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Cover
Title Page
Contributors
Preface
1 Veterinary Diagnostic Testing
1. 1.1 Introduction
2. 1.2 Diagnostic Sampling
3. 1.3 Collection, Preparation, and Handling
4. 1.4 Blood Sample Handling after Collection
5. 1.5 Centrifugation of Blood Samples
6. 1.6 Blood Culture Sampling
7. 1.7 Laboratory Validation of Blood Samples
8. 1.8 Specimens, Transport Containers, and Media for Various Disciplines
9. Further Reading
2 Basic Techniques and Procedures
1. 2.1 Introduction
2. 2.2 Essential Prerequisites for High‐Quality Bacteria Detection
3. 2.3 Microbiological Methods for Pathogen Detection
4. 2.4 Challenges to Current Detection Methods
5. References
3 Point‐of‐Care Testing
1. 3.1 Introduction
2. 3.2 Advantages of POC Testing
3. 3.3 Considerations for POC Testing
4. 3.4 Specific POC Tests to Consider
5. 3.5 Conclusion
6. References
4 Test Performance
1. 4.1 Introduction
2. 4.2 Analytical Validation
3. 4.3 Minimum Information for Diagnostic Tests
4. 4.4 Precision
5. 4.5 Accuracy
6. 4.6 Spiking Recovery and Linearity Checks
7. 4.7 Control Material
8. 4.8 Method Comparison
9. 4.9 Analytical Sensitivity and Specificity
10. 4.10 Additional Analytical Performance Tests
11. 4.11 Clinical Validation
12. 4.12 Study Design in the Clinical Validation Phase
13. 4.13 Diagnostic Sensitivity and Specificity
14. 4.14 Predictive Values
15. 4.15 Receiver‐Operating‐Characteristic (ROC) Curve
16. 4.16 Likelihood Ratios
17. Further Reading
5 Enzymes
1. 5.1 Introduction
2. 5.2 Sample Collection and Methodologic Considerations
3. 5.3 General Principles of Diagnostic Enzymology Data Interpretation
4. 5.4 Specific Diagnostic Enzymes and Their Interpretation
5. References
6 Kidney Function Tests
1. 6.1 Introduction
2. 6.2 Blood Urea Nitrogen (BUN)
3. 6.3 Creatinine (Cr)
4. 6.4 Classification of Azotemia
5. 6.5 Other Biochemical Analytes in Conditions of Decreased GFR
6. References
7 Carbohydrates
1. 7.1 Introduction and Physiology
2. 7.2 Glucose
3. 7.3 Ketones
4. References
8 Lipids
1. 8.1 Introduction
2. 8.2 Normal Metabolism
3. 8.3 Sample Collection and Methods
4. 8.4 Disorders of Lipid Metabolism
5. 8.5 Patterns of Dyslipidemia
6. References
9 Blood Gases
1. 9.1 Introduction
2. 9.2 Technical Aspects
3. 9.3 Acid‐Base
4. 9.4 Ventilation
5. 9.5 Oxygenation
6. 9.6 Arterial Oxygen Content
7. 9.7 Summary
8. References
10 Electrolytes
1. 10.1 Introduction
2. 10.2 Sample Handling and Analysis
3. 10.3 Sodium
4. 10.4 Chloride
5. 10.5 Potassium
6. 10.6 Calcium
7. 10.7 Phosphorus
8. 10.8 Magnesium
9. References
11 Miscellaneous Solutes
1. 11.1 Introduction
2. 11.2 Bilirubin
3. 11.3 Bile Acids
4. 11.4 Ammonia
5. 11.5 Lactate
6. References
12 Cardiac Troponin
1. 12.1 Introduction and Physiology
2. 12.2 Indications
3. 12.3 Sample Collection and Handling
4. 12.4 Immunoassays
5. References
13 Vitamin and Mineral Assessment
1. 13.1 Introduction
2. 13.2 Macrominerals
3. 13.3 Trace Minerals
4. 13.4 Vitamins
5. References
14 Toxicologic Diagnostics
1. 14.1 Introduction
2. 14.2 History
3. 14.3 Clinical Signs
4. 14.4 Clinicopathologic Testing
5. 14.5 Analytical Testing
6. 14.6 Selecting a Laboratory
7. 14.7 Diagnostic Considerations for Specific Equine Toxicants
8. References
15 Therapeutic Drug Monitorings
1. 15.1 Clinical Background
2. 15.2 Tests Available
3. 15.3 Sample Collection and Submission
4. 15.4 Possible Results
5. 15.5 Interpretation
6. 15.6 Case Example
7. References
16 Red Blood Cells
1. 16.1 Introduction
2. 16.2 Laboratory Diagnostics
3. 16.3 Effects of Age, Breed, Sex, and Physiologic Factors
4. 16.4 Anemia
5. 16.5 Erythrocytosis
6. References
17 Leukocytes
1. 17.1 Introduction
2. 17.2 Leukocyte Production and Kinetics
3. 17.3 Laboratory Diagnostics
4. 17.4 Leukocyte Morphology and Interpretation of Abnormal Values
5. 17.5 General Considerations
6. References
18 Platelets
1. 18.1 Platelet Production and Kinetics
2. 18.2 Laboratory Diagnostics
3. 18.3 Thrombocytopenia
4. 18.4 Thrombocytosis
5. 18.5 Von Willebrand Disease and Platelet Dysfuntion
6. References
19 Blood Proteins and Acute Phase Proteins
1. 19.1 Introduction
2. 19.2 Protein Measurement
3. 19.3 Interpretation of Abnormal Protein Concentrations
4. 19.4 Decreased Protein Concentrations
5. 19.5 Increased Protein Concentrations
6. 19.6 Acute Phase Proteins
7. References
20 Clotting Times (aPTT and PT)
1. 20.1 Clinical Background
2. 20.2 Test(s) Available
3. 20.3 Sample Collection and Submission
4. 20.4 Interpretation
5. 20.5 Case Example
6. Further Reading
21 Antithrombin
1. 21.1 Clinical Background
2. 21.2 Test(s) Available
3. 21.3 Sample Collection and Submission
4. 21.4 Interpretation
5. 21.5 Case Example
6. Further Reading
22 Fibrin and Fibrinogen Degradation Products (FDPs)
1. 22.1 Clinical Background
2. 22.2 Test(s) Available
3. 22.3 Sample Collection and Submission
4. 22.4 Interpretation
23 Coagulation Factors
1. 23.1 Clinical Background
2. 23.2 Test(s) Available
3. 23.3 Sample Collection and Submission
4. 23.4 Interpretation
5. Further Reading
24 Equine Infectious Anemia Virus
1. 24.1 Introduction
2. 24.2 Diagnostic Testing
3. References
25 Equine Influenza Virus
1. 25.1 Clinical Background
2. 25.2 Serological Tests Available
3. 25.3 Sample Collection and Submission
4. 25.4 Possible Results
5. 25.5 Interpretation and Case Examples
6. References
26 Alpha‐Herpesviruses (EHV‐1, EHV‐4)
1. 26.1 Clinical Background
2. 26.2 Serological Tests Available
3. 26.3 Sample Collection and Submission
4. 26.4 Possible Results
5. 26.5 Interpretation and Case Examples
6. References
27 Equine Rhinitis Viruses (ERAV, ERBV)
1. 27.1 Clinical Background
2. 27.2 Serological Tests Available
3. 27.3 Sample Collection and Submission
4. 27.4 Possible Results
5. 27.5 Interpretation and Case Examples
6. References
28 Interpretation of Testing for Common Mosquito Transmitted Diseases: West Nile Virus and Eastern and Western Equine Encephalitis
1. 28.1 Introduction
2. 28.2 Clinical Background
3. 28.3 Important Risk Factors
4. 28.4 Clinical Differentials
5. 28.5 Tests Available
6. 28.6 Sample Collection and Submission
7. 28.7 Interpretation of Results
8. 28.8 Case Example
29 Streptococcus equi ss equi
1. 29.1 Clinical Background
2. 29.2 Tests Available
3. 29.3 Sample Collection and Submission
4. 29.4 Possible Results
5. 29.5 Serological Results and Interpretation
6. 29.6 Case Discussions
7. Acknowledgments
8. References
30 Corynebacterium pseudotuberculosis
1. 30.1 Disease Overview
2. 30.2 Diagnostic Tests
3. 30.3 Summary
4. References
31 Neorickettisa risticii
1. 31.1 Introduction
2. 31.2 Diagnostic Testing
3. 31.3 Case Examples
4. References
32 Anaplasma phagocytophilum
1. 32.1 Introduction
2. 32.2 Routine Diagnostic Tests
3. 32.3 Specialized Diagnostic Tests
4. References
33 Lawsonia intracellularis
1. 33.1 Introduction
2. 33.2 Lawsonia intracellularis
3. 33.3 Equine Proliferative Enteropathy
4. 33.4 Comparison of Serological Assays
5. 33.5 Diagnostic Recommendations
34 Borrelia burgdorferia
1. 34.1 Overview of Lyme Disease in Horses
2. 34.2 Overview of Serologic Testing
3. 34.3 Interpretation of Results
4. 34.4 Available Tests
5. 34.5 Test Comparisons
6. 34.6 Summary of Recommendations
7. References
35 Clostridium difficile
1. 35.1 Clinical Background
2. 35.2 Tests Available
3. 35.3 Recommended Approach for Diagnostic Testing for Clostridium difficile Infection
4. 35.4 Sample Collection and Submission
5. 35.5 Possible Results
6. 35.6 Interpretation
7. 35.7 Case Example
8. References
36 Leptospira spp.
1. 36.1 Introduction
2. 36.2 Clinical History and Physical Examination
3. 36.3 Routine Diagnostic Tests
4. 36.4 Specialized Diagnostic Tests
5. 36.5 Response to Therapy
6. 36.6 Herd Health and Public Health Considerations
7. References
37 Fungal Pathogens
1. 37.1 Introduction
2. 37.2 Diagnostic Testing
3. References
38 Sarcocystis neurona and Neospora hughesi
1. 38.1 Introduction
2. 38.2 Overview of Serologic Testing
3. 38.3 Interpretation of Results
4. 38.4 Available Tests
5. 38.5 Test Comparisons
6. 38.6 Summary of Recommendations
7. References
39 Babesia caballi and Theileria equi
1. 39.1 Introduction
2. 39.2 Serological Tests Available
3. 39.3 Microscopy and Molecular Assays
4. 39.4 Selection of Diagnostic Tests
5. 39.5 Interpretation of Results
6. References
40 Assessment of Vaccination Status and Susceptibility to Infection
1. 40.1 Introduction
2. 40.2 Duration of Immunity
3. 40.3 Rationale for Serologic Testing
4. 40.4 Tetanus
5. 40.5 Rabies
6. 40.6 Eastern and Western Equine Encephalomyelits (EEE, WEE)
7. 40.7 Venezuelan Equine Encephalomyelitis (VEE)
8. 40.8 West Nile Virus (WNV)
9. 40.9 Influenza
10. 40.10 Equine Herpesvirus‐1 (EHV‐1) and EHV‐4
11. 40.11 Equine Viral Arteritis (EVA)
12. 40.12 Strangles (Streptococcus equi subsp. equi Infection)
13. 40.13 Botulism
14. 40.14 Equine Neorickettsiosis (Potomac Horse Fever)
15. 40.15 Equine Rotavirus
16. 40.16 Equine Rhinitis A (ERAV) and Equine Rhinitis B, types 1 and 2 (ERBV1 and ERBV2)
17. References
41 Immune‐Mediated Hemolytic Anemia
1. 41.1 Clinical Background
2. 41.2 Tests Available
3. 41.3 Sample Collection and Submission
4. 41.4 Direct Antiglobulin Test (Direct Coombs Test)
5. 41.5 Indirect Antiglobulin Test (Indirect Coombs Test)
6. 41.6 Possible Results and Interpretation
7. 41.7 Direct Immunofluorescence Flow Cytometry
8. 41.8 Enzyme‐Linked Antiglobulin Test
9. 41.9 Clinical Case
10. References
42 Equine Neonatal Isoerythrolysis
1. 42.1 Clinical Background
2. 42.2 Diagnosis and Prevention of NI
3. 42.3 Tests Available
4. 42.4 Sample Collection and Submission
5. 42.5 Blood Factor Assays (Blood Typing)
6. 42.6 Complement‐Mediated Hemolytic Assay
7. 42.7 Cross‐Match
8. 42.8 Direct Antiglobulin Test
9. 42.9 Jaundice Foal Agglutination Test
10. 42.10 Clinical Case
11. References
43 Immune‐Mediated Thrombocytopenia
1. 43.1 Clinical Background
2. 43.2 Tests Available
3. 43.3 Sample Collection and Submission
4. 43.4 Possible Results and Interpretation
5. 43.5 Direct Immunofluorescence Flow Cytometry
6. 43.6 Clinical Case
7. References
44 Neonatal Alloimmune Thrombocytopenia
1. 44.1 Clinical Background
2. 44.2 Tests Available
3. 44.3 Sample Collection and Submission
4. 44.4 Diagnosis and Prevention of NAIT
5. 44.5 Possible Results and Interpretation
6. 44.6 Clinical Case
7. References
45 Cellular Immunity
1. 45.1 Clinical Background
2. 45.2 Tests Available
3. 45.3 Sample Collection and Submission
4. 45.4 Possible Results and Interpretation: Immune Disorders of the Young Horse
5. 45.5 Possible Results and Interpretation: Immune Disorders of the Adult Horse
6. 45.6 Possible Results and Interpretation for Phagocyte Dysfunction
7. 45.7 Clinical Case
8. References
46 Immunoglobulins
1. 46.1 Clinical Background
2. 46.2 Tests Available
3. 46.3 Sample Collection and Submission
4. 46.4 Serum Immunoglobulin Concentrations
5. 46.5 Failure of Passive Transfer of Immunoglobulins in Foals
6. 46.6. Immunodeficiencies of the Young Horse
7. 46.7 Immunodeficiencies of the Adult Horse
8. 46.8 Monoclonal Gammopathies
9. 46.9 Clinical Case
10. References
47 Equine Blood Groups and Factors
1. 47.1 Clinical Background
2. 47.2 Tests Available
3. 47.3 Sample Collection and Submission
4. 47.4 Possible Results
5. 47.5 Interpretation
6. 47.6 Case Example
7. References
48 Bacteriology and Mycology Testing
1. 48.1 Introduction
2. 48.2 Preanalytical Variables
3. 48.3 Interpretation of the Gram Stain
4. 48.4 Upper Respiratory Infections
5. 48.5 Bronchopneumonia and Pleuropneumonia
6. 48.6 Peritonitis
7. 48.7 Enterocolitis
8. 48.8 Urogenital
9. 48.9 Septicemia
10. 48.10 Bacterial Meningitis
11. 48.11 Musculoskeletal Infections
12. 48.12 Dermatological and Subcutaneous Infections
13. 48.13 Lymph Node/Lymphatic Infections
14. 48.14 Ocular Infections
15. References
49 Antimicrobial Susceptibility Testing
1. 49.1 Clinical Background
2. 49.2 Test(s) Available
3. 49.4 Possible Results
4. 49.5 Interpretation
5. 49.6 Case Example
6. References
50 Parasite Control Strategies
1. 50.1 Introduction
2. 50.2 Useful Terminology and Concepts
3. 50.3 Fecal Flotation Assays
4. 50.4 Biology of Selected Equine Parasites of Concern
5. 50.5 Anthelmintic Mode of Action and Spectrum of Activity
6. 50.6 Environmental Control Strategies
7. 50.7 Risk Assessment: Age and General Husbandry
8. 50.8 Parasite Control Strategies for Mature Horses
9. 50.9 Parasite Control Strategies for Juvenile Horses
10. 50.10 Summary
11. References
51 Molecular Diagnostics for Infectious Pathogens
1. 51.1 Introduction
2. 51.2 Molecular Awareness and Panel Strategy
3. 51.3 Pre‐Analytical Variables and Quality Controls
4. 51.4 Blood‐Borne Pathogens
5. 51.5 Respiratory Pathogens
6. 51.6 Neurologic Pathogens
7. 51.7 Enteric Pathogens
8. 51.8 Abortogenic Pathogens
9. 51.9 Miscellaneous Pathogens
10. 51.10 Interpretation of qPCR Results for Common Pathogens
11. Further Reading
52 Equine Genetic Testing
1. 52.1 Introduction
2. 52.2 Hyperkalemic Periodic Paralysis (HYPP)
3. 52.3 Severe Combined Immunodeficiency (SCID)
4. 52.4 Ileocolonic Aganglionosis (Lethal White Foal Syndrome)
5. 52.5 Junctional Epidermolysis Bullosa (JEB)
6. 52.6 Glycogen Branching Enzyme Deficiency (GBED)
7. 52.7 Malignant Hyperthermia (MH)
8. 52.8 Hereditary Equine Regional Dermal Asthenia (HERDA)
9. 52.9 Glanzmann Thrombasthenia (GT)
10. 52.10 Type 1 Polysaccharide Storage Myopathy (Type 1 PSSM)
11. 52.11 Lavender Foal Syndrome (LFS) or Coat Color Dilution Lethal
12. 52.12 Cerebellar Abiotrophy (CA)
13. 52.13 Foal Immunodeficiency Syndrome (Immunodeficiency of Fell Ponies)
14. 52.14 Congenital Myotonia
15. 52.15 Multiple Ocular Defects (Anterior Segment Dysgenesis or Congenital Aniridia)
16. 52.16 Congenital Stationary Night Blindness (CSNB)
17. 52.17 Incontinentia Pigmenti
18. 52.18 Dwarfism
19. 52.19 Disorders of Sexual Development
20. 52.20 DNA Testing through Licensed Laboratories
21. References
53 Genetic Tests for Equine Coat Color
1. 53.1 Clinical Background
2. 53.2 Tests Available
3. 53.3 Sample Collection and Submission
4. 53.4 Interpretation of Test Results
5. References
54 Peritoneal Fluid
1. 54.1 Introduction
2. 54.2 Visual Inspection
3. 54.3 Cytological Evaluation
4. 54.4 Biochemical Evaluation
5. References
55 Respiratory Secretions
1. 55.1 Introduction
2. 55.2 How to Decide Which Sample to Take
3. 55.3 Performing the Tracheal Aspirate
4. 55.4 Performing the Bronchoalveolar Lavage
5. 55.5 Processing Fluid from the BAL or Tracheal Aspirate
6. 55.6 Cells and Cellular Products Seen on BAL or TA
7. 55.7 Non‐Cellular Elements Seen on BAL or TA
8. 55.8 Submitting Samples for Bacterial or Viral Culture
9. 55.9 Secretions of the Lower Respiratory System and Diagnosis of Disease
10. References
56 Pleural Fluid
1. 56.1 Introduction
2. 56.2 Causes of Pleural Effusion
3. 56.3 Pleurocentesis
4. 56.4 Assessment of Pleural Fluid
5. References
57 Urine Analysis
1. 57.1 Introduction
2. 57.2 Gross Evaluation
3. 57.3 Chemical Evaluation
4. 57.4 Sediment Evaluation
5. References
58 Synovial Fluid
1. 58.1 Introduction
2. 58.2 Sample Collection
3. 58.3 Fluid Analysis
4. 58.4 Diagnostic Imaging
5. 58.5 Polymerase Chain Reaction (PCR)
6. 58.6 Bacterial Culture and Sensitivity
7. 58.7 Osteoarthritis Biomarkers
8. References
59 Cerebrospinal Fluid
1. 59.1 Introduction
2. 59.2 Cerebrospinal Fluid Collection
3. 59.3 Cerebrospinal Fluid Constitution
4. 59.4 Cerebrospinal Fluid Analysis/Interpretation
5. 59.5 Other Diagnostic Tests in CSF
6. References
60 Laboratory Testing for Endocrine and Metabolic Disorders
1. 60.1 Introduction
2. 60.2 Pituitary Pars Intermedia Dysfunction
3. 60.3 Adrenal Disorders
4. 60.4 Adrenal Exhaustion (Steroid Withdrawal)
5. 60.5 Insulin Dysregulation and Equine Metabolic Syndrome
6. 60.6 Equine Hyperlipemia
7. 60.7 Parathyroid Hormone Disorders
8. 60.8 Thyroid Disorders
9. References
61 Endocrine Testing for Reproductive Conditions in Horses
1. 61.1 Introduction and Overview
2. 61.2 Diagnostic Reproductive Hormone Analytes
3. 61.3 Endocrine Diagnostic Aids for Cryptorchidism
4. 61.4 Endocrine Diagnostic Aids for Granulosa‐Cell Tumors (GCT)
5. 61.5 Pregnancy Diagnosis Aided by Estrone Sulfate and Progesterone Concentrations
6. 61.6 The Future of Endocrine Diagnostics for Reproductive Conditions in Horses
7. References
62 Foaling Predictor Tests
1. 62.1 Clinical Background
2. 62.2 Tests Available
3. 62.3 Sample Collection and Submission for FoalWatch Test Kit (CHEMetrics Inc., Calverton, VA)
4. 62.4 Interpretation of Test Results‐Sensitivity, Specificity, and Positive Predictive Values of Measuring Calcium Carbonate in a Mare’s Prepartum Mammary Secretions
5. 62.5 Case Example
6. References
Index
End User License Agreement

List of Tables

Chapter 05
1. Table 5.1 Summary of diagnostic enzymes, their tissues sources, mechanisms for increase, and basics of interpretation.
Chapter 06
1. Table 6.1 Classification of azotemia. Urine specific gravity (USG).
Chapter 09
1. Table 9.1 Age‐related values of arterial blood pH, bicarbonate (HCO₃), base excess (BE), partial pressure of carbon dioxide (PaCO₂) and oxygen (PaO₂) in premature foals.
2. Table 9.2 Age‐related values of arterial blood pH, bicarbonate (HCO₃), base excess (BE), partial pressure of carbon dioxide (PaCO₂) and oxygen (PaO₂) in healthy term foals and adult horses.
3. Table 9.3 Age‐related values of mixed venous blood pH, bicarbonate (HCO₃), base excess (BE), partial pressure of carbon dioxide (PvCO₂) and oxygen (PvO₂) in healthy 11 foals.
4. Table 9.4 Approximately predicted arterial oxygen partial pressure (PaO₂, mmHg) in humans as a function of the inspired oxygen fraction (FiO₂) for different shunt fractions incorporating a factor of V/Q mismatch.
Chapter 13
1. Table 13.1 Normal plasma mineral concentrations in adult horses.
2. Table 13.2 Normal plasma vitamin concentrations in adult horses.
3. Table 13.3 Methods of assessing vitamin A concentrations in the horse.
Chapter 14
1. Table 14.1 Testing considerations for selected equine toxicants.
Chapter 17
1. Table 17.1 Common leukogram patterns.
Chapter 18
1. Table 18.1 Estimating platelet count from a peripheral blood film.
Chapter 28
1. Table 28.1 Most common or known alphaviruses, flaviviruses, and bunyaviruses that cause encephalomyelitis in horses.
2. Table 28.2 Infectious and non‐infectious differential for viral encephalomyelitis.
3. Table 28.3 Summary of known CSF findings for arbovirus diseases.
4. Table 28.4 Antemortem and postmortem diagnostic tests for detection of arboviruses.
5. Table 28.5 Testing results for the case example.
Chapter 29
1. Table 29.1 Availability of serologic tests for Streptococcus equi ss equi. Source: Data from Robinson (2013) and Hobo (2008).
2. Table 29.2 Interpretation of SeM‐specific ELISA (IDEXX, EDS).
Chapter 32
1. Table 32.1 Features and interpretation for various types of diagnostic tests for equine granulocytic anaplasmosis.
Chapter 33
1. Table 33.1 Characteristics of three serological assays available for detecting humoral IgG for Lawsonia intracellularis in foals and horses.
2. Table 33.2 Number of positive results obtained for each serology test when testing sera from weanling and healthy horses with and without equine proliferative enteropathy. Agreements within each category are shown.
3. Table 33.3 Specificity and sensitivity results of the IPMA, SIPA, and ELISA using different serum dilutions or cut‐off units, respectively, from weanlings and healthy horses of various ages.
Chapter 34
1. Table 34.1 Serologic tests for Borrelia burgdorferi infection in horses.
Chapter 35
1. Table 35.1 Common causes of diarrhea in horses.
2. Table 35.2 Algorithm of diagnostic work‐up for Clostridium difficile infection.
Chapter 37
1. Table 37.1 Characteristics of relevant equine fungal pathogens.
2. Table 37.2 Distribution of IgG coccidioidal antibody level based on the different forms of the disease in 39 horses diagnosed with coccidioidomycosis.
Chapter 38
1. Table 38.1 Commercially available immunologic tests for antibodies against Sarcocystis neurona.
2. Table 38.2 Commercially available immunologic tests for antibodies against Neospora hughesi.
3. Table 38.3 Test comparisons, focusing on EPM caused by Sarcocystis neurona.
Chapter 40
1. Table 40.1 Antibody titers associated with protection, expected duration of protection and cautionary comments for various vaccine‐associated equine pathogens and toxins.
2. Table 40.2 Laboratories offering routine antibody testing for various equine vaccine pathogens or toxins.
Chapter 45
1. Table 45.1 Peripheral blood immunophenotyping and serum immunoglobulin concentrations in a filly with delayed cellular immune development.
Chapter 46
1. Table 46.1 Immunoglobulin isotypes of the horse.
Chapter 47
1. Table 47.1 Equine blood groups and factors.
Chapter 48
1. Table 48.1 Sterile anatomical sites.
2. Table 48.2 Media used for specimen transport.
3. Table 48.3 Possible causative organisms in cases of bronchopneumonia or pleuropneumonia.
Chapter 50
1. Table 50.1 Interpretation of fecal egg count reduction (FECR) values used to determine anthelmintic efficacy.
2. Table 50.2 Cyathostomin egg reappearance periods (ERP) for commonly used equine anthelmintics.
3. Table 50.3 Fecal diagnostic tests summary.
4. Table 50.4 Equine parasites: classification and diagnostic assays.
Chapter 51
1. Table 51.1 Testing considerations for selected blood‐borne pathogens.
2. Table 51.2 Testing considerations for selected respiratory pathogens.
3. Table 51.3 Testing considerations for selected neurologic pathogens.
4. Table 51.4 Testing considerations for selected enteric pathogens.
5. Table 51.5 Testing considerations for selected abortogenic pathogens.
6. Table 51.6 Interpretation of common qPCR results for selected equine pathogens.
Chapter 52
1. Table 52.1 Definitions of genetic terms.
2. Table 52.2 US laboratories offering licensed genetic testing for horses.
Chapter 53
1. Table 53.1 Genes, allelic variants, and molecular nature of coat color mutations. DNA changes are described in reference to location on the horse genome reference sequence assembly EquCab2.0.
2. Table 53.2 Partial list of service laboratories that provide horse coat color tests.
3. Table 53.3 Genotypes reported in coat color tests and mode of inheritance mutations.
4. Table 53.4 Coat color genotypes and genetic implications for color and breeding potential.
Chapter 59
1. Table 59.1 Protein content in CSF for atlanto‐occipital (AO) and lumbosacral (LS) spaces for adults and neonatal foals reported by several authors (Andrews et al., 1990, 1994, Kirk et al., 1974, Kristensen et al., 1977).
2. Table 59.2 Biochemical parameters of normal CSF. Values presented here are derived from various publications and should only be used as a guideline (Furr and Bender, 1994, Jackson et al., 1996, Rossdale et al., 1982, Toth et al., 2012).* = Values from neonatal foals during anesthesia with isoflurane in 100% oxygen (Geiser et al., 1996).
3. Table 59.3 Bacterial pathogens reported to cause meningitis/meningoencephalomyelitis in horses. F = facultative, all other anaerobic organisms are obligate anaerobes (Toth et al., 2012). Two other organisms reported in horses with sinusitis and meningitis but not isolated in CSF include Acinetobacter spp. and Prevotella spp.
Chapter 60
1. Table 60.1 Recommended diagnostic tests for pituitary pars intermedia dysfunction.
2. Table 60.2 Recommended diagnostic tests for equine metabolic syndrome.
Chapter 61
1. Table 61.1 Reference range from common hormones established at the Clinical Endocrinology Laboratory, School of Veterinary Medicine, University of California at Davis.
Chapter 62
1. Table 62.1 Available stall‐side tests.
2. Table 62.2 Case example calcium test results.

List of Illustrations

Chapter 01
1. Figure 1.1 Blood flow chart.
Chapter 04
1. Figure 4.1 A Receiver‐Operating‐Characteristic (ROC) curve can be plotted by creating the DSE‐DSP pairs over the range of selected cutoff values. Tests with poor performance and low discriminative power tend toward the diagonal line. Tests with good performance and discriminative power tend to bend upwards and to the left upper corner. The best performance, characterized by a DSE of 100% and DSP of 100% is located at the top left corner in the ROC graph.
Chapter 08
1. Figure 8.1 The sample on the left is serum from a Quarterhorse with hypertriglyceridemia and hyperbilirubinemia. Notice how the sample is opaque from the hyperlipemia. Anorexic horses often become hyperbilirubinemic, imparting the dark yellow to orange color to the sample. The sample on the right is serum from a normal horse.
Chapter 09
1. Figure 9.1 Application of a local anesthetic mixture topically to a shaved area to desensitize the skin and facilitate catheterization of the transverse facial artery in an awake horse. After approximately 20 min contact time, the area is scrubbed and the vessel is located via pulse palpation and subsequently punctured using aseptic technique.
2. Figure 9.2 Horses under injectable anesthesia breathing a fraction of inspired oxygen (FiO₂) of 21% (room air) frequently become severely hypoxemic (PaO₂ < 60 mmHg, Panels A and B). Ventilation (PaCO₂) may be normal (Panel A) or slightly decreased (Panels B and C) as evidenced by eucapnia (normal PaCO₂) or hypercapnia (increased PaCO₂). Increasing FiO₂ to approximately 30% via oxygen insufflation (15 l/min in adult horses) into the airway (nostril or orotracheal tube) will often ameliorate (Panels A and C) and sometimes fully correct (Panel B) hypoxemia. Higher FiO₂ may be needed to fully correct hypoxemia in some horses (Panel C), but it may not be practical in out‐of‐hospital situations.
3. Figure 9.3 Oxygen supplementation can be easily accomplished by using a portable source of oxygen to administer 15 l/min deep into the nostril. This will increase the fraction of inspired oxygen (FiO₂), which frequently offsets the severe hypoxemia commonly observed in anesthetized horses breathing room air (FiO₂ = 21%).
Chapter 16
1. Figure 16.1 (A–D) Equine peripheral blood films. Modified Wright‐Giemsa stain. (A) Rouleaux. (B) RBC containing a Howell‐Jolly body. (C) Two RBCs with Heinz bodies. (D) Eccentrocyte.
2. Figure 16.2 Diagnostic approach to anemia.
3. Figure 16.3 Diagnostic approach to erythrocytosis.
Chapter 17
1. Figure 17.1 (A–I) Peripheral blood films. Equine leukocytes. Modified Wright‐Giemsa stain. (A) Segmented neutrophil. (B–C) Toxic band neutrophils. (D) Morulae of Anaplasma phagocytophilum in a neutrophil. (E) Eosinophil. (F) Basophil. (G) Monocyte (left) and segmented neutrophil (right). (H) Small lymphocyte. (I) Small lymphocyte with cytoplasmic granules.
Chapter 18
1. Figure 18.1 Five equine platelets. Peripheral blood film. Modified Wright‐Giemsa stain.
2. Figure 18.2 Diagnostic approach to thrombocytopenia.
3. Figure 18.3 Diagnostic approach to thrombocytosis.
Chapter 20
1. Figure 20.1 Clinical presentation of a mare after consumption of a vitamin K antagonist rodenticide. Spontaneous hemorrhage from the gingiva (A) as well as sonographic evidence of hemoabdomen (B) were observed.
Chapter 29
1. Figure 29.1 The combined SEQ2190 (Antigen A) and SeM (Antigen C) serology can be used in unvaccinated horses to prescreen new animals prior to introduction into the herd. If an asymptomatic horse tests negative on serology, it is recommended that the horse be retested 2 weeks later before introducing the animal into the new herd. If the new arrival is positive on serology, then guttural pouch lavage qPCR and endoscopic examination is warranted. If guttural pouch examination is not possible, then three nasopharyngeal washes over a 2‐week period should be performed, though this is not ideal (Robinson et al., 2013).
2. Figure 29.2 The combined Antigen A and C serology can also be utilized in the control of outbreaks. Guttural pouch lavage and endoscopy should be performed on all previously clinical animals three weeks post the resolution of clinical signs. The asymptomatic nonexposed and exposed groups are then tested at that time with the combined iELISA assays to identify who requires additional screening via guttural pouch lavage and endoscopy to find subclinical carriers from these two groups (Robinson et al., 2013).
Chapter 30
1. Figure 30.1 Typical pectoral abscess due to Corynebacterium pseudotuberculosis infection, which is one of the most common clinical manifestations. Bacterial culture is all that is required to confirm infection.
2. Figure 30.2 Diagnostic flow chart for systemic infection caused by Corynebacterium pseudotuberculosis.
3. Figure 30.3 Photograph of the SHI serologic test for IgG antibodies to the bacterial exotoxin produced by Corynebacterium pseudotuberculosis.
4. Figure 30.4 Dot plot of log₂–transformed anti–Corynebacterium pseudotuberculosis toxin antibodies measured via serum SHI testing in 170 horses of various breeds (171 records; 92 cases of Corynebacterium pseudotuberculosis infection and 79 controls with no evidence of C. pseudotuberculosis infection). Case horses were grouped according to disease location (external abscess only [n = 49], internal abscess only [21], or external and internal abscesses [22]). Bars represent 95% confidence intervals. C = Control. EI = External and internal abscess. EO = External abscess only. IO = Internal abscess only.
Chapter 32
1. Figure 32.1 Timeline of clinical signs, CBC findings, and diagnostic detection of A. phagocytophilum infection in the horse.
2. Figure 32.2 Anaplasma phagocytophilum morula (arrow) within a neutrophil on a blood smear from a horse with equine granulocytic anaplasmosis (Wright‐Giemsa stain, 1000×).
Chapter 39
1. Figure 39.1 Babesia caballi merozoites appear pyriform shaped and occur in pairs within erythrocytes.
2. Figure 39.2 Theileria equi merozoites appear as four pyriform parasites in a Maltese cross formation within erythrocytes.
Chapter 41
1. Figure 41.1 Clinical signs of a horse with immune‐mediated hemolytic anemia. Pale mucous membranes (B) and depression (D) are signs of severe anemia; discolored serum (A, hemoglobulinemia) and urine (C, hemoglobinuria) indicate intravascular hemolysis.
2. Figure 41.2 Direct antiglobulin test (direct Coombs test). DAT tests for the presence of antibody‐coated red blood cells in the patient’s blood. Washed red blood cells from the patient are incubated with anti‐horse immunoglobulin (antibody reagent). (A) When the red blood cells are coated with immunoglobulin, antibody reagent binding promotes links between red blood cells and, consequently, agglutination (positive test). (B) In the absence of antibody‐coated red blood cells, the antibody reagent cannot promote agglutination (negative test). False‐positive and false‐negative tests are possible, as discussed in the text.
3. Figure 41.3 Indirect antiglobulin test (indirect Coombs test). IAT tests for the presence of antibodies against red blood cell surface molecules in the serum of the patient with hemolysis or a patient in need of a blood transfusion. Dilutions of the patient/recipient serum is mixed with washed red blood cells of known antigenic expression or washed red blood cells from a blood donor. (A) When antibodies against red blood cell antigens are present in the recipient’s serum, antibody‐red blood cell complexes are formed, and subsequently detected by agglutination with the addition of antibody reagent (anti‐horse immunoglobulin) (positive test). (B) In the absence of antibodies against red cell blood antigens in the serum of the patient/recipient, red blood cell link is not formed, and no agglutination is observed (negative test).
Chapter 42
1. Figure 42.1 Incompatible blood types between the mare and the stallion predisposes to neonatal isoerythrolysis. When the sire’s red blood cells express surface proteins that are not shared by the dam, the foal has a chance to inherit these proteins on their red blood cells. During gestation, the dam develops antibodies against the foal antigens, and transfers them to the colostrum. When that foal or a subsequent gestation foal (more likely) expressing the same incompatible antigen absorbs the antibodies in the colostrum, red blood cells become coated by these antibodies and hemolysis occurs.
2. Figure 42.2 Hemolytic assay to detect serum antibodies against red blood cell surface proteins. Different two‐fold dilutions (1:2 to 1:32) of the serum from the mare are mixed with red blood cells expressing different antigens (e.g., Aa or Qa). If antibodies are present in the mare’s serum, they bind to the red blood cells and, after adding exogenous complement, red blood cell lysis is induced. A negative control uses saline instead of mare’s serum. Serum dilutions above 1:16 for Aa and Qa that cause hemolysis in vitro may produce NI; therefore, withholding of the colostrum is recommended. Antibodies to Aa and Qa factors detected at 1:2 serum dilution require retest before foaling.
3. Figure 42.3 Jaundice foal agglutination test. This detects antibodies in the colostrum against the foal’s red blood cells, and should be run at parturition, before the ingestion of colostrum. In this test, two‐fold dilutions of the dam’s colostrum with saline (1 ml of 1:2 to 1:32 dilutions) are mixed with one drop of the foal’s whole blood. A 1 ml saline is used as a negative control, and the mare’s blood may be tested under the same conditions as another negative control. The test can be performed in tubes for centrifugation or on a glass slide.
Chapter 43
1. Figure 43.1 Direct immunofluorescence flow cytometry to detect antibody‐coated platelets. Flow cytometric analysis identifies the presence of IgG‐, IgM‐, and IgA‐coated platelets. Platelets from the patient are washed to remove unbound‐antibodies present in the blood, and a fluorescence‐conjugated anti‐IgG, anti‐IgM, or anti‐IgA is added for subsequent reading using a flow cytometer. (A) Platelets from the patient may be coated by (A1) auto‐immune antibodies that recognize a self cell‐surface molecule or (A3) irrelevant antibodies may bind non‐specifically to Fc receptors on the surface of platelets; in addition, (A2) Fc receptors may be free of antibodies. When fluorescence‐conjugated anti‐horse immunoglobulin is added to the platelet solution, (B) the reagent may (B1) bind specifically to an autoantibody recognizing a self‐antigen (true positive results), (B2) bind non‐specifically to a Fc receptor (false‐negative), or (B3) bind to an antibody linked non‐specifically to a Fc receptor (false‐positive). (C) In addition, in a true‐negative sample, there is no (C1) auto‐antibody bound to a platelet self‐antigen; yet, positive fluorescence is obtained with antibody reagent binding to (C2) an empty Fc receptor or (C3) an non‐specific antibody bound to a Fc receptor. Consequently, not all detected platelet‐associated antibody is anti‐platelet antibody.
Chapter 45
1. Figure 45.1 Peripheral blood lymphocyte subpopulation distribution and serum immunoglobulin concentrations in a filly with delayed cellular immunity development. An 8‐month‐old Quarter Horse filly presented for veterinary care with recurrent fevers and infections, including a non‐respiratory Rhodococcus equi abscess. Infection with a facultative intracellular bacterium at this age suggests impaired cellular immunity. Peripheral blood lymphocyte immunophenotyping performed every 2 months revealed CD4+ T cell lymphopenia, low CD4/CD8 ratio, and low percentage of lymphocytes expression the MHC class II molecule. When stimulated in vitro with a mitogen (PHA, phytohemagglutinin), the lymphocytes proliferated robustly, and flow cytometric analysis measured an increase in the percentage of lymphocytes expressing the MHC class II molecule, in comparison to freshly isolated lymphocytes and non‐stimulated lymphocytes. In this case, intrinsic lymphocyte dysfunction was not documented, and delayed cellular immunity development due to lack of appropriate stimulus in vivo is likely.
Chapter 46
1. Figure 46.1 Serum protein electrophoresis pattern. Protein electrophoresis separates blood proteins based on their net charge (positive or negative), and physical properties (size and shape) when exposed to an electric current: albumin, alphaglobulins, betaglobulins, and gammaglobulins. The gamma region comprises mostly of immunoglobulins, primarily IgG. Nevertheless, immunoglobulins can be found throughout the electrophoretic spectrum. (A) normal electrophoretic pattern; (B) electrophoretic pattern showing a monoclonal spike in the gamma region in a horse with B cell leukemia; note the low albumin levels; (C) electrophoretic pattern showing a monoclonal spike in the beta2 region in a horse with B cell leukemia; note the low albumin and gammaglobulin levels; (D) electrophoretic pattern showing increased alpha and beta inflammatory proteins, and decreased gammaglobulins in a horse with common variable immunodeficiency.
2. Figure 46.2 Transient hypogammaglobulinemia of the young. Serum IgG (left y‐axis) and IgM (right y‐axis) concentrations through time in a filly with history of recurrent fevers, hyperfibrinogenemia and pneumonia.
Chapter 48
1. Figure 48.1 Fruiting structure of Aspergillus spp. including conidia (arrows) observed in a cytological sample collected from an equine guttural pouch.
2. Figure 48.2 General algorithm for interpretation of aerobic bacterial culture results.
Chapter 50
1. Figure 50.1 Ascarid eggs are surrounded by a thick proteinaceous capsule.
2. Figure 50.2 Strongyle eggs.
3. Figure 50.3 Anoplocephala perfoliata eggs are typically D‐shaped.
4. Figure 50.4 Strongyle (red arrow) and cestode (black arrow) eggs.
5. Figure 50.5 Oxyuris equi eggs contain an operculum (black arrow) at one end.
6. Figure 50.6 Strongyloides westeri eggs are small (50 × 40 µm), thin‐shelled elliptical eggs that already contain a larva.
7. Figure 50.7 Chronological approach to parasite control for foals during the first 12 months of life.
Chapter 52
1. Figure 52.1 Sequencing chromatogram generated from an automated Sanger DNA sequencer of three horses. Each color represents a nucleotide. The pink arrow points to a single nucleotide variant where the first horse (top panel with arrow) is heterozygous (T/C) while the second (middle panel) and third (bottom panel) horses are homozygous T/T. The letter “N” may appear over these sites to denote that the sequencer was unable to determine only one base pair at this location.
Chapter 53
1. Figure 53.1 DNA profiles for each possible genotype for the Extension, Agouti, and Cream genes. Colored peaks in yellow, blue, and red are fluorescence‐labeled PCR products separated by laser‐assisted capillary electrophoresis followed by fragment size analysis of imaging data. For each gene, alleles are identified by the length in base pairs of PCR product (x‐axis). Signal intensity (y‐axis) only reflects yield of product in the PCR reaction.
2. Figure 53.2 American Miniature Horse mare with diluted color phenotype.
Chapter 54
1. Figure 54.1 Peritoneal fluid of a horse with blood contamination at collection (A) and a horse with a strangulating obstruction (B). Left sample is distilled water for comparison, middle sample is non‐centrifuged peritoneal fluid and right sample is centrifuged peritoneal fluid).
2. Figure 54.2 Peritoneal fluid from a horse with septic peritonitis due to a cecocentesis. Fluid was serosanguineous, had a high protein, and elevated number of nucleated cells.
3. Figure 54.3 Peritoneal fluid of a horse with rupture bowel. The fluid had a total of 0.1 g/dL protein, 420 nucleated cells/μL, and lactate total of 7.9 mmol/L (peripheral lactate was 13.7 mmol/L). There is heterogeneous population of bacteria and protozoa and the presence of intracellular bacteria within karyolitic neutrophils indicating rupture bowel.
4. Figure 54.4 Hand‐held lactate portable analyzers available in the United States. Peritoneal fluid was analyzed by the portable analyzers and compared to a bench top analyzer and to a chromogenic assay. The Lactate Pro analyzer has the highest level of agreement in peritoneal fluid of horses.
Chapter 55
1. Figure 55.1 Squamous cell with attached bacteria but no accompanying inflammatory cells indicates nasopharyngeal contamination.
2. Figure 55.2 Material routinely used to collect BAL fluid includes a Bivona Tube, a puffer, an infusion set, 60‐ml syringes, dilute lidocaine (0.66%), lubricant, and red top tubes.
3. Figure 55.3 These neutrophils appear degenerate, however, even very segmented neutrophils, when left in saline without the benefit of being in a pocket of mucus or adding protein to the sample in the form of serum, will become degenerate in appearance after several hours.
4. Figure 55.4 This BAL slide was not dried quickly and although there is an appropriate single cell layer, the cells have all shrunk and it is impossible to distinguish cell type. This is an example of “Blue Dot Disease.”
5. Figure 55.5 Dif‐Quik and other Romanowsky stains do not stain mast cells. On the left, a seemingly innocuous BAL stained with Dif‐Quik from a horse with pronounced airway hyper‐responsiveness. On the right, the same slide stained with Toluidine Blue. Mast cells are easy to detect with their magenta granules.
6. Figure 55.6 Pneumocystis jirovecci is considered an opportunistic infection which can be found in the lungs of even normal people and presumably normal horses. If the immune system is suppressed, the fungus can cause severe disease.
7. Figure 55.7 Typical BALF cytology from a normal horse. The predominant cells types are alveolar macrophages and lymphocytes.
8. Figure 55.8 Epithelial cells have a basally located nucleus and a columnar shape. These epithelial cells are easy to recognize because they are ciliated.
9. Figure 55.9 Goblet cells (arrow) may look unexpectedly round for an epithelial cell and would possibly be mistaken for a mast cell, but the granules are very large and stain dark blue.
10. Figure 55.10 Large numbers of cliated epithelial cells can be seen in horses with severe coughing, after viral disease, when the BAL is traumatic, or if a bronchial lavage has been performed rather than a bronchoalveolar lavage.
11. Figure 55.11 Clumps of reactive epithelial cells (arrow), also called creola, can be seen in horses with chronic airway inflammation.
12. Figure 55.12 Alveolar macrophages (arrows) are large cells with lacy cytoplasm. They should be the predominant cell in the normal BAL cytology.
13. Figure 55.13 The normal BAL cytology in the horse should have approximately 40% lymphocytes, and these will be a mixture of small lymphocytes with scant cytoplasm (black arrow) and larger lymphocytes with a lighter and more obvious cytoplasm (red arrow).
14. Figure 55.14 Neutrophil with pyknotic nucleus (black arrow) in a pool of mucus.
15. Figure 55.15 Mixed neutrophilic and eosinophilic inflammation.
16. Figure 55.16 When airway inflammation becomes chronic, mucus will become more fibrillar, forming long, tightly compacted strands.
17. Figure 55.17 Hypercellular mucus often contains large numbers of degenerate‐appearing neutrophils. This trapping of neutrophils can falsely decrease the reported neutrophil percentage.
18. Figure 55.18 Curschmann’s spirals are spiral‐shaped mucus plugs that reflect the shape of mucus gland ducts or bronchioles. They can be seen in cases with long‐standing mucus accumulation, and are not specific to any one disease.
19. Figure 55.19 Mucus and pollen (arrow) in a horse with a recent onset cough. Alveolar macrophages dominate the cell population but occasional neutrophils are also seen.
20. Figure 55.20 Giant cell containing many particulates (dark blue staining within cytoplasm) and a hay spore (arrow).
21. Figure 55.21 Birefringent particulates (arrow) can only be seen with a polarizing lens.
22. Figure 55.22 BAL cytology from a horse with EIPH that raced 10 days before sample collection. Note the dark black pigment within the hemosiderophage, and the lack of free red cells.
23. Figure 55.23 Within this giant cell are multiple scintillating refractile particles. This can only be seen with polarizing microscopy (Picture courtesy of Dr. Andrew Hoffman).
24. Figure 55.24 This BAL was taken from a horse that had been in a barn fire several months previously. Carbon particles (arrows) are still evident engulfed in alveolar macrophages. Alveolar macrophages are extremely long‐lived, and these particles will be evident on BAL for years.
Chapter 56
1. Figure 56.1 Pleural cytology from a horse with pleuropneumonia secondary to esophageal obstruction. Note the degenerate appearance of the neutrophils as well as a mixed population of intracellular bacteria.
Chapter 57
1. Figure 57.1 Urine with clearing myoglobin after an acute episode of myopathy. The urine was collected on the day of presentation and the subsequent 3 days of hospitalization (left to right).
2. Figure 57.2 Calcium oxalate crystals in the urine of a healthy horse. Unstained direct wet preparation, 200×.
Chapter 58
1. Figure 58.1 Synovial fluid collected from a horse with a dorsal carpal laceration. Fluid from the midcarpal joint (A) is cloudy yellow, with a total protein of 2.1 g/dL, good mucin clot, 2400 total nucleated cells/μL, and 60% neutrophils. Fluid from the radiocalrpal joint (B) is cloudy and pink, with a total protein of 5.3 g/dL, poor mucin clot, 86,800 total nucleated cells/μL, and 99% neutrophils. Samples were collected before antimicrobials were administered and bacterial cultures yielded no growth.
2. Figure 58.2 A and B. Synovial fluid sample (100×) from a tendon sheath showing increased cellularity with a pale pink finely stippled background and scattered erythrocytes. Neutrophils show moderate degeneration. Scattered neutrophils contain intracellular cocci and short rods. Rarely bacteria of similar morphology were also noted extracellularly.
3. Figure 58.3 Ultrasonographic image of a septic proximal interphalangeal joint. The image shows slightly echogenic effusion within the dorsal recess of the joint with moderate synovial thickening. A 19G needle was inserted under ultrasound guidance and was used to collect synovial fluid.
Chapter 59
1. Figure 59.1 Cerebrospinal fluid. Xanthochromic transparent CSF from a horse with herpesvirus myeloencephalopathy (A); Xanthochromic cloudy opaque CSF from a horse with bacterial meningitis (B).
2. Figure 59.2 Blood contamination of LS CSF. Note sequential aspirates until CSF became as clear as possible.
Chapter 62
1. Figure 62.1 SofCheck^TM test strips showing color change correlated to calcium levels from 0 ppm to 425 ppm.
2. Figure 62.2 pH paper.
3. Figure 62.3 FoalWatch^TM Kit displaying color change from clear to orange to blue.