. Creatinine is used asreference only.

Increased: - renal proteinuria, post renal proteinuria- severe increase: glomerulonephritis, renal amyloidosis- mild increase: interstitial nephritis, chronic nephropathies

Artefact: pyuria, haematuria

PPrrootteeiinn//CCrreeaattiinniinnee RRaattiioo 11 mmll UUrriinnee

UUrriinnee SSeeddiimmeenntt 55 mmll UUrriinnee

UUrriinnee AAnnaallyyssiiss 55 mmll UUrriinnee

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88..22 UUrriinnee TTeessttss

Indication: further differentiation of proteinuria

This test method is used to assess the urine protein patternas well as single protein excretion according to the molecularweight. Amount and composition of the urine proteins allowsassessment as to the localisation and the extent of renaldamage (differentiation between glomerular and tubulardamage). Post-renal proteinuria can be differentiated.

Normal: proteins > 67 000 D are held back by the basementmembrane, only a small amount is filtered by the glomerulus

proteins < 40 000 D are able to pass the basementmembrane, and is then mostly reabsorbed in the tubules

Pre-renal proteinuria: increase in llooww mmoolleeccuullaarr wweeiigghhtt proteinsdemonstration of Bence-Jones proteins, myoglobin,haemoglobin, α1-microglobulin

Glomerular proteinuria: increase in hhiigghh mmoolleeccuullaarr wweeiigghhtt proteinsGlomerular filtration: defectTubular reabsorption: intactGlomerular proteinuria occurs only once the tubular proteinreabsorption capacity is exhausteddemonstration of albumin and possibly IgG

Tubular proteinuria: increase in low molecular weight proteinsGlomerular filtration: intactTubular reabsorption: defectdemonstration of albumin, α1-microglobulin

Glomerular-tubular increase in llooww aanndd hhiigghh mmoolleeccuullaarr wweeiigghhtt proteinsproteinuria: Glomerular filtration: defect

Tubular reabsorption: defectdemonstration of IgG, albumin, α1-microglobulin

Post-renal proteinuria: increase in hhiigghh mmoolleeccuullaarr wweeiigghhtt proteins > 250 000 D (post-glomerular bleeding and lower urinary tract infections)

demonstration of IgG, albumin

UUrriinnee PPrrootteeiinnEElleeccttrroopphhoorreessiiss

55 mmll UUrriinnee

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88..22 UUrriinnee TTeessttss

Using infrared spectrometry the size, shape, appearance,and chemical structure are determined.

Aerobic culture allows detection of most pathogenic organisms.

Bacteriologic urine examination determines the type andnumber of bacteria. Additionally an inhibition test isperformed to detect the excretion of antibacterial agents.

Examination - step by step: - the sample is then cultured on selective culture media depending on the type and requirements of the pathogen

- the bacteria are also put in broth for enrichment. This allows the growth of damaged bacteria as well as growth from swabs with limited material

- aerobic culture incubation for a minimum of 48 hrs (longer if required; urine samples usually only require an incubation period of 24 hrs)

- the cultures are assessed daily and evaluated for further differentiation of pathogenic and facultatively pathogenic bacteria

BBaacctteerriioollooggyy,, AAeerroobbiicc UUrriinnee (sterile)

SSttoonnee AAnnaallyyssiiss UUrriinnaarryy ccaallccuulluuss

OOssmmoollaalliittyy 22 mmll UUrriinnee

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88..22 UUrriinnee TTeessttss

Transitional cell carcinoma (TCC) is the most frequentlyfound malignant neoplasia in the lower urinary tract in dogs.It may be isolated or multiple and later stages arecharacterised by metastasis into regional lymph nodes andother organs. The latex agglutination test detects urine pro-tein complexes associated with TCC (sensitivity 90%, speci-ficity 78%).

Please note: False positive results are possible due to- haematuria- severe proteinuria- severe glucosuria- pyuria

Sample stability: 48 hrs (if the sample will not reach the laboratory within this time, please submit the samplefrozen).

TT--CCeellll CCaarrcciinnoommaaSSccrreeeenniinngg (dog only)

11 mmll UUrriinnee

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99..11 MMuussccllee DDiisseeaasseess99..11..11 MMuussccllee DDiisseeaasseess __ IInnffeeccttiioouuss

�� NNeeoossppoorroossiissGGeenneerraall IInnffoorrmmaattiioonn

Neospora caninum is morphologically similar to Toxoplasma gondii, but serological crossreactions do not occur. Life cycle and mode of transmission are not yet known althoughexperiments with oral infection have been successful. The organism is known to occur indogs, horses and ruminants.

See → 13 Infectious Diseases

The test for Neospora caninum antibodies using an immuno-fluorescence test is the only in-vivo test that is practicablein routine diagnostics for a suspected infection. It can beperformed 14 days post infection at the earliest.

Please note: AAnnttiibbooddiieess against Neospora caninum in dogs can persist for years. A confirmative diagnosis is not possible in-vivo. Only the clinical findings in conjunction with a positive titer and the success of therapy may lead to thepresumptive diagnosis of neosporosis.

�� TTooxxooppllaassmmoossiissGGeenneerraall IInnffoorrmmaattiioonn

Toxoplasma gondii, the causative agent of toxoplasmosis, is prevalent worldwide. Only catsand related Felidae act as final hosts, while almost all warm-blooded animals, as well ashumans, may act as intermediate hosts.

Clinical disease in cats is rare and if at all, it is seen in very young or immunosuppressedanimals. Infection in cats occurs via ingestion of cyst-containing meat of intermediatehosts or via feline faeces containing infective oocysts. Almost every organ will becolonized and in cats the parasite can multiply in the intestinal epithelium. Approx. 3-9days post infection with muscle cysts the excretion of oocysts starts for a limited period oftime. In case of infection with sporulated oocysts approximately 20% of cats excreteoocysts 18-35 days post infection.

Infection of other warm-blooded animals and humans occurs via ingestion of inadequatelycooked, cyst-containing meat of intermediate hosts or via contact with infective oocystsoriginating from feline faeces. A short parasitaemia is observed as in cats and the parasitethen colonizes in all organs, with development of tissue cysts, but there is no enteral multiplication and no excretion.

See → 13 Infectious Diseases

NNeeoossppoorraa ccaanniinnuummAAnnttiibbooddiieess (IFT)

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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99..11..11 MMuussccllee DDiisseeaasseess __ IInnffeeccttiioouuss

The direct detection of toxoplasma oocysts in faeces usingthe flotation method is only useful in cats (as no otherspecies will excrete oocysts). Oocysts are ususally onlyexcreted in acute first infections, and re-infections do notnormally lead to excretion. The excretion may beintermittent, therefore re-testing may be necessary.

Please note: Collect several small samples from different places in thefaeces. It is advisable to submit a pooled sample from 3 con-secutive days.

A negative result does not rule out infection!

See → 13 Infectious Diseases

See → 17 Moleculargentical Tests

TTooxxooppllaassmmaa (PCR) AAssppiirraattee,, CCeerreebbrroossppiinnaall fflluuiidd,, MMuussccllee bbiiooppssiieess

TTooxxooppllaassmmaa AAnnttiibbooddiieess

TTooxxooppllaassmmaa DDiirreeccttDDeetteeccttiioonn

mmiinniimmuumm 00..55 SSAA ffaaeeccaall ttuubbee

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99..11..22 MMuussccllee DDiisseeaasseess __ NNoonn iinnffeeccttiioouuss

CK, LDH, AST (GOT), calcium

Please note: The sample material must not be haemolysed!

Indication: checking equine fitness state, myopathies

Occurrence: lactate is produced in the tissues (muscle) during anaerobicglucose metabolism. It is also increasingly produced byintestinal bacteria when feeding carbohydrate-rich diets

Increased: - increased anaerobic glycolysis- disturbed hepatic lactate metabolism

(e.g. due to shock) burns- leukosis- in newborns in the first 24 hrs- hard physical exercise- intestinal torsion, intestinal strangulation, intestinal

rupture (horse)- postoperatively

Artefact: whole blood

Please note: NaF blood should be used otherwise false high values arepossible.

Indication: myopathies, placental retention, fertility problems, Yellow Fat Disease (horse, cat)

Significance: antioxidant

Decreased: - low concentration in diet (poor storage conditions or spoilage)

- high concentration of unsaturated fatty acids- vitamin A and carotene deficiency- increased requirement (high performance, stress,

hepatopathy)- selenium deficiency

VViittaammiinn EE (Tocopherol) 22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

LLaaccttaattee 11 mmll NNaaFF bblloooodd,, ((00..22 mmll SSeerruumm))

MMuussccllee PPrrooffiillee 11 mmll SSeerruumm

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99..11..22 MMuussccllee DDiisseeaasseess __ NNoonn iinnffeeccttiioouuss

Indication: selenium imbalance, wasting, embryonic death, reducedperformance, fertility problems, increased susceptibility toillness, decreased immune response

Occurrence: antioxidants, metabolic function in prostaglandin synthesis,steroid and cholesterol metabolism

Decreased: - nutritional- increased requirement (growth, stress,

high milk production)- vitamin E deficiency- selenium antagonists (zinc, sulphur)

�� MMyyaasstthheenniiaa ggrraavviiss

Myasthenia gravis is due to a disturbance in the transmission of nervous signals at theneuromuscular end-plate, triggered by a reduction of acetylcholine receptors. Twodifferent types are found in dogs and cats:

1. Congenital type Lack of acetylcholine receptors. This type is mostly found inJack Russell Terriers, Fox Terriers, Springer Spaniels andSiamese cats. Symptoms often show as early as 6-8 weeksof age.

2. Acquired type Production of autoantibodies against acetylcholinereceptors. Breeds most frequently affected are German ShepherdDogs, Labrador and Golden Retrievers, Akita Inu Dogs, andAbyssinian and Somali cats. Onset of disease is often seenat the age of 2-3 years or 7-9 years. The cause for theproduction of autoantibodies is not yet known. Concurrentpresence of Myasthenia with neoplasias, esp. thymomas,has been described.

Diagnosis: Acetylcholine Receptor Antibodies

See → 14 Immunology

SSeelleenniiuumm 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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99..11..22 MMuussccllee DDiisseeaasseess __ NNoonn iinnffeeccttiioouuss

Should you require a higher sensitivity, there is the option toforward your sample to the University of San Diego, Califor-nia, USA. Please note this request clearly on the submissionform and allow for more time until you receive a result.Please also note that there is a considerably higher chargefor this test (depending on the exchange rate).

The autoantibody level in the congenital form of the diseaseis usually very low or not existent. In this case or in problemcases, it is recommended to perform the Tensilon® or Mestinon® (Pyridostigmine) test (i.e. diagnostic treatment ofMyasthenia gravis). Tensilon® or Mestinon®. The test is positive when there is immediate improvement in the clinicalsymptoms.

See → 15 Moleculargenetical Tests

HHYYPPPP 11 mmll EEDDTTAA bblloooodd

AAcceettyyllcchhoolliinnee RReecceeppttoorrAAnnttiibbooddiieess

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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99..22 SSkkeelleettaall DDiisseeaasseess

Indication: osteopathies

Occurrence: produced from 7-dihydro-cholesterol in the skin or absorbedfrom diet in the small intestine. Hydroxylation in the liver,forming 25-hydroxy-cholecalciferol, which is thentransformed to 1.25-dihydroxy-cholecalciferol in the kidneys

Decreased: - hepatopathies- nephropathies- phosphate over-supplementation- rapid growth- lack of UV exposure- chronic diarrhoea

Increased: - iatrogenic (application of 10 times the required dosage)- nutritional

See → Vitamin D3 (1.25-di-OH)

VViittaammiinn DD33 (25-OH) 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

VViittaammiinn DD33 (1.25-di-OH) 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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99..22 SSkkeelleettaall DDiisseeaasseess

�� BBoorrrreelliioossiissGGeenneerraall IInnffoorrmmaattiioonn

Six different genotypes of Borrelia are found in Europe (B. burgdorferi sensu stricto, B.afzelii, B. garinii, B. lusitaniae, B. valaisiana and B. bissettii), which constitute the group ofB. burgdorferi sensu lato. The pathogenicity in animals is still uncertain for most of theseserotypes. The organism is primarily transmitted by ticks of the genus Ixodes ricinus, andeffectively wherever the tick is prevalent, Borrelia is also found. Apart from humans, dogsare also susceptible to infection and may show clinical symptoms. Other animal speciesappear to be much less susceptible. Infections in horses have been described, but therelation to clinical symptoms is still being discussed.

See → 13 Infectious Diseases

See → 13 Infectious Diseases

See → 13 Infectious Diseases

BBoorrrreelliiaa AAnnttiibbooddiieess(Immunoblot)

00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

BBoorrrreelliiaa AAnnttiibbooddiieessIIggGG aanndd IIggMM (ELISA)

00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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99..33 JJooiinntt DDiisseeaasseess99..33..11 JJooiinntt DDiisseeaasseess __ IInnffeeccttiioouuss

See → 13 Infectious Diseases

See → 13 Infectious Diseases

See → 15 Moleculargenetical Tests

Cell count, total protein

profile I + cytology

profile II + bacteriology (aerobe + anaerobe)

See → 3.2 Special Screening Profiles.

SSyynnoovviiaall fflluuiidd pprrooffiillee IIIIII

SSyynnoovviiaall fflluuiidd pprrooffiillee IIII

SSyynnoovviiaall fflluuiidd pprrooffiillee II

BBoorrrreelliiaa (PCR)

BBoorrrreelliiaa CC66 AAnnttiibbooddiieessqquuaannttiittaattiivvee (ELISA)QQuuaanntt CC66™

00..55 mmll SSeerruumm

(dogs only)

BBoorrrreelliiaa CC66 AAnnttiibbooddiieessqquuaalliittaattiivvee (ELISA)

00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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99..33..11 JJooiinntt DDiisseeaasseess __ IInnffeeccttiioouuss

�� RRhheeuummaattooiidd PPoollyyaarrtthhrriittiissGGeenneerraall IInnffoorrmmaattiioonn

Rheumatoid polyarthritis is included amongst the immunoreactive polyarthritides. Immunemediated arthritic diseases are the most commonly found inflammatory joint diseases insmall animal practice. They all have in common that several joints are affected (minimum2-6) and that generalised symptoms are present. Rheumatoid arthritis is characterised by erosive damage to the joints. It commonly affectsdogs around the age of 5-6 years, mostly dwarf and toy breed dogs. The disease is causedby the production of abnormal antibodies against endogenous immunoglobulins, which arethen deposited in the joints.

See → 14 Immunology

The detection of circulating autoantibodies using theWaaler-Rose test is the method of choice in human medicineto diagnose rheumatoid arthritis. The method is based onthe ability of the antibodies to agglutinate in vitro sensitisederythrocytes. In fact the detection of rheumatoid arthritisfactors in veterinary medicine is characteristic but not specific, since they also occur in other diseases such asSLE, dirofilariasis, leishmaniasis, pyometra, etc. Therefore a positive result must always be interpreted in conjunctionwith the clinical symptoms, radiographic changes and ifpossible synovial fluid examination. With a sensitivity below90% false negative results are also possible. The blood sampleshould be taken during an acute phase of the disease.

RRhheeuummaattooiidd AArrtthhrriittiissFFaaccttoorr (Waaler-Rose test)

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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99..33..22 JJooiinntt DDiisseeaasseess __ NNoonn iinnffeeccttiioouuss

�� SSyysstteemmiicc LLuuppuuss EErryytthheemmaattoossuuss ((SSLLEE))GGeenneerraall IInnffoorrmmaattiioonn

Systemic lupus erythematosus is characterised by the production of autoantibodies againstmany cell structures, mostly against nuclear material. Erythrocytes, coagulation factorsand immunoglobulins may also be affected. The disease most commonly affects GermanShepherd Dogs, Beagles, Irish Setter, Bobtails, Poodles, Shelties and Collies. Breed predis-position: Siamese and Himalya cats.

See → 14 Immunology

The test for ANA using IFT can be performed in dogs andcats. It detects IgM and IgG antibodies which allows the differentiation between acute and chronic forms, but onlyabout 70% of animals develop clear antibody levels. A positive test does only prove lupus erythematosus in conjunction with corresponding clinical symptoms. Clinically asymptomatic animals may also show antibodies,or autoantibodies may be produced in the course of other diseases. The blood sample should be collected during anacute phase of the disease.

For the diagnosis of discoid lupus and other immune-mediatedskin diseases, a test for circulating antibodies is not veryuseful. In these cases it is recommended to submit a skinbiopsy for histological examination.

AAnnttiinnuucclleeaarr AAnnttiibbooddiieess(ANA test)

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1100..11 IInnffeeccttiioouuss

�� BBoorrnnaaGGeenneerraall IInnffoorrmmaattiioonn

Borna is a disease which occurs in horses, sheep and rabbits, but may also be seen inother vertebrates and humans. It is not considered a highly contagious disease. Transmis-sion occurs presumably via nasal secretion, saliva, urine and blood. In horses the diseasehas been described in Germany and Switzerland only.

Symptoms: The disease may be acute, chronic or clinically inapparent.- incoordination, lameness- compulsive movements- reduced consciousness- nystagmus- recumbency

In endemic areas the disease prevalence is up to 30%, withup to 70% in affected stables.

Therefore antibody detection in the blood using IFT does notprove disease!

Antibody detection from cerebrospinal fluid is usually onlysuccessful in clinically affected animals.

See → 13 Infectious Diseases

See → 15 Moleculargenetical Tests

BBoorrrreelliiaa (PCR)

BBoorrrreelliiaa AAnnttiibbooddiieess(Immunoblot/ELISA/EIA)

00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

BBoorrnnaa AAnnttiibbooddiieess(IFT)

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa,,CCeerreebbrroossppiinnaall fflluuiidd

10 Central Nervous System

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1100..11 IInnffeeccttiioouuss

�� CCAAEE

See → 13 Infectious Diseases

�� CCeerreebbrroossppiinnaall fflluuiidd ((CCSSFF))

Please note that only four hours after collection cerebrospinal fluid may have deterioratedleading to changes in the test results. The preparation of a smear from sediment is recom-mended for cytological examinations (centrifuge at 1000 rpm for 20 minutes).

Cell count, total protein

Cell count, total protein, bacteriology (aerobic + anaerobic)

See → 13 Infectious Diseases

See → 15 Moleculargenetical Tests and 13 Infectious Diseases

CCHHVV II ((CCaanniinnee hheerrppeessvviirruuss II)) (PCR)

CCHHVV II ((CCaanniinnee hheerrppeessvviirruuss II)) AAnnttiibbooddiieess (NT)

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

CCSSFF PPrrooffiillee IIII aapppprrooxx.. 33 mmll CCeerreebbrroossppiinnaall fflluuiidd

CCSSFF PPrrooffiillee II aapppprrooxx.. 33 mmll CCeerreebbrroossppiinnaall fflluuiidd

CCAAEE AAnnttiibbooddiieess 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa(Caprine arthritis encephalitis)

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1100..11 IInnffeeccttiioouuss

�� EEnncceepphhaalliittoozzoooonnoossiiss//NNoosseemmaattoossiissGGeenneerraall IInnffoorrmmaattiioonn

Encephalitozoon cuniculi is an intracellular protozoal organism which infects rabbits butalso other pets and humans. The route of infection is ingestion of spores excreted via urineand faeces.

Symptoms: the infection may be inapparent, acute or chronic- torticollis (screwneck), opisthotonus- paresis and paralysis- nystagmus- polydipsia/polyuria- anorexia, lethargy

Microscopic detection of spores in urine (intermittent excretion!) or detection of antibodies in serum using carbonsuspension test (Tusche test)

See → 13 Infectious Diseases

See → 15 Moleculargenetical Tests

See → 15 Moleculargenetical Tests

See → 13 Infectious Diseases

CCoorroonnaavviirruuss FFCCooVV 11 mmll SSeerruummIFT 1

CCoorroonnaavviirruuss FFCCooVV,, FFEECCVVPCR 1

FFHHVV II (Feline herpesvirus I)(PCR)

FFHHVV (Feline herpesvirus)AAnnttiibbooddiieess (VNT)

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

EEnncceepphhaalliittoozzoooonn DDeetteeccttiioonn(carbon suspension test)

00..55 mmll SSeerruumm,, UUrriinnee

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1100..11 IInnffeeccttiioouuss

See → 13 Infectious Diseases

See → 13 Infectious Diseases

�� TTiicckkbboorrnnee eenncceepphhaalliittiissGGeenneerraall IInnffoorrmmaattiioonn

Tickborne encephalitis is caused by a flavivirus. It is transmitted by Ixodes ricinus ticks. Indomesticated animals the disease has only been described in dogs. Known endemic areasare parts of Southern Germany, but a wide prevalence must also be suspected in Austriaand Switzerland.

Symptoms: - pyrexia- convulsions- paresis, ataxia- reduced consciousness- hyperaesthesia/hyperalgesia

The complement fixation test (CFT) is useful to detectseropositive animals. In endemic areas the prevalence ofantibodies is up to 30% in dogs. In the case of a suspectedinfection the examination of cerebrospinal fluid isrecommended.

See → 15 Moleculargenetical Tests

See → 17 Parasitology: Faecal samples

TTooxxooppllaassmmaa DDiirreeccttDDeetteeccttiioonn

FFaaeecceess 11

TTiicckkbboorrnnee EEnncceepphhaalliittiiss (PCR)

TTiicckkbboorrnnee EEnncceepphhaalliittiissAAnnttiibbooddiieess

00..55 mmll SSeerruumm

NNeeoossppoorraa AAnnttiibbooddiieess 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

MMaaeeddii//VViissnnaa AAnnttiibbooddiieess 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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See → 13 Infectious Diseases

See → 15 Moleculargenetical Tests

�� HHeeppaattiicc EEnncceepphhaallooppaatthhyy SSyynnddrroommee

Indication: hepatopathies, hepatic encephalopathy

Occurrence: (toxic) metabolites of protein metabolism, synthesized in theintestine, metabolized to urea (BUN) in the liver

Increased: - portosystemic shunt- severe chronic hepatopathies (fibrosis, cirrhosis)- severe acute hepatopathies (acute hepatitis, acute

liver cell necrosis)- uraemia- primary hyperammonaemia (rare)

Please note: Blood collection in pre-cooled collection tubes - close tubeimmediately. Centrifuge to gain plasma, submit plasmafrozen! The animal must be starved for 12 hrs prior tocollection.

For test performance and interpretation

See → 5 Biochemistry

�� TThheerraappeeuuttiicc MMoonniittoorriinngg ooff AAnnttii--eeppiilleeppttiicc DDrruuggss

BBrroommiiddee 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

PPhheennoobbaarrbbiittoonnee 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

AAmmmmoonniiaa TToolleerraannccee TTeesstt 22 xx 11 mmll EEDDTTAA ppllaassmmaa ffrroozzeenn

AAmmmmoonniiaa 11 mmll EEDDTTAA ppllaassmmaa ffrroozzeenn

TTooxxooppllaassmmaa ggoonnddiiii (PCR)

TTooxxooppllaassmmaa AAnnttiibbooddiieess 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

1100..22 NNoonn iinnffeeccttiioouuss

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1111..11 AAlllleerrggiicc//IInnffeeccttiioouuss SSkkiinn DDiisseeaasseess

�� AAlllleerrggyy TTeessttiinngg

See → 14 Immunology and Allergy

�� EEccttooppaarraassiitteess

Submit skin biopsies from affected areas.

See → 17 Parasitology

Collect sufficient sample material from several differentsites within the affected area. In suspected mite infestation,skin scapings should be taken at hairless or shaved sites,deep enough to cause slight capillary bleeding.

�� LLeeiisshhmmaanniiaassiiss

See → 13 Infectious Diseases and 15 MoleculargeneticalTests

EEccttooppaarraassiitteess (scraping) SSkkiinn ssccrraappiinngg

EEccttooppaarraassiitteess (biopsy) TTiissssuuee iinn ffoorrmmaalliinn

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1111..11 AAlllleerrggiicc//IInnffeeccttiioouuss SSkkiinn DDiisseeaasseess

�� MMiiccrroobbiioollooggyy

Aerobic culture allows for the detection of most pathogenicorganisms.

Examination steps: - the sample is then cultured on selective media depending on the type and requirements of the material

- the organism is further enriched in broth. This allows for growth of partly damaged organisms or growth from a swab with low pathogen content

- the cultures undergo aerobic incubation for a minimum of 48 hrs (longer if required)

- the cultures are examined daily and evaluated for further differentiation of pathogenic and facultative pathogenic bacteria

Ear swabs: The examination of ear swabs includes aerobic bacterialculture (see above), as well as yeast culture for detection of Malassezia.

BBaacctteerriioollooggyy,, aaeerroobbiicc SSwwaabb,, ttiissssuuee,, ootthheerr

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1111..11 AAlllleerrggiicc//IInnffeeccttiioouuss SSkkiinn DDiisseeaasseess

Dermatomycoses are fungal infections that affect the super-ficial layers of the skin. The most common dermatomycoticinfections are caused by the dermatophytes Trichophytonspp. and Microsporum spp.

Sample material: - dermatophyte hyphae invade into the skin, therefore a skin scraping is the material of choice

- plucked hair may also be useful - pre-incubated dermatophyte cultures may also be

submitted for dermatophyte identification

Collecting the sample: - the sample should be taken in the transitional area between affected skin and healthy skin

- disinfection of the skin area prior to sample collection will prohibit bacterial overgrowth of the dermatophyte culture

Examination: 1. A native microscopic slide is prepared and examined immediately after receipt of the sample.

2. Cultivation on special dermatophyte medium. 3. Regular evaluation of the culture and differentiation of

fungi in the case of dermatophyte growth.

Please note: Dermatophytes grow very slowly. Plates will be incubatedfor up to four weeks.

Yeasts and moulds may participate in various diseaseprocesses, for example otitis, genital infections, mastitis andair sac infections.

Sample collection: - use a swab in transport medium which is usually submitted for bacterial culture

Examination: 1. A microscopic slide is prepared and examined immediately after receipt of the sample.

2. Incubation on special agar plates. 3. Regular evaluation of the culture and differentiation

of fungi in the case of growth of pathogenic or facultative pathogenic yeasts or moulds.

Please note: Ear swab examination always includes mycological culture.When submitting an ear swab there is therefore no need foran extra request.

YYeeaassttss aanndd MMoouullddss SSwwaabb,, ootthheerr

DDeerrmmaattoopphhyytteess SSkkiinn ssccrraappiinngg,, HHaaiirr

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1111..11 AAlllleerrggiicc//IInnffeeccttiioouuss SSkkiinn DDiisseeaasseess

�� SSaarrccoopptteess GGeenneerraall IInnffoorrmmaattiioonn

Canine mange is caused by the mange mite Sarcoptes canis. Excessive pruritus is typicalof this disease which does not or only minimally, respond to glucocorticoid administration.Initially symptoms are seen on the skin of the abdomen, sternum, lateral limbs and earsbefore becoming widespread.

In chronic cases it is often difficult if not impossible to find the mites in skin scrapings.With previous sensitisation an infection with very few mites is sufficient for the symptomsto continue. The sensitivity of skin scrapings is approx. 30-50%.

Sarcoptes antibody detection in dogs is highly specific(97%) and highly sensitive (92%).

No cross reaction occurs with house mites, storage mites,demodex mites or cheyletiella mites. The antibody test canbe performed 3-4 weeks post infection. A negative resultdoes not rule out infection since 5-10% of dogs will not pro-duce antibodies.

The antibody titer persists over a long period of time; there-fore antibody testing has limited use as a means oftherapeutic assessment.

Please also note our examination → 17 Ectoparasites in skinbiopsies

SSaarrccoopptteess AAnnttiibbooddiieess(ELISA)

00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1111..22 NNoonn iinnffeeccttiioouuss SSkkiinn DDiisseeaasseess

See → 14.1 Immunology, Autoimmune Diseases

See → 12 Endocrinology

Indication: alopecia, disturbed keratinisation

See → 5 Biochemistry

See → 5 Biochemistry

ZZiinncc 22 mmll SSeerruumm,, HHaaiirr

VViittaammiinn HH (Biotin) 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

TThhaalllliiuumm 22 mmll SSeerruumm,, 55 mmll UUrriinnee,, HHaaiirr

EEnnddooccrriinnee SSkkiinn DDiisseeaasseess

AAnnttiinnuucclleeaarr AAnnttiibbooddiieess 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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�� HHiissttoollooggiiccaall SSkkiinn EExxaammiinnaattiioonnss

Skin Profile 1 - 7 See → 3.2 Special Screening Profiles

1111..33 HHiissttoollooggiiccaall SSkkiinn EExxaammiinnaattiioonnss

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1122..11 AAddrreennaall GGllaanndd1122..11..11 AAddrreennaall GGllaanndd __ HHyyppeerraaddrreennooccoorrttiicciissmm

�� HHyyppeerraaddrreennooccoorrttiicciissmm ((CCuusshhiinngg’’ss SSyynnddrroommee))GGeenneerraall IInnffoorrmmaattiioonn

Cushing’s syndrome is one of the most common endocrine diseases in dogs, whereas it is rare in cats. In horses hypophyseal adenomas are increasingly being diagnosed. The disease usually affects older animals (> 6 years). There is no obvious gender predisposition. The disease is classified according to the aetiology:

A. PPiittuuiittaarryy ddeeppeennddeenntt hhyyppeerraaddrreennooccoorrttiicciissmm ((PPDDHH))::A hypophyseal disturbance with chronically increased ACTH secretion leads to bilateral adrenal hyperplasia and subsequently increased cortisol secretion. This form accounts for 80-85% of all Cushing cases in dogs.

B. FFuunnccttiioonnaall aaddrreennooccoorrttiiccaall ttuummoouurr ((FFAATT))::In approx. 15-20% of the cases the increased cortisol production is due to the presence of an adrenal adenoma or adenocarcinoma.

C. IIaattrrooggeenniicc CCuusshhiinngg’’ss ssyynnddrroommee::Administration of exogenous glucocorticoids over an extended period of time can lead to the characteristic clinical symptoms.

Various non specific parameters as well as endocrinological function tests may be used todiagnose Cushing’s syndrome.

The determination of a single cortisol value is not useful fordiagnosing Cushing’s disease because of the episodicsecretion of cortisol in dogs, and it is extremely stress-dependant in cats. In horses, resting cortisol levels are notor very slightly elevated, but the circadian rhythm is lost.

CCoorrttiissooll 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa,, UUrriinnee

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1122..11..11 AAddrreennaall GGllaanndd __ HHyyppeerraaddrreennooccoorrttiicciissmm

Test principle: Animals with Cushing’s syndrome show an elevated serumcortisol level and elevated cortisol excretion. Creatinine isused as reference value only, since the cortisol level mayalso be elevated in a metabolic state that is not pathological.The test is highly sensitive (95-99%) and therefore suitablefor ruling out Cushing’s syndrome. On the other hand it has alow specificity (pathological levels may be found in diabetesmellitus, diabetes insipidus, pyometra, hypercalcaemia,renal disease, liver disease, etc). Pathological results shouldtherefore be confirmed with further function tests (e.g. dex-amethasone low dose test). The urine should always be col-lected in a stress-free environment (preferably at home andnot in the practice).

Test procedure: aa.. CCuusshhiinngg’’ss ddiiaaggnnoossiiss- day 1: collection of morning urine = first sample

bb.. DDiiffffeerreennttiiaattiioonn FFAATT//PPDDHH- day 2: collection of morning urine = second sample

Administration of dexamethasone 3 x 0.1 mg/kg body weight p.o. every 8 hrs

- day 3: collection of morning urine = third sample

Interpretation - cortisol/creatinine ratio 4 -10 x 106: normal(one determination): - cortisol/creatinine ratio 11 -16 x 106: borderline

- cortisol/creatinine ratio > 16 x 106: suspicious of Cushing’s syndrome

Interpretation - take the mean value of the ratios of days 1 and 2 (three determinations): (interpretation: see above)

- the ratio of day 3 is used to differentiate between FAT and PDH:

cortisol/creatinine ratio < 50% of the mean value of the ratios of days 1 and 2: PDH

cortisol/creatinine ratio > 50% of the mean value of the ratios of days 1 and 2: PDH or FAT

CCoorrttiissooll//CCrreeaattiinniinnee RRaattiioo 11 ddeetteerrmmiinnaattiioonn:: 11 xx 33 mmll UUrriinnee22 ddeetteerrmmiinnaattiioonnss:: 22 xx 33 mmll UUrriinnee33 ddeetteerrmmiinnaattiioonnss:: 33 xx 33 mmll UUrriinnee

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1122..11..11 AAddrreennaall GGllaanndd __ HHyyppeerraaddrreennooccoorrttiicciissmm

Test principle: This test allows evaluation of the secretory capacity of theadrenal cortex. The ACTH stimulation test is the method ofchoice for the diagnosis of iatrogenic Cushing’s syndrome.

Test procedure: 1. First blood sample = basal cortisol level2. Injection of ACTH (e.g. Synacthen®) i.v/i.m.

(cat 0.125 mg; dog 0.25 mg)(0.125 mg/animal = 12.5 IU; 0.25 mg/animal = 25 IU)

3. Second blood sample 1 hour post injection = stimulation level

Interpretation (dog): - basal level < 0.5-2 µg/dl or 13.8-55.2 nmol/land stimulation level < 0.5-2 µg/dl or 13.8-55.2 nmol/l: iatrogenic

Cushing’s syndrome or suspectedAddison’s disease

AACCTTHH SSttiimmuullaattiioonn TTeesstt 22 xx 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1122..11..11 AAddrreennaall GGllaanndd __ HHyyppeerraaddrreennooccoorrttiicciissmm

�� TTeesstt ttoo ddiiffffeerreennttiiaattee bbeettwweeeenn PPDDHH aanndd FFAATT

It is essential to submit the sample frozen. Please contactyour Regional Manager or the laboratory before sending asample.

Test principle: The determination of ACTH is used to differentiate betweenadrenal and pituitary dependant Cushing’s syndrome.Adrenocortical tumours will cause a suppression of ACTHsecretion due to the negative feedback mechanism, where-as in PDH excessive ACTH secretion is found.

Due to the irregular ACTH secretion and the influence ofstress, result interpretation can be difficult. The blood sam-ple must be taken into a pre-cooled EDTA sample tube, spunand the separated plasma must be frozen immediately.

Interpretation: - ACTH level 35-60 pg/ml: normal- ACTH level < 10 pg/ml: suspected FAT or Addison’s Disease- ACTH level > 45 pg/ml: in 85-90% of the dogs with PDH- ACTH level > 100 pg/ml: in 35% of the dogs with PDH

Please note: The sample must be submitted frozen!

AACCTTHH 00..55 mmll EEDDTTAA ppllaassmmaa ffrroozzeenn

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1122..11..11 AAddrreennaall GGllaanndd __ HHyyppeerraaddrreennooccoorrttiicciissmm

�� FFuunnccttiioonn tteesstt ttoo ddiiffffeerreennttiiaattee bbeettwweeeenn PPDDHH aanndd FFAATT

Test principle: The test is based on the fact that in PDH the negative feed-back mechanism is not completely blocked, whereas in FATthe glucocorticoid secretion cannot be influenced. Thismeans:

- low-dose administration of dexamethasone (0.01 mg/kg) leads to no, or only a mild decrease, in the cortisol level in both PDH and FAT.

- high-dose administration of dexamethasone (0.1 mg/kg) leads, in most cases, to a significant suppression of the cortisol level in PDH, but to no or only a mild suppression in FAT.

Please note: Approx. 15-20% of the animals with PDH do not react with asignificant suppression of cortisol levels, even in the high-dose test.

Test procedure: 1. First blood sample = basal cortisol level2. Injection of dexamethasone 0.1 mg/kg i.v.3. Second blood sample 8 hours after injection of

dexamethasone = suppression level (an additional samplemay be taken 4 hours post injection)

Interpretation: Suppression level < 50% of the basal levelor < 1.5 µg/dl or < 40 nmol/l: PDHSuppression level > 50% of the basal levelor > 1.5 µg/dl or > 40 nmol/l: FAT

DDeexxaammeetthhaassoonnee HHiigghh--ddoossee TTeesstt (HDDS)

22 ccoorrttiissooll vvaalluueess:: 22 xx 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1122..11..11 AAddrreennaall GGllaanndd __ HHyyppeerraaddrreennooccoorrttiicciissmm

�� FFuunnccttiioonn tteesstt ttoo ddiiaaggnnoossee hhyyppeerraaddrreennooccoorrttiicciissmm

Test principle: ACTH from the pituitary gland, controlled by thehypothalamus, stimulates the adrenal cortex to produce cortisol. The rising cortisol level leads to a reduced ACTHsecretion via a negative feedback mechanism. This alsohappens when dexamethasone is administered exogenously.

Normal result: After approx. 2-3 hours ACTH secretion is suppressed due tothe negative feedback mechanism. The suppression lasts forapprox. 24-48 hours. The adrenal cortex produces less cortisol, the cortisol level drops.

Functional adrenocortical Tumours of the adrenal cortex produce cortisol autonomously.tumour (FAT) Dexamethasone suppresses the ACTH secretion, but does not

lead to a suppression of the cortisol secretion. The cortisol level drops only mildly or not at all.

Pituitary dependant The pituitary gland in sick animals will show little or no hyperadrenocorticism (PDH) response to dexamethasone. The ACTH secretion will not be

suppressed at all or only for a short period of time, then it resumes and therefore the cortisol secretion in the adrenal cortex is stimulated. The cortisol level drops not at all, only very little, or only for a short period of time.

The sensitivity of the test is 80-96%, the specificity is 60-90%.

Test procedure (dog, cat): 1. First blood sample = basal cortisol level2. Injection of dexamethasone dog: 0.01 mg/kg i.v. / cat: 0,1 mg/kg i.v.3. Second blood sample 8 hrs post injection = suppression

level (an additional blood sample may be taken 4 hrs post injection)

Test procedure (horse): 1. First blood sample (approx. 5 pm) = basal cortisol level2. Injection of dexamethasone 40 µg/kg i.m.3. Second blood sample approx. 19 hours post

injection = suppression level (an extra blood sample may be taken 15 hours post injection)

DDeexxaammeetthhaassoonnee LLooww--ddoossee TTeesstt (LDDS)

22 ccoorrttiissooll vvaalluueess:: 22 xx 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

33 ccoorrttiissooll vvaalluueess:: 33 xx 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1122..11..11 AAddrreennaall GGllaanndd __ HHyyppeerraaddrreennooccoorrttiicciissmm

Interpretation (dog): - 4 hr level- and- 8 hr level < 1.0 µg/dl or 28 nmol/l: normal

- 4 hr level- and - 8 hr level > 1.4 µg/dl or 40 nmol/l: suspicious of

Cushing’s syndrome

Interpretation to differentiatePDH/FAT (dog): - 4 hr level < 1.4 µg/dl or < 40 nmol/l:

- and - 8 hr level > 1.4 µg/dl or > 40 nmol/l: suspicious of PDH

- 4 hr level < 50% above basal level- and - 8 hr level > 1.4 µg/dl or > 40 nmol/l: suspicious of PDH

- 8 hr level < 50% of basal level,> but > 1.4 µg/dl or > 40 nmol/l: suspicious of PDH

Interpretation (horse): - 15 hr level- and - 19 hr level < 0.5 µg/dl or < 14 nmol/l: normal

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1122..11..11 AAddrreennaall GGllaanndd __ HHyyppeerraaddrreennooccoorrttiicciissmm

�� NNoonn--ssppeecciiffiicc ppaarraammeetteerrss iinn CCuusshhiinngg’’ss DDiiaaggnnoossttiiccss

Various biochemical parameters, as well as changes in haematology and urine, mayindicate Cushing’s syndrome. The final diagnosis may only be made performing the functiontests mentioned above or possibly using imaging methods. The following general changesmay be found in Cushing’s syndrome:

Increased: - AP/heat stable APendogenous and exogenous glucocorticoids lead specifically to an induction of the heat stable fraction of the enzyme. Bone, liver and kidney AP on the other hand are heat unstable. The heat stable AP is determined after heating the serum to 65°C.

- GPT- triglycerides- glucose- bile acids- insulin- glucose (urine)- protein (urine)

Decreased: - urea (BUN)- T4- specific gravity (urine)

Hematology: - characteristic ‘stress leukogram’:leukocytosis, neutrophilia (without left shift), lymphopenia, eosinopenia, monocytosis, thrombocytosis

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1122..11..11 AAddrreennaall GGllaanndd __ HHyyppeerraaddrreennooccoorrttiicciissmm

�� TTrreeaattmmeenntt ooff CCuusshhiinngg’’ss SSyynnddrroommee

Adrenal tumour, adrenal - surgical tumour removalCushing’s syndrome (FAT) - initial treatment with Mitotane or Ketoconazole,

followed by surgery- treatment with o,p´DDD (mitotane)- therapy with ketoconazole- treatment with trilostane (Modrenal®, Vetoryl®)

Pituitary dependent Cushing’s - hypophysectomySyndrome (PDH) - adrenalectomy

- treatment with o,p´DDD (mitotane)- treatment with ketoconazole- treatment with trilostane (Modrenal®, Vetoryl®)- radiation therapy

EExxaammppllee ooff ttrreeaattmmeenntt pprroottooccooll uussiinngg LLyyssooddrreenn®

1. PPaarrttiiaall, drug-iinndduucceedd ddeessttrruuccttiioonn of the adrenal cortex

Initial phase: - 50 mg/kg Lysodren® per day, divided into at least 2 doses- ACTH stimulation test after 4-8 days, depending on the

clinical symptoms:Cortisol stimulation level > 4 µg/dl or > 110 nmol/l: continue daily Lysodren®

Cortisol stimulation level 2-4 µg/dl or 55–110 nmol/l: continue with maintenance dosageCortisol stimulation level < 1 µg/dl or < 27 nmol/l: discontinue treatment for 2 - 3 weeks

Maintenance phase: - 50 mg/kg (15-75 mg/kg) Lysodren® per week, divided dose to be given on 2 days

- ACTH stimulation test approx. every 3-6 months, depending on the clinical symptoms (aim for cortisol stimulation level 2-4 µg/dl or 55–110 nmol/l)

Patients with FAT may need doses as high as 100 mg/kg.

2. TToottaall, drug-induced ddeessttrruuccttiioonn of the adrenal cortex

Initial phase: - 50-75 mg/kg Lysodren® per day, divided into 3-4 doses, for 25 days

- 2 mg/kg cortisone per day, divided into 2 doses, starting on day 3 (possibly adequate dosage of prednisolone)

- 0.01 mg/kg fludrocortisone per day, starting on day 3

Maintenance phase: - generally no further medication with Lysodren® necessary- maybe maintenance dose of Lysodren® as described above

for the partial destruction of the adrenal cortex

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1122..11..11 AAddrreennaall GGllaanndd __ HHyyppeerraaddrreennooccoorrttiicciissmm

EExxaammppllee ooff ttrreeaattmmeenntt sscchheemmee uussiinngg kkeettooccoonnaazzoollee

(described to be ineffective in approx. 50% of patients)

- initially 5 mg/kg twice daily for 7 days- 10 mg/kg twice daily for 7 days- ACTH stimulation test:

Increase dosage to 15 mg/kg twice daily if the cortisol poststimulation level is > 5 µg/dl or 140 nmol/l.

EExxaammppllee ooff ttrreeaattmmeenntt sscchheemmee uussiinngg ttrriilloossttaannee ((VVeettoorryyll®,, MMooddrreennaall®))

Initial dosage: 5 kg body weight 30 mg orally once daily in the morning5-20 kg body weight 60 mg orally once daily in the morning> 20 kg body weight 120 mg orally once daily in the morning

Control: - ACTH stimulation test (4-6 hrs after trilostane administration) after 1, 3, 6 weeks, according to published references aim for cortisol stimulation level should be 1-2,5 µg/dl (= 28-69 nmol/l) or 1-4 µg/dl (= 28-110 nmol/l)

- further tests after 3, 6, 12 months, according to published references aim for cortisol stimulation level should be 1-2,5 µg/dl (= 28-69 nmol/l) or 1-4 µg/dl (= 28-110 nmol/l)

See datasheet or wwwwww..aarrnnoollddss..ccoo..uukk for more details

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1122..11..22 AAddrreennaall GGllaanndd __ HHyyppooaaddrreennooccoorrttiicciissmm

�� HHyyppooaaddrreennooccoorrttiicciissmm GGeenneerraall IInnffoorrmmaattiioonn

Hypoadrenocorticism is a relatively rare endocrine disorder. The cause can be adrenocortical(primary hypoadrenocorticism, Addison’s Disease) or a reduced secretion of ACTH or CRH(secondary hypoadrenocorticism). Primary hypoadrenocorticism usually affects both glucocorticoid and mineralocorticoid synthesis, while secondary hypoadrenocorticism usually affects glucocorticoid synthesis only. There is a gender predisposition for females(70%). In the majority of cases the affected animals are medium to large breeds and middle aged.

The most frequently found type in veterinary medicine is iatrogenic hypoadrenocorticismas a result of long term exogenous glucocorticoid administration or medication with o,p´-DDD (mitotane) in the treatment of Cushing’s syndrome.

Various non-specific changes may or may not be found in laboratory diagnostics, such asmild anaemia, azotaemia, hypercalcaemia or hypoglycaemia, whereas a change of thesodium/potassium ratio is frequently seen (only if mineralocorticoid synthesis is affected).The normal ratio is 27:1 - 40:1, whereas in hypoadrenocorticism ratios below 27:1 are often found.

Single cortisol determination is not useful as healthy animals may also show cortisol levels < 0.5 µg/dl or < 14 nmol/l.

See → above

AACCTTHH SSttiimmuullaattiioonn TTeesstt 22 xx 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1122..11..22 AAddrreennaall GGllaanndd __ HHyyppooaaddrreennooccoorrttiicciissmm

A single aldosterone determination is of little diagnostic value. Interpretation should bemade after performing an ACTH stimulation test (Follow the protocol used for cortisol leveldetermination in the diagnosis of Cushing’s syndrome. See → ACTH stimulation test).

Indications: - selective aldosterone deficiency (hyponatraemia and hyperkalaemia at normal basal cortisol level and normal cortisol levels after ACTH stimulation test respectively)

- primary hyperaldosteronism

Occurrence: Aldosterone is produced in the zona glomerulosa of theadrenal cortex. It is regulated by the renin-angiotensin-aldosterone system and the serum potassium concentration.

Increased: - increase or over stimulation respectively: primary hyperaldosteronism: overactivity of the adrenal gland, (secondary hyperaldosteronism: disturbance in aldosterone breakdown)

Decreased: - little or no stimulation: hypoaldosteronism

AAllddoosstteerroonnee 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1122..22 TThhyyrrooiidd GGllaanndd1122..22..11 TThhyyrrooiidd GGllaanndd __ IInnddiivviidduuaall PPaarraammeetteerrss

Total T4 consists of a free fraction and a protein-bound fraction, which are both exclusively produced in the thyroidgland.

Please note: Non specific decrease may be seen due to non-thyroidal ill-nesses (NTI) or due to medication.

NNTTII::Diabetes mellitus, hyperadrenocorticism,hypoadrenocorticism, renal disease, liver disease, acuteinfections, neuromuscular diseases, pyoderma,hypoproteinaemia, congestive heart failure, etc..

MMeeddiiccaattiioonn::NSAID´s, glucocorticoids, mitotane, anabolic steroids,halothane, thiopentone, methoxyflurane, furosemide, fattyacids, phenobarbitone, phenytoin, sulfonamides, etc..

T4 values in the middle or upper reference range rule outhypothyroidism with a high probability. Values in the lowerreference range or below should be verified using furthertests (FT4, TSH, TRH stimulation test).

Free T4 is not bound to transport proteins and it is thebiologically active form of total T4. The FT4 concentration isreponsible for the feedback mechanism. It may beinfluenced by external factors (see → T4).

Using the equilibrium dialysis method, T4 is separated fromserum proteins and protein-bound T4, and then determinedin the dialysate. This method has the advantage thatdiseases that cause a change in the serum protein/serumalbumin levels have less influence on the result.

FFTT44 (equilibrium dialysis) 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

FFTT44 00..33 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

TT44 00..33 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1122..22..11 TThhyyrrooiidd GGllaanndd __ IInnddiivviidduuaall PPaarraammeetteerrss

External factors influence the T3 level to an even greaterextent than they influence T4, therefore this parameter is notvery useful in the diagnosis of hypothyroidism in the dog.

A decreased T4 level leads to an increased TSH secretiondue to the missing negative feedback mechanism.

Interpretation: - T4 and FT4 decreased, TSH increased 1 primary hypothyroidism

- T4 and FT4 decreased, TSH normal 1 secondary hypothyroidism or other reason for T4/FT4 decrease (NTI, etc.)

Please note: 25% of all hypothyroid dogs show normal TSH concentration.

CCaanniinnee TTSSHH (dog only) 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

TT33 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1122..22..11 TThhyyrrooiidd GGllaanndd __ IInnddiivviidduuaall PPaarraammeetteerrss

Calculation of the FT4/Cholesterol ratio (‘K-value’) accordingto Larsson.

Hypothyroid dogs often have an increased fasting serumcholesterol level. Using the Larsson formula and includingthe FT4 value it may give an indication as to suspectedhypothyroidism. It must be noted that hypothyroidism is notalways associated with hypercholesterolaemia and thathypercholesterolaemia may also be observed for other rea-sons (food intake, liver disease etc.).

Larsson formula: K = 0.7 x FT4 (pmol/l) - serum cholesterol (mmol/l)

Conversion factors: FT4 conventional → SI: x 12.78Cholesterol conventional → SI: x 0.02

Interpretation: K = < -4 1 suspected hypothyroidismK = -4 - 1 1 borderlineK = > 1 1 normal

During the course of hypothyroidism which has developedfollowing lymphocytic thyroiditis, antibodies againstthyroglobulin will be produced among other things. Theseantibodies are not as useful in diagnosing the disease as in actually determining the aetiology. Please note that up to 15 % of healthy dogs and up to 25 % of all dogs with non-thyroidal illness may be positive for TAB. Raised TABconcentration may be an early sign of lymphocytic thyroiditisand in this case a regular check-up is recommended. As thedisease progresses and more and more of the thyroid tissueis destroyed, the autoantibody concentration may decreasedue to the lack of antigenic stimulant.

TThhyyrroogglloobbuulliinn AAnnttiibbooddiieess(TAB)

00..33 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

FFTT44//CChhoolleesstteerrooll RRaattiioo(dog only)

00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1122..22..22 TThhyyrrooiidd GGllaanndd __ HHyyppootthhyyrrooiiddiissmm ((ffuunnccttiioonn tteesstt))

�� HHyyppootthhyyrrooiiddiissmmGGeenneerraall IInnffoorrmmaattiioonn

Primary hypothyroidism is caused by lymphocytic thyroiditis, idiopathic follicular atrophy or(rarely) due to thyroid neoplasia. Secondary hypothyroidism (TSH deficiency) and tertiaryhypothyroidism (TRH deficiency) have been described but are rare. The clinical symptomsare caused by a deficiency of circulating thyroid hormones.

The disease is most commonly found in middle-aged, medium to large breed dogs. A breedpredisposition has been described for the Golden Retriever, Dobermann, Beagle,Dachshund, Irish Setter, Miniature Schnauzer, Great Dane, Boxer, Chow Chow, CockerSpaniel and Airedale Terrier.

Non specific parameters, such as increased serum cholesterol and neutral fats, as well asmild anaemia, may only give an indication of possible hypothyroidism.

This test determines the increase of serum T4 after stimula-tion. Please note: The stimulation result may be impaireddue to non-thyroidal ilnesses (NTI’s) or medication (see: T4).Also, healthy dogs may occasionally show insufficient stimulation.

Test procedure: 1. First blood sample = basal thyroxine value2. Injection of TRH (200 µg /animal) i.v. (e.g. Protirelin®)3. (Possibly sample collection after 2 hours = first

stimulation value)4. Blood sample after 4 hours = second stimulation value

Interpretation: - stimulation in the euthyroid (= normal) range (T4 stimulationvalue > 1.5 µg/dl or > 20 nmol/l) → euthyroid

- mild or no stimulation (T4 basal value and stimulation < 1.5 µg/dl or < 20 nmol/l) → hypothyroid/NTI

TTRRHH SSttiimmuullaattiioonn TTeesstt (dog)22 TT44 vvaalluueess 33 TT44 vvaalluueess

22 xx 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa33 xx 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1122..22..33 TThhyyrrooiidd GGllaanndd __ HHyyppeerrtthhyyrrooiiddiissmm ((ffuunnccttiioonn tteesstt))

�� HHyyppeerrtthhyyrrooiiddiissmmGGeenneerraall iinnffoorrmmaattiioonn

Hyperthyroidism is an endocrine disorder often seen in cats mostly caused by a thyroidadenoma. Thyroid carcinomas, on the other hand, are rarely seen in cats, but are the mostfrequent cause of this rare disease in dogs. Sometimes middle-aged, but more often olderanimals are affected. The clinical symptoms are due to an excessive amount of circulatingthyroid hormones.

Hyperthyroidism is primarily diagnosed by determining an increase in T4 concentration. In the initial phase of the disease or in mild cases T4 and FT4 concentrations may only bemildly increased or not increased at all. To confirm the diagnosis a T3 suppression test may be performed.

Test principle: In healthy cats the secretion of T4 is suppressed significantly following the administration of T3. In hyperthy-roid cats there is mild or no suppression due to an autonomic secretion of T4.

Test procedure: 1. First blood sample = basal thyroxine value2. Administration of liothyronine (e.g. Thybon®, Tertroxin®)

7 x 25 µg every 8 hrs p.o.3. Second blood sample 2 - 4 hrs after the last dose of

liothyronine = suppression value

Interpretation: - suppression > 50% of the basal value 1 euthyroid- suppression < 50% of the basal value 1 hyperthyroid

TT33 SSuupppprreessssiioonn TTeesstt (cat)22 TT44 vvaalluueess 22 xx 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1122..22..33 TThhyyrrooiidd GGllaanndd __ HHyyppootthhyyrrooiiddiissmm ((ffuunnccttiioonn tteesstt))

Test principle: This test determines the T4 increase in serum. With normalthyroid function, a TRH injection will induce an increase inTSH and ultimately in T4. In hyperthyroid animals, the TSH is suppressed due to the high T4 level, which results in mild or no increase in TSH and T4.

Please note: The stimulation may be affected by non-thyroidal illnessesor medication (see → T4).

Test procedure: 1. First blood sample = basal thyroxine value2. Injection of TRH (100 µg/animal) i.v. (e.g. Protirelin®)3. Second blood sample after 4 hours = stimulation value

Calculation of the Relative stimulation (%) stimulation: = T4 after stimulation - basal T4 value x 100

basal T4 value

Interpretation: - Stimulation > 60% of the basal value = euthyroid- Stimulation < 50% of the basal value = suspected hyperthyroid- Stimulation 50-60% of the basal value = borderline

TTRRHH SSttiimmuullaattiioonn TTeesstt22 TT44 vvaalluueess33 TT44 vvaalluueess

22 xx 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa33 xx 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1122..33 SSeexx hhoorrmmoonneess//PPrreeggnnaannccyy

Indications: - determination of the phase of the cycle- diagnosis of the abnormal cycle- diagnosis of sertoli cell tumours

Oestradiol concentration fluctuates markedly depending on the phase of the cycle (approx. 5-10 ng/l in anoestrus, up to 50-100 ng/l in pro-oestrus). Oestradiol can be used todiagnose an abnormal cycle in combination withprogesterone determination.In entire males oestradiol determination can be used todetect sertoli cell tumours.

Indications: - pregnancy diagnosis (mare 18-21 days after covering)- determination of the optimum time for mating (bitch)- diagnosis of the abnormal cycle

Pregnancy diagnosis: The test can be performed on day 18-21 after covering the mare.

Interpretation: value > 2 ng/ml indicates pregnancyvalue < 2 ng/ml does not indicate pregnancy

Optimum time for mating: In bitches the progesterone level from day 9 of heat(oestrus) onwards can be used to determine the optimumtime for mating.

Interpretation: The hormone levels in individual bitches can vary significantly!

The progesterone level during anoestrus and during most ofprooestrus is < 1.0 ng/ml. Around day 10 of prooestrus thelevel will rise to approx. 2.0 ng/ml due to preovulatory luteinisation of the ovaries. The following day the level willbe at approx. 3.0 ng/ml and on the day of ovulation the levelwill be approx. 4.0-8.0 ng/ml. The optimum time for matingwill be approx. 2-3 days after ovulation. At this time theprogesterone level will rise above 10 ng/ml.

In cases where no history is given regarding previous cyclesor pregnancies, the first determination of the progesteronelevel is recommended on day 6-8 of heat (oestrus). If thevalue is < 1.0 ng/ml then samples should be taken at 3-4 dayintervals until the level reaches 1.0-8.0 ng/ml. Depending onthe exact concentration further samples may be necessaryevery 1-3 days.

PPrrooggeesstteerroonnee 00..33 mmll SSeerruumm,, HHeeppaarriinn ppllaassmmaa

OOeessttrraaddiiooll (17 β-) 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1122..33 SSeexx hhoorrmmoonneess//PPrreeggnnaannccyy

Indications: - checking androgen levels- differentiation between neutered and cryptorchid animals

A single testosterone determination is often not significantenough to differentiate between neutered and cryptorchidanimals. To confirm the diagnosis an HCG stimulation testmay be performed.

Test procedure (dog, cat): 1. First blood sample = basal testosterone value2. Injection of 50 IU HCG/kg i.v.3. Second blood sample 1 hour post

injection = stimulation value

Test procedure (horse): 1. First blood sample = basal testosterone value2. Injection of 5,000 - 10,000 IU HCG per animal i.v.3. Second blood sample 1 hour post

injection = first stimulation value4. Possibly a third blood sample 24 hours post

injection = second stimulation value

Interpretation: - mild or no stimulation indicates there is no functioning testicular tissue.

- a marked stimulation indicates there is functioning testicular tissue.

Indications: - pregnancy diagnosis (from day 82 in mares)- proof of intact pregnancy- diagnosis of cryptorchidism (stallion)

OOeessttrroonnee SSuullpphhaattee 11 mmll SSeerruumm,, 55 mmll UUrriinnee ((eeqquuiinnee))

HHCCGG SSttiimmuullaattiioonn TTeesstt22 TTeessttoosstteerroonnee vvaalluueess33 TTeessttoosstteerroonnee vvaalluueess

22 xx 00..33 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa33 xx 00..33 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

TTeessttoosstteerroonnee 00..33 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1122..33 SSeexx hhoorrmmoonneess//PPrreeggnnaannccyy

Indication: PMSG/eCG is produced between day 40 and 120 in the endometrial cups, but the best time to test for it, is between day 45 and day 90 post ovulation. In mares, where the foetusis absorbed, the endometrial cups still produces, which can causes "false positive" results. Therefore a positive result should always be accompanied by an oestronsulfate test after the 100. day of pregnancy.

PPMMSSGG // eeCCGG22 11 mmll SSeerruumm

(pregnant mare serum gonadotropin; eCG = equines choriongonadotropin)

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1122..44 OOtthheerr hhoorrmmoonneess

Indication: Diabetes insipidus

In diabetes insipidus, ADH determination can help to differ-entiate between the central form (absolute ADH deficiency)and the renal form (reduced response of the renal tubularepithelium).

Decreased: Central diabetes insipidus

Please note: The sample must be submitted frozen!

Indications: - diabetes mellitus (additional determination of glucose and fructosamine!)

- insulinoma

Occurrence: Insulin is produced in the ß-cells of the pancreas.- Type I diabetes: absolute insulin deficiency- Type II diabetes: characterized by an insulin resistance

of the peripheral tissue. The insulin level may be normal or increased compared to Type I diabetes.

Decreased: - Type I diabetes

Increased: - insulinoma (insulin-producing tumours of the pancreatic β-cells). Repeated blood glucose levels < 60 mg/dl or < 3.3 mmol/l in conjunction with an insulin level in the upper reference range or above are indicative of insulinoma.

Please note: The sample must be submitted frozen!

IInnssuulliinn 00..55 mmll SSeerruumm ffrroozzeenn

AADDHH (Vasopressin) 11 mmll EEDDTTAA ppllaassmmaa ffrroozzeenn

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1122..44 OOtthheerr hhoorrmmoonneess

Indications: - dwarfism- acromegaly

Occurrence: IGF I (somatomedine C) is synthesized in the liver. The rateof secretion is highly dependant on the secretion of growthhormone. But unlike growth hormone, IGF I is secreted verysteadily, therefore it is much more suitable for diagnosticpurposes.

Decreased: - proportional dwarfism (congenital growth hormone deficiency)

Increased: - acromegaly

Please note: The sample must be submitted frozen!

SSoommaattoommeeddiinnee (IGF I) 00..55 mmll SSeerruumm ffrroozzeenn

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See → Infectious canine hepatitis

See → Ehrlichia phagocytophila

AAnnaappllaassmmaa (Ehrlichia)pphhaaggooccyyttoopphhiilluummAAnnttiibbooddiieess

00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

AAddeennoovviirruuss AAnnttiibbooddiieess(dog)

00..55 mmll SSeerruumm

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�� BBaabbeessiioossiiss ((ccaanniinnee))GGeenneerraall IInnffoorrmmaattiioonn

Most cases of babesiosis in dogs are caused by Babesia canis, in rare cases by B. gibsoni.The transmission in Europe takes place via Rhipicephalus spp. and Dermacentor spp. ticks.The organism is prevalent in the entire Mediterranean region, Hungary, Austria and in partsof Germany. Further spread is likely. Direct detection of the organism is possible in bloodsmears and by PCR, as well as antibody detection.

Symptoms: depending on the pathogenicity of the Babesia spp. and theimmune status of the dog, the course of the disease may beacute or chronic. Usually the characteristic symptomsdevelop after an incubation period of several days to 3 (-5)weeks.

- pyrexia (above 40°C)- anaemia, haemoglobinaemia and haemoglobinuria- jaundice, bilirubinuria- hepatomegaly, splenomegaly- DIC, consumption coagulopathy- anorexia, lethargy

�� BBaabbeessiioossiiss ((eeqquuiinnee))GGeenneerraall IInnffoorrmmaattiioonn

Babesiosis or piroplasmosis infection in horses is caused by Babesia caballi and/or Theileria equi. The infection may be peracute to chronic and the prevalence is almost thesame as for B. canis.Direct detection of the organism is also possible in the horse, but the method of choice isantibody detection. Antibody detection using CFT and IFT are currently available, and anELISA test is in preparation.

The intra-erythrocytic, pear-shaped trophozoites are foundin Giemsa stained blood smears using an opticalmicroscope. Ideally the blood smear should be made fromcapillary blood. The first parasitaemia occurs 1-2 days postinfection and lasts for approx. 4 days. The second, moreintensive parasitaemia, occurs after approx. 10-14 days. In chronic cases resting and parasitaemic stages alternate.

Direct detection is therefore not always possible!

BBaabbeessiiaa DDiirreecctt DDeetteeccttiioonn 00..55 mmll EEDDTTAA bblloooodd ++ BBlloooodd ssmmeeaarr

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See → Babesiosis (equine)

The demonstration of Babesia antibodies is possible, at the earliest, 10-14 days post infection. Therefore it is notsuitable to detect early stages of babesiosis, but chronic or latent infections.

The IFT in dogs detects B. canis antibodies. In case ofsuspicion of infection with B. gibsoni, please contact the lab or your Regional Manager before submitting a sample.

Please also refer to our special profiles:→ 3.2 Travel Disease Profile , → 17.3 Blood parasites

PCR testing is much more sensitive than direct detection ofthe organism in a blood smear using an ocular microscope.

See → 15 Moleculargenetical Tests

See → Leukosis Virus, Bovine

�� BBoorrddeerr DDiisseeaasseeGGeenneerraall IInnffoorrmmaattiioonn

The Border disease virus (BDV) is an RNA virus of the pestivirus family. It is involved inintrauterine foetal infections. Adult sheep and goats are rarely affected, but they shedlarge amounts of infectious agent. The virus is closely related to the BVD virus (bovinevirus diarrhoea) and the virus that causes European Swine Fever.

BBLLVV AAnnttiibbooddiieess 11 mmll SSeerruumm

BBaabbeessiiaa sspppp.. (PCR) 00..55 mmll EEDDTTAA bblloooodd

BBaabbeessiiaa AAnnttiibbooddiieess (IFT)(canine + equine)

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

BBaabbeessiiaa AAnnttiibbooddiieess (CFT)(equine only)

11 mmll SSeerruumm

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The main reservoir for BDV is sheep. Infection before day 60 of the pregnancy and beforethe establishment of foetal immune response leads to early abortion. Infection betweendays 50 and 70 leads to the typical clinical picture of “hairy shakers” (lambs have hairy,discoloured wool and muscle tremors at birth). Infection between day 60 and 85 leads tosevere brain and/or skeletal abnormalities. After day 85 of the pregnancy, the foetussurvives as healthy and shows high antibody titres. Adult ewes in endemic areas show astable immunity and deliver healthy lambs.

Antibody detection using a virus neutralisation test.

�� BBoorrnnaa DDiisseeaassee ((BBDD))GGeenneerraall IInnffoorrmmaattiioonn

Borna disease occurs in horses, sheep and rabbits, as well as in other vertebrates andhumans. Contagion rate is low. Transmission occurs supposedly via nasal secretion, saliva,urine and blood. In horses, the disease has been reported in Germany and Switzerland only.

Symptoms: the course of the disease may be acute to chronic, or inapparent- ataxia, lameness- compulsive movements- reduced consciousness- nystagmus- recumbency

In endemic areas the disease prevalence is up to 30%, withup to 70% in affected stables.Therefore antibody detection in the blood using IFT does notprove disease!Antibody detection from cerebrospinal fluid is usually onlysuccessful in clinically affected animals.

See → 15 Moleculargenetical Tests

BBoorrnnaa (PCR)

BBoorrnnaa AAnnttiibbooddiieess (IFT) 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa,,CCeerreebbrroossppiinnaall fflluuiidd

BBoorrddeerr DDiisseeaassee (BDV)AAnnttiibbooddiieess (sheep)

00..55 mmll SSeerruumm

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�� BBoorrrreelliioossiissGGeenneerraall IInnffoorrmmaattiioonn

In Europe, six of the eleven known genotypes of Borrelia are found (B. burgdorferi sensustricto, B. afzelii, B. garinii, B. lusitaniae, B. valaisiana and B. bissettii), which constitute thegroup of B. burgdorferi sensu lato. The pathogenicity in animals is still uncertain for most ofthese serotypes. The organism is primarily transmitted by ticks of the genus Ixodes ricinus,and effectively wherever the tick is prevalent, Borrelia is also found. Apart from humans,paticularly dogs are also susceptible to infection and may show clinical symptoms. Other ani-mal species appear to be much less susceptible. Infections in horses have been described,but the clinical significance is still being discussed.

In humans, the disease progresses in three stages. Initially a localized infection is evident,often as chronic migrating erythema. It is followed by dissemination of the infection into thebody with the expression of a variety of different clinical manifestations. The third, chronicstage is dominated by arthritis and chronic dermatitis. This pattern of symptoms is not, orrarely, found in dogs.

Symptoms (dependent on the severity of infection):- pyrexia- anorexia, lethargy- intermittent lameness, swollen joints, polyarthrititis

Further symptoms in conjunction with borreliosis are being discussed: - myocarditis- neurological disorders (paresis, convulsions)- nephritis, glomerulonephritis and renal failure in

certain canine breeds

See → 9.3.1 Joint Diseases - Infectious

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IgG antibody detection is usually the method of choice tosubstantiate suspected Borrelia infection. IgG antibodydetection is possible approx. 4-6 weeks post infection. A major part of the canine population demonstrates antibodies, therefore a positive titre does not necessarilyconfirm borreliosis.

Also, false positive results are possible due to cross-reactions with other spirochaetes and post vaccination antibody detection. Therefore confirmation of positive andborderline results using an immunoblot is recommended(two-tiered approach).High IgG titres may persist for longperiods of time, which makes this test unsuitable fortreatment control.

In humans IgM antibodies are detectable from approx. 3 weeks post infection and indicate acute disease.

In dogs IgM antibodies appear to persist even without acute disease, and re-infection does not always trigger anIgM response. An IgM titre does therefore not necessarilyindi-cate acute borreliosis.Cross-reaction can not be ruled out.

Please note: IgG antibody detection can be performed in dogs andhorses, IgM antibody detection can only be performed indogs.

The immunoblot (western blot) test is recommended in thecase of a positive or borderline result with the ELISA test.The immunoblot determines IgG antibodies.

Please note that this test does not allow for a statementregarding the titre level and is therefore designed as a con-firmatory test only.

BBoorrrreelliiaa AAnnttiibbooddiieess(Immunoblot)

00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

BBoorrrreelliiaa AAnnttiibbooddiieessIIggGG aanndd IIggMM (ELISA)

00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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The qualitative detection of Borrelia burgdorferi anti C6 anti-bodies is the latest development in testing for Borrelia infec-tion and can be used as a screening method.

The distinct advantage of this technology is its highspecificity - no cross reactivity with antibodies against otherspirochaetes or vaccine induced antibodies is described.Positive results do not need further confirmation by westernblot.

In some cases it is possible to detect anti C6 antibodies asearly as 3 weeks post infection. The bacterial load appearsto correlate with the level of anti C6 antibodies, as shortlyafter infection an increase in anti C6 antibodies isdetectable, with the levels dropping significantly after treat-ment. However, this indicates limited use of the test in ananimal recently treated with antibiotics and/orcorticosteroids.

Please note: The test is accredited for dogs only, but can also be used incats and horses.

As the bacterial load shows a good correlation with thelevel of anti C6 antibodies, this test can be used for monitor-ing successful treatment. A baseline antibody level shouldbe determined directly following a positive qualitative result.In the case that the animal shows symptoms directly relatedto lyme disease, treatment should be considered. The testshould be repeated after six months to show a significantdecrease in C6 antibody levels as an indication for success-ful therapy.

See → 15 Moleculargenetical Tests

BBoorrrreelliiaa bbuurrggddoorrffeerriisseennssuu llaattoo (PCR)

BBoorrrreelliiaa CC66 AAnnttiibbooddiieessqquuaannttiittaattiivvee (ELISA)QQuuaanntt CC66™ (dogs only)

00..55 mmll SSeerruumm

BBoorrrreelliiaa CC66 AAnnttiibbooddiieessqquuaalliittaattiivvee (ELISA)

00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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�� BBoovviinnee HHeerrppeessvviirruuss IInnffeeccttiioonn ((BBHHVV))See → Herpesvirus infection, bovine

�� BBoovviinnee VViirruuss DDiiaarrrrhhooeeaa ((BBVVDD//MMDD))GGeenneerraall IInnffoorrmmaattiioonn

BVD in cattle is caused by a togavirus. The course of the disease varies dependant on theage of the affected animal, the time of infection and the type of virus (cytopathogenic ornon-cytopathogenic).Infection of a pregnant animal with the cytopathogenic virus before day 120 postconception will usually lead to embryonic death and abortion. Infection with the non-cytopathogenic virus during the same period will lead to the development of an animal withpersistent viraemia, which does not produce any antibodies against the virus. Infectionwith either virus type after day 120 post conception will lead to the development ofimmunocompetent healthy calves. Young animals aged 3-24 months usually contract the acute enteric form of the diseasewith high mortality, whereas older animals are more likely to suffer from the chronic formof the disease. When it comes to a super-infection of persistently viraemic animals withthe cytopathogenic virus the clinical symptoms of Mucosal Disease are seen.

Symptoms: - pyrexia, lethargy, inappetence- diarrhoea- nasal and ocular discharge- mucous membrane changes- abortion

Antibody detection using an ELISA test.

Antigen detection using an ELISA test.

BBVVDD AAnnttiiggeenn (ELISA) 22 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa

BBVVDD AAnnttiibbooddiieess (ELISA) 11 mmll SSeerruumm

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BRSV is a pneumovirus (family paramyxovirus) and plays arole in Enzootic Bronchopneumonia in cattle and other ruminants. Clinically inapparent BRSV infections withpermanent or intermittent excretion are seen. Clinical signs,for example pyrexia and respiratory symptoms, become evident in cases of stress and other concurrent pathogens.Adult cattle mostly have serum antibodies which protectthem from clinical illness, but not from infection, virus multiplication and virus spread in the body. Maternalantibodies are passed on via colostrum. Calves aged 2-5months are particularly prone to infection, but occasionallyolder calves and adult cattle may develop disease.

�� BBrruucceelllloossiissGGeenneerraall IInnffoorrmmaattiioonn

There are several specifically relevant types in the genus Brucella: B. abortus (bovine brucellosis), B. melitensis (ovine and caprine brucellosis), B. suis(porcine brucellosis), B. ovis and B. canis. There is no species specificity, therefore otheranimals as well as humans can be infected. Transmission occurs via the oral or genitalroute. The main source of infection is latently infected pathogen-shedding animals.

Symptoms: - pyrexia- anorexia, lethargy- abortion in the last trimester- testicular and epididymal infections- sterility in male animals

Detection of Brucella abortus antibodies using ELISA.

BBrruucceellllaa aabboorrttuussAAnnttiibbooddiieess (ELISA)

11 mmll SSeerruumm

BBRRSSVV (Bovine Respiratory Syncytial virus)AAnnttiibbooddiieess(bovine only) 11 mmll SSeerruumm

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Serum agglutination is used for the detection of Brucella canis antibodies in dogs. Antibodies can be found from day 21 post infection.

Serum Slow Agglutination is the method used to detect Brucella suis antibodies.

�� CCaalliicciivviirruussGGeenneerraall IInnffoorrmmaattiioonn

Feline calicivirus is one of the causative agents of the feline respiratory disease complex.The infection is transmitted by direct contact with saliva or nasal secretion. The incubationperiod is 3-5 days. Depending on the immune status of the animal the infection may varyfrom clinically inapparent to acute. Animals that have survived the infection often shed thevirus for a long period of time.

Symptoms: - pyrexia- anorexia, lethargy- conjunctivitis- rhinitis- stomatitis and ulceration of the oral mucosa- bronchopneumonia- ‘rheumatoid form’ including lameness and joint swelling

The method of choice for the detection of antibodies is usually the virus neutralisation test (VNT). Antibodies maybe found from 14 days post infection. It is not possible to differentiate between antibodies produced by vaccinationand infection.

CCaalliicciivviirruuss AAnnttiibbooddiieess (VNT) 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

BBrruucceellllaa ssuuiissAAnnttiibbooddiieess (SSA)

11 mmll SSeerruumm

BBrruucceellllaa ccaanniissAAnnttiibbooddiieess (SA)

11 mmll SSeerruumm

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See → 15 Moleculargenetical Tests

�� CCaapprriinnee AArrtthhrriittiiss EEnncceepphhaalliittiiss ((CCAAEE))GGeenneerraall IInnffoorrmmaattiioonn

CAE in goats is caused by a lentivirus. The virus shows a low level of contagion. Transmis-sion occurs mainly via the milk, less frequently by direct contact.

Symptoms: most affected animals are 2-9 years old- arthritis- wasting, emaciation- mastitis- CNS symptoms

Antibodies can be detected from a few weeks up to severalyears post infection. Therefore a negative antibody testdoes not entirely rule out infection.

�� CChhllaammyyddoopphhiillaaGGeenneerraall IInnffoorrmmaattiioonn

Recent studies have lead to the term Chlamydia only being used for Chl. suis and Chl. trachomatis. The pathogens formerly named Chlamydia psittaci are now calledChlamydophila abortus (sheep), Chlamydophila caviae (guinea pigs), Chlamydophila psittaci(birds), Chlamydophila felis (cats) and Chlamydophila pneumoniae. A definite differentiationcan only be done by genome sequence analysis and is usually not clinically relevant.

Chlamydophila are obligate intracellular organisms and therefore difficult to diagnose. The normal route of infection is oronasal, and also genital (mating) in sheep.

Symptoms: the symptoms vary strongly between species andindividuals. Often the infection is latent rather than acute or chronic- sheep: abortion- cats: conjunctivitis, involved in the feline respiratory

disease complex- birds: ocular and nasal discharge, diarrhoea, weight loss

CCAAEE AAnnttiibbooddiieess (ELISA) 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

CCaalliicciivviirruuss AAnnttiiggeenn (PCR)(cat)

SSwwaabb ((ddrryy))

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The detection of Chlamydia (Chlamydophila) antibodies ispossible in all species with the exception of birds, but unfor-tunately differentiation is not possible.

See → 15 Moleculargenetical Tests

See → Herpesvirus, canine

See → 15 Moleculargenetical Tests

See → Feline Coronavirus

See → 15 Moleculargenetical Tests

CCoorroonnaavviirruuss (PCR)

CCoorroonnaavviirruuss,, FFeelliinnee

CCHHVV II (PCR)

CCHHVV II AAnnttiibbooddiieess (VNT) 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

CChhllaammyyddoopphhiillaa sspppp.. (PCR)

CChhllaammyyddoopphhiillaaAAnnttiibbooddiieess (CFT)

11 mmll SSeerruumm

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�� DDiirrooffiillaarriiaassiissGGeenneerraall IInnffoorrmmaattiioonn

Dirofilariasis in the dog and cat is mainly caused by D. immitis, rarely by D. repens.Transmission occurs via mosquitoes of the genus Culex, Anopheles, and others. Theparasite is prevalent in the entire Mediterranean region (esp. Spain, Italy) and in Hungary.

Symptoms: the symptoms vary depending on the worm burden- subclinical carrier without symptoms- chronic coughing - dyspnoea, tachypnoea- reduced performance- right heart hypertrophy- oedema, ascites- anaemia- vena cava syndrome

The detection of macrofilaria antigen using an ELISA test ispossible, at the earliest, 5-6 months post infection with Dirofilaria immitis. Infection with one or very few adultworms may lead to false negative results.

The direct detection of microfilaria is performed afterenrichment using a light-optical microscope (Knott method).It is advisable to take capillary blood in the late afternoon orevening. The earliest possible direct detection of microfilar-ia is six months post infection, the sensitivity is approx. 60%.Therefore direct detection is not always possible!

Negative results are also possible in cases of infectionswith adult worms of the same sex.

MMiiccrrooffiillaarriiaa DDiirreeccttDDeetteeccttiioonn (Knott)

11 mmll EEDDTTAA bblloooodd

MMaaccrrooffiillaarriiaa AAnnttiiggeenn(Dirofilaria immitis)

00..55 mmll SSeerruumm

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�� DDiisstteemmppeerrGGeenneerraall IInnffoorrmmaattiioonn

Canine distemper is a highly contagious, acute to subacute or chronic infectious disease.The pathogen is a morbillivirus which is found in dogs, wild Canidae, Mustelidae andraccoons. Transmission occurs via droplet infection. The virus is found in all secretionsand excretions. The incubation period is 3-7 days.

Symptoms: depending on the virus strain and the immune status of theanimal distemper can be very diverse. Many of thesymptoms are caused by secondary bacterial infections due to the immunosuppressive properties of the virus:- pyrexia- gastrointestinal symptoms (vomiting, diarrhoea)- respiratory symptoms (rhinitis, conjunctivitis, coughing,

pneumonia)- CNS symptoms (convulsions, ataxia, paresis)- characteristic changes in dentition- hard pad disease, dermatitis- old dog encephalitis

The distemper antibody test using virus neutralisation canbe performed 10-14 days post infection at the earliest.Differentiation between vaccination titre and infection titreis not possible. Acutely infected dogs usually show no orvery low antibody titres. In chronic cases the antibody titrerises slowly. In these cases it is recommended to re-testafter 14 days to prove an increasing titre. To check the vaccination status a single test is sufficient. A titre equal or above 1:100 is considered protective.

See → 15 Moleculargenetical Tests

See → Trypanosoma spp.

DDoouurriinnee

DDiisstteemmppeerrvviirruuss (PCR)

DDiisstteemmppeerrvviirruuss AAnnttiibbooddiieess (VNT)

00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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�� EEhhrrlliicchhiioossiiss

GGeenneerraall IInnffoorrmmaattiioonnEEhhrrlliicchhiiaa ccaanniiss is the causal organism of monocytic ehrlichiosis. Ehrlichia can be foundthroughout the mediterranean region and is widespread in tropical and subtropical regions.It is transmitted by the brown dog tick Rhipicephalus sanguineus in Europe and by theAmerican dog tick Dermacentor variabilis in America respectively.

AAnnaappllaassmmaa (formerly Ehrlichia) ppllaattyyss is the causative agent of cyclic thrombocytopenia.The vector is not quite clear. There are indications that it is also Rhipicephalus sanguineus.

AAnnaappllaassmmaa pphhaaggooccyyttoopphhiilluumm is the most common causative agent of canine granulocyticehrlichiosis in Europe. It is transmitted by the pasture tick Ixodes ricinus and thereforemostly occurs in the northern parts of Europe. There are cases reported in Sweden and inSwitzerland; further studies may reveal cases in other European countries.

OOtthheerr Ehrlichia species are being discussed with respect to infection in dogs, mostly in the United States, but case reports are rare. In the case of suspicion of infection withEhrlichia spp. other than those described above, please contact the lab or your RegionalManager prior to submitting a sample.

Symptoms of monocytic ehrlichiosis: the incubation period of up to three weeks is followed by

a 2-4 week period of acute illness

it is characterised by:- pyrexia (above 40°C)- anaemia- leukopenia- thrombocytopenia- hepatomegaly and splenomegaly- oedema- anorexia, lethargy

following a subclinical phase of varying length, the illnesspasses into a chronic phase

- excessive loss of weight- tendency to bleed (epistaxis, petechiae, blood in

faeces and urine)- pancytopenia- hyperalbuminaemia, hypergammaglobulinaemia- proteinuria- hyperbilirubinaemia

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The detection of Ehrlichia canis antibodies is possible 10-14days post infection at the earliest.

Please also refer to our special profiles: → 3.2 Travel Disease Profile → 4.4 Comprehensive blood parasites

Seroprevalence of approx. 20% have been described inendemic areas. A positive antibody titre does therefore not necessarily indi-cate clinical disease.

The direct detection of the organism in blood cells is onlypossible during the acute stage of the disease. A Giemsastained blood smear is prepared and examined with a light-ocular microscope. Ideally, capillary blood should be used.

A negative result does not rule out infection!

This is a more sensitive test than the direct detection in ablood smear.However a negative result does not rule out infection!

See → 15 Moleculargenetical Tests

EEhhrrlliicchhiiaa ccaanniiss (PCR) 22 mmll EEDDTTAA bblloooodd

EEhhrrlliicchhiiaa DDiirreecctt DDeetteeccttiioonn BBlloooodd ssmmeeaarr ++ EEDDTTAA bblloooodd

EEhhrrlliicchhiiaa (Anaplasma)pphhaaggooccyyttoopphhiilluummAAnnttiibbooddiieess (dog only)

00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

EEhhrrlliicchhiiaa ccaanniiss AAnnttiibbooddiieess(dog)

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Detection of Ehrlichia and Anaplasma DNA, including themain pathogens; however no differentiation betweenspecies.

Please note: A negative result does not rule out infection!

EEhhrrlliicchhiiaa//AAnnaappllaassmmaa sspppp..(PCR)

11 mmll EEDDTTAA bblloooodd

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�� EEnncceepphhaalliittoozzoooonnoossiiss//NNoosseemmaattoossiissGGeenneerraall IInnffoorrmmaattiioonn

Encephalitozoon cuniculi is a single-celled, intracellular organism, which infects rabbits aswell as other domestic animals and humans. The route of infection is ingestion of sporesthat are passed via faeces and urine.

Symptoms: Infections are often inapparent, but may be acute to chronic.- torticollis, opisthotonos- paresis, paralysis- nystagmus- polydipsia/polyuria- anorexia, lethargy

Detection of spores in urine (intermittent shedding!) or anti-bodies in serum, using IFA and a light-optical microscope.

See → Herpesvirus, Equine

See → Infectious Anaemia, Equine

See → Influenza, Equine

See → Viral Arteritis, Equine

EEqquuiinnee VViirraall AArrtteerriittiiss (EVA)

EEqquuiinnee IInnfflluueennzzaa

EEqquuiinnee IInnffeeccttiioouussAAnnaaeemmiiaa (EIA)

EEqquuiinnee HHeerrppeessvviirruuss

EEnncceepphhaalliittoozzoooonnccuunniiccuullii

00..55 mmll SSeerruumm,, UUrriinnee

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�� FFeelliinnee CCoorroonnaavviirruuss IInnffeeccttiioonn//FFIIPPGGeenneerraall IInnffoorrmmaattiioonn

Feline coronavirus (FCoV) infection is prevalent throughout the feline population. Approx.10-50% of cats in single-cat households and 80-90% of cats in catteries have antibodiesagainst FCoV. The virus is excreted via faeces. The route of infection is oronasal: directlyor indirectly. The differentiation between FCoV and the FIP-causing mutant is not possibleat present (there is a 99% genetic correspondence between the two viruses). Also the theory which postulated that the harmless coronavirus is located in the intestines and onlythe pathogenic mutant is carried off into the body can no longer be upheld. Due to the factthat every virus replication produces copy mistakes, each coronavirus may turn into apathogenic mutant. This is the reason why, apart from the individual immune status, crowding of animals is thought to be one of the most important factors in the developmentof FIP. Continuous re-infection leads to accumulation of virus in such populations and inturn the associated high virus load of the individual animal leads to an increased likelihoodof mutation. The occurrence of pathogenic mutants and the influence of immunosuppressivefactors favour massive virus replication in the macrophages and spread of the pathogeninto every organ. Antibody production is unable to eliminate the virus and subsequently the animal develops an immune complex mediated disease.

Symptoms: deposition of antigen-antibody complexes leads to vasculitis or polyserositis (exudative form) and/or togranulomatous inflammation (dry form). Many differentsymptoms are seen:- recurrent pyrexia, resistant to treatment- lethargy, anorexia- ascites, thoracic and pericardial effusion- dyspnoea- glomerulonephritis- liver damage- CNS symptoms- uveitis

The diagnosis of FIP is problematic and is not 100% reliable in the living animal. Only the combination of different diagnostic methods may increase the probability of the diagnosis ‘FIP’.

The high prevalence of FCoV in the feline population makesit difficult to judge the disease using antibody detection.

FFCCooVV AAnnttiibbooddiieess (FIP Antibodies)

11 mmll SSeerruumm

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A positive titre merely indicates that the animal has beenexposed to coronavirus. Sero-conversion in cats may evenbe seen in infection with canine coronavirus or, in singlecases, after FIP vaccination. Therefore the detection of antibodies is not sufficient to diagnose FIP in an animal with clinical symptoms. In these cases we recommend aScreening Profile which frequently demonstrates hyperproteinaemia, hypergammaglobulinaemia, reducedalbumin/globulin ratio, increased liver enzymes, neutrophilia and anaemia.

Likewise a negative result does not rule out FIP becausemassive virus replication leads to excess antigen leaving noantibodies available for detection.

In healthy animals antibody detection may aid in identifyingsero-positive cats which are potential shedders. This maybe of interest when trying to establish a sero-negative popu-lation (i.e. for breeding).

Please note our profiles → 3.3 Species Specific Profiles

See → 15 Moleculargenetical Tests

See → Herpesvirus Infection, Feline

FFeelliinnee HHeerrppeessvviirruuss IInnffeeccttiioonn

FFeelliinnee CCoorroonnaavviirruuss (PCR)

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�� FFeeLLVVGGeenneerraall IInnffoorrmmaattiioonn

FeLV is an oncovirus from the retroviridae family. Due to mutation and recombination withcellular DNA there are several FeLV subtypes (e.g. subtype B and C, FeSV). However thesesubtypes often show replication defects. Therefore a co-infection with the infectioussubtype A is essential. The prevalence in the feline population varies due to the region.Transmission occurs either horizontally via saliva or vertically via the placenta or milk. The course of infection varies depending on the immune status and age of the animal aswell as on the infectious dosage and virulence of the pathogen. In about 30% of infectedcats the immune status is good and they can eliminate the virus before it leads to viraemia(regressor cats/abortive infection). No FeLV virus can be detected in these cats. Another30% of infected cats show transient viraemia for up to 16 weeks, if the pressure ofinfection is high. During this time the virus will be shed and antigen can be detected in theblood. At the same time neutralising antibodies will be produced which will either eliminatethe virus or merely prevent further virus replication. In this situation the virus may retreatinto the bone marrow cells and the animal remains latently infected. Antigen cannot bedetected. During the first few years immune suppressing factors will favour thereoccurrence of viraemia. However, the virus will eventually be eliminated in most cases. Afurther 30% of infected cats will be unable to produce sufficient neutralising antibodies.These cats remain permanently viraemic and usually die within 3-5 years due to FeLV-asso-ciated diseases. In the remaining 10% of infected cats the infection takes an atypicalcourse with localised replication without participation of the bone marrow.

Symptoms: depending on the course of disease the following symptoms can occur:- tumours: lymphoma, leukaemia, myeloid tumours,

fibrosarcomas- FeLV associated diseases: pyrexia, anorexia, lethargy,

stomatitis, gingivitis, abscesses, respiratory symptoms, gastrointestinal symptoms

- bone marrow suppression: leukopenia, esp. neutropenia, non-regenerative anaemia, thrombocytopenia

- immune-mediated diseases: autoimmune haemolytic anaemia, glomerulonephritis, uveitis, polyarthritis

- reproductive disorders: abortion, stillbirth, fading kitten syndrome

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The detection of free eexxttrraacceelllluullaarr FeLV-p27 antigen is pos-sible from approx. 3 weeks post infection. Latently infectedcats may show false negative results. A positive result indi-cates to a certain extend transient or persistent viraemia,therefore the test should be repeated after 6 weeks. Shouldthe second test be positive, a third test should be performedafter another 16 weeks. If it is positive persistent viraemiamust be assumed. Negative repeat tests indicate virus elimi-nation or transition into the latently infected stage.Vaccination does not lead to viraemia, therefore false positive results are not possible.

Alternatively an IFA can be performed 6 weeks after the firstpositive result (see below).

Please note our profiles → 3.3 Species Specific Profiles

The test detects iinnttrraacceelllluullaarr FeLV p27 antigen inthrombocytes and neutrophils. However the detection canonly be successful once the infection involves the bonemarrow, therefore it is recommended to use the IFA test notbefore six weeks after a positive test for extracellular p27antigen (see FeLV ELISA test).

The IFA test allows, to a certain degree, prognostic assump-tions. A positive result very likely indicates persistentviraemia. However a negative result does not rule out infec-tion, as latent infections cannot be detected. Also, thechance of detection is highly dependent on the number ofinfected thrombocytes and neutrophils.

Please note: Do not submit heparin blood as the test can only be run with EDTA blood.

See→ 15 Moleculargenetical Tests

FFeeLLVV PPrrooggeennoommee (PCR) 11--22 mmll EEDDTTAA BBlloooodd

FFeeLLVV AAnnttiiggeenn (IFA) 11 mmll EEDDTTAA BBlloooodd

FFeeLLVV AAnnttiiggeenn (ELISA) 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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�� FFIIVV ((FFeelliinnee IImmmmuunnooddeeffiicciieennccyy VViirruuss))GGeenneerraall IInnffoorrmmaattiioonn

FIV is a lentivirus from the retroviridae family. The prevalence in the feline populationvaries between 2 and 8%. Transmission occurs mainly via bite wounds, but also when mating, via the placenta or milk. Similar to HIV infection in humans, the formation ofneutralising antibodies will not lead to virus elimination. Mostly CD4+ lymphocytes areaffected by the virus replication, which, together with other factors, eventually leads to marked immunosuppression.

Symptoms: FIV infection can be divided into four stages:

1. Acute stage: lasts weeks to months- pyrexia- neutropenia- lymphadenopathy

2. Asymptomatic stage: lasts 3-5 (-10) years3. Stage of non-specific symptoms:

- pyrexia- lymphadenopathy- leukopenia, anaemia, thrombocytopenia- lethargy, anorexia, emaciation- stomatitis, gingivitis, rhinitis, enteritis- behavioural changes

4. AIDS-like stage: same as stage 3- opportunistic infections- neoplasias- CNS symptoms

The method of choice as a screening test for routinediagnostics is the detection of antibodies against the coreprotein p24 or the envelope protein gp40. Sero-conversionoccurs approx. 2-4 weeks post infection. The specificity ofthe test is approximately 90%. False positive results are pos-sible. Therefore all clinically healthy cats that are testedpositive should be re-tested within 14 days or a PCR antigentest should be performed. Maternal antibodies may be foundup to the age of 16 weeks.

Please note our profiles → 3.3 Species Specific Profiles

FFIIVV AAnnttiibbooddiieess (ELISA) 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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The western blot is recommended as a confirmatory test forfurther evaluation of positive results in the ELISA antibodytest.

See → 15 Moleculargenetical Tests (Feline Immunodeficiency Virus)

�� GGllaannddeerrssGGeenneerraall IInnffoorrmmaattiioonn

Glanders is caused by Burkholderia (Pseudomonas) mallei. The disease is considerederadicated in Europe. The pathogen can be found in all secretions and excretions.

Symptoms: Infections affecting the nose, lungs or skin can be differentiated clinically.- pyrexia- nodules/ulceration in the mucous membranes and skin- lymphadenopathy- nasal discharge

Please note that Glanders is a notifiable disease in severalcountries!

Antibody detection using a complement fixation test.

See → Mycoplasma General Information

HHaaeemmoobbaarrttoonneelllloossiiss

GGllaannddeerrss AAnnttiibbooddiieess (CFT) 11 mmll SSeerruumm

FFIIVV PPrrooggeennoommee (PCR)

FFIIVV AAnnttiibbooddiieess (Westernblot)

00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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�� HHeelliiccoobbaacctteerr IInnffeeccttiioonnGGeenneerraall IInnffoorrmmaattiioonn

The pathogenicity of helicobacter infection in animals is difficult to evaluate and the availabledata is often contradictory. Helicobacter spp. can be isolated from the gastric mucosa indogs and cats with gastritis, chronic vomiting or enteritis. But it can also be isolated inhealthy animals. The prevalence might therefore reach 90-100%. Apart from H. pylori, thefollowing helicobacter species can be found in dogs and cats: H. heilmanni, H. felis, H. canis or H. mustelae. Genome sequencing is the only way to differentiate betweenthese. It is being disputed whether pets play a role in the infection of humans.

Symptoms: bearing in mind the above mentioned uncertainties,helicobacter positive animals may show the following symptoms:- vomiting- diarrhoea- gastric ulceration- gastric carcinoma

See → 15 Moleculargenetical Tests

�� HHeerrppeessvviirruuss,, BBoovviinnee (IBR/IPV)GGeenneerraall IInnffoorrmmaattiioonn

Bovine herpesvirus I (BHV I) leads to two different disease complexes in cattle: a respiratory form and a genital form. As in all herpesvirus infections, the infected animalremains a lifelong carrier and the virus may be excreted intermittently via secretions orfaeces.

Symptoms: - pyrexia- salivation, nasal discharge- coughing- meningoencephalitis (calves)- vaginitis, balanoposthitis, abortion

HHeelliiccoobbaacctteerr (PCR)

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Bovine herpesvirus I antibody detection using an ELISA test.

Please note that the genital form of the disease is notifiablein some countries.

Differentiation between Bovine Herpesvirus I field virus and marker virus.

A further test offers the differentiation between thefield/marker virus and the vaccination virus.

�� HHeerrppeessvviirruuss,, CCaanniinneeGGeenneerraall IInnffoorrmmaattiioonn

Canine herpesvirus I (CHV I) leads to a generally lethal infection in puppies. Older animalsusually only show mild respiratory signs or are asymptomatic, but they play an importantrole as virus shedders. The route of infection is oronasal, mostly in the birth canal. Theincubation period is 4-6 days. Animals who survive the infection remain lifelong carriers.

Symptoms: - anorexia, lethargy- salivation, nasal discharge- crying/distress- diarrhoea- CNS symptoms- abortion

The virus neutralisation test is the method of choice for theidentification of subclinical carriers. Antibodies may bedetected as early as 3-4 weeks post infection. Fordiagnosing acute infection in puppies it is recommended touse direct detection of antigen with PCR.

See → 15 Moleculargenetical Tests (Canine Herpesvirus I)

CCHHVV II (PCR)

CCHHVV II AAnnttiibbooddiieess (VNT) 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

BBHHVV II (field virus/marker virus)

11 mmll SSeerruumm

BBHHVV II AAnnttiibbooddiieess (ELISA) 44 mmll SSeerruumm

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�� HHeerrppeessvviirruuss,, EEqquuiinneeGGeenneerraall IInnffoorrmmaattiioonn

At present, eight species of herpesvirus have been described in horses. EHV 1 isconsidered the pathogen responsible for abortion, but it may also cause respiratory andCNS symptoms. EHV 2 and possibly EHV 5 cause keratitis, EHV 3 causes coital exanthemaand EHV 4 causes rhinopneumonitis. As in all herpesvirus infections, the infected animalsremain lifelong carriers.

See → 15 Moleculargenetical Tests (Equine Herpesvirus 1,2,4,5)

Antibody detection using virus neutralisation test.

Please note that only EHV 1 and EHV 4 antibodies can bedetected. It is not possible to differentiate between vaccina-tion titre and infection titre.

�� HHeerrppeessvviirruuss,, FFeelliinneeGGeenneerraall IInnffoorrmmaattiioonn

Feline Herpesvirus I (FHV I) or rhinotracheitis virus is primarily responsible for the cat fludisease complex. The infection is transmitted by direct contact with saliva or nasal secre-tions. The incubation period is 2-4 days. Infected animals remain lifelong carriers.Symptom-free phases will alternate with clinical phases.

Symptoms: - pyrexia- anorexia, lethargy- keratoconjunctivitis- rhinitis- bronchopneumonia- abortion (rare)

HHeerrppeessvviirruuss,, EEqquuiinneeAAnnttiibbooddiieess (VNT)

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

HHeerrppeessvviirruuss,, EEqquuiinnee (PCR)

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The virus neutralisation test is the method of choice for theidentification of subclinical carriers. Antibodies may bedetected as early as 3-4 weeks post infection.Differentiation between vaccination titre and infection titreis not possible. For diagnosing acute infections it isrecommended to use the direct detection of antigen by PCR.

See → 15 Moleculargenetical Tests (Feline Herpesvirus I)

�� IIBBRR//IIPPVV

See → Herpesvirus Infection, Bovine

�� IInnffeeccttiioouuss AAnnaaeemmiiaa,, EEqquuiinnee ((EEIIAA))GGeenneerraall IInnffoorrmmaattiioonn

Infectious Equine Anaemia is caused by a lentivirus. Transmission occurs via infectiousblood e.g. blood sucking insects or intrauterine. The anaemia evolves from autoimmuneprocesses which lead to haemolysis. The Coggins test is used for antibody detection.

Symptoms: the course of disease varies from acutely fatal to chronicrelapsing - pyrexia, lethargy- anaemia- icterus- oedema

Please note that EIA is a notifiable disease in certain countries!

EIA antibody detection using immunodiffusion (Coggins test). The specificity is approx. 95%.

CCooggggiinnss TTeesstt 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

FFHHVV II (PCR)

FFHHVV II AAnnttiibbooddiieess (VNT) 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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�� IInnffeeccttiioouuss CCaanniinnee HHeeppaattiittiiss ((IICCHH))GGeenneerraall IInnffoorrmmaattiioonn

In dogs canine adenovirus I (CAV I) is the causal agent of ICH. It is closely related to theCAV II serotype, which is involved in the kennel cough complex. The virus is shed with allsecretions and excretions (up to 6 months via urine).

Symptoms: clinical signs are seen after an incubation period of 2-7 days. The severity depends on the degree of celldestruction due to virus replication.- pyrexia- anorexia, lethargy- tonsillitis, pharyngitis- oedema, ascites- haemorrhagic diathesis- corneal opacity, uveitis

CFT is the method used for the detection of adenovirus anti-bodies in dogs. Antibodies may be found 10-14 days post infection at theearliest. It is not possible to differentiate between CAV I andCAV II antibodies or between vaccination titre and infectiontitre. A titre rise within 10-14 days demonstrates infection.

�� IInnfflluueennzzaa,, EEqquuiinneeGGeenneerraall IInnffoorrmmaattiioonn

Equine influenza is an acute, highly contagious viral disease particularly affecting the res-piratory tract. Subtype A equi 1 and A equi 2 can be distinguished. Transmission occurs viaaerosol droplet infection.

Symptoms: - pyrexia, lethargy, inappetence- coughing- bronchopneumonia- early abortion

AAddeennoovviirruuss AAnnttiibbooddiieess(dog)

00..55 mmll SSeerruumm

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Antibody detection using virus neutralisation test. Thefollowing strains can be differentiated: Prague, Miami,Fontainebleau, Kentucky and Solvalla. It is not possible todifferentiate between vaccination titre and infection titre.

�� LLeeiisshhmmaanniiaassiissGGeenneerraall IInnffoorrmmaattiioonn

Canine leishmaniasis is predominantly caused by an infection with L. infantum. Thetransmission occurs via sand flies of the genus Phlebotomus or Lutzomyia. The pathogen is prevalent across the entire Mediterranean region, Hungary and Romania.In France infections may even occur in the region around Paris.

Symptoms: the incubation period may be weeks to months. Thedifferentiation between a visceral and a cutaneous type, asused in humans, is usually not possible in dogs. The clinicalsymptoms in dogs vary widely:- weight loss- anorexia, lethargy, enteritis- hyperkeratosis, alopecia (starting periorbitally),

dermatitis; fissures on the foot pads- excessive claw growth, paronychia- generalized lymph node enlargement- hyperproteinaemia, hypoalbuminaemia,

hypergammaglobulinaemia- hepatomegaly, splenomegaly- glomerulonephritis- polyarthritis- keratoconjunctivitis, uveitis, iritis

The test for leishmania antibodies can be performed 14 dayspost infection at the earliest. Often a titer can only bedetected months post infection, therefore re-testing may benecessary.

Please also note our profiles:→ 3.2 Special Screening Profiles (Travel Disease Profiles)→ 17.3 Blood parasites, comprehensive

LLeeiisshhmmaanniiaa AAnnttiibbooddiieess (IFT)(dog only)

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

IInnfflluueennzzaa,, EEqquuiinneeAAnnttiibbooddiieess (VNT)

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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Direct detection of Leishmania is only useful from lymphnode or bone marrow aspirates or from skin impressionsmears (sensitivity 30-50%). Detection in a blood smear isusually not successful.A negative result does not rule out infection!

See → 15 Moleculargenetical Tests

LLeeiisshhmmaanniiaa sspppp.. (PCR)

LLeeiisshhmmaanniiaa DDiirreeccttDDeetteeccttiioonn

SSmmeeaarr,, BBiiooppssyy

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�� LLeeppttoossppiirroossiissGGeenneerraall IInnffoorrmmaattiioonn

Leptospirosis is caused by the following serotypes: L. australis (bratislava), L. autumnalis,L. canicola, L. copenhageni (icterohaemorrhagiae), L. grippotyphosa, L. saxkoebing, L. sejroe and L. tarassovi.Transmission occurs directly via contact with shedders (urine) or indirectly via contaminatedwater. The pathogen is transported via the bloodstream into the body, especially into theliver and kidneys.

Symptoms: following an incubation period of 4-12 days the followingsymptoms can occur:- pyrexia- anorexia, vomiting, enteritis- polydipsia/polyuria- haemolysis, icterus- haemorrhagic diathesis- chronic liver and kidney disease- uveitis, retinitis

Microagglutination reaction (MAR) is usually the method ofchoice for the detection of leptospira antibodies in cases ofsuspected infection. The test should be performed 14 dayspost infection at the earliest. In dogs, all eight above mentioned serotypes are tested.Horses are tested for L. grippotyphosa, L. copenhageni, L. pomona, L. australis and L. autumnalis only. The titre maygive limited information for the differentiation between vaccination titre and infection titre (titre value). Vaccinescontain only the serotypes L. canicola and L. copenhageni(icterohaemorrhagiae), but cross reactions with otherserotypes are possible.

See → 15 Moleculargenetical Tests

LLeeppttoossppiirraa (PCR)

LLeeppttoossppiirraa AAnnttiibbooddiieess 11 mmll SSeerruumm

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�� LLeeuukkaaeemmiiaa VViirruuss IInnffeeccttiioonn,, FFeelliinnee

See → FeLV

�� LLeeuukkoossiiss VViirruuss,, BBoovviinnee ((BBLLVV))GGeenneerraall IInnffoorrmmaattiioonn

Bovine leukosis can be subdivided into four clinically different forms. Skin leukosis,juvenile leukosis and mast cell reticulosis are spontaneously occurring diseases, whereasenzootic lymphatic leukosis is caused by a retrovirus. Transmission usually occurs shortlyafter birth via colostrum or milk. Horizontal infection is also possible.

Symptoms: - lethargy, inappetence- oedema- anaemia, lymphocytosis- lymphadenopathy- splenomegaly

Bovine Leukosis Virus antibody detection using ELISA.

Please note that Bovine leucosis is notifiable in some countries.

�� LLiisstteerriioossiiss

See → 15 Moleculargenetical Tests

�� MMaaccrrooffiillaarriiaa//MMiiccrrooffiillaarriiaa

See → Dirofilariasis

LLeeuukkoossiiss VViirruuss,, BBoovviinnee(BLV) AAnnttiibbooddiieess

11 mmll SSeerruumm

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�� MMaaeeddii//VViissnnaaGGeenneerraall IInnffoorrmmaattiioonn

The Maedi/Visna virus leads to interstitial pneumonia or demyelinating encephalitis in sheep.

Symptoms: - dyspnoea, coughing- ataxia, lameness- decreased milk production- emaciation- splenomegaly, possibly hepatomegaly

Antibody detection using ELISA. Antibodies occur severalweeks to years post infection.Therefore a negative result does not rule out infection.

MMaaeeddii//VViissnnaa AAnnttiibbooddiieess 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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�� MMyyccooppllaassmmaa hhaaeemmooffeelliiss ++ CCaannddiiddaattuuss MMyyccooppllaassmmaa hhaaeemmoommiinnuuttuumm((pprreevviioouussllyy HHaaeemmoobbaarrttoonneellllaa ffeelliiss))GGeenneerraall IInnffoorrmmaattiioonn

H. felis has been reclassified as a Mycoplasma and there are 3 strains - Mycoplasmahaemofelis and Candidatus Mycoplasma haemominutum. M. haemofelis is generallyconsidered the most pathogenic.Cand. M. haemominutum in immunocompetent animals does not normally cause anyclinical symptoms, but in rare cases, mild transient febrile conditions are possible. Howev-er, concurrent infection with FeLV is of importance (see below). In these animals, Cand. M.haemominutum can cause similar symptoms as with M. haemofelis infection.

Feline haemobartonellosis is an acute or chronic disease often associated with haemolyticanaemia. Untreated it often leads to the death of the animal. Untreated animals may becomecarriers if they survive the infection. They may have intermittent parasitaemia. Mycoplasmamay also be found in clinically healthy cats. Predisposing factors for the development ofdisease are FeLV infection, splenectomy or long-term corticosteroid treatment.

The mode of transmission appears to be via blood-sucking insects and bite wounds, but it isnot yet certain. The organism is apparently widespread and may be found in blood smearsof asymptomatic cats. Immunosuppression promotes the occurrence of symptoms.

Symptoms: depending on the pathogenicity of the organism and theimmune status of the animal the course of the diseasevaries from acute to chronic/latent- pyrexia (above 40°C)- immune-mediated haemolytic anaemia- icterus, bilirubinuria- hepatomegaly, splenomegaly- anorexia, lethargy

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The epicellular organism is found in a Giemsa stained blood smear using a light-optical microscope. In the chroniccourse of the disease asymptomatic and parasitaemic phases will alternate.

Direct detection of the organism is therefore not alwayspossible!

Please note our profiles: → 3.2 Special Screening Profiles (Travel Disease Profile)→ 17.3 Blood parasites, comprehensive

�� MMyyccooppllaassmmaa sspppp.. ((HHaaeemmoobbaarrttoonneellllaa)) ((PPCCRR))

See → 15 Moleculargenetical Tests

�� NNeeoossppoorraa ccaanniinnuummGGeenneerraall IInnffoorrmmaattiioonn

Neospora caninum is morphologically similar to Toxoplasma gondii. Serological cross reac-tions especially in dogs cannot be completely ruled out. The development cycle and trans-mission are still unknown, although oral infections are possible experimentally. Neosporais found in dogs, horses and cattle.

Symptoms: N. caninum shows an affinity to nervous tissuethus the following symptoms are described

in ddooggss:- dysphagia, coughing, hoarseness- protrusion of the nictitating membrane- reduced reflexes- paralysis

in ccaattttllee:- abortion

MMyyccooppllaassmmaa (Haemobartonella)DDiirreecctt DDeetteeccttiioonn BBlloooodd ssmmeeaarr ++ EEDDTTAA bblloooodd

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The test for Neospora caninum antibodies using an immuno-fluorescence test is the only in-vivo test that is practicablein routine diagnostics for a suspected infection. It can beperformed 14 days post infection at the earliest.

Please note: AAnnttiibbooddiieess against Neospora caninum in dogs can persist for years. A confirmative diagnosis is not possible in-vivo. Only the clinical findings in conjunction with a positive titer and the success of therapy may lead to thepresumptive diagnosis of neosporosis.

�� PPaarraattuubbeerrccuulloossiissGGeenneerraall IInnffoorrmmaattiioonn

The infection with the acid-fast bacillus Mycobacterium avium subsp. paratuberculosisoccurs in ruminants and is also called Johne’s Disease. After a long incubation period ofup to 2-6 years the affected animals suffer from chronic enteritis and emaciation with fatalconsequences.

Antibody detection using a complement fixation test (CFT).

PPaarraattuubbeerrccuulloossiiss AAnnttiibbooddiieess (bovine)

11 mmll SSeerruumm

NNeeoossppoorraa ccaanniinnuummAAnnttiibbooddiieess (IFT)

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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�� PPaarrvvoovviirruuss//PPaannlleeuukkooppeenniiaaGGeenneerraall IInnffoorrmmaattiioonn

The pathogens causing canine parvovirus enteritis (CPV) and feline parvovirus enteritis(FPV) are very closely related. More recent strains of CPV may cause clinical disease incats. Transmission occurs oronasally by contact with infected faeces or contaminatedobjects. The course of disease varies from clinically inapparent to peracute, depending onthe age and immune status of the animal. Virus replication takes place in all tissues with ahigh cell multiplication rate, especially intestinal mucosa, bone marrow, lymphatic systemand myocardium, in cats also in the retina and cerebellum.

Symptoms: in puppies usually the following symptoms are seen:- pyrexia/hypothermia- anorexia, lethargy- vomiting, diarrhoea (haemorrhagic)- dehydration- leukopenia- dyspnoea, cardiac symptoms- abortion, mummification, cerebellar hypoplasia (cats)

Parvovirus antibody detection in cats and dogs using ahaemagglutination inhibition test (HI) is possible approx. 4-6days post infection. Differentiation between vaccinationvirus and field virus is not possible. A titre increase within10-14 days confirms infection. During acute infection directdetection of parvovirus antigen in faeces is recommended.

See → 16.2 Faecal examinations (Virological examination using electron microscopy)

In dogs and cats, direct detection of parvovirus antigen ispossible from a small faecal sample or a rectal swab, usingimmunochromatography. Excretion of the antigen starts 3-4days post infection and lasts approximately 7-10 days, insingle cases much longer. Certain vaccines will lead toexcretion of virus approx. 3-12 days post vaccination. It isnot possible to differentiate between vaccination virus andfield virus. A negative result in the direct detection does notrule out infection!

PPaarrvvoovviirruuss DDiirreeccttDDeetteeccttiioonn

FFaaeecceess,, RReeccttaall sswwaabb

PPaarrvvoovviirruuss AAnnttiibbooddiieess (HI) 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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See → 15 Moleculargenetical Tests

�� PPRRRRSS ((PPoorrcciinnee RReepprroodduuccttiivvee aanndd RReessppiirraattoorryy SSyynnddrroommee))GGeenneerraall IInnffoorrmmaattiioonn

The causing agent of PRRS is a highly infectious arterivirus. The disease is associated with abortion and reproductive disorders. Male pigs can also be affected, often showinggeneral symptoms such as inappetence, and can shed the virus with sperm. Howeverdisease occurrence without any clinical symptoms is possible.

Detection of antibodies using an ELISA test. One week post infection serum antibodies are detectable,with maximum titres after 3-5 weeks. Virus neutralizing antibodies develop not until 4-8 weeks post infection. It is recommended to test at least 5-10 animals perherd/population.

�� QQ FFeevveerrGGeenneerraall IInnffoorrmmaattiioonn

Q fever is a zoonotic disease caused by a species of bacteria called Coxiella burnetii. Itdoes not play a major role in animals, but affected animals constitute a risk of infection forhumans. Apart from ruminants, horses, dogs and cats are susceptible.

Symptoms: - pyrexia, lethargy, inappetence- conjunctivitis- bronchopneumonia- arthritis- abortion

Antibody detection using a complement fixation test.

QQ FFeevveerr AAnnttiibbooddiieess (CFT) 11 mmll SSeerruumm

PPRRRRSS AAnnttiibbooddiieess (porcine) 11 mmll SSeerruumm

PPaarrvvoovviirruuss (PCR)

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�� RRaabbiieessGGeenneerraall IInnffoorrmmaattiioonn

Travelling with a dog, cat or ferret is since 3. July 2004 governed by EU regulation Nr. 998/2003 from the European Parliament and the European commission of 26. May 2003.Compliance with this regulation has been compulsory since 1.10.2004.

When entering some countries it is compulsory to show proof of antibody titres againstthe rabies virus. This can only be done at laboratories certified by die EU commission ofwhich Vet Med Lab is one.

It is necessary that the pets have an EU pet passport. The regulations for the differentcountries can vary, it is therefore important to inquire well ahead of time what the exactrequirements are. Information can be found on the internet side of the country or itsembassy.

Please use the ssppeecciiaall ssuubbmmiissssiioonn ffoorrmm supplied by the lab (www.vetmedlab.comdownloads). To ensure prompt issuance of the certificate we kindly request that allinformation be completed legibly. NNoo ootthheerr tteesstt can be performed from the same material.

�� RRoottaavviirruussGGeenneerraall IInnffoorrmmaattiioonn

Rotaviruses are found in almost all animal species. The virus has a high affinity to the smallintestinal epithelium. Virus replication leads to massive destruction of epithelial villi,leading to malabsorption and hypersecretion. Severe watery diarrhoea is found especiallyin young animals. The infectious route is oral, older animals act as a virus reservoir.

Symptoms: clinical symptoms occur after an incubation period of 1-2 days:- watery diarrhoea- vomiting- dehydration

RRaabbiieess AAnnttiibbooddiieess (IFT) 11mmll SSeerruumm

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Virus excretion via the faeces usually lasts 3-10 days andcan be detected using immunochromatography on a smallfaecal sample. The test can be performed in all animalspecies.

See → 16.2 Faecal examinations (Virological examination using electron microscopy)

�� SSaarrccoopptteessGGeenneerraall IInnffoorrmmaattiioonn

Canine mange is caused by Sarcoptes canis. Severe pruritus is characteristic for thisdisease. There is no or little response to treatment with glucocorticoids. Initially thechanges in the skin are

Seen on the abdomen, sternum, lateral limbs and ears, before they generalise. The detection of mites in skin scrapes is often unsuccessful in chronic cases, as due tosensitization even very low numbers of mites continue to cause clinical symptoms. Thesensitivity of skin scrapes is approx. 30-50%.

The method for detecting sarcoptes antibodies in dogs usingan ELISA test is highly specific (92.6%) and highly sensitive(83.3%). No cross reactions occur with storage mites,demodex mites or cheyletiella mites. The antibody test canbe performed approx. 3-4 weeks post infection. A negativeresult does not entirely rule out infection, since 5-10% ofdogs will not produce antibodies.

Antibody titres persist over a long period of time; thereforethey are not very useful in treatment control.

See → 17.2 Ectoparasites

SSaarrccoopptteess AAnnttiibbooddiieess (ELISA)(dog only) 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

RRoottaavviirruuss AAnnttiiggeenn FFaaeecceess

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�� TTiicckkbboorrnnee EEnncceepphhaalliittiiss

Tickborne encephalitis is caused by a flavivirus which is transmitted by the pasture tickIxodes ricinus. Endemic areas have been identified in Southern Germany, Austria, Switzer-land, Hungary, Poland, Slovakia, Czech Republic, Russia, the Baltic States and parts ofSouthern Scandinavia.In domestic animals the disease has been predominantly described in dogs.

Symptoms: - pyrexia- convulsions- paresis, ataxia- reduced consciousness- hyperaesthesia/hyperalgesia

The complement fixation test is useful for the detection ofsero-positive animals. In endemic areas the antibody preva-lence in dogs may be as high as 30 %. If infection is stronglysuspected clinically it is recommended to examinecerebrospinal fluid for antigen using PCR.

See → 15 Moleculargenetical Tests

�� TTooxxooppllaassmmoossiissGGeenneerraall IInnffoorrmmaattiioonn

Toxoplasma gondii, the causative agent of toxoplasmosis, is prevalent worldwide. Only catsand related Felidae act as final hosts, while almost all warm-blooded animals, as well ashumans, may act as intermediate hosts.

Clinical disease in cats is rare and if at all, it is seen in very young or immunosuppressedanimals. Infection in cats occurs via ingestion of cyst-containing meat of intermediatehosts or via feline faeces containing infective oocysts. Almost every organ will becolonized and in cats the parasite can multiply in the intestinal epithelium. Approx. 3-9days post infection with muscle cysts the excretion of oocysts starts for a limited period oftime. In case of infection with sporulated oocysts approximately 20% of cats excreteoocysts 18-35 days post infection.

TTiicckkbboorrnnee EEnncceepphhaalliittiiss VViirruuss (PCR)

TTiicckkbboorrnnee EEnncceepphhaalliittiissAAnnttiibbooddiieess (CFT)

11 mmll SSeerruumm

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Infection of other warm-blooded animals and humans occurs via ingestion of inadequatelycooked, cyst-containing meat of intermediate hosts or via contact with infective oocystsoriginating from feline faeces. A short parasitaemia is observed as in cats and the parasitethen colonizes in all organs, with development of tissue cysts, but there is no enteral multi-plication and no excretion.

Symptoms: the infection is usually clinically inapparent, but the following symptoms may be observed:- pyrexia (usually non responsive to antibiotics)- anorexia, lethargy, enteritis- retinopathies- abortion (humans, sheep, goats)- encephalitis- pneumonia- lymph node enlargement- anorexia/lethargy/hypothermia and sudden death in

congenitally infected kittens

The detection of toxoplasma antibodies using an immunoflu-orescence test is usually the method of choice to confirmtoxoplasma infection in dogs and cats. It can be performed14 days post infection at the earliest for IgG and 1-2 weekspost infection for IgM. Prevalence in the feline and caninepopulation is worldwide, and depending on age up to 80-90%.

However, the high prevalence of antibodies againsttoxoplasma in dogs and cats restricts the use of serology inthe diagnosis. Only high IgM titers and a negative or low IgGtiter, or a rising IgG titer gives a clear indication for acuteinfection, which could be accompanied by faecal oocystshedding in cats. Most infected animals remain seropositive(IgG) at high levels for several years or for life, which caneven make it difficult to judge paired serum samples.

TTooxxooppllaassmmaa AAnnttiibbooddiieess(IFT) IIggMM//IIggGG

IIggMM:: 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaaIIggGG:: 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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The direct detection of toxoplasma oocysts in faeces usingthe flotation method is only useful in cats (as no otherspecies will excrete oocysts). Oocysts are ususally onlyexcreted in acute first infections, and re-infections do notnormally lead to excretion. The excretion may beintermittent, therefore re-testing may be necessary.

Please note: Collect several small samples from different places in thefaeces. It is advisable to submit a pooled sample from 3 con-secutive days.

A negative result does not rule out infection!

The PCR test cannot be performed on faeces, but other sam-ple material, based on clinical symptoms, can be used todetect infection. Despite the high sensitivity false negativeresults can occur.

See → 15 Moleculargenetical Tests

�� TTrryyppaannoossoommaa sspppp..GGeenneerraall IInnffoorrmmaattiioonn

Infection with Trypanosoma spp. essentially does not play a role in domestic animals in our latitude. Merely the causal agent of ddoouurriinnee in horses (Trypanosoma equiperdum) isprevalent worldwide.

Please note that dourine in horses is a notifiable disease in certain countries!

Detection of T. equiperdum antibodies using a complementfixation test.

TTrryyppaannoossoommaa eeqquuiippeerrdduummAAnnttiibbooddiieess (CFT)

00..55 mmll SSeerruumm

TTooxxooppllaassmmaa ggoonnddiiii (PCR)

TTooxxooppllaassmmaa DDiirreeccttDDeetteeccttiioonn

mmiinniimmuumm 00..55 SSAA ffaaeeccaall ttuubbee

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Using a light-optical microscope, the pathogen can be foundin blood smears or smears from genital secretion.

Direct detection is not always possible!

�� VViirraall AArrtteerriittiiss,, EEqquuiinnee (EVA)GGeenneerraall IInnffoorrmmaattiioonn

Equine Viral Arteritis is caused by an arterivirus. The disease occurs worldwide, the preva-lence in Germany is approx. 20%. The disease leads to damage of the vascularendothelium.

Symptoms: The disease is usually clinically inapparent.- pyrexia, lethargy, inappetence- haemorrhage, oedema- coughing, dyspnoea- conjunctivitis- early abortion

Detection of Equine Viral Arteritis antibodies using a virusneutralisation test.

See → 15 Moleculargenetical Tests

�� VViirruuss DDiiaarrrrhhooeeaa,, BBoovviinnee

See → Bovine Virus Diarrhoea

EEVVAA (PCR)

EEVVAA AAnnttiibbooddiieess (VNT) 55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

TTrryyppaannoossoommaa DDiirreeccttDDeetteeccttiioonn

EEDDTTAA bblloooodd,, SSmmeeaarr

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1144..11 AAuuttooiimmmmuunnee DDiisseeaasseess

�� SSyysstteemmiicc LLuuppuuss EErryytthheemmaattoossuuss ((SSLLEE))

Systemic lupus erythematosus is characterized by the production of autoantibodies againstmany cell structures, mostly against nuclear material. Erythrocytes, coagulation factorsand immunoglobulins may also be affected. The disease most commonly affects GermanShepherd Dogs, Poodles, Shelties and Collies.

Symptoms: cats, like humans, usually show several symptomcomplexes, whereas in most dogs one symptompredominates- pyrexia- polyarthritis- haemolytic anaemia, icterus, haemoglobulinuria- thrombocytopenia, neutropenia- glomerulonephritis- hydropic degeneration of the skin and hyperkeratosis

(discoid lupus)

The test for ANA using IFT can be performed in dogs andcats. It detects IgG antibodies, but only about 70% of animalsdevelop clear antibody levels. A positive test does only provelupus erythematosus in conjunction with corresponding clinical symptoms, because clinically asymptomatic animalsmay show antibodies too, or autoantibodies may be producedin the course of other diseases. The blood sample should becollected during an acute phase of disease. For the diagnosisof discoid lupus and other immune mediated skin diseases, atest for circulating antibodies is not very useful. In thesecases it is recommended to submit a skin biopsy for histological examination.

AAnnttiinnuucclleeaarr AAnnttiibbooddiieess (ANA test)

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1144..11 AAuuttooiimmmmuunnee DDiisseeaasseess

�� MMyyaasstthheenniiaa ggrraavviiss

Myasthenia gravis is due to a disturbance in the transmission of nervous signals at theneuromuscular end-plate, triggered by a reduction of acetylcholine receptors. Twodifferent types are found in dogs and cats: 1. Congenital type: Lack of acetylcholine receptors. This type is mostly found in JackRussell Terriers, Fox Terriers, Springer Spaniels and Siamese cats. Symptoms often showas early as 6-8 weeks of age.2. Acquired type: Production of autoantibodies against acetylcholine receptors. Breeds most frequently affected are German Shepherd Dogs, Labrador Retrievers, GoldenRetrievers, Akita Inu Dogs, and Abyssinian and Somali cats. An onset of disease is oftenseen at the age of 2-3 years or 7-9 years. The cause for the production of autoantibodies isnot yet known. Concurrent presence of myasthenia with neoplasias, esp. thymomas, hasbeen described.

Symptoms: three courses of the disease can be differentiated:focal form: - dysphagia

- megoesophagus- regurgitation- aspiration pneumonia

acute form: - acute muscle weakness- dyspnoea

chronic form: - progressive weakness- megoesophagus- regurgitation- aspiration pneumonia

a megoesophagus is not observed in the congenital type

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1144..11 AAuuttooiimmmmuunnee DDiisseeaasseess

The detection of circulating autoantibodies using IFT is themethod of choice for diagnosing myasthenia gravis. Thesensitivity is approx. 85%, therefore 15% are false negativeresults.Should you require a higher sensitivity, there is the option toforward your sample to the University of San Diego, California,USA. Please note this request clearly on the submissionform and allow more time to receive a result. Please alsonote that there is a considerably higher charge for this test(depending on the exchange rate).The autoantibody level in the congenital form of the diseaseis usually very low or not existent. In this case or in problematiccases, it is recommended to perform the Tensilon® or Mestinon® (Pyridostigmine) test (i.e. diagnostic treatment ofMyasthenia gravis). Tensilon® or Mestinon®. The test is pos-itive in case of immediate improvement of the clinical symp-toms.

AAcceettyyllcchhoolliinnee RReecceeppttoorrAAnnttiibbooddiieess

11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1144..11 AAuuttooiimmmmuunnee DDiisseeaasseess

�� RRhheeuummaattooiidd PPoollyyaarrtthhrriittiiss

Rheumatoid polyarthritis is counted among the immunoreactive polyarthritides. Immunemediated arthritic diseases are the most commonly found inflammatory joint diseases insmall animal practice. They have in common that several joints are affected (minimum 2-6)and that generalised symptoms are present. Rheumatoid arthritis is characterised by erosive damage to the joints. It commonly affectsdogs at the age of 5-6 years, mostly dwarf and toy breed dogs. The disease is caused bythe production of abnormal antibodies against endogenous immunoglobulins, which arethen deposited in the joints.

Symptoms: - inappetence, lethargy- pyrexia- stiff gait, lameness- increased amount of synovial fluid (esp. carpal and

tarsal joints)- joint deformation in chronic cases

The detection of circulating autoantibodies using theWaaler-Rose test is the method of choice in humanmedicine to diagnose rheumatoid arthritis. The method isbased on the ability of the antibodies to agglutinate in vitrosensitized erythrocytes. In fact the detection of rheumatoidarthritis factors in veterinary medicine is characteristic butnot specific, as they also occur in other diseases for exam-ple SLE, dirofilariasis, leishmaniasis, pyometra, etc.Therefore a positive result must always be interpreted inconjunction with the clinical symptoms, radiographicchanges and if possible synovial fluid examination. Withsensitivity below 90% false negative results are alsopossible. The blood sample should be taken during an acutephase of the disease.

Please also see our special profiles:18.2 Aspirate Profile I+II

RRhheeuummaattooiidd AArrtthhrriittiissFFaaccttoorr (Waaler-Rose test)

11 mmll SSeerruumm ,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1144..11 AAuuttooiimmmmuunnee DDiisseeaasseess

�� AAuuttooiimmmmuunnee HHaaeemmoollyyttiicc AAnnaaeemmiiaa

Autoimmune processes are the most frequent cause of haemolytic anaemia in dogs. A dif-ferentiation is made between a primary, idiopathic form and a secondary form. Thesecondary form is caused by an underlying disease e.g. babesiosis, ehrlichiosis, dirofilaria-sis, leishmaniasis, viral or bacterial infection, neoplasia, SLE or drugs such as penicillin,sulfonamides, cephalosporins, levamisole, NSAID´s or vaccines.Cats rarely have immune-mediated anaemia, and if they have it is most frequently due toFeLV or haemobartonella infection. Mostly young and middle aged animals are affected. Indogs, breed predispositions are described in the American Cocker Spaniel, SpringerSpaniel, Irish Setter and Poodle.

Symptoms: - inappetence, lethargy, weakness- pyrexia, dyspnoea- anaemia, icterus, haemoglobulinuria- splenomegaly, possibly hepatomegaly

The direct Coombs test or direct antiglobulin test is used todetect antibodies or complement on the erythrocyte surface.Low antibody titres may lead to false negative results. Sec-ondary haemolytic anaemias, e.g. due to babesiosis, maylead to positive results. For more secure diagnosis it istherefore additionally necessary to find evidence of sphero-cytes in the blood smear, and possibly also microscopic oreven macroscopic autoagglutination.

DDiirreecctt CCoooommbbss TTeesstt 11 mmll EEDDTTAA bblloooodd

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1144..22 AAlllleerrggyy DDiiaaggnnoossttiiccss

�� AAlllleerrggyyGGeenneerraall IInnffoorrmmaattiioonn

Allergies are inherited or acquired specific changes of the immune system’s ability torespond towards external, intrinsically innocuous substances, which are recognized asallergens. Allergies are always preceded by a phase of sensitization, during which there isrepeated contact with one or several allergens.

A differentiation is made between four types of allergic reactions. In veterinary medicineonly type I (immediate type) and type IV (cell mediated type) are important.

The following allergy forms can be differentiated in animals, based on the cause:- flea bite allergy- atopy- allergic skin reactions towards food components- allergic contact dermatitis- allergic skin reactions to staphyloccocus or malassezia- allergic reactions towards insect allergens

FFlleeaa bbiittee and fflleeaa ssaalliivvaa allergies are one of the most common allergies in dogs and cats.Sensitization occurs against saliva allergen and probably against excretion products. Theallergic reaction is not necessarily limited to the site of the flea bite, but may be found allover the body. Fleas cannot always be found. In sensitized animals one single flea biteevery 10-14 days is sufficient to maintain the symptoms. Similar mechanisms seem to playa role in sarcoptes infestation (see → Sarcoptes).

AAttooppyy is an allergic overreaction (immediate type) towards environmental allergens. Inmost cases there is a genetic predisposition. The allergens are mostly taken uppercutaneously. Once in the skin these allergens become recognised by the immunesystem by ‘antigen presenting cells’. This leads to the production of specific IgE antibodieswhich bind to the surface of mast cells. In the event of a new contact with the allergen,bridge-forming of the IgE antibodies occurs which leads to the release of histamine andother biogenic amines from the mast cells. Subsequently the classical symptoms ofpruritus occur, followed by erythema and alopecia.The allergy usually starts between one and three years of age. Certain breeds show agenetic predisposition for atopic disease: West Highland White Terrier, Bull terrier, ChowChow, Boxer, German Shepherd, etc. Cats and horses, less often dogs, may develop asthma-like symptoms or allergic rhinitisand conjunctivitis.

In ffoooodd aalllleerrggiieess, the immediate allergic reaction with the production of IgE antibodiesplays a minor role. These are type IV allergies: neutrophils and eosinophils migrate into theskin where they release inflammatory mediators. Symptoms such as those found in atopicdermatitis are seen, as well as gastrointestinal symptoms.The pathogenesis of food allergies restricts the use of diagnostic serological IgE testing. Ifdietary mediated allergies are suspected it is advisable to perform an elimination diet over8-10 weeks, followed by provocation testing. Ideally the owners should prepare the dietthemselves. The diet should consist of a single protein source (horse, game, turkey) and a

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1144..22 AAlllleerrggyy DDiiaaggnnoossttiiccss

single carbohydrate source (potato). Deficiencies need not be considered for a period ofup to three months.

Late type allergic reactions are seen in ccoonnttaacctt ddeerrmmaattiittiiss. The symptoms are primarilyfound in body areas where contact with the allergen has occurred (ventral abdomen, headetc.). The testing for IgE is not very useful, but the suspected allergens should be eliminatedfrom the animal’s immediate environment.

Allergic reactions against ssttaapphhyyllooccooccccuuss and mmaallaasssseezziiaa aannttiiggeennss appear to be commonin animals. But both organisms belong to the normal skin flora and are primarily non-patho-genic. Only when the pH of the skin changes due to other diseases, massive multiplicationof staphylococcus and malassezia may occur, leading to sensitization. Staphylococcus andmalassezia allergies cannot be diagnosed serologically. Bacterial culture is recommended.

Cats and dogs rarely have allergic reactions to iinnsseecctt aalllleerrggeennss. In horses on the otherhand the insect allergens play a role in the development of summer eczema.

Allercept™ (Fcεε-receptor technology)

The Allercept™ test for dogs, cats an horses is an improve-ment compared to the former used Topscreen™ test as faras specificity and sensitivity is concerned. This test systemuses Fc-epsilon receptors (FcεRI) for the detection of aller-gen specific IgE. These receptors represent the bindingsites for IgE on mast cells and neutrophils.

The Screening-Test is a reliable and low price screeningtest for cats, dogs and horses. A positive group result canbe followed by individual allergen determination andimmunotherapy. Hyposensitisation solution can be orderedvia the laboratory.

AAlllleerrggeennss aarree tteesstteedd wwiitthhiinn tthhee iitteemmiisseedd ggrroouuppss::

•• MMiitteess // MMoouullddss,, FFuunngguuss // FFlleeaa ssaalliivvaa ((oonnllyy ddoogg//ccaatt))•• TTrreeeess•• GGrraasssseess //HHeerrbbss

SSccrreeeenniinngg--TTeesstt AAlllleerrcceepptt™™ 00..55 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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1144..22 AAlllleerrggyy DDiiaaggnnoossttiiccss

Specific single allergen determination can be performed fol-lowing a positive Allercept™ Screening-Test. The test is per-formed using any of the 3 groups (see page 209) thatshowed a positive result. Once a single allergen has beenidentified it can be eliminated or specific immune therapycan be started.

MMiitteess // MMoouullddss,, FFuunngguuss // FFlleeaa ssaalliivvaa ((1122 aalllleerrggeennss))

• Penicillium notatum• Aspergillus fumigatus• Cladosporium herbarum• Alternaria alternata• Cockcroach (Blatella germanica)• Flea saliva (only dog/cat)• Cat epithelia (only dog)• Acarus siro (storage mite)• Lepidoglyphus (storage mite)• Tyrophagus putrescentiae (storage mite)• Dermatophagoides farinae

(house dust mite)• Dermatophagoides pteronyssinus

(house dust mite)

GGrraasssseess // HHeerrbbss ((1122 aalllleerrggeennss))

• 6 grasses (see above)• Agrostis alba (redtop)• Cynodon dactylon (bermuda grass)• Sorghum halpense (sorghum)• Rumex crispus (sheep sorrel)• Artemisia spp. (mugwort)• Plantago lanceolata (ribwort)• Chenopodium spp. (lambs quarter)• Urtica dioica (nettel)• Parietaria jud. (parietaria)• Salsola kali ssp. ruthenica

(russian thistle)

SSiinnggllee AAlllleerrggeenn DDeetteerrmmiinnaattiioonn -- LLAARRGGEE(Allercept™™) ffoorr ddoogg//ccaatt//hhoorrssee

00..55 mmll//ggrroouupp SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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TTrreeeess ((1122 aalllleerrggeennss))

• Betula (birch)• Alnus (alder)• Quercus (oak)• Cupressus (cypress)• Corylus (hazel)• Ulmus (elm)• Fagus sylvatica (beech)• Populus (poplar)• Acer (japanese maple)• Salix (willow)• Olea (olive)• Cedrus (ceder)

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1144..22 AAlllleerrggyy DDiiaaggnnoossttiiccss

Specific single allergen determination can be performed fol-lowing a positive Allerceptä Screening-Test. The test is per-formed using any of the 3 groups (see page 209) thatshowed a positive result. Once a single allergen has beenidentified it can be eliminated or specific immune therapycan be started.The SMALL panels are only available for catsand dogs.

MMiitteess // MMoouullddss,, FFuunngguuss ((66 aalllleerrggeennss))

• Alternaria + Aspergillus• Cladosporium + Penicillin• Dermatophagoides farinae

(house dust mite)• Dermatophagoides pteronyssinus

(house dust mite)• Tyrophagus putrescentiae

(storage mite)• Acarus siro

(storage mite)

Note: No Flea saliva tested!

Simulium sp. (blackfly)Culex sp. (mosquito)Tabanus sp. (horse fly)Stomoxys calcitrans (stable fly)Culicoides sp. (biting midge)

IInnsseecctt AAlllleerrggyy TTeesstt(Equine)

33 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

SSiinnggllee AAlllleerrggeenn DDeetteerrmmiinnaattiioonn -- SSMMAALLLL(Allercept™™) for ddoogg//ccaatt

00..55 mmll//ggrroouupp SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

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TTrreeeess // GGrraasssseess // HHeerrbbss((88 aalllleerrggeennss))

• Mix of 6 grasses:- Dactylis glomerata (cocksfoot)- Festuca pratensis (meadow fescue)- Poa pratensis (blue grass anual)- Lolium perenne (perennial ryegrass)- Phleum pratense (timothy grass)- Holcus lanatus (common velvet grass)

• Secale cereale (rye)• Artemisia spp. (mugwort)• Plantago lanceolata (ribwort)• Betula (birch)• Salix (willow)• Urtica dioica (nettel)• Rumex crispus (sheep sorrel)

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In order to produce a hyposensitisation solution a veterinaryprescription is required. The starter pack includes 3 bottlesin ascending concentrations and is sufficient for about 6months. A dosage scheme is included.

Usually 2-3 repeat orders can be prepared from a singlebatch of hyposensitisation solution without the need to submit new material.

HHyyppoosseennssiittiissaattiioonn SSoolluuttiioonn --RReeppeeaatt OOrrddeerr (if required)

HHyyppoosseennssiittiissaattiioonn SSoolluuttiioonn(dog, cat, horse)

1144..22 AAlllleerrggyy DDiiaaggnnoossttiiccss

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1155..11 GGeenneerraall IInnffoorrmmaattiioonn oonn PPCCRR

�� PPCCRRGGeenneerraall IInnffoorrmmaattiioonn

The diagnostic advantage of PCR (polymerase chain reaction) is based on the principlethat specific segments of the various nucleic acids (DNA and RNA) contained in a samplemay be increased (amplified), so that they become measurable or able to be sequenced forfurther identification. The amplified nucleic acid is usually derived from pathogen specificDNA or RNA, or in the case of hereditary diseases it is from gene sections wheremutations are located. For sex identification, the specific genome sequence is amplifiedwhich contains the different gene sequences for the male and female gender.

PPCCRR tteecchhnniiqquuee

PCR runs in three reaction steps:In the ffiirrsstt sstteepp the DNA which is to be amplified is heated to 94 °C, which denaturates itand splits it into two complementary single strands. The temperature is reduced in the sseeccoonndd sstteepp, so that a specific complementary oligonu-cleotide (primer) can attach to each DNA single strand (template DNA). The region of thetemplate DNA between the two primers is the region which will be amplified. The primersserve as contacts for the heat-stable DNA polymerase (taq-polymerase).In the tthhiirrdd sstteepp, the taq-polymerase joins the single nucleotides, which were added to thetest preparation along with the template DNA to form a complementary strand. Now twoidentical double strands have been produced.A new heating sequence separates these new DNA double strands so that the newlyformed single strands can again act as template DNA.These three reaction steps are repeated many times to gain a large number of identicalcopies of the original DNA segment.

Several modifications to the test protocol expand the range of the use of PCR:

- amplification of RNA to detect RNA viruses (reverse transcription into DNA required)- increased specificity by using an additional specific primer pair (‘nested PCR’),

hybridisation probes or RFLP analysis- quantification of the original DNA/RNA by using internal standards

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1155..11 GGeenneerraall IInnffoorrmmaattiioonn oonn PPCCRR

TTeesstt iinntteerrpprreettaattiioonn

A ppoossiittiivvee PCR result indicates the presence of the sought-after nucleic acid in the testedmaterial. However it is not possible to distinguish whether or not the pathogen found isviable and able to multiply. Conventional PCR techniques also do not allow quantification of nucleic acid. Suitable methods for quantitative PCR are currently being implemented at our lab.Please note that due to the high sensitivity ffaallssee ppoossiittiivvee PCR results are possible if the sample is even slightly contaminated with the sought-after nucleic acid.

A nneeggaattiivvee PCR result indicates that at the time of sampling the sought-after nucleic acid could not be amplified, either because there was no such nucleic acid present in the sample or the amount was insufficient to be amplified.

FFaallssee nneeggaattiivvee results are possible when using unsuitable material, e.g. sample materialcontaining inhibitory substances (such as heparin) or inadequate handling of the samplebefore/during transport (e.g. repeated freezing and defrosting). However, inhibitorysubstances will be detected during PCR analysis and either removed, or if not possible,commented on. Therefore, false negative PCR results due to inhibition can be completely avoided.

SSaammppllee mmaatteerriiaall

Suitable samples for PCR are those that are expected to contain as much of the sought-after pathogen as possible. Before sampling it should therefore be decided

- whether the animal is presently in the bacteraemic/viraemic stage - whether the pathogen has already reached its target organ and if so,

which would be its most likely location considering the clinical symptoms- whether there could be a latency organ to which the pathogen retreats

outside of acute phases of disease (e.g. EHV 1 in leukocytes)

Possible sample material which can be used for PCR:

- SSwwaabbssUse a sterile, dry swab. Do not use transport medium or a coated sample tube. Please note: no bacterial culture can be performed on these samples!

- BBiioollooggiiccaall fflluuiiddss(synovial fluid, cerebrospinal fluid, body cavity aspirates, aqueous humour, urine etc.)Use a sterile, uncoated sample tube. An amount of 0.5 - 2.0 ml material is required, depending on the desired test. Urine samples require 5 ml. If the sample is guaranteed to arrive at the lab within 48 hours of sampling, please store the sample at + 4°C prior to sending, and do not freeze for transportation. If the transportation time is expected to take any longer, the sample should be frozen (- 20°C) and sent to the lab wwiitthhoouutt ddiissrruuppttiioonn ooff tthhee ccoolldd cchhaaiinn throughout transportation. However, for detection of intracellular organisms (i.e. Babesia, etc.), freezing of the sample should be avoided, but if necessary storage at - 4°C is acceptable.

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1155..11 GGeenneerraall IInnffoorrmmaattiioonn oonn PPCCRR

Please clearly state on the outside packaging if you are sending a frozen sample. Defrosting and refreezing must be avoided!

- BBiiooppssiieess,, oorrggaann ppaarrttss,, aabboorrttiioonn mmaatteerriiaallUse a sterile, uncoated sample tube and fill it with an adequate amount of normal saline solution to cover the sample. In cases where the sample would not reach the lab within 48 hours of sampling, please do not cover the sample with saline solution, but freeze it and send it to the lab wwiitthhoouutt ddiissrruuppttiioonn ooff tthhee ccoolldd cchhaaiinn. Please clearly state on the outside packaging that this is a frozen sample. Thawing and refreezing must be avoided!

- EEDDTTAA bblloooodd,, cciittrraatteedd bbllooooddThe amount of sample material needed varies depending on the desired test and the phase of disease. Do not send frozen blood samples. DDoo nnoott sseenndd hheeppaarriinn bblloooodd.

- FFaaeecceessUse a sterile, uncoated sample tube. Usually 2 g faeces are sufficient.

PPrreeccaauuttiioonnaarryy mmeeaassuurreess wwhheenn hhaannddlliinngg ssaammppllee mmaatteerriiaall

- Due to the high sensitivity of the PCR method it is extremely important to use sterile tubes and collection equipment. Avoid contamination due to handling of the sample (e.g. decanting or packaging).

- Send the sample unfrozen if it is guaranteed to reach the lab within 48 hours of sampling, but store the sample at +4°C until you send it.

- If longer transport times cannot be avoided, freeze the sample and send it frozen (except EDTA/citrated plasma), ensuring an undisrupted cold chain (e.g. use dry ice). If this is not possible, it is better not to freeze the sample at all. Thawing and refreezing must be avoided!

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1155..22 PPaatthhooggeenn DDeetteeccttiioonn uussiinngg PPCCRR

Serologically, infection with Babesia spp. can be detected10-14 days post infection at the earliest. In rare cases seroconversion does not take place at all. In the early stageof infection, Babesia spp. can be found microscopically inblood smears. False negative results are possible due to the fact that often only a small percentage of erythrocytescontain the pathogen. PCR presents an alternative method with a high sensitivityto clarify suspected Babesia spp. infection before theformation of specific antibodies.

B. henselae infection in cats is usually asymptomatic. A connection to localised or generalised lymphadenopathyis currently being discussed. Infected cats can remain bacteraemic for months or years, with varying amounts of bacteria in the blood stream.The disease is of interest when a contact person developssuspicious clinical symptoms (‘cat scratch disease’). In 90% of the human cases, the disease shows as a benign,self-limiting lymphadenopathy. Complications are only seenin rare cases, mainly in immunosuppressed individuals, andconsist of encephalopathy, arthritis and pneumonia.Cat bites and scratches are not the only means by whichhumans can become infected with Bartonella. There areproven cases of human bartonellosis that have had no contact with cats at all.

BBaarrttoonneellllaa hheennsseellaaee,,qquuiinnttaannaa ((DDNNAA))(cat scratch disease)

00..55 mmll EEDDTTAA bblloooodd,, LLyymmpphh nnooddee aassppiirraattee

BBaabbeessiiaa sspppp.. ((DDNNAA)) 00..55 mmll EEDDTTAA bblloooodd

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1155..22 PPaatthhooggeenn DDeetteeccttiioonn uussiinngg PPCCRR

Due to the high seroprevalence in the dog population it isoften difficult to interpret the results. Only a significantincrease in the titre level or an extremely high initial titrecan be suggestive for an acute infection. Should clinicalsymptoms be present, the PCR test for detection of the antigen is therefore a fast method to confirm the clinicalsuspicion (in the case of a positive PCR). Yet a negativeresult can not rule out infection because the pathogen may be elsewhere in the body. It is therefore vital to choose the sample material very carefully!Horses in endemic areas show B. burgdorferi antibodytitres, but the clinical relevance of the infection is debatable.Lameness, polyarthritis and panuveitis have been describedin conjunction with Borrelia infection in horses. Generally it is possible to detect the pathogen in the affected organsusing PCR.

Virus excretion in the faeces is highest during the first weekpost infection and then it decreases rapidly. After 15 days p. i. it is usually not possible to detect the virus. Therefore a rectal swab should be taken as soon as first symptoms are seen.CCV infection usually causes a moderate, self-limitinggastroenteritis. PCR diagnostics are particularly interestingto identify sick animals early and to detect virus sheddingindividuals in breeding populations. Naturally the detection of coronavirus in faeces does notrule out other pathogens for the cause of diarrhoea.

CCaanniinnee CCoorroonnaavviirruuss(CCV) ((RRNNAA))

GGaassttrrooeenntteerriittiiss:: RReeccttaall sswwaabbAAccuuttee ffeebbrriillee ssttaattee:: 00..55 mmll EEDDTTAA bblloooodd

CCaalliicciivviirruuss ((RRNNAA))(cat)

SSwwaabb ((ddrryy))

BBoorrrreelliiaa bbuurrggddoorrffeerrii(sensu lato) ((DDNNAA))

LLaammeenneessss:: 00..55 mmll JJooiinntt aassppiirraatteeCCNNSS ssyymmppttoommss:: 00..55 mmll CCeerreebbrroossppiinnaall fflluuiiddAAccuuttee ddiisseeaassee//ppyyrreexxiiaa:: 55 mmll UUrriinnee,, 00..55 mmll EEDDTTAA bbllooooddOOtthheerr:: TTiicckk

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1155..22 PPaatthhooggeenn DDeetteeccttiioonn uussiinngg PPCCRR

It is important for dog breeders to clarify possibleherpesvirus involvement in the event of acute deaths in puppies < 3 weeks of age in the breeding population, inorder to prevent further spreading of the disease. Due to the fulminant progession of the disease animals do not have the chance to produce antibodies. In this case PCR is the method of choice to diagnose CHV I infection.

The most meaningful results are obtained if material iscollected with the first onset of symptoms. Chlamydia areobligate intracellular pathogens, therefore it is important toobtain swabs with as much cellular material as possible. A positive PCR result confirms the involvement of Chlamydia spp. in the disease process, whereas a negativeresult does not rule out chlamydial involvement.

CChhllaammyyddoopphhiillaa ffeelliiss(Chlamydia felis) ((DDNNAA))

CCoonnjjuunnccttiivviittiiss:: CCoonnjjuunnccttiivvaall sswwaabbRReessppiirraattoorryy ssyymmppttoommss:: SSwwaabb ffrroomm nnoossee,, tthhrrooaattAAbboorrttiioonn:: VVaaggiinnaall sswwaabb

CCaanniinnee HHeerrppeessvviirruuss II(CHV I) ((DDNNAA))

AAccuuttee ppuuppppyy ddeeaatthh:: TTiissssuuee ffrroomm lliivveerr,, lluunnggss,, kkiiddnneeyyss,, sspplleeeenn

GGeenniittaall iinnffeeccttiioonnss:: VVaaggiinnaall sswwaabbAAbboorrttiioonn:: AAbboorrttiioonn mmaatteerriiaallRReessppiirraattoorryy ssyymmppttoommss:: SSwwaabb ffrroomm nnoossee,,

tthhrrooaatt,, ttoonngguuee

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1155..22 PPaatthhooggeenn DDeetteeccttiioonn uussiinngg PPCCRR

Birds infected with Chlamydophila psittaci can remain withoutsymptoms for a long period of time or show only nonspecificsymptoms. Occasionally it takes years before chlamydiosisappears. The faecal excretion of the pathogen starts 3 dayspost infection and can last for months, often intermittently.Latently infected animals may start shedding again ifimmunosuppressed (stress, illness). Stressed and sickanimals shed a larger amount of pathogen and they shed it more frequently.It is important to identify infected birds, especially permanentshedders, because they constitute the main danger of infection to other birds and to humans (zoonosis!). Cloacalswabs are most suitable for testing. In the case of clinicalsuspicion but a negative test result the test should berepeated to allow for the intermittent shedding of thepathogen.

Virus replication takes place from the 8th day post infectionin the epithelial cells of different organs (respiratory tract,digestive tract, urogenital tract, skin) and in the CNS.Clinical symptoms reflect the location of the virus replication.At this time PCR can be used on the affected organs. Withthe exception of chronic infection, virus excretion ceaseswith the fading of clinical symptoms and virus is no longerdetectable.As opposed to antibody detection, the high percentage ofvaccinated animals does not pose a major problem for PCRtesting, because the vaccination virus is only detectable 8-21 days after inoculation and it remains in the lymphatictissues.

DDiisstteemmppeerrvviirruuss ((RRNNAA)) FFeebbrriillee ssttaattee:: 22 mmll EEDDTTAA bbllooooddCCoonnjjuunnccttiivviittiiss:: CCoonnjjuunnccttiivvaall sswwaabbCCNNSS ssyymmppttoommss:: 00..55 mmll CCeerreebbrroossppiinnaall fflluuiiddGGaassttrrooeenntteerriittiiss:: RReeccttaall sswwaabbRReeppiirraattoorryy ssyymmppttoommss:: NNaassaall sseeccrreettiioonnss

CChhllaammyyddoopphhiillaa ppssiittttaaccii(Chlamydia psittaci) ((DDNNAA))

CCllooaaccaall sswwaabb,, FFaaeecceess

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1155..22 PPaatthhooggeenn DDeetteeccttiioonn uussiinngg PPCCRR

Dogs infected with E. canis can be tested successfullyapprox. 4 days post infection using PCR. This allows for testing even before antibodies are found. PCR also allowschecking for pathogen elimination during antibiotic therapy,whereas serology would be less useful because antibodiescirculate much longer.

A positive PCR result confirms a suspected infection with E. canis, but a negative result does not rule out infection:the pathogen might not have been in the blood at the time of sampling, there might not have been sufficient pathogenin the blood at the time of sampling, or there could be aninfection with a different Ehrlichia species.

No differentiation between species.

EEhhrrlliicchhiiaa//AAnnaappllaassmmaa sspppp..((DDNNAA))

11 mmll EEDDTTAA bblloooodd

EEhhrrlliicchhiiaa ccaanniiss ((DDNNAA)) 11 mmll EEDDTTAA bblloooodd

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1155..22 PPaatthhooggeenn DDeetteeccttiioonn uussiinngg PPCCRR

The interpretation of serological test results can be difficult, especially in herpesvirus infections. Some of the reasons are:

1. Virus persistence, which is characteristic for herpesvirus, leading to reactivation of the virus under stress conditions so renewing antibody production.

2. Serum antibodies do not lead to a stable immunity, therefore even high antibody levels do not protect from reinfection.

3. Antibody production may be insufficient especially in the respiratory form of the disease. In the EHV infection defence mechanism cellular immunity plays a more important role than humoral immunity.

Using PCR allows the direct detection of the pathogen in the affected organ and subsequently the assurance of theaetiological correlation between the acute disease and a herpesvirus infection. The examination of amniotic fluid and uterine mucosa is the method of choice, especially in abortions, as a foetus from a herpesvirus abortion may be virus negative (abortion due to under-nourishment via the placenta)!A positive PCR result from blood is no evidence for theinvolvement of herpesvirus in acute disease, becauseherpesvirus can persist in leukocytes after a previous infection.

Please note: The test used does routinely differentiate between EHV-1 and EHV-4!

EEqquuiinnee HHeerrppeessvviirruuss 11(EHV-1) ((DDNNAA))EEqquuiinnee HHeerrppeessvviirruuss 44(EHV-4) ((DDNNAA))

RReessppiirraattoorryy ssyymmppttoommss:: NNaassaall//tthhrrooaatt sswwaabb,, NNaassaallsseeccrreettiioonn,, TTrraacchheeaall sseeccrreettiioonn

CCoonnjjuunnccttiivviittiiss:: CCoonnjjuunnccttiivvaall sswwaabbAAbboorrttiioonn:: AAmmnniioottiicc fflluuiidd,,

EEnnddoommeettrriiuumm,, FFeettuussCCNNSS ssyymmppttoommss:: 00..55 mmll CCeerreebbrroossppiinnaall fflluuiidd

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1155..22 PPaatthhooggeenn DDeetteeccttiioonn uussiinngg PPCCRR

Once again, using PCR allows the direct detection of the pathogen in the affected organ and subsequently the assurance of the aetiological correlation between the acute disease and a herpesvirus infection.

Although EHV-5 detection using PCR is possible the clinical relevance is not quite clear.

Various sample material is suitable for EVA detection usingPCR (0.5 ml of fluid or 0.5 g of tissue is required):

- sperm, seminal plasma- vaginal swab, vaginal wash- nasal secretion, tracheal wash- EDTA blood, citrated blood,- tissue: lymph node, spleen, lung, placenta, foetal- (urine)

EEqquuiinnee VViirraall AArrtteerriittiiss (EVA) ((DDNNAA))

VVaarriioouuss ((sseeee bbeellooww))

EEqquuiinnee HHeerrppeessvviirruuss 55(EHV-5) ((DDNNAA))

CCeerreebbrroossppiinnaall fflluuiidd,, SSwwaabb

EEqquuiinnee HHeerrppeessvviirruuss 22(EHV-2) ((DDNNAA))

OOccuullaarr ssyymmppttoommss:: CCoorrnneeaall sswwaabb,, CCoonnjjuunnccttiivvaall sswwaabb

RReessppiirraattoorryy ssyymmppttoommss:: NNaassaall sswwaabb,, NNaassaall//TTrraacchheeaallsseeccrreettiioonn

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1155..22 PPaatthhooggeenn DDeetteeccttiioonn uussiinngg PPCCRR

Using PCR, it is currently not possible to differentiatebetween FIPV (feline infectious peritonitis virus) and FECV(feline enteric coronavirus), which can mutate in the body to FIPV.

The detection of FCoV (feline coronavirus) in an aassppiirraatteeor in cceerreebbrroossppiinnaall fflluuiidd suggests the diagnosis of FIP, especially when concurrent clinical symptoms and othercorresponding laboratory findings are present (serology,clinical chemistry).

Qualitative detection of FCoV in ffaaeecceess does prove infectionwith FCoV, but it does not give evidence of FIP disease. Itcan merely be used to identify virus shedders. In the case of a negative result the test should be repeated becauseshedding may be intermittent. Possible future quantificationof virus shed via faeces (an appropriate PCR test is underdevelopment) may be a helpful diagnostic aid in the identification of ‘heavy’ shedders in a feline population,which would pose a threat for other animals.

It is suggested that all feline coronaviruses can causeviraemia. Therefore the detection of FCoV in bblloooodd is of little significance for FIP diagnosis.

Acutely infected animals excrete virus in large quantities.However, chronically infected animals only excrete virusintermittently or in small quantities. The high sensitivity ofPCR allows the identification of these chronic virus carriers.In the case of a negative result, the test should be repeatedas the virus is excreted intermittently.

FFeelliinnee HHeerrppeessvviirruuss II(FHV I) ((DDNNAA))

KKeerraattooccoonnjjuunnccttiivviittiiss:: SSwwaabb ffrroomm ccoorrnneeaall//ccoonnjjuunnccttiivvaall lleessiioonn

RRhhiinnoottrraacchheeiittiiss:: NNaassaall sswwaabb,, TThhrrooaatt sswwaabbGGeenniittaall iinnffeeccttiioonn:: VVaaggiinnaall sswwaabbAAbboorrttiioonn:: AAbboorrttiioonn mmaatteerriiaall

FFeelliinnee CCoorroonnaavviirruuss(FCoV/FECV)((RRNNAA))

BBooddyy ccaavviittyy eeffffuussiioonn:: 00..55 mmll AAssppiirraatteeCCNNSS ssyymmppttoommss:: 00..55 mmll CCeerreebbrroossppiinnaall fflluuiiddPPyyrreexxiiaa ((vviirraaeemmiicc pphhaassee)):: 00..55 mmll EEDDTTAA bbllooooddVViirruuss eexxccrreettoorrss:: FFaaeecceess oorr RReeccttaall sswwaabb

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1155..22 PPaatthhooggeenn DDeetteeccttiioonn uussiinngg PPCCRR

The safest method for proving FIV infection is a PCR test ona blood sample at the very onset of clinical symptoms,because the clinical symptoms are usually accompanied byviraemia. As the amount of circulating virus can be belowPCR detection limits the test applied will only screen for FIVprogenome (i.e. FIV nucleic acid incorporated intolymphocyte genomic DNA).

PCR may be used to clarify doubtful positive or negativeserological results: - infected animals may show false negative serological

results in the early stage of disease (not all animals show antibodies 2-4 weeks p.i.) or in the late stage of the disease (amount of antibodies falling below detection limits)

- false positive serological results are possible e. g. in kittens up to the age of 16 weeks when maternal antibodies will still interfere

Viral DNA integrated in the host cell genome is known asprogenome or provirus, which can be detected using PCR.This test is highly specific and can therefore be used toconfirm doubtful results with other methods.

Latent infections can possibly be diagnosed, which usuallyshow negative results with other test methods. The sensitiv-ity of PCR is highly dependent on the number of infectedcells (provirus load), which is why a negative result does notentirely rule out infection.

FFeelliinnee LLeeuucceemmiiaa VViirruuss(FeLV) Progenome ((DDNNAA))

22 mmll EEDDTTAA bblloooodd oorr bboonnee mmaarrrrooww

FFeelliinnee IImmmmuunnooddeeffiicciieennccyyVViirruuss (FIV) Progenome((DDNNAA))

22 mmll EEDDTTAA bblloooodd,, LLyymmpphh nnooddee aassppiirraattee ((eennllaarrggeedd llyymmpphh nnooddeess))

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1155..22 PPaatthhooggeenn DDeetteeccttiioonn uussiinngg PPCCRR

The pathogenicity of helicobacter infection in animals is not quite clear. The data available is often contradictory. It is possible to isolate Helicobacter spp. from the gastricmucosa in dogs and cats suffering from gastritis, chronicvomiting or enteritis. However, Helicobacter spp. can also be isolated in healthy animals and there is a strongsuspicion that the prevalence in the canine and feline population is 90-100%.In rodents tested positive forHelicobacter spp. DNA it is possible to differentiate betweeninfections with H. bilis, H. hepaticus and H. muridarium (onrequest only).

The highest success rate is gained from lymph node andbone marrow aspirates.The great advantage of pathogen detection using PCR is tobe able to identify healthy carriers, whose antibody titresare often below detection limits. PCR on bone marrow maybe used for treatment control.

Pathogen detection using PCR is done on EDTA blood in thefirst two weeks (possibly up to two months) post infection,but after two weeks detection in urine is more effective. The pathogen can be found in urine for month or years, but the excretion can occur intermittently.Compared to serology, PCR has the advantage of being ableto confirm a clinical suspicion even before antibodies occur(approx. 10 days p.i.). It is also possible to identify chronicshedders, even if they are vaccinated. A negative test resultcan occur and should be repeated, since the pathogen isshed intermittently.

LLeeppttoossppiirraa sspppp.. ((DDNNAA)) 00..55 mmll EEDDTTAA bblloooodd,, 55 mmll UUrriinnee,, 00..55 mmll CCSSFF

LLeeiisshhmmaanniiaa sspppp.. ((DDNNAA)) SSkkiinn lleessiioonnss:: SSkkiinn bbiiooppssyyLLyymmpphhaaddeennooppaatthhyy:: LLyymmpphh nnooddee aassppiirraatteeRRhhiinniittiiss:: NNaassaall sswwaabbOOtthheerr:: BBoonnee mmaarrrrooww,, LLiivveerr//SSpplleeeenn bbiiooppssyy

HHeelliiccoobbaacctteerr sspppp.. ((DDNNAA)) GGaassttrriicc bbiiooppssyy,, FFaaeecceess

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1155..22 PPaatthhooggeenn DDeetteeccttiioonn uussiinngg PPCCRR

Using PCR for Listeria detection is a sensitive method foridentifying permanent shedders. Apart from feed andenvironmental contamination, these pose an importantfactor in pathogen distribution.

Haebartonella felis has been reclassified as a Mycoplasmaand there are 2 strains - Mycoplasma haemofelis and Candi-datus Mycoplasma haemominutum. M. haemofelis is gener-ally considered the most pathogenic.Cand. M. haemominutum in immunocompetent animals doesnot normally cause any clinical symptoms, but in rare cases,mild transient febrile conditions are possible. However, concurrent infection with FeLV is of importance (see below).In these animals, Cand. M. haemominutum can cause similarsymptoms as with M. haemofelis infection.

Feline haemobartonellosis is an acute or chronic diseaseoften associated with haemolytic anaemia. Untreated itoften leads to the death of the animal. Untreated animalsmay become carriers if they survive the infection. They mayhave intermittent parasitaemia. Mycoplasma may also befound in clinically healthy cats. Predisposing factors for thedevelopment of disease are considered FeLV infection,splenectomy or long-term corticosteroid treatment.

The mode of transmission appears to be via blood-suckinginsects and bite wounds, but it is not yet certain. PCR detectionof Mycoplasma is much more specific and sensitive thandirect detection in a blood smear (the organism can easilyseparate from the erythrocyte which makes it very difficultto identify in a blood smear).

MMyyccooppllaassmmaa hhaaeemmooffeelliiss++ CCaannddiiddaattuuss MMyyccooppllaassmmaa hhaaeemmoommiinnuuttuumm ((DDNNAA))

00..55 mmll EEDDTTAA bblloooodd

LLiisstteerriiaa mmoonnooccyyttooggeenneess((DDNNAA))

CCNNSS ssyymmppttoommss:: 00..55 mmll CCeerreebbrroossppiinnaall fflluuiiddAAbboorrttiioonn:: AAbboorrttiioonn mmaatteerriiaallSSeeppttiiccaaeemmiiaa:: 22 mmll EEDDTTAA bbllooooddPPeerrmmaanneenntt sshheeddddeerr:: FFaaeecceessDDiiaarrrrhhooeeaa:: FFaaeecceess

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1155..22 PPaatthhooggeenn DDeetteeccttiioonn uussiinngg PPCCRR

Direct detection of parvovirus is possible in faeces or rectalswabs from cats and dogs. An additional test can differenti-ate between the field virus and the vaccination virus in thedog. This is of diagnostic value as the vaccination virus maybe excreted 5-12 days post vaccination. Excretion of thefield virus starts 3-4 days post infection and usually lasts for 7-10 days. Longer excretion is possible in single cases.

A negative PCR test does not rule out infection.

The pathogen causing PBFD (psittacine beak and featherdisease) is a circovirus. Initial virus replication occurs inlymphatic tissue, gastrointestinal tract and liver, but the target organ is the epidermis.

The acute form affects mostly hatchlings which showdiarrhoea, possibly hepatitis and in particular deformedfeathers. Many young birds overcome the acute disease and develop a chronic infection. The chronic form is characterised by growth of deformed feathers after moulting and changes on the beak.

Latently infected animals and animals in the incubation period pose the biggest threat for introducing the virus to a population. PCR is the method of choice to identify theseanimals. But a positive PCR test in not proof of active infection, since inactive virus DNA is detectable in the bloodfor up to three months. PCR-positive animals that do notshow clinical symptoms should therefore be isolated and re-tested after three months. If they are still positive afterthree months, they must be considered chronically infected,posing a threat to other birds.

PPBBFFDD VViirruuss ((DDNNAA)) DDiiaarrrrhhooeeaa:: CCllooaaccaall sswwaabbFFeeaatthheerr ddeeffoorrmmaattiioonn:: DDeeffoorrmmeedd ffeeaatthheerrssPPoosstt mmoorrtteemm:: KKiiddnneeyy,, SSpplleeeenn,, LLiivveerrCChhrroonniicc ffoorrmm:: 00..55 mmll EEDDTTAA bblloooodd

PPaarrvvoovviirruuss (dog, cat)((DDNNAA))

FFaaeecceess,, RReeccttaall sswwaabb

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1155..22 PPaatthhooggeenn DDeetteeccttiioonn uussiinngg PPCCRR

Vertical spread and virus spread by clinically inapparentanimals are the main means of transmission of BFD(budgerigar fledgling disease). Carriers can be identified by testing several cloacal swabs using PCR, in three monthintervals, to be able to detect even intermittently sheddinganimals. When feather deformities are present, clinical suspicion can be confirmed using PCR on deformed feathers.The liver, spleen and kidneys can be used from young birdsthat have died acutely.

Should an animal from an endemic area show CNSsymptoms, antigen detection using PCR is a useful test in addition to serological testing of cerebrospinal fluid.The virus can also be detected directly in the tick.

TTiicckkbboorrnnee EEnncceepphhaalliittiissVViirruuss ((RRNNAA))

TTiicckk,, 00..55 mmll CCeerreebbrroossppiinnaall fflluuiidd

PPoollyyoommaavviirruuss(BFD-Virus) ((DDNNAA))

DDiiaarrrrhhooeeaa:: CCllooaaccaall sswwaabbFFeeaatthheerr ddeeffoorrmmaattiioonn:: DDeeffoorrmmeedd ffeeaatthheerrssPPoosstt mmoorrtteemm:: KKiiddnneeyy,, SSpplleeeenn,, LLiivveerrCChhrroonniicc ffoorrmm:: 00..55 mmll EEDDTTAA bblloooodd

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1155..22 PPaatthhooggeenn DDeetteeccttiioonn uussiinngg PPCCRR

The high prevalence of antibodies against toxoplasma indogs and cats greatly restricts the use of serology in thediagnosis. Only increased IgM titres give a clear indicationfor acute infection, which is often accompanied by faecaloocyst shedding in cats. Usually the body is unable to eliminate the pathogen, therefore most infected animalsremain seropositive (IgG) - often with high titres due to prolonged exposure, which even makes it difficult to judge paired serum samples.

Please note that a positive PCR test does not prove acuteinfection with Toxoplasma gondii. The pathogen has beenisolated from cerebrospinal fluid and aqueous humour inclinically healthy animals! PCR testing of faecal samples is not very useful, because it is very difficult to extract DNA from the hard-shelled oocysts that are shed. Normal chemical preparations cannot extract the DNA (a specialprotocol is being worked on).In order to rule out the shedding of oocysts in particular circumstances, e.g. pregnancy of the owner, classical methods such as serology and microscopic faecal examination must be performed.

TTooxxooppllaassmmaa ggoonnddiiii((DDNNAA))

CCNNSS ssyymmppttoommss:: 00..55 mmll CCSSFFAAbboorrttiioonn ((ddoogg,, ssmmaallll rruummiinnaannttss)):: VVaaggiinnaall ssmmeeaarr,,

PPllaacceennttaa,, FFooeettaall CCNNSS

RReessppiirraattoorryy ssyymmppttoommss:: BBrroonncchhiiaall wwaasshhOOccuullaarr ssyymmppttoommss ((eesspp.. ccaattss)):: AAqquueeoouuss hhuummoouurrPPyyrreexxiiaa:: 00..55 mmll EEDDTTAA bblloooodd

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1155..33 HHeerreeddiittaarryy DDiisseeaasseess

�� HHeerreeddiittaarryy DDiisseeaasseessGGeenneerraall IInnffoorrmmaattiioonn

Hereditary diseases are due to genetic mutations. The mutation can be passed on fromparents to offspring.

FFuunnddaammeennttaall ggeenneettiiccss::Sexual reproduction means that the offspring receives a double set of chromosomes. Oneset of chromosomes each originates from the mother and father respectively. Thereforeeach gene is found in duplicate, meaning as two alleles.

- if both alleles carry the same characteristic or the same defect, the individual is hhoommoozzyyggoottiicc for that defect

- if only one of the alleles carries the characteristic or the defect, the individual is hheetteerroozzyyggoottiicc

The phenotype of the individual is the result of the gene expression. For hereditary disease this implies:

- ddoommiinnaanntt genes will be expressed even if only one of the two alleles is affected by the defect. Thus, the hereditary disease will be expressed in the offspring if the mother or the father passes on the mutant gene.

- rreecceessssiivvee genes are only expressed when both alleles are affected by the defect. This means that both mother and father must both pass the mutant gene to the offspring. If an animal carries only one allele for the recessive hereditary disease, it will not express the disease all its life. But it is a carrier and can pass on the gene to its offspring. If two recessive carriers are matched, the offspring may receive two defective alleles and subsequently express the disease.

- XX--cchhrroommoossoommaall gene expression: male animals will express the hereditary disease, because the defect is located on the gene that is responsible for the x-chromosome. Female individuals can be carriers or if they are homozygote also express the hereditary disease.

- aauuttoossoommaall gene expression: the responsible gene is not located on the x-chromosome, therefore the hereditary disease can be expressed by both male and female individuals and they can both pass it on to their offspring.

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1155..33 HHeerreeddiittaarryy DDiisseeaasseess

�� MMoolleeccuullaarrggeenneettiiccaall TTeessttiinngg ffoorr HHeerreeddiittaarryy DDiisseeaasseess

Moleculargenetical testing can be performed at an early age, before the expression ofhereditary disease occurs. It is suitable for identifying carriers of genetic defects. Theseanimals can then be excluded from breeding.PCR is used for hereditary disease testing. The DNA which contains the possible mutantgene is amplified and the sequence is compared to the same sequence of a geneticallysound animal.

The following results are possible:

1. The animal is genetically sound in respect of the disease tested. Neither of the two alleles carries the mutation in question. The animal cannot express the hereditary disease, nor can it pass it on.

2. The animal is heterozygous in respect of the mutation in question. It carries a mutant gene either from the mother or the father. Autosomal dominant gene expression will lead to phenotypic expression of the gene: the animal will express the hereditary disease. Autosomal recessive gene expression will not lead to an expression of the disease. In both cases, the animal can pass on the genetic defect to its offspring.

3. The animal is homozygous in respect of the genetic defect in question. Both alleles are mutants. The animal will express the hereditary disease and it will pass on the genetic defect to its offspring.

BLAD (Bovine leukocyte adhesion deficiency) leads to fatalimmunodeficiency in calves and young cattle.

Occurrence: Holstein cattle

Symptoms: - recurrent infections of the respiratory and gastrointestinal tract, as well as the nasopharyngeal region

- low birth weight- delayed wound healing, necrosis, gangrene

Laboratory findings: leukocytosis

Gene expression: autosomal recessive

BBLLAADD 11 mmll EEDDTTAA bblloooodd

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1155..33 HHeerreeddiittaarryy DDiisseeaasseess

Also called Canine Stress Syndrome. It is caused by asudden severe rise in body temperature during or after general anaesthesia and results in death in up to 70% ofcases. The severity of the symptoms varies. Genetic predisposition and the use of depolarizing muscle relaxantsor volatile anaesthetic agents leads to disturbance in calciumhomeostasis and subsequent increased prolonged musclecontractions, resulting in tachycardia, tachypnoea, musclerigidity, increased lactic acid, hypercalcaemia andmyoglobinuria.

Homozygous aanndd heterozygous carriers can develop the disease.

Gene expression: autosomal dominant

A mutation of MC1R (melanocyte stimulating hormonereceptor) appears to be responsible for the chestnut colour.

Genetic test possible: horse

Symptoms: lack of pigment formation (brown/black)

Gene expression: autosomal recessive

A mutation in the gene which codes for a leukocyteadhesion protein leads to a disturbance in leukocyte functionand subsequently to CLAD (Canine leukocyte adhesiondeficiency), a usually fatal immunodeficiency in Irish Setters.

Occurrence: Irish Setter

Symptoms: - susceptibility to infections (phlebitis, fever, gingivitis, osteomyelitis, osteopathy esp. of metaphyses and jaw bones).

- enlargement of superficial lymph nodes

Laboratory findings: severe neutrophilia

Gene expression: autosomal recessive

CCLLAADD 11 mmll EEDDTTAA bblloooodd

CChheessttnnuutt CCoolloouurr GGeennee 11 mmll EEDDTTAA bblloooodd

CCaanniinnee MMaalliiggnnaanntt HHyyppeerrtthheerrmmiiaa

11 mmll EEDDTTAA bblloooodd

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1155..33 HHeerreeddiittaarryy DDiisseeaasseess

Copper storage hepatopathy is due to a disturbance in copper excretion, which leads to an accumulation of copperin the liver with subsequent damage of the liver cells. Forthe detection of this disease, a DNA microsatellite marker is used, which is closely linked to the responsible genemutation.

Occurrence: Bedlington Terrier

Symptoms: severe liver damage, tremors, possibly haemolytic anaemia

Gene expression: autosomal recessive

A mutation on the gene SCL3A1 leads to a disturbance ofcystine reabsorption in the renal tubuli in Newfoundlanddogs. The increased cystine excretion may lead to theformation of cystine calculi. The DNA test enables thedetection of homozygous animals with this reabsorption disturbance which can then be adequately treatedprophylactically to prevent stone formation, as well as theidentification of clinically healthy carriers of the mutatedgene. This is important for breeding purposes asheterozygous carriers may only be mated with genetically healthy animals.

Genetic test possible: Newfoundland and Landseer dogs

Gene expression: autosomal recessive

CCyyssttiinnuurriiaa iinn tthheeNNeewwffoouunnddllaanndd ddoogg

00..55 mmll EEDDTTAA bblloooodd

CCooppppeerr SSttoorraaggeeHHeeppaattooppaatthhyy

11 mmll EEDDTTAA bblloooodd

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1155..33 HHeerreeddiittaarryy DDiisseeaasseess

Fucosidosis is characterized by the deposit of fucose-containing complex molecules in the nervous system, butalso in the liver, kidneys, lungs, lymph nodes and bone marrow. Due to a genetically determined deficiency of theenzyme alpha-L-fucosidase, these substrates can not bebroken down.

First neurological symptoms are seen at the age of 12-18months (behavioural changes, locomotor disorders, blindness,deafness), eventually leading to the death of the animal.

Genetic test possible: English Springer Spaniel

Genetic expression: autosomal recessive

Gangliosidosis is an autosomal recessive hereditary lipidstorage disease. Gangliosides accumulate in lysosomesbecause of the absence of the necessary enzymes for theirbreakdown. Gangliosidosis is seen in certain dog and catbreeds and in humans. Two main forms are differentiated,depending on the stored ganglioside or the missing enzymerespectively. GM1-gangliosidosis is characterized by thelack of β-galactosidase, and GM2-gangliosidosis is characterized by the absence of β-hexosaminidase.

Both forms lead to severe progressive CNS disorders with tremor and paralysis. GM1-gangliosidosis is expressedearlier and the clinical symptoms progress more quicklythan in GM2-gangliosidosis. Both forms are expressed in the first few months of life.

The Korat cat expresses both forms of the disease. Thegenome for GM2-gangliosidosis is widespread in the Koratcat population, which poses a serious problem for breeders.All cats should be tested before they are used for breedingto avoid breeding with genetic carriers.

Genetic test possible: Korat cats

Symptoms: - CNS symptoms- tremor- paralysis

Gene expression: autosomal recessive

GGaanngglliioossiiddoossiissiinn tthhee KKoorraatt CCaatt

11 mmll EEDDTTAA bblloooodd

FFuuccoossiiddoossiiss 00..55 mmll EEDDTTAA bblloooodd

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1155..33 HHeerreeddiittaarryy DDiisseeaasseess

Globoid cell leukodystrophy (Krabbe disease) is found iscertain dog and cat breeds and in humans. It is a hereditarylipid storage disease. The lack of the lysosomal enzymegalactocerebrocide-β-galactosidase leads to the depositionof of cerebrosides in the CNS. As a consequence the whitematter is demyelinated.In West Highland White and Cairn Terriers the defectfollows an autosomal recessive expression. First symptomsare usually seen at the age of 2-6 months. The animal hassigns of ataxia, paresis of the hind legs, tremor (head),changes in behaviour, reduced spinal reflexes and muscleatrophy.

Genetic test possible: West Highland White Terrier, Cairn Terrier

Symptoms: CNS symptoms such as ataxia/paresis of the hind legs, head tremor.

Gene expression: autosomal recessive

HYPP (Hyperkalaemic periodic paralysis) is a musculardisease that is probably due to disturbed electrolytetransportation in the muscle cell membrane. The responsiblemutation lays on the gene which codes for the sodium channels in the muscle cells. Potassium-induced attacks of skeletal muscle paralysis occur.

Occurrence: American Quarter horse and their cross-breeds

Symptoms: increased breathing sounds, muscle weakness, muscle tremor, collapse;

during training: laryngospasm, hypoxia, hypercapnia, arrhythmias

Gene expression: autosomal co-dominant (more severe symptoms in homozygous animals than in heterozygous animals)

HHYYPPPP 11 mmll EEDDTTAA bblloooodd

MMDDRR 11 00..55 mmll EEDDTTAA bblloooodd

GGlloobbooiidd CCeellllLLeeuukkooddyyssttrroopphhyy

11 mmll EEDDTTAA bblloooodd

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1155..33 HHeerreeddiittaarryy DDiisseeaasseess

The disease is caused by a mutation in the gene coding forthe ryanodine receptor in skeletal muscle. It occurs mainlyin pig breeds with increased muscle and reduced fatproportions. This genetic defect induces increased releaseof calcium from the sarcoplasmic reticulum of themyelocytes in stress situations and under inhalation anaesthetic. This leads to contraction of muscles, followed by increased anaerobic glycolysis, lactic acidosis and hyperthermia.The genetic test allows detection of healthy animals andcarriers of one or two pathological alleles, which is of interest to breeders. Nevertheless the expression of the disease is polygenetically determined.

Genetic test possible: all pig breeds

MDR 1 defect (multidrug-resistance/ivermectine sensitivity).In the 80ties it was already reported that Collies showedneurotoxicity after administration of ivermectin. Recentlyscientists in Germany and in the United States discovered agenetic defect causing this sensitivity. The defect affectsthe building of the Multidrugresistance-1 transporter. The MDR 1-transporter forms part of the blood-brain barrierand is normally responsible for limiting toxic substances(e.g. ivermectine) to enter the neurological tissue. Whenthere is a genetic defect the MDR 1-transporter is notformed properly and looses its protective function. High concentrations of toxic substances can enter the neu-rological tissue. Dependent on the substances you can getvarious symptoms e.g. in-coordination, shivering, enlargedpupils and sometimes they can even die. Other drugs poten-tially causing problems are e.g. dexamethasone, digoxine,loperamide, vincristine, doxorubicin, cyclosporine A,grepafloxacin.

Genetic test possible Collie, Shetland Sheepdog (Sheltie), Bearded Collies, OldEnglish Sheepdog , Australian Sheperd, Australian cattledog

Gene expression: autosomal recessive

MMaalliiggnnaanntt HHyyppeerrtthheerrmmiiaaSSyynnddrroommee (porcine)

00..55 mmll EEDDTTAA bblloooodd

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1155..33 HHeerreeddiittaarryy DDiisseeaasseess

Mucopolysaccharidosis VII occurs in German ShepherdDogs, Beagles, Welsh Corgis and their cross-breeds and is also known in cats, mice and humans. It is caused by adeficiency in the enzyme beta-D-glucuronidase, which contributes to normal cellular function. Affected individualssuffer from progressive lysosomal accumulation ofglucosaminoglycans in certain tissue, leading to variousclinical symptoms (bone malformation, reduced body weight, mental retardation, ocular and cardiac disease,hepatosplenomegaly, etc.). Life span is reduced.

Gene expression: autosomal recessive

Myotonia congenita is not only known in miniature Schnau-zer but also in other dog breeds (Chow Chow, StaffordshireBull Terrier), and cats, horses, sheep, goats, mice andhumans. A mutation in the gene causes changes in the chlo-ride channel in the skeletal muscle membrane. The electrical stimulation of the muscle is impaired and thisleads to delayed muscle relaxation. Puppies already showsymptoms at a few weeks of age

A deletion in the RPE65 gene, which codes for the protein inthe stratum pigmentosum of the retina, is responsible for thedefect. Young puppies show signs of night blindness.Progressively the blindness also extends to daytime.

Occurrence: Berger de Briard dog

Symptoms: night blindness, gradual day blindness

Gene expression: autosomal recessive

NNiigghhtt BBlliinnddnneessss iinnBBrriiaarrddss

11 mmll EEDDTTAA bblloooodd

MMyyoottoonniiaa ccoonnggeenniittaa 00..55 mmll EEDDTTAA bblloooodd

MMuuccooppoollyyssaacccchhaarriiddoossiissVVIIII

00..55 mmll EEDDTTAA bblloooodd

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1155..33 HHeerreeddiittaarryy DDiisseeaasseess

American Paint and other horses with overo-spotted coatcolouring can be heterozygous carriers of a defect in thegene for the endotheline-receptor B. This receptor isinvolved in the development of certain neural tube cells,which later develop into intestinal ganglia. Breeding withtwo heterozygous carriers can lead to the birth ofhomozygous white foals that die of OLWS (Overo LethalWhite Syndrome), a defect of the innervation of thegastrointestinal tract, within days. OLWS also calledCongenital Intestinal Aganglionosis.Occasionally, entirely white foals from affected breeds areborn genetically healthy with regard to OLWS. In suspiciouscases, a moleculargenetical test is always recommended.

Occurrence: offspring from American Paint Horses, Appaloosa, Pinto,Quarter Horses, Thoroughbreds, American MiniatureHorses, Mustangs, Half-Arabs

Symptoms: the foals are born white and develop lethal completeintestinal obstruction

Gene expression: autosomal recessive

Phosphofructokinase is a glycolytic enzyme that is involvedin the energy supply to erythrocytes and myelocytes. Hereditary phosphofructokinase deficiency leads to chronichaemolysis (chronic hyperbilirubinaemia, increased reticulocyte count with normal haematocrit). However, stresssituations will lead to a haemolytic crisis (brown/red urinedue to haemoglobinuria and hyperbilirubinuria, icterus,severe anaemia, lethargy) and to stress myopathies(reluctance to move, convulsions). With adequate good care and rest, animals may have a normal life span.

The disease is caused by a point mutation in the muscletype phosphofructokinase gene.

Genetic test possible: English Springer Spaniel

Gene expression: autosomal recessive

PPhhoosspphhooffrruuccttookkiinnaasseeDDeeffiicciieennccyy

00..55 mmll EEDDTTAA bblloooodd

OOLLWWSS 11 mmll EEDDTTAA bblloooodd

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1155..33 HHeerreeddiittaarryy DDiisseeaasseess

PKD was first discovered in 1967 in Persians. Polycystic Kid-ney Disease is a genetic disease with a worldwide distribu-tion, about 40% of Persians suffer from it. The disease isslowly progressive in affected cats and will cause terminalrenal failure. The symptoms are generally the same as inchronic renal insufficiency and can only be treated sympto-matically.Moleculargenetical testing is superior to the ultrasound as itallows a dependable early diagnose, when their still kittens.It is also possible to detect healthy heterozygous carriers.The healthy carriers should not be used for breedingpurposes to try and reduce the incidence of the disease inthe breed.

Genetic test possible: Persians, Himalayan, Siamese, Ragdolls, British Shorthair,Domestic Shorthair, American Shorthair, Exotic Shorthair

Gene expression: autosomal dominant.

PRA (Progressive retinal atrophy) occurs in various dog andcat breeds. The disease is due to a degeneration or dysplasiaof the retinal photoreceptors. The different forms of PRAshow similar clinical symptoms (night blindness, reducedday vision) and ophthalmological pictures (hyper-reflectivityof the tapetum lucidum, thin retinal vessels, atrophy of opticpapilla, decreased areas of pigmentation in the tapetum-freefundus), but the age of manifestation of clinical symptoms isdifferent. They are caused by different genetic mutations,few of which are known.

PPRRAA iinn tthhee IIrriisshh SSeetttteerr:: The genetic mutation for an early type of PRA, the rod-conedysplasia type 1, could be identified in the Irish Setter. Thegene expression is autosomal recessive, therefore only animals with two mutated genes will develop disease. Ophthalmological detection is usually possible from the ageof 4 months. Molecularbiological detection is possible at any age to determine whether the animal is a geneticallyhealthy heterozygous carrier or homozygous carrier that will develop the disease.

PPRRAA 00..55 mmll EEDDTTAA bblloooodd

PPKKDD 00..55 mmll EEDDTTAA bblloooodd

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1155..33 HHeerreeddiittaarryy DDiisseeaasseess

PPRRAA iinn tthhee CCaarrddiiggaann The gene mutation leading to PRA in the Welsh Corgi is WWeellsshh CCoorrggii:: known: the rod-cone dysplasia type 3. The gene expression is

autosomal recessive, therefore only animals with two mutatedgenes will develop the disease. Ophthalmological detection isusually possible from the age of 6 weeks. Molecularbiologicaldetection is possible at any age to determine whether the animal is a genetically healthy heterozygous carrier or homozygous carrier that will develop the disease.

Genetic test possible: Irish Setter, Cardigan Welsh Corgi

Gene expression: autosomal recessive

The deletion of a base pair in the pyruvate kinase gene prevents the formation of functional enzyme. Pyruvatekinase deficiency leads to insufficient glycolysis in theerythrocytes and therefore a reduced life span of thesecells. The affected animals develop chronic regenerativehaemolytic anaemia, progressive myelofibrosis andosteosclerosis. Most affected animals die before the age of 5 years.

Genetic test possible: Basenji dogs

Gene expression: autosomal recessive

PPyyrruuvvaattee KKiinnaassee DDeeffiicciieennccyy iinn BBaasseennjjii ddooggss

00..55 mmll EEDDTTAA bblloooodd

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1155..33 HHeerreeddiittaarryy DDiisseeaasseess

Pyruvate kinase deficiency is well researched in Basenjidogs and West Highland White Terriers, but it also occurs in other dog breeds (Cairn Terrier, Beagle, Miniature Poodle,etc.), cats and humans. The lack of the enzyme, which playsan important role in red blood cell metabolism, leads to premature breakdown and destruction of red blood cells.The affected individual subsequently develops chronicregenerative haemolytic anaemia and has a much reducedlife span. The onset of disease is between the ages of fourto twelve months.

Symptoms: - lack of energy and reduced exercise tolerance- slow growth- progressive osteosclerosis- myelofibrosis- hepatopathy

Genetic test possible: West Highland White Terrier, Cairn Terrier

Gene expression: autosomal recessive

SCID (Severe combined immunodeficiency) in the Arab foalis probably due to a defect in the lymphoid stem cells, which leads to disturbed maturation of the B- and T-celllymphocytes, resulting in severe lymphopenia. Affectedfoals develop disease at the age of approximately 1 monthand the majority of them die within 5 months of birth, due to opportunistic infections. The disease is based on the deletion in a gene that codesfor DNA-dependent protein kinase. Only foals that carry twocopies of the gene will develop disease. The genetic testcan detect diseased foals as well as clinically healthy carriers, which is important for breeding purposes.

Occurrence: Arab horse

Symptoms: susceptibility to infection

Gene expression: autosomal recessive

SSCCIIDD 11 mmll EEDDTTAA bblloooodd

PPyyrruuvvaattee KKiinnaasseeDDeeffiicciieennccyy iinn WWHHWWTT

00..55 mmll EEDDTTAA bblloooodd

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1155..33 HHeerreeddiittaarryy DDiisseeaasseess

Scrapie is a non febrile, chronic progressive degenerativeCNS disorder in sheep, rarely seen in goats and cattle. It iscaused by the formation of an endogenous glycoprotein onthe neuronal surface which folds incorrectly and can there-fore not break down. This results in the formation of amyloidaggregates which deposit in certain tissues, causing CNSsymptoms. In sheep, horizontal and vertical transmission can occur.Whether or not an individual is susceptible to Scrapie isdetermined by the prion protein gene (PrP). Moleculargenetical testing of the gene make it possible to assess the risk for the animal to develop Scrapie.

Genetic test possible: all sheep breeds

The Von Willebrand factor (vWF) mediates the adhesion ofthrombocytes to the subendothelial cells of a damagedblood vessel. It also acts as a carrier protein for Factor VIIof the plasma coagulation system and protects it frompremature proteolytic decomposition. Reducedconcentration or complete absence of functional vWF leadsto coagulation disorders of various degrees of severity.Characteristic symptoms are bleeding from the mucus mem-branes and vigorous bleeding during teething, oestrus andtrauma.There are three types of Von Willebrand Disease, two ofwhich can be genetically determined: type 1 and type 3.

vvWWFF ttyyppee 11 Often a milder course of the disease. The gene expression isaauuttoossoommaall iinnccoommpplleetteellyy ddoommiinnaanntt, e.g. heterozygous animalspossess moderate vWF plasma concentrations and may beclinically inapparent, whereas homozygous animals possesslow vWF plasma concentrations and therefore show clinicalsymptoms more clearly.

Genetic test possible: Dobermann Pinscher, Poodle, Manchester Terrier

vvoonn WWiilllleebbrraanndd DDiisseeaassee(vWF)

00..55 mmll EEDDTTAA bblloooodd

SSccrraappiiee 00..55 mmll EEDDTTAA bblloooodd

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1155..33 HHeerreeddiittaarryy DDiisseeaasseess

vvWWFF ttyyppee 33 The most severe course of the disease. The gene expressionis aauuttoossoommaall rreecceessssiivvee. Homozygous animals possess nodetectable vWF plasma concentrations and suffer fromsevere coagulation disorders, heterozygous animalspossess reduced vWF plasma concentrations and are carriers of the disease, but usually do not show any clinicalsymptoms.

Genetic test possible: Scotch Terrier, Sheltie

X-SCID (X-linked severe combined immunodeficiency) in thedog is caused by a defect in the γ-chain of the interleukin-2receptor. The cellular and humoral immune systems aremarkedly impaired. Only male dogs are affected by thedisease, female dogs are only carriers. Recurring andchronic infections due to opportunistic pathogens start once maternal antibody protection decreases. Most affected puppies die at the age of three to four months.

Occurrence: Welsh Corgi, Basset

Symptoms: developmental disorders, thymic dysplasia, susceptibility to infections, inadequately formed peripheral lymph nodes

Laboratory findings: lymphopenia, reduced IgG and IgA levels, variable IgM levels

Gene expression: x-chromosome bound

XX--SSCCIIDD 11 mmll EEDDTTAA bblloooodd

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1155..44 AAvviiaann SSeexx IIddeennttiiffiiccaattiioonn

�� GGeenneerraall IInnffoorrmmaattiioonn

Avian sex identification is performed using the DNA extracted from feather pulp or fromEDTA blood. A specific region of the DNA is amplified using PCR. Then two different molecularbiological methods are employed to identify the gender-specific polymorph gene sequences of the sex chromosomes.

This test can be used in several hundred avian species. Unfortunately it can not be used in the ratites emu, ostrich, nandu and kiwi, but it can be used in cassowaries.

EDTA blood: only 2-3 drops are required

Feathers: Several small feathers or one large feather can besubmitted, but it is important that the quill is intact. Growingfeathers contain more DNA than mature feathers, which iswhy they are most suitable for sex identification, but it isalso possible to use mature feathers or even feathers thathave recently been moulted. Clear identification of thesource of the feathers must be ensured and contaminationwith foreign genetic material (cage dust or sand) must beavoided. Bloody feathers should be submitted in a steriletube, the vane (top part) of the feather may be shortened.Dry feathers can be sent in a sealed plastic bag.

Egg shells: Isolation of DNA from the egg membrane is possible; therefore the egg shell should be mostly intact. A drop ofblood taken from the egg shell with a sterile swab is evenmore suitable. Please make sure the egg shell is assigned to the correct individual.

Please note: - In order to avoid false or doubtful results, the sample material must be protected from contamination with other material which may contain DNA.

- The sample material (blood or feather pulp) can be stored at 4-8 °C for several days.

- Dry feathers can be stored at room temperature for several weeks.

- Detailed identification must be applied to the sample at submission, including the accurate avian species (scientific name if possible), the ring number and the date of collection.

AAvviiaann SSeexx IIddeennttiiffiiccaattiioonn EEDDTTAA bblloooodd,, FFeeaatthheerrss,, EEgggg sshheellllss

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1155..55 PPaarreennttaaggee VVeerriiffiiccaattiioonn

�� GGeenneerraall IInnffoorrmmaattiioonn

Parentage verification is sometimes required to verify that the parents are the true parents of the offspring. Parentage verification is done using microsatellite analysis.

PPrriinncciippllee::Genetic material contains a large number of DNA segments, so-called microsatellites,which consist of multiple repeated copies of short DNA sections. The number of copiesand the length of the microsatellites vary from one individual to another. The humangenome is estimated to contain up to 100,000 of these microsatellite gene sites. Eachindividual therefore possesses a unique genome and there are practically no two identical individuals (except monozygotic twins).

In principle, offspring inherit 50% of its genetic material from its mother and 50% from its father. This means that any variation of the genome (e.g. in the highly variablemicrosatellite sequence) that is not inherited from the mother must be inherited from the father.

In the case of the detection of microsatellites in offspring where the mother is known,which cannot be found in the genome of the mother nor in the genome of the suspectedfather, fatherhood can be ruled out with a high probability.

Detection safety increases with the comparison of several microsatellite gene sites. Which is why 12 microsatellites are examined in horses, 10 in cats and 10 in dogs (17 in dogs with a high degree of inbreeding) which are recommended by ISAG(International Society for Animal Genetics).

For parentage verification sample material from theoffspring is required as well as sample material from eachof the suspected parents. Please ensure proper labelling of the samples!

Example: The mother is known, but there are two different fathersconsidered.

Submit the sample materials clearly marked as:1. Offspring2. Mother3. Potential father A4. Potential father B

PPaarreennttaaggee VVeerriiffiiccaattiioonn 22 mmll EEDDTTAA bblloooodd

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1155..55 PPaarreennttaaggee VVeerriiffiiccaattiioonn

The ‘genetic fingerprint’ is the only forgery-proof means ofidentification of an individual. It is much more reliable thantatoos and implanted microchips. It uses the individual variability of the genetic information and allows doubt freeidentification after death.

The results of the ‘genetic fingerprint’ are electronicallystored at our laboratory and can be recalled at any time ifnecessary (loss of the animal, damage caused by animals,stolen animals, etc.). The animal owner will receive a certificate with the DNA profile of his animal.

Genetic test possible: dog, cat, horse

Each individual has an unmistakable genome (with theexception of identical twins). Therefore a DNA profile of two submitted materials will determine whether they arefrom the same animal. Genetic identity determination is themethod of choice for forensic purposes (damage, theft, etc).

Genetic test possible: dog, cat, horse

GGeenneettiicc IIddeennttiittyy DDeetteerrmmiinnaattiioonn

00..55--11 mmll EEDDTTAA bblloooodd,, HHaaiirr,, CCllaaww,, TTiissssuuee,, SSppeerrmm,, BBlloooodd ttrraaccee

GGeenneettiicc FFiinnggeerrpprriinntt 00..55--11 mmll EEDDTTAA bblloooodd

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1166..11 GGeenneerraall BBaacctteerriioollooggyy

�� OOvveerrvviieeww ooff tteessttiinngg ttiimmeess aanndd cchhaarrggeess

Bacteriological examinations require a variable amount of material and time which takesinto account bacterial growth and the number of differentiations.

Unless otherwise stated, the charge for a sample therefore comprises of (for exceptions see below):

11.. ccuullttuurree

++ 22.. ppoossss.. ddiiffffeerreennttiiaattiioonn((ss)) (only when pathogenic bacteria are detected)

++ 33.. ppoossss.. aannttiibbiiooggrraamm((ss)) (only at special request)

== TToottaall cchhaarrggee ffoorr ssaammppllee

BBaacctteerriiaall ccuullttuurree::

* The duration of bacteriological cultures depends on the bacteria to be demonstrated and their growth rate. Most animal pathogenic bacteria are detected within the times stated above. In special cases it may be necessary to cultivate for a longer period of time(e.g. Nocardia: approx. 7 days). Occasionally routine cultures may take longer than stated,e.g. in case subcultures are necessary for extraction of pure cultures, or if an enrichmentis needed.

CCuullttuurree ffoorr DDaayyss TTiimmee** IInncclluuddeedd iinn cchhaarrggeeBacteriology - aerobic Mon-Sat 2-3 daysEar swab Mon-Sat 2-3 days mycological culture (Malassezia)Cervical swab, mare Mon-Sat 2-3 days mycological culture and differentiationTaylorella equigenitalis (CEM) Mon-Sat 7 daysMilk sample, bovine Mon-Sat 2-3 days mycological culture,

differentiation and antibiogram

Urine sample Mon-Sat 1-2 days Inhibition test and bacterial countBacteriology - anaerobic Mon-Fri 3-4 daysBlood cultureaerobic/anaerobic

Mon-Sat 10 days

Enteropathogenic organismsfrom faecal samples

Mon-Sat 3-4 days

Salmonella Mon-Sat 3-4 daysClostridia in faeces(quantitatively)

Mon-Fri 2-3 days

Mycobacteria Mon-Fri 8 weeks Please contact the lab prior tosending a sample!

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1166..11 GGeenneerraall BBaacctteerriioollooggyy

Aerobic bacterial culture allows for the identification of alarge number of pathogenic bacteria.

Examination steps: - the sample is cultured on selective agar plates depending on the type and requirements of the sample material

- enrichment of the pathogen in broth. This allows for growth of damaged pathogens or pathogens from a swab that contains only limited numbers of pathogens

- aerobic incubation of the culture for a minimum of 48 hours(longer if required). Urine cultures usually only require 24 hours incubation

- daily assessment of the cultures and further differentiationin the case of detection of pathogenic and facultatively pathogenic bacteria

Special treatment:

Ear swab: The examination of ear swabs includes aerobic bacterialculture (see above), as well as yeast culture for detection of malassezia.

Cervical swab (Equine): The ‘mare-swab’ includes aerobic bacterial culture (see above), as well as mycological culture.

Please note: The examination for Taylorella equigenitalis (CEM:contagious equine metritis) must be requested separately.Submission in transport medium is necessary and thesample must reach the lab within 48 hours. Please ensureadequate labelling of the sample, including the date of sampling!

Milk samples (Bovine): Bacterial culture includes aerobic bacterial culture,mycological culture, differentiation and antibiogram, all for afixed price.

Urine samples: Bacterial urine examination includes identification andquantification of bacteria as well as an inhibition test todetect excretion of antibacterial substances.

BBaacctteerriioollooggyy ((aaeerroobbiicc)) SSwwaabb,, BBooddyy fflluuiiddss,, TTiissssuuee

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1166..11 GGeenneerraall BBaacctteerriioollooggyy

The examination for anaerobic organisms is recommendedin addition to the aerobic culture from the following samplematerials: abscess material, pus, wound swabs (especiallyfrom bite wounds), body fluids (aspirates, synovial fluid,cerebrospinal fluid, etc.), swabs from inner organs andserous membranes, paronychia. Please note that swabsmust be sent in transport medium!

Examination steps: - culture on special nutrient medium- enrichment of the bacteria in nutrient broth- anaerobic incubation of the culture for a minimum of

72 hrs (longer if required)- regular assessment of the cultures and further

differentiation in the case of detection of pathogenic and facultatively pathogenic anaerobic bacteria

In case of bacteraemia or suspected bacteraemia, blood is collected from the patient in a sterile manner andtransferred into special blood culture bottles directly in thesurgery. These bottles, plus the necessary blood collectionset, are provided by the lab free-of-charge on request. The bottles are incubated for 10 days. A detection systemrecognises and reports any bacterial growth.

Handling: - always use one aerobic and one anaerobic bottle for culture

- thorough disinfection of the collection site is necessary to prevent contamination with bacteria from the skin

- use a syringe or collection set for blood collection- fill each bottle with 3-10 ml (optimum 8-10 ml) of blood.

First fill the aerobic bottle and then the anaerobic bottle.If you are not using a blood collection set, please inject the blood through the rubber plug into the bottle.

- collect the blood and submit your sample at the beginning of the week if possible

- inoculated bottles should be stored at room temperature (not in the fridge)

BBlloooodd CCuullttuurree BBlloooodd mmuusstt bbee sseenntt iinn ssppeecciiaall ccoonnttaaiinneerrss

BBaacctteerriioollooggyy ((aannaaeerroobbiicc)) SSwwaabbss,, BBooddyy fflluuiiddss,, TTiissssuuee

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1166..22 FFaaeeccaall EExxaammiinnaattiioonnss

In carnivores a quantitative increase of Clostridium is a signfor imbalance of the intestinal flora. The faecal sample isspecifically diluted, followed by anaerobic culture on aselective medium to determine the number of Clostridiumper gram of faeces.

C. perfringens enterotoxin can cause diarrhoea in cats and dogs.

Canine faecal Elastase-1 is produced in the pancreas andreleased into the small intestine as part of the pancreaticsecretion during digestion. It is stable in the intestine and remains detectable unaltered for some period of time in faeces. See → 7.3 Exocrine Pancreatic Diseases

Species: Dog only

Indication: Suspected exocrine pancreatic insufficiency

Please note: Enzyme substitution does not have to be discontinued fortesting, as the results are not influenced by enzymesubstitution. Watery faeces may have a dilution effect,resulting in false low test results.

EEllaassttaassee (dog only) 00..55 SSAA FFaaeeccaall ttuubbee

CClloossttrriiddiiuumm ppeerrffrriinnggeennssEEnntteerroottooxxiinn

00..55--11 SSAA FFaaeeccaall ttuubbee

CClloossttrriiddiiuumm (quantitatively) 00..55--11 SSAA FFaaeeccaall ttuubbee

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1166..22 FFaaeeccaall EExxaammiinnaattiioonnss

Bacteriological faecal - examination for enteropathogenic bacteriaexamination

Mycological faecal - (semiquantitatively)examination

Parasitological faecal - Detection of cestode eggs, nematode eggs, coccidia oocyts;examination additionally in large animals: rumen fluke and liver fluke

eggs, lungworm larvae

Giardia - (dog and cat only)

Diarrhoea Profile E corresponds to ‘Diarrhoea Profile C’ butalso includes canine faecal elastase-1:

Bacteriological faecal examination, mycological faecal examination, parasitological faecal examination, giardia, canine faecal elastase-1

Faecal samples and rectal swabs are examined forenteropathogenic organisms using selective media andenrichment methods.

The culture includes: - Salmonella- Thermophilic Campylobacter species (Campylobacter

jejuni, Campylobacter coli, Campylobacter lari)- Yersinia enterocolitica- Species specific pathogenic and facultative pathogenic

FFaaeeccaall BBaacctteerriioollooggyy(enteropathogenic germs)

FFaaeecceess,, RReeccttaall sswwaabb

DDiiaarrrrhhooeeaa PPrrooffiillee EE (dog only)

MMiinniimmuumm 11 ffuullll SSAA ffaaeeccaall ttuubbee

DDiiaarrrrhhooeeaa PPrrooffiillee CC(dog/cat)DDiiaarrrrhhooeeaa PPrrooffiillee CC(horse/cattle/pig)

SSmmaallll aanniimmaallss:: mmiinniimmuumm 11 ffuullll SSAA ffaaeeccaall ttuubbee

LLaarrggee aanniimmaallss:: mmiinniimmuumm 11 ffuullll LLAA ffaaeeccaall ttuubbee

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1166..22 FFaaeeccaall EExxaammiinnaattiioonnss

enterobacteriaceae (e.g. Klebsiella spp., haemolytic and mucoid E. coli strains, Proteus spp.)

- Coagulase-positive staphylococci (Staphylococcus aureus, Staphylococcus intermedius)

- Pseudomonas aeruginosa- Yeasts (semiquantitative detection in the case of

excessive growth)

In carnivores the composition of the faecal flora is judgedsemiquantitatively. A quantitative increase in gram positiveor gram negative bacteria could be a sign of imbalance ofthe large intestinal flora.

Detection of undigested dietary components in the faeces:fatty acid globules, neutral fat, muscle fibres and starch.

Species: Carnivores and omnivores

Indication: Suspected maldigestion e.g. due to exocrine pancreaticinsufficiency

Artefacts: - faecal digestion is dependent on the composition of the diet, e.g. fatty acid globules and muscle fibres can be found when feeding raw meat

- diarrhoea (i.e. reduced faecal passage time) will lead to poor faecal digestion results

Viruses which are excreted in the faeces can be detectedand classified using electron microscopy.

GGeenneerraall FFaaeeccaall VViirroollooggyy(electron microscopy)

00..55 SSAA FFaaeeccaall ttuubbee

FFaaeeccaall DDiiggeessttiioonn TTeesstt 00..55 SSAA FFaaeeccaall ttuubbee

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1166..22 FFaaeeccaall EExxaammiinnaattiioonnss

No meat must be fed for three days prior to sampling foroccult blood testing to avoid possible false positive results.

The faecal sample is examined exclusively for Salmonella.Pooled faecal samples can be used.

SSaallmmoonneellllaa OOnnllyy FFaaeecceess,, RReeccttaall sswwaabb

OOccccuulltt BBlloooodd 00..55 SSAA FFaaeeccaall ttuubbee

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1166..33 MMyyccoollooggyy

�� OOvveerrvviieeww ooff tteessttiinngg ttiimmeess aanndd cchhaarrggeess

Similar to bacteriological examination, the charge for mycological examination comprises of:

11.. ccuullttuurree

++ 22.. ppoossss.. ddiiffffeerreennttiiaattiioonn((ss)) (only when pathogenic fungi are detected)

++ 33.. ppoossss.. aannttiimmyyccooggrraamm((ss)) (only for yeasts and only at special request)

== TToottaall cchhaarrggee ffoorr ssaammppllee

MMyyccoollooggiiccaall ccuullttuurree::

* The duration of mycological culture depends on the organism to be demonstrated andtheir growth rate. Most animal pathogenic fungi are detected within the times statedabove. In special cases it may be necessary to cultivate for a longer period of time (e.g.Malassezia: 5 days, Cryptococcus neoformans: 7 days).

CCuullttuurree ffoorr DDaayyss TTiimmee**Dermatophytes Mon-Fri approx. 4 weeksYeasts and moulds Mon-Sat 2-3 daysYeasts in faeces, quantitatively Mon-Fri 2-3 days

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1166..33 MMyyccoollooggyy

Dermatomycosis is a fungal infection which is restricted tothe superficial skin layers. Two of the most commondermatomycotic infections are caused by Trichophyton andMicrosporum.

Sample material: - skin scrapings are most effective for testing due to dermatophyte hyphae which invade the skin

- plucked hair may also be used- pre-incubated dermatophyte cultures can be submitted

for species identification

Collection of material: - the sample should be taken in the transitional area between affected skin and healthy skin

- disinfection prior to collection will prevent bacterial overgrowth of the dermatophyte culture

Examination: 1. A slide preparation is prepared immediately once the sample arrives, followed by microscopic examination.

2. Culture on special agar plates.3. Regular assessment of the culture and differentiation of

the fungal species in the case of dermatophyte growth.

Please note: Dermatophytes grow very slowly. The sample will beincubated for up to 4 weeks.

DDeerrmmaattoopphhyytteess//FFuunnggaall SSkkiinn DDiisseeaassee

SSkkiinn ssccrraappiinnggss,, HHaaiirr

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1166..33 MMyyccoollooggyy

Yeasts and moulds may participate in various infectious diseases, for example otitis, genital infections, mastitis, air sac infections.

Collection of material: Use a swab in medium as used for bacterial culture. When taking mucous membrane swabs from the mouth,nasopharynx or genitals pay attention to membranous orfibrous coverings, because often the pathogen can beisolated from these. For diagnosis of avian aspergillosis, an air sac swab can be submitted, however biopsy material is even more suitable.

Examination: 1. A slide preparation is prepared immediately once the sample arrives, followed by microscopic examination.

2. Culture on special agar plates.3. Regular assessment of the culture and differentiation.

of the fungal species in the case of growth of pathogenic or facultatively pathogenic yeasts or moulds.

Please note: Mycological examination is routinely included in the examination of ear swabs, cervical swabs from mares and milk samples.

Various immunosuppressive influences or antibiotictherapies can lead to excessive multiplication of intestinalyeasts (esp. Candida spp.), resulting in diarrhoea. In order to make a diagnosis a quantitative test for the pathogen isnecessary.

Examination: 1. Quantitative dilution of the faecal sample.2. Culture on special agar plates.3. Estimation of the number of colonies. Calculation of

the number of yeasts per gram of faeces.

YYeeaassttss iinn FFaaeecceess (quantitative)

00..55 SSAA FFaaeeccaall ttuubbee

YYeeaassttss aanndd MMoouullddss SSwwaabbss,, BBooddyy fflluuiiddss,, eettcc..

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1166..44 AAuuttoovvaacccciinneess

�� AAuuttoovvaacccciinneess AAggaaiinnss VViirraall oorrttBBaacctteerriiaall PPaatthhooggeennss

The sample material is cultured, followed by isolation and differentiation of the bacteria.After further multiplication of the pathogen a vaccine can be produced.

SShhoouulldd yyoouu wwiisshh ttoo rreeqquueesstt tthhee pprreeppaarraattiioonn ooff aann aauuttoovvaacccciinnee ffoolllloowwiinngg aa rroouuttiinnee bbaacctteerriioo--llooggiiccaall eexxaammiinnaattiioonn,, pplleeaassee ccoonnttaacctt uuss iimmmmeeddiiaatteellyy..

Animals which suffer from chronic, treatment resistant diar-rhoea often respond well to E. coli autovaccine. Studieshave shown that the use of an autovaccine can lead to animprovement or cure of the diarrhoea. The vaccine is anoral vaccine to be taken daily for 10 days.

The use of autovaccines has proved itself in treatmentresistant ENT (ear-nose-throat) infections caused byPseudomonas aeruginosa. The vaccine combines oraladministration and s.c. injections.

This vaccine is used in animals with treatment resistantStaphylococcus pyoderma. It is administered as four subcu-taneous injections.

Vaccine production requires at least an almond-size pieceof tissue, submitted in sterile saline solution. For furtherinformation, e.g. about autovaccines for dam/herdprotection, please contact your Regional Manager.

PPaappiilllloommaa AAuuttoovvaacccciinnee//EEqquuiinnee SSaarrccooiidd AAuuttoovvaacccciinnee 33--55 gg TTiissssuuee iinn ssaalliinnee ssoolluuttiioonn

SSttaapphhyyllooccooccccuussAAuuttoovvaacccciinnee

SSwwaabb

PPsseeuuddoommoonnaass aaeerruuggiinnoossaaAAuuttoovvaacccciinnee

SSwwaabb

EE.. ccoollii AAuuttoovvaacccciinnee FFaaeecceess

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1166..55 HHyyggiieennee CCoonnttrrooll

�� HHyyggiieennee CCoonnttrrooll

HHyyggiieennee ccoonnttrrooll iinn cclliinniiccss aanndd pprraaccttiicceess::

In veterinary practice it is important to regularly check the effectiveness of sterilizers and autoclaves. This is possible using test organisms. The test organisms are placed in the sterilizer or autoclave and exposed to the conditions of your equipment. Vet�Med�Labwill provide you with the necessary kits needed for heat or steam sterilization. Followingexposure the kits are sent to Vet�Med�Lab for evaluation.

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1177..11 FFaaeeccaall EExxaammiinnaattiioonn ffoorr PPaarraassiitteess

�� NNoottiiccee

When submitting a faecal sample for parasites please make sure that you collect materialfrom different areas of the faeces.

Flotation method: Detection of cestode eggs, thin and thickwalled nematode eggs, coccidia oocysts (includingToxoplasma oocysts).

Please note: Collect several small samples from different places in thefaeces. For detection of Toxoplasma it is advisable to submita pooled sample from 3 consecutive days.

Including: - native preparation, stained and unstained: protozoa (flagellates, amoeba, ciliates, microsporidia), nematode larvae, trematodes

Flotation method: nematode eggs, cestode eggs, pentastomid eggs, coccidia oocysts

To examine further for lungworms and trematodes, the sedimentation and larval migration methods are recommended.

EEnnddooppaarraassiitteess (reptile)

mmiinniimmuumm 22 gg ffrreesshh FFaaeecceess

EEnnddooppaarraassiitteess (dog/cat/bird/rabbit/small pets)

mmiinniimmuumm 00..55 SSAA ffaaeeccaall ttuubbee

GGiiaarrddiiaa AAnnttiiggeenn (ELISA) 22--33 gg FFaaeecceess

CCrryyppttoossppoorriiddiiaa AAnnttiiggeenn(ELISA)

22--33 gg FFaaeecceess

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1177..11 FFaaeeccaall EExxaammiinnaattiioonn ffoorr PPaarraassiitteess

Including: - flotation method: cestode eggs, thin and thick walled nematode eggs, coccidia oocysts

- sedimentation method (not horse, please request separately if necessary): rumen/liver fluke eggs

- larval migration method (Baermann method): lungworm larvae

Detection of lungworm larvae; also detection of GInematode larvae or larvae of free-living nematodes (incidental findings).

It is advisable to submit a pooled sample from 3 consecutive days.

Detection of rumen and liver fluke eggs.

SSeeddiimmeennttaattiioonn MMeetthhoodd 11 LLAA ffaaeeccaall ttuubbee

LLaarrvvaall MMiiggrraattiioonn TTeesstt(Baermann method)

mmiinniimmuumm 00..55 -- 11 SSAA ffaaeeccaall ttuubbee

EEnnddooppaarraassiitteess(horse, cattle, pig)

mmiinniimmuumm 11 ffuullll LLAA ffaaeeccaall ttuubbee

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1177..22 EEccttooppaarraassiitteess

Submit skin biopsies from several different sites within andbordering the affected area. Serial microtome sections arethen prepared and specifically examined for ectoparasites.A histological examination can be requested separately.

Collect sufficient sample material from several differentsites within and bordering the affected area. In suspectedmite infestation, skin scrapings should be taken at hairlessor shaved sites, deep enough to cause slight capillarybleeding.

EEccttooppaarraassiitteess (scraping) SSkkiinn ssccrraappiinngg

EEccttooppaarraassiitteess (biopsy) TTiissssuuee iinn ffoorrmmaalliinn

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1177..33 BBlloooodd PPaarraassiitteess

See → 13 Infectious Diseases

See → 13 Infectious Diseases

See → 15 Moleculargenetical Tests

See → 13 Infectious Diseases

See → 13 Infectious Diseases

See → 15 Moleculargenetical Tests

No differentiation between species.

See → 13 Infectious Diseases

LLeeiisshhmmaanniiaa AAnnttiibbooddiieess 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

EEhhrrlliicchhiiaa//AAnnaappllaassmmaasspppp.. (PCR)

11 mmll EEDDTTAA bblloooodd

EEhhrrlliicchhiiaa ccaanniiss (PCR) 22 mmll EEDDTTAA bblloooodd

EEhhrrlliicchhiiaa DDiirreecctt DDeetteeccttiioonn BBlloooodd ssmmeeaarr ++ EEDDTTAA bblloooodd

EEhhrrlliicchhiiaa AAnnttiibbooddiieess 11 mmll SSeerruumm,, EEDDTTAA ppllaassmmaa,, HHeeppaarriinn ppllaassmmaa

BBaabbeessiiaa sspppp.. (PCR) 00..55 mmll EEDDTTAA bblloooodd

BBaabbeessiiaa DDiirreecctt DDeetteeccttiioonn BBlloooodd ssmmeeaarr,, EEDDTTAA bblloooodd

BBaabbeessiiaa AAnnttiibbooddiieess (dog, horse)

11 mmll SSeerruumm

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1177..33 BBlloooodd PPaarraassiitteess

See → 13 Infectious Diseases

See → 15 Moleculargenetical Tests

See → 13 Infectious Diseases

See → 13 Infectious Diseases

See → 13 Infectious Diseases and 15 Moleculargenetical Tests

See → 13 Infectious Diseases

See → 13 Infectious Diseases

TTrryyppaannoossoommaa DDiirreeccttDDeetteeccttiioonn

BBlloooodd ssmmeeaarr,, EEDDTTAA bblloooodd

TTrryyppaannoossoommaa AAnnttiibbooddiieess(CFT)

00..55 mmll SSeerruumm

MMyyccooppllaassmmaa ((HHaaeemmoobbaarrttoonneellllaa)) DDiirreecctt DDeetteeccttiioonn oorr PPCCRR

BBlloooodd ssmmeeaarr,, 11 mmll EEDDTTAA bblloooodd ((ddiirreecctt))11 mmll EEDDTTAA bblloooodd ((PPCCRR))

MMiiccrrooffiillaarriiaa DDiirreeccttDDeetteeccttiioonn

11 mmll EEDDTTAA bblloooodd

MMaaccrrooffiillaarriiaa AAnnttiiggeenn(Dirofilaria)

00..55 mmll SSeerruumm

LLeeiisshhmmaanniiaa sspppp.. (PCR) 22 mmll EEDDTTAA bblloooodd,, IImmpprreessssiioonn ssmmeeaarr,, BBiiooppssyy,, eettcc..

LLeeiisshhmmaanniiaa DDiirreeccttDDeetteeccttiioonn

SSmmeeaarr,, BBiiooppssyy,, eettcc..

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1188..11 HHiissttooppaatthhoollooggiiccaall EExxaammiinnaattiioonnss

Notice: Please also see the General Advice on HistopathologicalExaminations, chapter 2.

Histopathology, bacteriology (aerobic)

Histopathology, mycology

Histopathology, bacteriology (aerobic), mycology

Histopathology, sarcoptes antibodies

Histopathology, production of an autogenous vaccine (following diagnosis of equine sarcoid)

Please note: Approx. 3-5 g tissue is needed for preparation of the autogenous vaccine. Please contact us if vaccine for species other than the horse is required.

SSkkiinn PPrrooffiillee 55 (horse only)

TTiissssuuee iinn NNaaCCll ++ TTiissssuuee iinn ffoorrmmaalliinn

SSkkiinn PPrrooffiillee 44 (dog only) TTiissssuuee iinn ffoorrmmaalliinn ++ 11 mmll SSeerruumm

SSkkiinn PPrrooffiillee 33 TTiissssuuee iinn ffoorrmmaalliinn ++ SSkkiinn ssccrraappiinngg ++ SSwwaabb

SSkkiinn PPrrooffiillee 22 TTiissssuuee iinn ffoorrmmaalliinn ++ SSkkiinn ssccrraappiinngg

SSkkiinn PPrrooffiillee 11 TTiissssuuee iinn ffoorrmmaalliinn ++ SSwwaabb

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1188..11 HHiissttooppaatthhoollooggiiccaall EExxaammiinnaattiioonnss

Histopathology, preparation of an autogenous vaccine (following diagnosis of papilloma)

See → Skin Profile 5

Histopathology, allergy test (Allercept™)

Please note that a higher fee is charged for vveerryy llaarrggee samples, samples containing several tumours or sseevveerraall ssaammpplleess from the same animal, as well as for mmoorree tthhaann ssiixx skin biopsies from a single animal. This is due to the increase in timerequired for processing the sample, as well as the larger number of sections and possibly diagnoses that have to be made.

Detection of ectoparasites in skin biopsy (selective examination of sample for ectoparasites only).

EEccttooppaarraassiitteess BBiiooppssyy iinn ffoorrmmaalliinn

TTiissssuuee SSaammpplleess TTiissssuuee iinn ffoorrmmaalliinn

FFiinnee NNeeeeddllee AAssppiirraattee//CCyyttoollooggiiccaall EExxaammiinnaattiioonn

SSmmeeaarr,, AAssppiirraattee

SSkkiinn PPrrooffiillee 77(dog and cat only)

TTiissssuuee iinn ffoorrmmaalliinn ++ 11 mmll SSeerruumm

SSkkiinn PPrrooffiillee 66(dog, cattle)

TTiissssuuee iinn NNaaCCLL ++ TTiissssuuee iinn ffoorrmmaalliinn

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1188..22 BBiioollooggiiccaall FFlluuiiddss

�� CCeerreebbrroossppiinnaall FFlluuiidd ((CCSSFF))

Brain and meningeal disease may have all kinds of causes, often they are bacterial (e.g. borreliosis) or viral (e.g. tickborne encephalitis).Neoplastic disease must also be considered. Changes in cell count, cell type and protein content can give valuable clues about the nature of the problem.

Normal CSF is a clear fluid. If the CSF sample obtained is cloudy, a bacteriologicalexamination is indicated.

Please note that only four hours after collection cerebrospinal fluid may have deterioratedleading to changes in the test results. The preparation of a smear from sediment is recommended for cytological examinations (centrifuge at 1000 rpm for 20 minutes).

Various pathogens can be identified in CSF using the PCR technique.

See → 15 Moleculargenetical Tests

Cell count, total protein

Please note: As early as four hours after sampling the results may beinfluenced by transport and aging. For cytology it isrecommended to prepare a smear of the sediment(centrifuge at 1000 rpm for 20 minutes).

Cytology, total protein, See → CSF Profile Ibacteriology (aerobic + anaerobic)

See → 3.2. Special Screening Profiles

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Synovial fluid is usually clear and virtually cell free. In joint disease the determination of the type of cells and the protein content can give information about the type and origin of the disease.

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CCSSFF PPrrooffiillee II aapppprrooxx.. 33 mmll CCeerreebbrroossppiinnaall fflluuiidd

18 Histopathology

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Cell count, total protein

Profile I + cytology

Profile II + bacteriology (aerobe + anaerobe)

See → 3.2. Special Screening Profiles

Cytology, total protein, specific gravity

Please note: As early as four hours after sampling the results may beinfluenced by transport and aging. For cytology it isrecommended to prepare a smear of the sediment(centrifuge at 1000 rpm for 20 minutes).

Cytology, total protein, See → Aspirate Profile Ispecific gravity, bacteriology (aerobic + anaerobic)

See → 3.2. Special Screening Profiles

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AAssppiirraattee PPrrooffiillee II aapppprrooxx.. 33 mmll AAssppiirraattee

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SSyynnoovviiaall fflluuiidd pprrooffiillee II 22 mmll SSeerruumm

18 Histopathology

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