A unique collection of photographic illustrations of the major equine disorders, providing both qualified practitioners and veterinary students with an invaluable guide to greater diagnostic accuracy, treatment options, and a wider understanding of the processes and signs of equine disorders. The systematic presentation of disorders along with the icon-based key points system of evaluation gives unparalleled ease of access and use. Conditions presented are gathered from around the world, making for a resource of universal application that is a major aid to the rapid visual recognition and interpretation of clinical signs that are vital elements of success in veterinary practice.
- Many new conditions added
- Over 300 new colour illustrations
- Brand new design with icon-based key points boxes.
- Systematic presentation of text with emphasis gives greater ease of access.
- Treatment options and prognoses now included.
- Includes access to online database of all disorders
- Two upcoming top experts brought in to build on the foundation of Derek Knottenbelt and Reg Pascoe's milestone text.
A unique collection of photographic illustrations of the major equine disorders, providing both qualified practitioners and veterinary students with an invaluable guide to greater diagnostic accuracy, treatment options, and a wider understanding of the processes and signs of equine disorders. The systematic presentation of disorders along with the icon-based key points system of evaluation gives unparalleled ease of access and use. Conditions presented are gathered from around the world, making for a resource of universal application that is a major aid to the rapid visual recognition and interpretation of clinical signs that are vital elements of success in veterinary practice. Many new conditions added Over 300 new colour illustrations Brand new design with icon-based key points boxes. Systematic presentation of text with emphasis gives greater ease of access. Treatment options and prognoses now included. Two upcoming top experts brought in to build on the foundation of Derek Knottenbelt and Reg Pascoe's milestone text.
Front cover 1
Half title page 2
Dedication 3
Knottenbelt and Pascoe's Color Atlas of Diseases and Disorders of the Horse 4
Copyright page 5
Foreword 6
Preface 8
Acknowledgements 8
Contributors 10
Table of Contents 12
1 Gastrointestinal system 14
Chapter Contents 14
Part 1: The mouth 14
Developmental disorders 14
Cleft palate (Figs. 1.1–1.3) 14
Diagnosis 14
Treatment 14
Cleft tongue and mandible (Fig. 1.4A,B) 14
Parrot mouth (brachygnathia) (Figs. 1.5–1.7) 14
Sow mouth (prognathia) (Figs. 1.8 & 1.9)
Diagnosis and treatment of parrot mouth/sow mouth 16
Shear mouth 16
Missing and malerupted teeth (Figs. 1.10–1.18) 16
Oligodontia 16
Maleruptions 18
Persistent temporary dentition 18
Supernumerary teeth 18
Diagnosis of missing/malerupted teeth 19
Treatment 19
Wolf teeth (Fig. 1.19) 19
Dentigerous cysts (Figs. 1.20 & 1.21)
Diagnosis and treatment 19
Non-infectious disorders 20
Dental tartar (Figs. 1.22 & 1.23)
Diagnosis and treatment 20
Ossifying alveolar periostitis (Fig. 1.24) 20
Diagnosis and treatment 20
Lampas/inflammation of the hard palate (Fig. 1.25) 20
Diagnosis and treatment 21
Fractures of the maxilla and mandible (Figs. 1.26–1.30) 21
Diagnosis and treatment 21
Dental disease 21
Abnormal wear patterns (Figs. 1.31–1.38) 21
Periodontal disease (Figs. 1.39–1.41) 25
Dental caries (Fig. 1.42) 25
Infection of the dental pulp 26
Diagnosis 26
Treatment 27
Part 2: The tongue 27
Position and function 27
Diagnosis and treatment of abnormal tongue position/function 28
Traumatic lesions involving the tongue (Figs. 1.45 & 1.46)
Hyperkeratinized oral mucosa (Fig. 1.47) 28
Stomatitis (Figs. 1.48–1.50) 29
Diagnosis and treatment 30
Part 3: The salivary glands and ducts 30
Developmental disorders 30
Salivary mucocele (Fig. 1.51) 30
Diagnosis and treatment 30
Non-infectious disorders 30
Idiopathic sialadenitis (Fig. 1.52) 30
Diagnosis and treatment 30
Sialoliths (Figs. 1.53 & 1.54)
Diagnosis and treatment 31
Ptyalism (Fig. 1.55) 31
Differential diagnosis 31
Diagnosis and treatment 32
Infectious disorders 32
Sialadenitis 32
Diagnosis and treatment 32
Part 4: The esophagus 32
Developmental disorders 32
Congenital intramural and esophageal duplication cysts (Figs. 1.56 & 1.57)
Diagnosis and treatment 32
Non-infectious disorders 33
Intraluminal obstruction (Figs. 1.58–1.63) 33
Diagnosis 34
Treatment 34
Esophageal strictures (Figs. 1.64–1.70) 35
Diagnosis 36
Esophageal dilatation/megaesophagus (Figs. 1.71–1.74) 36
Causes/differential diagnosis 36
Clinical signs and diagnosis 37
Treatment 37
Esophagitis (Figs. 1.75 & 1.76)
Diagnosis 38
Treatment 38
Esophageal diverticula (Fig. 1.77) 38
Diagnosis and treatment 39
Esophageal perforation (Figs. 1.78–1.81) 39
Diagnosis 39
Treatment 39
Esophageal fistulae (Figs. 1.82 & 1.83)
Diagnosis and treatment 40
Infectious disorders 40
Oropharyngeal necrosis (Fig. 1.84) 40
Diagnosis and treatment 40
Esophageal abscesses (Fig. 1.85) 40
Diagnosis and treatment 41
Part 5: The gastrointestinal tract 41
Congenital/developmental disorders 41
Intestinal atresia: atresia ani (Fig. 1.86) / atresia coli (Fig. 1.87) 41
Diagnosis: 41
Treatment and prognosis 42
Inguinal hernia (see also p. 48) (Figs1.88 & 1.89)
Diagnosis and treatment 42
Lethal white syndrome (Figs. 1.90 & 1.91)
Diagnosis and treatment 42
Meconium impaction (Figs. 1.92–1.95) 43
Diagnosis 43
Treatment 44
Meckel’s diverticulum (Fig. 1.96) 44
Mesodiverticular bands (Fig. 1.97) 44
Herniation of bowel through the umbilicus (Fig. 1.98) 44
Diagnosis and treatment 45
Congenital diaphragmatic hernias 45
Non-infectious disorders 45
Colic (Figs. 1.99–1.117) 45
Obstructive disorders: Simple non-strangulating obstructive lesion 48
Ileal impaction (Figs. 1.118–1.120) 49
Diagnosis 49
Ileal hypertrophy (Fig. 1.121) 50
Large intestine simple obstruction (Figs. 1.122 & 1.123)
Diagnosis and treatment 50
Sand impactions of the large colon (Fig. 1.124) 50
Diagnosis and treatment 50
Cecal impactions (Figs. 1.125 & 1.126)
Diagnosis and treatment 53
Foreign body impactions (Fig. 1.127) 53
Fecaliths and enteroliths (Figs. 1.128–1.132) 53
Diagnosis and treatment 55
Intramural lesions and abdominal abscesses (Figs. 1.133–1.138) 55
Diagnosis and treatment 55
Submucosal hematomas (Fig. 1.139) 56
Diagnosis and treatment 56
Obstructive disorders: Non-strangulating obstructions (Figs. 1.140–1.143) 56
Diagnosis and treatment 58
Large colon displacements 58
Diagnosis 59
Treatment 60
Ischemic disorders: Strangulating obstructions 60
Small intestinal strangulation 60
Umbilical hernia entrapment (Figs. 1.149–1.152) 60
Inguinal hernia entrapment (Figs. 1.153–1.157) 61
Epiploic foramen entrapment 61
Intussusceptions (Figs. 1.158–1.163) 61
Acquired (or developmental) defects in the diaphragm or mesentery (Figs. 1.164–1.166) 64
Mesodiverticular bands (see Fig. 1.97) and pedunculated lipomas (Figs. 1.167–1.169) 64
Rotation of segments of jejunum or ileum (Figs. 1.170–1.173) 65
Rotation of the mesenteric root about its axis 66
Torsion of the cecum (Fig. 1.174) 66
Strangulating displacements (torsion) of the large bowel (Figs. 1.175 & 1.176)
Diagnosis 67
Treatment 67
Prolapse of the rectum (Figs. 1.177–1.179) 67
Diagnosis and treatment 69
Rectal tears (Figs. 1.180–1.185) 69
Diagnosis and treatment 70
Grass sickness (Figs. 1.186–1.193) 71
Diagnosis, treatment and prognosis 73
Infiltrative bowel diseases (Figs. 1.194 & 1.195)
Diagnosis 73
Granulomatous enteritis 74
Lymphocytic-plasmacytic enterocolitis 74
Multisystemic eosinophilic epitheliotropic disease 74
Idiopathic focal eosinophilic enterocolitis 74
Intestinal lymphoma 74
Prognosis 74
Gastric and gastroduodenal ulceration (Figs. 1.196–1.206) 74
Gastric ulcers 75
Diagnosis 76
Treatment 76
Gastric distension (Figs. 1.207–1.210) 78
Diagnosis 79
Treatment 79
Gastric rupture (Figs. 1.211 & 1.212)
Diagnosis 80
Infectious disorders 80
Viral disease 80
Rotavirus (Fig. 1.213) 80
Diagnosis and treatment 80
Equine coronavirus 80
Diagnosis and treatment 80
Bacterial diseases (Figs. 1.214–1.216) 81
Acute equine colitis 81
Salmonellosis 81
Equine intestinal clostridiosis 81
Clostridium perfringens 82
Clostridium difficile 82
Neorickettsia risticii (Potomac horse fever) 82
Diagnosis 82
Treatment 82
Public health 82
Lawsonia intracellularis infection (Figs. 1.217–1.220) 82
Diagnosis 83
Treatment 83
Miscellaneous disorders 83
Intestinal hyperammonemia 83
Diagnosis 83
Treatment 84
Peritoneal disorders 84
Peritonitis (Figs. 1.221–1.227) 84
Diagnosis 85
Treatment 85
Omental prolapse 85
Treatment 85
Parasitic diseases 85
Diagnostic methods 85
Clinical diagnosis 86
Parasite surveillance (Figs. 1.228 & 1.229)
Anthelmintic resistance 86
Detection of anthelmintic resistance 87
Tapeworm diagnosis 87
Fecal examination for tapeworm eggs 87
Tapeworm serum ELISA 87
Manifestations of parasitic disease 88
Ascarid impaction (Figs. 1.230–1.232) 88
Diagnosis 88
Treatment and prognosis 89
Larval cyathostominosis (Figs. 1.233–1.235) 89
Diagnosis 90
Treatment and prognosis 90
Thromboembolic colic (Figs. 1.236–1.238) 90
Diagnosis 91
Treatment and prognosis 91
Tapeworm-associated colic (Fig. 1.239) 91
Diagnosis 91
Treatment and prognosis 91
Principles for equine parasite control 91
Part 6: Neoplastic disorders 92
The mouth (Figs. 1.240–1.245) 92
Diagnosis 93
Treatment 94
Salivary glands (Figs. 1.246 & 1.247)
Diagnosis and treatment 94
The esophagus 94
Lower gastrointestinal tract (Figs. 1.248–1.251) 94
Diagnosis 96
References and further reading 96
2 Conditions of the liver, spleen and pancreas 97
Chapter Contents 97
Developmental disorders 97
Hepatic disorders 97
Portosystemic shunt 97
Diagnosis and treatment 97
Biliary atresia 97
Diagnosis 97
Hyperammonemia of Morgan foals 97
Diagnosis and treatment 97
Hepatic insufficiency 97
Icterus (Figs. 2.1 & 2.2)
Hepatic encephalopathy (HE) (Figs. 2.3–2.6) 98
Weight loss (Fig. 2.7) 100
Colic, diarrhea, edema, tenesmus, ascites and steatorrhea (Fig. 2.8) 100
Hepatogenic photosensitization (Figs. 2.9 & 2.10)
Hemorrhagic diathesis 101
Hemolysis 101
Pruritis and seborrhea 101
Endotoxemia 101
Polydipsia, polyuria and the hepatorenal system 101
Diagnosis of liver disease 101
Treatment of hepatic insufficiency 101
Secondary hepatic failure 102
Chronic fibrosing hepatitis (Figs. 2.11–2.15) 103
Diagnosis and treatment 103
Non-infectious disorders 103
Toxic hepatopathy 103
Hepatotoxic plants (Figs. 2.16–2.22) 103
Chemical hepatotoxins 104
Mycotoxins (Fig. 2.23) 104
Diagnosis and treatment 105
Theiler’s disease (Fig. 2.24) 105
Diagnosis and treatment 106
Liver failure in foals following neonatal isoerythrolysis 106
Diagnosis and treatment 106
Bile duct obstruction 106
Diagnosis 106
Treatment and prognosis 106
Cholelithiasis (Figs. 2.25–2.29) 106
Diagnosis 107
Treatment 107
Hepatic lipidosis (Figs. 2.30–2.34) 107
Diagnosis and treatment 108
Infectious disorders 109
Tyzzer’s disease (Fig. 2.35) 109
Diagnosis and treatment 109
Equine herpes virus 1 hepatitis (Fig. 2.36) 109
Diagnosis 109
Treatment 110
Infectious necrotic hepatitis 110
Diagnosis and treatment 110
Bacterial cholangiohepatitis (Fig. 2.37) 110
Diagnosis and treatment 110
Liver abscessation/scarring (Figs. 2.38 & 2.39)
Umbilical vein abscess into the liver (Fig. 2.40A,B) 111
Diagnosis and treatment 111
Parasitic diseases (Figs. 2.41–2.43) 111
Neoplastic disorders 112
Diagnosis 113
Pancreatic disorders 113
Pancreatitis 113
Diagnosis 114
Treatment 114
Splenic disorders (Figs. 2.53–2.60) 114
Splenic neoplasms 114
Splenic hematoma 114
Splenic abscess 115
Splenomegaly 115
Splenic rupture 116
Splenic neoplasia 116
References and further reading 116
3 Conditions of the respiratory tract 118
Chapter Contents 118
Congenital/developmental disorders 118
Wry nose (Fig. 3.1) 118
Diagnosis 118
Treatment 118
Epiglottic and pharyngeal cysts (Figs. 3.2–3.6) 118
Diagnosis and treatment 118
Guttural pouch tympany (Figs. 3.7–3.10) 119
Diagnosis 120
Treatment 121
Tracheal collapse (Figs. 3.11 & 3.12)
Diagnosis and treatment 121
Hypoplasia of the nasal turbinate bones 121
Epidermal inclusion cysts (atheroma) (Fig. 3.13) 121
Diagnosis and treatment 121
Choanal atresia (Fig. 3.14) 121
Diagnosis and treatment 122
Branchial cysts (Fig. 3.15) 122
Diagnosis and treatment 122
Maxillary sinus cysts (Figs. 3.16–3.19) 122
Diagnosis and treatment 124
Maxillary mucocele 124
Diagnosis and treatment 124
Epiglottic hypoplasia (Fig. 3.20) 124
Diagnosis and treatment 124
Fourth branchial arch defects 124
Diagnosis and treatment 124
Non-infectious disorders 124
Foreign bodies (Figs. 3.21 & 3.22)
Clinical signs 124
Diagnosis and treatment 125
Facial trauma (Fig. 3.23) 125
Clinical signs 125
Diagnosis and treatment 125
Arytenoid chondritis (Figs. 3.24–3.26) 125
Clinical signs 126
Diagnosis and treatment 126
Tracheal perforation (Figs. 3.27–3.29) 127
Clinical signs 127
Diagnosis and treatment 128
Tracheal chondroma (Figs. 3.30 & 3.31)
Diagnosis and treatment 128
Pneumothorax (Figs. 3.32–3.34) 128
Diagnosis and treatment 128
Exercise-induced pulmonary hemorrhage (EIPH) (Figs. 3.35–3.44) 129
Clinical signs 129
Diagnosis 130
Treatment and control 132
Prognosis 132
Recurrent airway obstruction and inflammatory airway disease (Figs. 3.45–3.49) 132
Clinical signs 134
Diagnosis 134
Treatment 134
Laryngeal hemiplegia (Figs. 3.50–3.56) 134
Diagnosis 135
Treatment 136
Dorsal displacement of the soft palate (Figs. 3.57 & 3.58)
Diagnosis 136
Treatment and prognosis 136
Epiglottic entrapment (Figs. 3.59–3.63) 136
Clinical signs and diagnosis 137
Treatment and prognosis 138
Lymphoid hyperplasia (Figs. 3.64–3.67) 138
Diagnosis and treatment 139
Amyloidosis (Fig. 3.68) 139
Diagnosis and treatment 139
Ethmoid hematomas (Figs. 3.69–3.71) 139
Diagnosis 140
Treatment and prognosis 140
Infectious disorders 141
Nasal discharges (Figs. 3.72–3.83) 141
Viral diseases (Fig. 3.84) 141
Clinical signs 141
Diagnosis 141
Equine influenza 141
Diagnosis 144
Treatment and prevention 144
Equine herpes virus (Fig. 3.85) 145
Diagnosis 145
Treatment and prevention 145
Other viral infections 145
Diagnosis 147
Treatment and control 147
Bacterial diseases 147
Rhodococcus equi pneumonia (Figs. 3.91–3.99) 147
Diagnosis 149
Treatment 150
Streptococcus equi var. equi (strangles) (Figs. 3.100–3.113) 150
Diagnosis 154
Treatment 154
Sequelae 154
Control of an outbreak 155
Prevention 155
Sinusitis (Figs. 3.114–3.117) 155
Diagnosis 156
Treatment and prognosis 156
Bacterial pneumonia (Figs. 3.118–3.122) 156
Diagnosis 157
Treatment 158
Pleuritis (Figs. 3.123–3.139) 158
Diagnosis 159
Treatment 162
Mycobacterial infection 162
Glanders 162
Clinical signs 162
Diagnosis 163
Treatment 163
Fungal diseases 163
Guttural pouch mycosis (see Figs. 3.140–3.146) 163
Diagnosis and treatment 163
Fungal rhinitis (Figs. 3.147 & 3.148)
Fungal pneumonia 165
Clinical signs 165
Diagnosis 166
Treatment 166
Secondary opportunistic pathogens in horses (Figs. 3.149 & 3.150)
Clinical signs 166
Diagnosis and treatment 166
Equine multinodular pulmonary fibrosis (Figs. 3.151 & 3.152)
Diagnosis 167
Treatment 168
Parasitic diseases 168
Parascaris equorum 168
Diagnosis 168
Dictyocaulus arnfieldi 168
Diagnosis and treatment 168
Pulmonary hydatidosis 169
Neoplastic disorders 169
Upper respiratory tract 169
Clinical signs 169
Diagnosis and treatment 169
Pulmonary neoplasms (Figs. 3.153–3.156) 169
Clinical signs 170
Diagnosis 171
Treatment 171
References and further reading 171
4 Disorders of the cardiovascular system 172
Chapter Contents 172
Part 1: The heart and blood vessels 172
Developmental disorders 172
Persistent neonatal pulmonary hypertension 172
Diagnosis and treatment 172
Congenital cardiac abnormalities 172
Patent ductus arteriosus (PDA) (Fig. 4.1) 172
Diagnosis and treatment 173
Ventricular septal defect (VSD) (Figs. 4.2–4.5) 173
Diagnosis 173
Treatment and prognosis 174
Atrial septal defect (ASD) (Fig. 4.6) 174
Diagnosis and treatment 175
Tetralogy of Fallot (Figs. 4.7 & 4.8)
Diagnosis and treatment 175
Tricuspid atresia 175
Diagnosis and treatment 175
Great vessel transposition (Fig. 4.9) 175
Diagnosis and treatment 175
Truncus arteriosus (Fig. 4.10) 175
Clinical signs 176
Treatment 176
Non-infectious disorders 176
Dysrhythmias: atrial fibrillation (Fig. 4.11) 176
Diagnosis and treatment 177
Prognosis 177
Premature atrial beats (PAB) (Fig. 4.12) 177
Diagnosis and treatment 178
Ventricular premature contractions (VPC) (Figs. 4.13 & 4.14)
Diagnosis 178
Treatment 178
Acquired valvular heart disease 178
Clinical signs 178
Diagnosis 179
Ruptured chordae tendinae (Figs. 4.15 & 4.16)
Clinical signs, diagnosis and treatment 179
Endocarditis (Figs. 4.17–4.24) 179
Clinical signs 182
Diagnosis and treatment 182
Prognosis 182
Pericarditis (Figs. 4.25–4.30) 182
Diagnosis 183
Treatment and prognosis 184
Myocardial disease (Figs. 4.31–4.32) 185
Diagnosis 185
Treatment and prognosis 185
Rupture of major vessels 186
Arteriovenous fistula (Figs. 4.35 & 4.36)
Diagnosis 188
Treatment 188
Mucous membranes (Figs. 4.37–4.46) 188
Vasculitis (Figs. 4.47–4.53) 188
Treatment 191
Prognosis 192
Infectious disorders 192
Viral diseases 192
Equine viral arteritis (see also Chapter 12, pp. 474, 490 and 511) 192
Diagnosis and treatment 192
Equine infectious anemia (EIA) 192
Diagnosis and management 193
African horse sickness 193
Thrombophlebitis (Figs. 4.54–4.61) 193
Clinical signs 193
Diagnosis and treatment 194
Prognosis 195
Aorto-iliac thrombosis (Fig. 4.62) 195
Diagnosis 195
Treatment 195
Parasitic diseases (Fig. 4.63) 196
Neoplastic disorders 196
Part 2: The blood, lymphatic vessels and lymph nodes 196
Developmental disorders 196
Coagulation defects (Figs. 4.64 & 4.65)
Clinical signs 196
Diagnosis 197
Treatment and prognosis 197
Thrombocytopenia 197
Disseminated intravascular coagulopathy (Figs. 4.66–4.69) 197
Diagnosis 198
Treatment 199
Immune-mediated thrombocytopenia (IMTP) 199
Clinical signs 199
Diagnosis 199
Idiopathic thrombocytopenia (Fig. 4.70) 199
Clinical signs 199
Diagnosis 199
Treatment 200
Hemolytic anemia (Fig. 4.71) 200
Intravascular hemolysis 200
Diagnosis 200
Treatment and prognosis 200
Other causes of intravascular hemolysis 200
Extravascular hemolysis 201
Immune-mediated hemolytic anemia 201
Diagnosis 201
Treatment 201
Anemia as a result of nutritional deficiencies 201
Polycythemia 201
Diagnosis 201
Treatment 201
Ulcerative lymphangitis (Figs. 4.72–4.75) 201
Diagnosis, treatment and prognosis 203
Protozoal diseases 203
Potomac horse fever 203
Piroplasmosis (Figs. 4.76–4.78) 203
Diagnosis 203
Treatment 204
Equine ehrlichiosis 204
Diagnosis and treatment 204
Trypanosomal infections (Figs. 4.79 & 4.80)
Surra 204
Neoplastic disorders 205
Lymphoma (Figs. 4.81–4.86) 205
Generalized (multicentric) lymphosarcoma 206
Alimentary (intestinal) lymphosarcoma 206
Mediastinal lymphosarcoma 206
Extranodal lymphosarcoma 207
Diagnosis and treatment 207
Myeloid leukemias 207
Diagnosis and treatment 207
Lymphangioma (Figs. 4.87 & 4.88)
Plasma cell myeloma (Figs. 4.89 & 4.90)
Diagnosis and treatment 208
Hemangiosarcoma 208
Further reading 208
5 Urinary tract disorders 209
Chapter Contents 209
Developmental disorders 209
Renal agenesis, hypoplasia and dysplasia (Figs. 5.1 & 5.2)
Treatment 210
Renal cysts (Figs. 5.3–5.6) 210
Polycystic kidney disease and glomerulocystic disease 210
Diagnosis, treatment and prognosis 210
Hereditary nephropathies 210
Vascular anomalies 210
Diagnosis and treatment 210
Pendulent kidney 210
Diagnosis and treatment 210
Rectourethral and rectovaginal fistulae (Figs. 5.7 & 5.8)
Diagnosis and treatment 211
Ectopic ureter (Fig. 5.9) 211
Diagnosis and treatment 211
Patent urachus (Fig. 5.10) 212
Diagnosis and treatment 212
Uroperitoneum (Figs. 5.11–5.18) 212
Clinical signs 213
Diagnosis 214
Treatment 214
Prognosis 215
Non-infectious disorders 215
Bladder rupture (Fig. 5.19) 215
Diagnosis and treatment 215
Polyuria/polydipsia (Fig. 5.20) 215
Diabetes insipidus 215
Cushing’s disease 215
Sepsis and endotoxemia 215
Diabetes mellitus 215
Iatrogenic causes of polyuria 215
Psychogenic polydipsia 215
Diagnosis and differentiation 216
Treatment 216
Displacements of the urinary bladder (Figs. 5.21–5.23) 216
Diagnosis and treatment 217
Urinary incontinence and bladder dysfunction (Fig. 5.24–5.28) 217
Diagnosis 219
Treatment 219
Obstructive disorders of the urinary tract 219
Urethral calculi (Figs. 5.29–5.31) 219
Clinical signs and diagnosis 220
Treatment and prognosis 220
Cystic calculi (Figs. 5.32–5.34) 220
Diagnosis and treatment 220
Nephrolithiasis (Figs. 5.35–5.39) 221
Diagnosis 221
Treatment 222
Acute renal failure (Figs. 5.40–5.44) 222
Clinical signs 223
Diagnosis 224
Chronic renal failure (Figs. 5.45–5.50) 224
Clinical signs 224
Diagnosis 225
Treatment 225
Vascular disorders 225
Urinary tract infection (Figs. 5.51 & 5.52)
Cystitis (Figs. 5.53–5.55) 226
Diagnosis 227
Treatment and prognosis 227
Pyelonephritis (Figs. 5.56–5.59) 227
Diagnosis and treatment 227
Neoplastic disorders 228
Renal neoplasia (Figs. 5.60–5.63) 228
Diagnosis and treatment 228
Bladder neoplasia 228
Diagnosis and treatment 228
References and further reading 229
6 Disorders of metabolism, nutrition and endocrine diseases 231
Chapter Contents 231
Developmental disorders 231
Hypocalcemia 231
Synchronous diaphragmatic flutter 231
Hypocalcemic tetany 231
Hypocalcemic seizures 231
Ileus 231
Retained placenta 231
Diagnosis and treatment of hypocalcemia 231
Hypercalcemic disorders 231
Primary hyperparathyroidism (Figs. 6.1–6.4) 231
Diagnosis 232
Secondary hyperparathyroidism (Figs. 6.5–6.7) 233
Nutritional secondary hyperparathyroidism (bran disease, big-head, Miller’s disease) 233
Diagnosis and treatment 234
Iron deficiency 234
Diagnosis and treatment 234
Thyroid disease 234
Hyperthyroidism 234
Diagnosis and treatment 234
Hypothyroidism (Figs. 6.8–6.10) 234
Diagnosis 235
Treatment 235
Non-thyroidal illness syndrome (euthyroid sick syndrome) 235
Thyroid gland enlargement and neoplasia (Fig. 6.11) 235
Diagnosis and treatment 236
Nutritional and other disorders 236
Nutritional myodegeneration/vitamin E and selenium deficiency/white muscle disease (Figs. 6.12–6.14) 236
Diagnosis 237
Treatment and prognosis 237
Biotin and/or methionine deficiencies (Fig. 6.15) 237
Anhidrosis (Figs. 6.16 & 6.17)
Diagnosis 238
Treatment 238
Equine metabolic syndrome (Figs. 6.18–6.20) 238
Diagnosis 239
Differentiating EMS from pituitary pars intermedia dysfunction (PPID equine Cushing’s disease)
Treatment 239
Poor body condition (Figs. 6.21–6.23) 239
Neoplastic diseases 240
Pituitary pars intermedia dysfunction (Figs. 6.24–6.28) 240
Diagnosis 240
Treatment 242
Tumors of the adrenal medulla (pheochromocytoma) 242
Further reading 242
7 Skeletal disorders 243
Chapter Contents 243
Developmental disorders 243
Deformities of the axial skeleton (Figs. 7.1–7.4) 243
Deformities of the vertebral column 243
Diagnosis and treatment 243
Polydactyly (Fig. 7.5) 243
Diagnosis and treatment 244
Congenital deformities of the limbs and joints (arthrogryposis) (Figs. 7.6 & 7.7)
Diagnosis and treatment 245
Collapse of carpal and/or tarsal bones and incomplete ossification (Figs. 7.8–7.11) 245
Diagnosis and treatment 245
Congenital luxation of the patella (Fig. 7.12) 245
Diagnosis and treatment 246
Fractured ribs (Figs. 7.13–7.16) 246
Diagnosis 247
Treatment 247
Hereditary multiple exostoses (multiple osteochondroma, multiple cartilagenous exostosis, diaphyseal aclasis or endochondromatosis) (Fig. 7.17) 247
Diagnosis and treatment 248
Developmental disorders: Acquired conditions 248
Osteochondrosis (Figs. 7.18–7.24) 248
Diagnosis and treatment 250
Prognosis 250
Angular limb deformities (Figs. 7.25–7.28) 250
Diagnosis and treatment 251
Epiphysitis and physitis (Figs. 7.29 & 7.30)
Diagnosis, treatment and prognosis 251
Sesamoiditis (Figs. 7.31–7.35) 252
Diagnosis 252
Treatment 253
Non-infectious/traumatic disorders 254
Bucked shins (Figs. 7.36 & 7.37)
Diagnosis and treatment 254
Pedal bone fractures (Figs. 7.38 & 7.39)
Diagnosis 254
Treatment 254
Fractures of the proximal sesamoids (Figs. 7.40–7.45) 255
Diagnosis 257
Treatment 257
Exostoses of the second and fourth metacarpal bones (splints) (Figs. 7.46–7.49) 257
Diagnosis and treatment 257
Splint bone fractures (Fig. 7.50) 258
Diagnosis and treatment 259
Chronic proliferative synovitis (villonodular synovitis) (Figs. 7.51 & 7.52)
Diagnosis 259
Treatment and prognosis 259
Pelvic fractures (Figs. 7.53–7.59) 260
Diagnosis 261
Treatment and prognosis 261
Sacroiliac disease (Figs. 7.60–7.63) 261
Diagnosis and treatment 262
Stifle joint (Figs. 7.64–7.66) 263
Diagnosis 263
Treatment 263
Tibial stress fractures (Fig. 7.67) 263
Diagnosis and treatment 264
Condylar fractures of the third metacarpal bone (Fig. 7.68) 264
Diagnosis, treatment and prognosis 264
Salter Harris fractures (Figs. 7.69–7.73) 265
Diagnosis and treatment 265
Osteoarthritis (Figs 7.74–7.80) 265
Diagnosis 266
Treatment 267
Tarsus 267
Tarsocrural synovitis (bog spavin) 267
Diagnosis 267
Intertarsal synovitis/osteoarthritis (bone spavin) 268
Diagnosis 269
Treatment and prognosis 269
Non-infectious disorders 269
Laminitis (Figs. 7.81–7.88) 269
Diagnosis 272
Treatment and prognosis 272
Navicular (Figs. 7.89 & 7.90)
Diagnosis 273
Impingement of dorsal spinous processes (kissing spines/overriding dorsal spinous processes) (Figs. 7.91–7.93) 273
Diagnosis 274
Treatment 274
Ringbone (Figs. 7.94 & 7.95)
Diagnosis, treatment and prognosis 274
Sidebone (Figs. 7.96–7.98) 275
Diagnosis 275
Ischemic necrosis of the medial femoral condyle (Figs. 7.99 & 7.100)
Diagnosis, treatment and prognosis 276
White line disease and seedy toe (Figs. 7.101 & 7.102)
Diagnosis 277
Treatment and prognosis 277
Hoof wall cracks (Figs. 7.103–7.106) 277
Diagnosis, treatment and prognosis 277
Coronary band and hoof wall avulsions (Figs. 7.107 & 7.108)
Diagnosis, treatment and prognosis 278
Hypertrophic osteopathy (Marie’s disease, pulmonary osteopathy) (Figs. 7.109–7.111) 279
Diagnosis, treatment and prognosis 279
Nail blind 279
Diagnosis and treatment 279
Solar bruising 280
Diagnosis and treatment 281
Infectious disorders 281
Septic arthritis/osteomyelitis/osteitis (Figs. 7.112–7.120) 281
Diagnosis 282
Treatment 283
Sequestrum (Figs. 7.121–7.123) 283
Diagnosis and treatment 283
Foreign body penetration of the sole (Figs. 7.124 & 1.125)
Diagnosis and treatment 284
Subsolar abscess (Fig. 7.126) 285
Thrush (Fig. 7.127) 286
Diagnosis and treatment 286
Canker (Fig. 7.128) 286
Diagnosis, treatment and prognosis 286
Quittor (Fig. 7.129) 286
Diagnosis and treatment 287
Neoplastic disorders (Figs. 7.130–7.132) 287
Keratoma 287
Diagnosis and treatment 288
Tendons, ligaments and bursae: Developmental disorders 288
Flexural laxity (Fig. 7.133) 288
Diagnosis and treatment 289
Congenital contracted tendons (Figs. 7.134–7.136) 289
Diagnosis and treatment 289
Rupture of the extensor tendons (Fig. 7.137) 290
Diagnosis and treatment 290
Acquired contracted tendons (Figs. 7.138–7.140) 290
Diagnosis, treatment and prognosis 291
Tendons, ligaments and bursae: Non-infectious disorders 291
Rupture of the extensor carpi radialis tendon (Fig. 7.141) 291
Diagnosis, treatment and prognosis 291
Rupture of the peronius tertius tendon (Fig. 7.142) 291
Superficial digital flexor tendon injury (Figs. 7.143–7.149) 292
Clinical signs 292
Diagnosis and treatment 292
Suspensory desmitis (Figs. 7.150–7.158) 293
Proximal suspensory desmitis 294
Diagnosis 294
Treatment and prognosis 294
Desmitis of the suspensory ligament body 295
Diagnosis, treatment and prognosis 296
Suspensory branch desmitis 296
Diagnosis, treatment and prognosis 296
Deep digital flexor tendonitis (Figs. 7.159 & 7.160)
DDFT tendonitis within the digital sheath (Fig. 7.160) 297
Diagnosis and treatment 297
DDFT injuries within the foot 298
Diagnosis 298
Inferior check ligament desmitis (accessory ligament of the deep digital flexor tendon) 299
Diagnosis, treatment and prognosis 299
Sesamoidean ligament desmopathy 299
Diagnosis 299
Treatment and prognosis 299
Tenosynovitis of the tarsal sheath (thoroughpin) 299
Diagnosis 299
Treatment and prognosis 299
Curb (Fig. 7.161) 299
Diagnosis, treatment and prognosis 300
Traumatic injuries to flexor tendons and suspensory apparatus (Fig. 7.162) 300
Extensor tendon injury (Fig. 7.163) 300
Diagnosis and treatment 301
Dislocation of the superficial flexor tendon (Fig. 7.164) 301
Annular ligament syndrome (annular ligament constriction, stenosis of the fetlock canal, stenosing palmar ligament desmitis) (Fig. 7.165) 301
Diagnosis 302
Treatment 302
Upward fixation of the patella (Fig. 7.166) 303
Diagnosis 303
Treatment and prognosis 303
Synovial bursae (Figs. 7.167 & 7.168)
Diagnosis and treatment 304
Non-infectious bursitis 304
Diagnosis and treatment 304
Tendons, ligaments and bursae: Infectious disorders 304
Infectious bursitis (Fig. 7.169) 304
Diagnosis and treatment 305
Tendons, ligaments and bursae: Neoplastic disorders 305
References and further reading 305
8 Muscle 306
Chapter Contents 306
Congenital/developmental disorders 306
Hyperkalemic periodic paralysis (HYPP) (Fig. 8.1) 306
Diagnosis and treatment 306
Control 306
Prognosis 306
Myotonia congenita (Fig. 8.2) 306
Diagnosis 306
Treatment 306
Prognosis 306
Glycogen branching enzyme deficiency 306
Diagnosis and treatment 307
Polysaccharide storage myopathy (PSSM) (Figs. 8.3 & 8.4)
Diagnosis and treatment 309
Management 309
Recurrent exertional rhabdomyolysis (RER) 309
Diagnosis 309
Treatment 309
Management 309
Malignant hyperthermia 310
Diagnosis and treatment 310
Non-infectious/traumatic disorders 310
Gastrocnemius muscle rupture (Fig. 8.5) 310
Treatment and prognosis 310
Exertional rhabdomyolysis (Figs. 8.6 & 8.7)
Diagnosis and treatment 310
Post-anesthetic myelopathy (Fig. 8.8) 311
Post-anesthetic myopathy 311
Diagnosis and treatment 311
Traumatic injuries to the muscles (Figs. 8.9–8.15) 311
Diagnosis 311
Treatment 312
Muscle necrosis (Figs. 8.16–8.19) 313
Diagnosis and treatment 314
Fibrotic myopathy 314
Treatment 314
Immune-mediated myopathies (Fig. 8.20) 315
Acute rhabdomyolysis caused by S. equi 315
Diagnosis 315
Treatment and prognosis 315
Infarctive purpura hemorrhagica 315
Diagnosis, treatment and prognosis 315
Immune-mediated polymyositis 315
Diagnosis, treatment and prognosis 315
Atypical myopathy/pasture-associated myopathy 316
Diagnosis and treatment 316
Masseter myopathy (Fig. 8.21) 316
Diagnosis and treatment 316
Muscle atrophy (Fig. 8.22) 316
Neoplastic disorders (Fig. 8.23) 316
Diagnosis and treatment 316
References and further reading 317
9 The integumentary system 318
Chapter Contents 318
Congenital/developmental disorders 318
Epitheliogenesis imperfecta (Figs. 9.1 & 9.2)
Diagnosis and treatment 318
Epidermolysis bullosa (Fig. 9.3) 318
Diagnosis and treatment 318
Congenital equine cutaneous mastocytosis 319
Diagnosis and treatment 319
Congenital vascular hamartoma/cavernous hemangioma (Fig. 9.4) 319
Diagnosis and treatment 320
Congenital papillomatosis (neonatal wart/epidermal nevus) (Fig. 9.5) 320
Diagnosis and treatment 320
Linear keratosis/alopecia (Figs. 9.6 & 9.7)
Diagnosis and treatment 320
Hereditary equine regional dermal asthenia (HERDA hypoelastosis cutis
Diagnosis and treatment 320
Dermoid cysts (Fig. 9.10) 320
Diagnosis and treatment 320
Hypotrichosis/mane and tail dystrophy (follicular dysplasia) (Fig. 9.11) 320
Diagnosis and treatment 321
Arabian fading syndrome (pinky Arab syndrome) (Fig. 9.12) 321
Diagnosis and treatment 321
Non-infectious disorders 322
Calcinosis circumscripta (Figs. 9.13 & 9.14)
Diagnosis and treatment 322
Equine axillary nodular necrosis (Fig. 9.15) 322
Diagnosis and treatment 322
Wounds 322
Foreign body wounds 323
Self-inflicted trauma (Fig. 9.16) 323
Pressure sores (Fig. 9.17) 323
Thermal injury (Fig. 9.18) 324
Endocrine diseases with cutaneous manifestations 324
Nutritional diseases with cutaneous manifestations 325
Diagnosis, treatment and prognosis of selenium poisoning 325
Chemicals, toxic plants and heavy metals 325
Chemical trauma (Fig. 9.21) 325
Diagnosis, treatment and prognosis 326
Skin scalding (Figs. 9.22 & 9.23)
Diagnosis, treatment and prognosis 326
Actinic dermatitis (Figs. 9.24 & 9.25)
Diagnosis 327
Treatment and prognosis 327
Arsenic poisoning (chronic) 327
Diagnosis and treatment 327
Mercury poisoning 327
Diagnosis and treatment 328
Plant poisoning (leucaenosis/mimosine toxicity) 328
Diagnosis and treatment 328
Zootoxicosis (Figs. 9.26–9.29) 328
Disorders of pigmentation and hair density 328
Acquired persistent leukoderma/leukotrichia (Fig. 9.30) 328
Diagnosis and treatment 328
Idiopathic depigmentation or vitiligo (Figs. 9.31 & 9.32)
Diagnosis 330
Treatment 330
Variegated or reticulated leukotrichia (Figs. 9.33 & 9.34)
Diagnosis and treatment 330
Hyperaesthetic leuko(melano)trichia 330
Diagnosis, treatment and prognosis 331
Anhidrosis (Fig. 9.35) 331
Immune-mediated skin diseases 331
Urticaria and angioedema (Figs. 9.36–9.39) 331
Diagnosis and treatment 332
Atopy (Fig. 9.40) 332
Diagnosis 333
Treatment 333
Autoimmune skin conditions 333
Pemphigus foliaceus (Figs. 9.41–9.46) 333
Clinical signs 334
Diagnosis 334
Treatment 334
Bullous pemphigoid (Figs. 9.47 & 9.48)
Diagnosis and treatment 334
Equine sarcoidosis (Fig. 9.49) 336
Diagnosis 336
Treatment 336
Multisystemic eosinophilic epitheliotropic disease/generalized eosinophilic disorder (Figs. 9.50 & 9.51)
Diagnosis 336
Treatment 336
Systemic lupus erythematosus-like syndrome (SLE) (Fig. 9.52) 336
Diagnosis 336
Treatment 337
Immune vasculitis 337
Diagnosis 337
Treatment 337
Equine cutaneous amyloidosis (Fig. 9.53) 337
Diagnosis, treatment and prognosis 337
Infectious diseases 337
Virus diseases 337
Equine genital herpes virus (coital exanthema) (Fig. 9.54) 337
Diagnosis, treatment and prognosis 338
Horsepox virus 338
Diagnosis and treatment 338
Equine molluscum contagiosum (Figs. 9.55 & 9.56)
Diagnosis and treatment 338
Viral papular dermatitis 338
Diagnosis and treatment 338
Viral papillomatosis (Figs. 9.57 & 9.58)
Diagnosis and treatment 339
Pinnal acanthosis (hyperplastic aural dermatitis/aural plaques/fungal plaques) (Fig. 9.59) 339
Diagnosis and treatment 339
Bacterial diseases 339
Dermatophilosis (rain scald/mud fever/rain rot) (Figs. 9.60–9.62) 339
Diagnosis 340
Treatment 340
Bacterial folliculitis and furunculosis (Fig. 9.63) 340
Diagnosis, treatment and prognosis 341
Botryomycosis (Fig. 9.64) 341
Diagnosis, treatment and prognosis 341
Streptococcal dermatitis/folliculitis (Figs. 9.65 & 9.66)
Diagnosis, treatment and prognosis 341
Pigeon fever (pigeon chest, Wyoming strangles or false strangles) (Fig. 9.67) 342
Clostridium species infection (see Chapter 8, p. 300) 342
Glanders (farcy) (Fig. 9.68) 342
Diagnosis 342
Treatment 342
Fungal diseases 342
Dermatophytosis (Figs. 9.69 & 9.70)
Diagnosis 344
Treatment and prognosis 344
Eumycetic mycetoma 344
Diagnosis and treatment 344
Phaeohyphomycosis 344
Diagnosis and treatment 344
Sporotrichosis (Fig. 9.71) 344
Diagnosis 344
Treatment 345
Pythiosis (phycomycosis, bursatti, swamp cancer, Florida horse leeches, hyphomycosis) (Fig. 9.72) 345
Diagnosis 345
Treatment and prognosis 345
Systemic mycoses (Fig. 9.73) 345
Histoplasmosis (epizootic lymphangitis, pseudoglanders, African farcy) 346
Diagnosis, treatment and prognosis 346
Ectoparasitic diseases 346
Pediculosis (louse infestation) (Figs. 9.74 & 9.75)
Diagnosis 346
Treatment 346
Mange mites 347
Psoroptic mange (Figs. 9.76 & 9.77)
Diagnosis and treatment 347
Chorioptic mange (Figs. 9.78 & 9.79)
Diagnosis and treatment 347
Sarcoptic mange (Fig. 9.80) 348
Diagnosis and treatment 348
Demodectic mange 348
Diagnosis and treatment 348
Other mites (Fig. 9.81) 348
Diagnosis and treatment 349
Ticks (Fig. 9.82) 349
Diagnosis and treatment 349
Flies and other biting insects 349
Family tabanidae 349
Family Muscidae 349
Family Muscidae 350
Diagnosis and treatment 350
Family Ceratopogonidae 350
Family Simulidae 350
Family Culicidae 350
Family Glossinidae 350
Equine ventral midline dermatitis (Fig. 9.83) 350
Diagnosis and treatment 350
Equine insect hypersensitivity (Figs. 9.84 & 9.85)
Diagnosis 351
Treatment and control 351
Family Apidae (Apis mellifera, bee) 351
Non-biting flies 351
Myiasis flies (Fig. 9.86) 351
Diagnosis and treatment 352
Hypoderma spp. (warble flies) (Fig. 9.87) 352
Diagnosis and treatment 352
Gasterophilus spp. (horse bots) (Figs. 9.88 & 9.89)
Diagnosis and treatment 352
Nematode parasites causing skin disease 352
Habronema spp. (Figs. 9.90–9.92) 352
Diagnosis and treatment 353
Onchocerca cervicalis (Fig. 9.93) 354
Diagnosis and treatment 354
Parafilariasis 354
Diagnosis 354
Oxyuris equi (pinworm) (Figs. 9.94 & 9.95)
Diagnosis and treatment 354
Neoplastic disorders 355
Equine sarcoid (Figs. 9.96–9.100) 355
Occult sarcoid 355
Verrucose (warty) sarcoid 355
Nodular sarcoid 355
Fibroblastic sarcoid 356
Mixed (verrucose, fibroblastic and nodular) sarcoids 357
Diagnosis 357
Treatment 357
Squamous cell carcinoma (Figs. 9.101 & 9.102)
Diagnosis and treatment 360
Melanoma and melanosarcoma (Figs. 9.103–9.106) 360
Diagnosis 360
Neurofibroma (schwannoma, neurilemoma, neurinoma) (Fig. 9.107) 360
Diagnosis and treatment 361
Fibromas and fibrosarcomas (Fig. 9.108) 363
Diagnosis, treatment and prognosis 363
Lipomas (Fig. 9.109) 363
Diagnosis and treatment 363
Cutaneous lymphosarcoma (Fig. 9.110) 363
Mastocytomas (mast cell tumors) (Fig. 9.111) 364
Diagnosis and treatment 364
Reference and further reading 364
10 Disorders of the eye 365
Chapter Contents 365
Part 1 Orbit and globe 365
Congenital/developmental conditions 365
Microphthalmos/anophthalmos (Figs. 10.1–10.4) 365
Diagnosis and treatment 365
Anterior segment dysgenesis (Figs. 10.5 & 10.6)
Diagnosis and treatment 366
Non-infectious conditions 367
Phthisis bulbi (Figs. 10.7–10.9) 367
Diagnosis and treatment 367
Orbital fat prolapse (Fig. 10.10) 367
Diagnosis and treatment 367
Orbital neoplasia (Figs. 10.11–10.15) 368
Diagnosis 368
Treatment 369
Orbital trauma (Fig. 10.16) 369
Sinusitis and sinus neoplasia 369
Part 2 Eyelids, third eyelids, conjunctiva and nasolacrimal diseases 369
Congenital/developmental disorders 369
Entropion (Figs. 10.17 & 10.18)
Diagnosis 370
Treatment 370
Cilia disorders (Fig. 10.19) 370
Diagnosis 370
Treatment 370
Nasolacrimal duct atresia (Figs. 10.20 & 10.21)
Diagnosis 371
Treatment 371
Non-infectious disorders 371
Eyelid injury (Figs. 10.22–10.25) 371
Diagnosis, treatment and prognosis 371
Acquired nasolacrimal duct obstruction (Figs. 10.26–10.29) 372
Diagnosis 372
Treatment 372
Non-infectious/infectious disorders 373
Blepharitis (Figs. 10.30–10.34) 373
Diagnosis 373
Treatment 374
Horner’s syndrome and facial nerve paralysis 374
Neoplasia 374
Eyelid sarcoids (Figs. 10.35–10.37) 374
Diagnosis 374
Treatment 375
Squamous cell carcinoma of the eyelid and third eyelid (Figs. 10.38–10.42) 375
Diagnosis 376
Treatment 376
Other adnexal tumors (Figs. 10.43–10.51) 376
Part 3 Cornea 378
Congenital/developmental conditions 378
Dermoids (Fig. 10.52) 378
Diagnosis, treatment and prognosis 378
Linear keratopathy (Fig. 10.53) 378
Diagnosis and treatment 378
Non-infectious disorders 379
Corneal trauma (Figs. 10.54–10.60) 379
Diagnosis 380
Treatment and prognosis 380
Corneal foreign bodies (Figs. 10.61–10.67) 380
Diagnosis, treatment and prognosis 382
Non-infectious/infectious disorders 382
Ulcerative keratitis 382
Superficial corneal ulceration (Figs. 10.68–10.71) 382
Treatment 383
Non-healing superficial corneal ulceration (Figs. 10.72 & 10.73)
Diagnosis 383
Treatment 383
Stromal and deep corneal ulceration (Figs. 10.74–10.77) 383
Diagnosis 384
Treatment 385
Melting corneal ulcer (Figs. 10.78–10.81) 385
Diagnosis 385
Treatment 386
Eosinophilic keratitis (Figs. 10.82–10.84) 386
Diagnosis and treatment 386
Immune-mediated keratitis (Figs. 10.85–10.91) 386
Diagnosis 388
Treatment 388
Calcific keratopathy (Figs. 10.92 & 10.93)
Diagnosis 389
Treatment 389
Infectious disorders 389
Multifocal punctate keratopathy (viral keratitis) (Figs. 10.94–10.96) 389
Diagnosis 390
Treatment 390
Fungal keratitis (keratomycosis) (Figs. 10.97–10.103) 390
Diagnosis 391
Treatment and prognosis 392
Stromal abscess (Figs. 10.104–10.106) 392
Diagnosis 392
Treatment and prognosis 392
Part 4 Uvea 393
Congenital/developmental conditions 393
Iris coloboma (Figs. 10.107 & 10.108)
Diagnosis, treatment and prognosis 393
Iris hypoplasia (‘iris stromal cysts’) (Figs. 10.109–10.111) 393
Anterior uveal cysts/cystic corpora nigra (Figs. 10.112–10.114) 394
Diagnosis and treatment 394
Non-infectious/infectious disorders 394
Equine recurrent uveitis (Figs. 10.115–10.121) 394
Diagnosis 396
Treatment 396
Anterior uveitis (Figs. 10.122–10.130) 396
Diagnosis 398
Treatment 398
Prognosis 398
Neoplasia 398
Intraocular melanoma (Figs. 10.131–10.137) 398
Diagnosis 400
Treatment 400
Part 5 Lens and glaucoma 400
Congenital/developmental conditions 400
Cataracts (Figs. 10.138–10.153) 400
Diagnosis 403
Treatment 403
Non-infectious disorders 403
Lens luxation (Figs. 10.154–10.157) 403
Treatment 404
Glaucoma (Figs. 10.158–10.161) 404
Diagnosis 405
Treatment and prognosis 405
Part 6 Posterior segment 405
Normal ocular fundus and variations of normal 405
Congenital/developmental conditions 406
Colobomas of the retinal pigment epithelium (Figs. 10.164 & 10.165)
Congenital stationary nightblindness 406
Diagnosis and treatment 406
Retinal hemorrhages 407
Non-infectious disorders 407
Asteroid hyalosis (Figs. 10.166 & 10.167)
Retinal detachment (Figs. 10.168–10.170) 407
Treatment 407
Equine motor neuron disease (Figs. 10.171 & 10.172)
Diagnosis and treatment 408
Treatment 408
Senile retinopathy (Figs. 10.173–10.175) 408
Optic nerve atrophy (Fig. 10.176) 408
Diagnosis 409
Treatment and prognosis 409
Ischemic optic neuropathy 409
Traumatic optic neuropathy (Figs. 10.177 & 10.178)
Diagnosis 410
Treatment and prognosis 410
Proliferative and exudative optic neuropathy (Fig. 10.179) 410
Non-infectious/infectious disorders 410
Chorioretinitis (Figs. 10.180–10.182) 410
Diagnosis 410
Treatment 411
Optic neuritis (Fig. 10.183) 411
Treatment and prognosis 411
Neoplasia of the retina and optic disc 412
Diagnosis 412
Prognosis 412
References and further reading 412
11 Disorders of the nervous system 413
Chapter Contents 413
Developmental disorders 413
Hydrocephalus (Figs. 11.1–11.3) 413
Diagnosis and treatment 413
Myelodysplasias (Figs. 11.4 & 11.5)
Diagnosis and treatment 413
Cerebral hypoplasia 413
Diagnosis and treatment 413
Cerebellar hypoplasia (Fig. 11.6) 414
Diagnosis and treatment 414
Cerebellar abiotrophy 415
Diagnosis and treatment 415
Occipitoatlantoaxial malformation (OAAM) (Fig. 11.7) 415
Diagnosis and treatment 416
Juvenile epilepsy (Fig. 11.8) 416
Clinical signs 416
Treatment 416
Lavender foal syndrome/coat color dilution lethal (Fig. 11.9) 416
Diagnosis and treatment 417
Deafness (Fig. 11.10) 417
Diagnosis and treatment 417
Hypoxic ischemic encephalopathy (neonatal maladjustment syndrome) (Fig. 11.11) 417
Diagnosis 417
Treatment and prognosis 418
Narcolepsy/cataplexy 418
Diagnosis and treatment 418
Non-infectious disorders 418
Cervical vertebral malformation/cervical vertebral stenotic myelopathy (Figs. 11.12–11.15) 418
Diagnosis 419
Treatment 419
Traumatic injuries 420
Cerebral trauma (Figs. 11.16–11.20) 420
Basioccipital and basisphenoid fractures (Figs. 11.21 & 11.22)
Petrous temporal bone fractures (Figs. 11.23–11.30) 421
Fractures involving the base of the cranium 422
Fractures which affect the optic or vestibulo-cochlear nerves 422
Diagnosis 422
Treatment 423
Prognosis 424
Cord trauma 425
Clinical signs 425
Cervical spine (Figs. 11.31–11.34) 425
Thoracic spine (Figs. 11.35–11.38) 425
Lumbar spine (Figs. 11.39–11.41) 428
Sacrococcygeal spine 428
Clinical pathology and radiographic findings 428
Treatment 429
Prognosis 429
Other cranial nerve disorders 429
The trigeminal nerve (CN-V) (Fig. 11.42) 429
Clinical signs 430
Diagnosis 430
Facial nerve (VII) (Fig. 11.43) 430
Clinical signs 431
Treatment and prognosis 431
Horner’s syndrome (Figs. 11.44 & 11.45)
Diagnosis and treatment 432
Peripheral nerve damage 432
Suprascapular nerve ‘Sweeney’ (Fig. 11.46) 432
Diagnosis, treatment and prognosis 432
Radial nerve paralysis (Figs. 11.47 & 11.48)
Femoral nerve (Fig. 11.49) 434
Sciatic nerve (Fig. 11.50) 434
Obturator nerve (Fig. 11.51) 434
Stringhalt (Figs. 11.52 & 11.53)
Diagnosis and treatment 435
Polyneuritis equi (cauda equina neuritis) (Fig. 11.54) 435
Diagnosis, treatment and prognosis 436
Shivers (Fig. 11.55) 436
Diagnosis, treatment and prognosis 436
Gomen disease 436
Diagnosis 436
Cholesterol granuloma (Fig. 11.56) 436
Diagnosis and treatment 437
Nutritional and metabolic conditions resulting in neurological disease 437
Hypoglycemia 437
Hyponatremia (Fig. 11.57) 437
Hypernatremia 437
Hypocalcemia 437
Thiamine deficiency 437
Diagnosis and treatment 437
Toxic plants (Fig. 11.58) 437
Sorghum toxicity (see Chapter 5, p. 205) (Fig. 11.59) 437
Nigropallidal encephalomalacia 438
Diagnosis and treatment 440
Mycotoxicosis 440
Diagnosis 440
Yew poisoning 440
Diagnosis 440
Equine motor neuron disease (EMND) (Figs. 11.60 & 11.61)
Diagnosis 441
Treatment 441
Prognosis and prevention 441
Equine degenerative myeloencephalopathy 441
Diagnosis, treatment and prognosis 441
Neuroses 441
Crib-biting and wind-sucking 441
Self-mutilation syndrome 442
Head shaking (Fig. 11.62) 442
Diagnosis and treatment 442
Infectious disorders 442
Otitis media-interna/temporohyoid osteoarthropathy (Figs. 11.63–11.65) 442
Borna disease (Near Eastern encephalitis) 443
Diagnosis and treatment 443
Alphavirus (Togaviridae) encephalitis of horses (Figs. 11.66–11.69) 443
Clinical signs 444
Diagnosis 445
Treatment and prevention 445
West Nile virus 445
Diagnosis 445
Treatment, prognosis and prevention 445
Other arboviral diseases 445
Rabies (Figs. 11.70 & 11.71)
Diagnosis 446
Treatment and prevention 446
Equine herpes virus myeloencephalopathy (Fig. 11.72) 446
Clinical signs 447
Diagnosis 447
Treatment 447
Prevention 447
Listeriosis 448
Diagnosis and treatment 448
Meningoencephalomyelitis (Figs. 11.73 & 11.74)
Clinical signs 448
Treatment 448
Borreliosis (Lyme disease) 448
Diagnosis 449
Treatment 449
Equine protozoal myeloencephalitis (Figs. 11.75 & 11.76)
Diagnosis 450
Treatment 450
Trypanosomiasis 450
Botulism (Fig. 11.77) 450
Diagnosis 451
Treatment and prognosis 451
Prevention 451
Ehrlichiosis 451
Tetanus (Figs. 11.78–11.80) 451
Clinical signs and diagnosis 452
Treatment 452
Prevention 453
Cerebral abscess (Fig. 11.81) 453
Diagnosis 453
Treatment 453
Vertebral osteomyelitis (Fig. 11.82) 453
Clinical signs and diagnosis 453
Treatment 454
Fungal granulomas (Figs. 11.83 & 11.84)
Parasitic diseases 454
Verminous meningoencephalomyelitis 454
Neoplastic disorders 454
Diagnosis 455
References and further reading 455
12 Reproductive disorders 456
Chapter Contents 456
1 The mare 456
Clinical examination of the mare (Figs. 12.1–12.2) 456
The estrous cycle (Figs. 12.3–12.20) 456
The ovary 461
Developmental disorders 461
Turner’s syndrome (63X0) 461
XY sex-reversal syndrome (64X0) 461
Clinical signs 461
Autosomal chromosome abnormalities (Figs. 12.22–12.24) 461
Diagnosis of chromosomal abnormalities 461
Diagnosis and treatment 463
Non-infectious disorders 463
Anovulatory follicles (Fig. 12.25) 463
Diagnosis 463
Treatment 463
Lack of follicular development (anestrus) (Figs. 12.26 & 12.27)
Clinical signs 463
Diagnosis and treatment 464
Ovarian hematoma (Figs. 12.28 & 12.29)
Diagnosis and treatment 464
Ovarian tumors (Figs. 12.30 & 12.31)
Diagnosis and treatment 466
Cyst adenoma (Fig. 12.31C) 466
Treatment 466
Pituitary Pars Intermedia dysfunction (PPID) 466
Diagnosis and treatment 466
Epithelial inclusion cysts 466
The oviduct 466
Salpingitis 466
Diagnosis and treatment 466
Oviduct blockage (Fig. 12.32) 466
Diagnosis 466
Treatment 467
The uterus 467
Developmental disorders 467
Non-infectious disorders (barren mares) 467
Endometrial cysts (Figs. 12.33–12.37) 467
Diagnosis 467
Treatment 468
Persistent endometrial cups (Figs. 12.38–12.40) 468
Diagnosis 469
Treatment 469
Non-infectious disorders (pregnant mares) 469
Uterine torsion (Figs. 12.41 & 12.42)
Diagnosis 469
Treatment 470
Peripaturient hemorrhage (Figs. 12.43–12.46) 470
Diagnosis 471
Treatment 471
Vestibulo/vaginal varicosities (Fig. 12.47) 472
Clinical signs 472
Diagnosis and treatment 472
Hydrops allantois/hydrops amnios (Figs. 12.48–12.51) 473
Clinical signs 473
Diagnosis 474
Treatment 474
Ruptured prepubic tendon or abdominal hernia (Fig. 12.52) 474
Clinical signs 474
Diagnosis 475
Treatment 475
Fescue toxicosis (Fig. 12.53) 475
Clinical signs 475
Treatment and prevention 475
Non-infectious disorders (post-partum mares) 476
Retained placenta (Figs. 12.54–12.56) 476
Clinical signs 476
Diagnosis 476
Treatment 477
Uterine prolapse (Figs. 12.57 & 12.58)
Clinical signs and diagnosis 477
Treatment 477
Uterine tear (Figs. 12.59–12.61) 478
Diagnosis 478
Treatment 479
Infectious/inflammatory disorders (non-pregnant) 479
Persistent post-mating-induced endometritis (Figs. 12.62 & 12.63)
Clinical signs and diagnosis 479
Treatment 479
Chronic endometritis (Figs. 12.64–12.68) 480
Diagnosis 481
Treatment 481
Endometriosis (Fig. 12.69) 483
Diagnosis and treatment 483
Contagious equine metritis (CEM) (Figs. 12.70 & 12.71)
Clinical signs and diagnosis 483
Treatment 484
Other sexually transmitted bacterial infections 484
Infectious/inflammatory disorders (pregnant) 484
Placentitis (Figs. 12.72–12.77) 484
Clinical signs and diagnosis 485
Treatment 486
Herpes virus (Fig. 12.77D) 486
Clinical signs and diagnosis 486
Treatment 486
Equine viral arteritis (EVA) 487
Clinical signs and diagnosis 487
Treatment and prevention 488
Infectious/inflammatory disorders (post-partum) 488
Metritis (Fig. 12.78) 488
Clinical signs and diagnosis 488
Treatment 488
Neoplastic disorders (Fig. 12.79) 488
Leiomyoma (Fig. 12.79B) 488
Clinical signs and diagnosis 489
Treatment 489
The cervix 489
Cervical lacerations (Fig. 12.80) 489
Diagnosis and treatment 489
Cervical adhesions (Fig. 12.81) 489
Diagnosis and treatment 489
Failure of cervical relaxation 489
Clinical signs and treatment 489
The vagina, vestibule and vulva 489
Developmental disorders 489
Non-infectious disorders 489
Mating and foaling accidents (Figs. 12.82 & 12.83)
Trauma to the vagina during foaling 490
Diagnosis and treatment 491
Trauma to the vagina during breeding 491
Clinical signs and diagnosis 491
Treatment 491
False cover 491
Vaginal prolapse (Fig. 12.84) 491
Vesico-vaginal reflux (urine pooling) (Fig. 12.85 & 12.86)
Clinical signs and diagnosis 491
Treatment 492
Pneumovagina 492
Clinical signs and diagnosis 492
Treatment 493
Physical injury to the vulva (Fig. 12.87) 493
Perineal lacerations (Fig. 12.88) 493
Clinical signs 493
Treatment 493
Infectious disorders (Fig. 12.89) 494
Viral diseases 494
Bacterial diseases 494
Protozoal diseases 494
Clinical signs 494
Diagnosis and treatment 494
Neoplastic disorders (Figs. 12.90 & 12.91)
Mammary glands 495
Developmental disorders 495
Non-infectious disorders (Figs. 12.92 & 12.93)
Agalactia 496
Clinical signs and diagnosis 496
Treatment 496
Infectious disorders 496
Acute, chronic and indurative mastitis (Fig. 12.94) 496
Clinical signs 496
Diagnosis and treatment 496
Neoplastic disorders (Fig. 12.95) 497
2 The stallion and gelding 497
Clinical examination of the stallion (or gelding) (Figs. 12.96–12.99) 497
The testis, scrotum and spermatic cord (Figs. 12.100–12.103) 499
Developmental disorders 499
Cryptorchidism 499
Clinical signs (Figs. 12.104–12.106) 500
Diagnosis and treatment 500
Other developmental abnormalities 500
Non-infectious disorders 501
Testicular hematoma or abscess (Fig. 12.108) 501
Clinical signs and diagnosis 501
Treatment and prognosis 501
Orchitis (Fig. 12.109) 501
Clinical signs 501
Diagnosis and treatment 501
Testicular degeneration 502
Clinical signs and diagnosis 502
Treatment 502
Epididymitis 502
Clinical signs and diagnosis 502
Complications arising from castration (Figs. 12.110–12.115) 502
Infectious disorders (Figs. 12.116–12.119) 503
Scirrhous cord (Figs. 12.116–12.118) 504
Scirrhous cord 504
Clinical signs 504
Treatment 505
Neoplastic disorders (Fig. 12.120) 505
Seminomas (Figs. 12.121 & 12.122)
Clinical signs, diagnosis and treatment 505
Interstitial cell tumors 505
The penis and prepuce (Figs. 12.123 & 12.124)
Developmental/congenital disorders 505
Intersex 506
Male pseudohermaphrodite 506
Clinical signs 506
Diagnosis and treatment 506
Non-infectious disorders 506
Traumatic damage to the penis (Figs. 12.126 & 12.127)
Paraphimosis (Figs. 12.128–12.130) 507
Clinical signs and treatment 507
Penile/preputial hematoma (Figs. 12.131–12.136) 507
Clinical signs 509
Diagnosis 509
Treatment and prognosis 509
Occlusion of the urethra (Figs. 12.136–12.138) 509
Priapism (Fig. 12.139) 510
Clinical signs 510
Diagnosis and treatment 510
Hemospermia (Fig. 12.140) 510
Clinical signs 510
Diagnosis and treatment 510
Infectious disorders 511
Coital exanthema 511
Clinical signs 511
Diagnosis and treatment 511
Bacterial urethritis (Figs. 12.141) 511
Diagnosis 511
Bacterial infections 511
Contagious equine metritis 511
Clinical signs 511
Diagnosis and treatment 511
Pseudomonas aeruginosa and Klebsiella pneumoniae 511
Clinical signs 511
Diagnosis and treatment 511
Dourine (Fig. 12.142) 512
Clinical signs 512
Diagnosis and treatment 512
Parasite infestation 512
Clinical signs 512
Diagnosis and treatment 512
Neoplastic disorders 512
Squamous cell carcinomas (Figs. 12.143–12.147) 512
Clinical signs 512
Diagnosis and treatment 513
Melanoma 513
Nodular and fibroblastic sarcoids (Fig. 12.148) 513
3 The placenta 514
Non-infectious disorders 517
Twinning (Figs. 12.163–12.169) 517
Placental defects (Figs. 12.170–12.176) 518
Physical disorders of the placenta (Figs. 12.177–12.186) 521
Fetal resorption (Figs. 12.187–12.189) 523
Body pregnancy (Figs. 12.190 & 12.191)
Premature placental separation (Fig. 12.192) 523
Infectious diseases (see Placentitis) 524
Viral diseases 524
Systemic bacterial diseases (Figs. 12.193 & 12.194)
Fungal diseases (Figs. 12.195–12.197) 525
Mare reproductive loss syndrome (Figs. 12.198 & 12.199)
Clinical signs 525
Diagnosis and treatment 526
References and further reading 526
Index 528
A 528
B 529
C 529
D 531
E 531
F 533
G 534
H 534
I 535
J 536
K 536
L 536
M 536
N 538
O 538
P 539
Q 541
R 541
S 541
T 543
U 544
V 545
W 545
X 545
Y 545
Z 545
Part 5: The gastrointestinal tract
Congenital/developmental disorders
Intestinal atresia: atresia ani (Fig. 1.86) / atresia coli (Fig. 1.87)
Both disorders are uncommon congenital abnormalities. Atresia coli, although rare, is the most common type of intestinal atresia and may be related to vascular accidents during intestinal development; it usually occurs in the region of the pelvic flexure, that is between the left ventral and left dorsal colon, but may affect any site in the large or small colon. Foals affected by either condition are born normally and appear to be normal for the first 24 hours of life. As feces and gas accumulate proximal to the blind-ended anus or section of colon, progressive signs of abdominal pain and distension develop. Atresia coli is associated with more severe and earlier onset signs than atresia ani. In some fillies with atresia ani, development of rectovaginal fistula will be associated with some relief of pain, depending on the amount of feces and gas that can be passed. In cases of atresia coli in which intestinal rupture occurs, there may be a transient period of improvement, based on lessening of intraintestinal pressure, followed by rapid deterioration within hours as septic peritonitis ensues.
Figure 1.86 Atresia ani. Fortunately in this foal it was only the external opening of the anus that was absent and surgical creation of an opening yielded a good result.
Differential diagnosis: other causes of progressive abdominal distension with failure to pass feces:
• Meconium impaction
• Lethal white syndrome.
Figure 1.87 Atresia coli. The large colon in this case ends in a blind sac with subsequent enlargement in size due to failure of passage of contents.
Diagnosis:
• Atresia ani. The perineum should be examined for evidence of a normal anus. In some cases, the anus is absent. In others, an external anus is visible but not patent. If feces are present in or around the vulva, vaginal examination for a rectovaginal fistula should be performed. If an external anus is present, a blind-ended structure may be palpable within the rectum. Proctoscopy can be used to confirm that a palpable obstruction is indeed atresia ani. Foals should be examined for other congenital abnormalities. Rarely, deformities (or absence) of the tail or vagina may also be present.
• Atresia coli. Diagnosis is more difficult because the lesion is not evident grossly; meconium impaction is often suspected initially because of the failure to pass feces and progressive abdominal pain and distension. Digital rectal examination may be highly suggestive as there will be no fecal ‘staining’ of the glove and only mucus evident in the rectum. A blind-ended lesion may be evident with proctoscopy/colonoscopy. Distension of the proximal intestine may be evident radiographically. Contrast radiographs (barium enema, barium series) can confirm an obstruction but not necessarily atresia coli. Exploratory laparotomy may be required for definitive diagnosis. Thorough examination for other congenital problems that may accompany atresia coli (i.e. renal aplasia or hypoplasia, hydrocephalus, cerebellar dysplasia) should be performed.
Treatment and prognosis
• Atresia ani. Prompt surgical correction is required, and has been successful in some cases. The prognosis with surgery is dependent, in part, on the amount of intestine involved and whether concurrent abnormalities are present. The prognosis is better when the anal sphincter is normal and the obstruction is only a thin, bulging layer of tissue. Affected horses should not be bred because of the possibility of a genetic basis.
• Atresia coli. This condition should be regarded as fatal. Intestinal motility problems or failure of the anastomosis have resulted in poor outcomes in cases in which surgical correction has been attempted.
Inguinal hernia (see also p. 48) (Figs1.88 & 1.89)
Most congenital inguinal hernias are indirect, with the intestines passing through an intact vaginal ring and contained within the parietal layer of the vaginal tunic. Indirect hernias are usually reducible, are not life-threatening and usually resolve with manual reduction within a few days. A direct hernia occurs when the parietal vaginal tunic or the peritoneum in the vaginal ring region tears and the intestines become positioned under the skin. Direct hernias are normally irreducible, contain large amounts of intestine, are life-threatening and regarded as a surgical emergency.
Figure 1.88 Congenital indirect inguinal hernia. Reproduced from McAuliffe SB, Slovis NM (eds), Color Atlas of Diseases and Disorders of the Foal (2008), with permission from Elsevier.
Figure 1.89 Congenital direct inguinal hernia. This foal had its entire colon herniated through the inguinal ring and was lying in a subcutaneous position.
An uncomplicated hernia is any type of hernia which either does not contain intestine or contains non-incarcerated intestine. A complicated hernia is any type of hernia which contains incarcerated or strangulated intestine.
Diagnosis and treatment
• Hernias are usually apparent visually or detected by palpation. Individual loops of small intestine may be apparent under the skin in foals with direct inguinal hernias. The inguinal skin is thin and associated stretching may result in tearing of the skin or disruption of dermal circulation.
• Signs of colic are often but not always observed when strangulation has occurred but will develop as intestinal compromise progresses and intestinal distension develops.
• Direct inguinal hernias and complicated hernias are regarded as a surgical emergency. Indirect hernias depending on their size may be managed conservatively with frequent reduction or bandaging to facilitate reduction although bandage sores are a frequent complication.
Lethal white syndrome (Figs. 1.90 & 1.91)
Also known as ileocolonic aganglionosis, lethal white syndrome is an inherited, congenital condition that occurs in foals that are homozygous for the lethal white gene. It is an autosomal recessive condition that means that if two carriers (heterozygotes) are bred approximately 1 in 4 of their offspring will be homozygous or affected. Heterozygotes usually have the Overo color pattern, which is most common in American Paint horses but may also be found in Quarter Horses, Pintos and Saddlebreds. Most affected foals are entirely white with white irises, but some may have small areas of pigmentation on the forelock and tail. Within 4–24 hours of life, abdominal distension and pain develop. These signs are progressive and become very severe. Minimal feces are passed.
Figure 1.90 Lethal white foal showing early signs of colic.
Differential diagnosis: other causes of progressive abdominal distension with passage of little or no feces:
• Atresia ani/coli
• Impending enteritis
• Peritonitis
• Meconium impaction.
Figure 1.91 Colonic hypoplasia. No histopathology was performed in this case but it was believed that the etiology may have been some form of ileocolonic aganglionosis (similar to that found in lethal white foals). This was a 2-day-old TB foal that presented with early colic signs (at 24?h). Serial ultrasound examinations showed progressive small intestinal distension with no intestinal motility detectable on ultrasound or auscultation.
Diagnosis and treatment
• A white foal born to an Overo–Overo mating with progressive abdominal distension and minimal fecal production is highly suggestive. This history and progression of clinical signs is typically used to make a diagnosis. It should not be confused with colic in white foals born to non-Overo parents.
• Diagnostic imaging (ultrasound, radiography) demonstrates gaseous intestinal distension.
• Genetic testing can determine whether the foal is homozygous for the condition but is impractical considering the time delay.
• There is currently no treatment; this is an invariably fatal condition and affected foals should be promptly euthanized.
Meconium impaction (Figs. 1.92–1.95)
Normally, meconium is passed within a few hours of birth....
Erscheint lt. Verlag | 13.4.2014 |
---|---|
Sprache | englisch |
Themenwelt | Medizin / Pharmazie |
Veterinärmedizin ► Klinische Fächer | |
Veterinärmedizin ► Pferd | |
ISBN-10 | 0-7020-5421-6 / 0702054216 |
ISBN-13 | 978-0-7020-5421-1 / 9780702054211 |
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