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Equine II Flashcards

1
Q

What are the major viral causes of equine encephalitis?

A

West Nile Virus (WNV)

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2
Q

What are the key distinguishing features of viral encephalitides?

A

Mental depression

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3
Q

What is the primary mode of transmission for equine viral encephalitides?

A

Mosquito-borne transmission

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4
Q

How can viral encephalitides be prevented?

A

Vaccination and mosquito control.

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5
Q

What is the general treatment approach for viral encephalitides?

A

Supportive care

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6
Q

When are viral encephalitides most commonly seen in temperate climates?

A

June-November.

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7
Q

What is the enzootic cycle of West Nile Virus?

A

Transmission between birds and mosquitoes.

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8
Q

What are common clinical signs of WNV in horses?

A

Depression

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9
Q

How is WNV diagnosed?

A

IgM capture ELISA

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10
Q

What CSF abnormalities are seen in WNV?

A

Elevated protein concentration and mononuclear pleocytosis.

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11
Q

What is the prognosis for WNV in horses?

A

Variable; one study reported a mortality rate of 33%.

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12
Q

What is the primary reservoir for Togaviridae encephalitis viruses?

A

Infected but asymptomatic wild birds and small mammals.

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13
Q

What are the clinical signs of EEE

A

WEE

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14
Q

How is Togavirus encephalitis diagnosed?

A

Clinical signs

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15
Q

What is the mortality rate of EEE?

A

75-100%.

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16
Q

What is the mortality rate of WEE?

A

20-50%.

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17
Q

What is the mortality rate of VEE?

A

40-80%.

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18
Q

What treatment is available for EEE

A

WEE

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19
Q

What long-term effects can occur in horses that survive Togavirus encephalitis?

A

Residual neurologic deficits may persist.

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20
Q

What is White Muscle Disease (WMD)?

A

A myodegenerative disease caused by vitamin E and/or selenium deficiency.

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21
Q

Which species are affected by WMD?

A

Horses

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22
Q

What are the two main clinical forms of WMD?

A

Cardiac form and skeletal muscle form.

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23
Q

Which age group is most commonly affected by WMD?

A

Young

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24
Q

What is the primary cause of oxidative damage in WMD?

A

Deficiency of vitamin E and/or selenium leading to impaired control of reactive oxygen species.

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25
Q

What is the role of selenium in preventing WMD?

A

Selenium is a co-factor for glutathione peroxidase

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26
Q

What is the role of vitamin E in preventing WMD?

A

Vitamin E (alpha-tocopherol) is a lipid-soluble antioxidant that protects cell membranes from lipid peroxidation.

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27
Q

Why are muscle cells particularly prone to oxidative damage?

A

They have high metabolic activity

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28
Q

What is the typical presentation of the cardiac form of WMD?

A

Sudden onset

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29
Q

What are key clinical signs of the cardiac form of WMD?

A

Depression

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30
Q

What is the prognosis for the cardiac form of WMD?

A

Poor; affected animals often die within 24 hours despite treatment.

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31
Q

What are key clinical signs of the skeletal form of WMD?

A

Muscular weakness

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32
Q

Which muscle groups are commonly affected in skeletal WMD?

A

Biceps

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33
Q

What is the prognosis for the skeletal form of WMD?

A

Better than the cardiac form; it responds to treatment if diagnosed early.

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34
Q

What laboratory findings are seen in acute WMD?

A

Elevated AST

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35
Q

What other diagnostic markers indicate WMD?

A

Decreased serum selenium

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36
Q

What gross histologic changes are seen in WMD?

A

Gray to white muscle discoloration in limbs

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37
Q

What microscopic findings are characteristic of WMD?

A

Bilaterally symmetric myodegeneration

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38
Q

What is the primary treatment for WMD?

A

Vitamin E and selenium supplementation.

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39
Q

What supportive therapies can aid WMD recovery?

A

Limiting physical activity

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40
Q

How can WMD be prevented?

A

Ensuring adequate vitamin E and selenium levels in at-risk regions.

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41
Q

What management strategy helps prevent WMD in neonates?

A

Supplementing pregnant animals with vitamin E and selenium to ensure sufficient fetal stores.

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42
Q

What is another name for Cervical Vertebral Malformation (CVM)?

A

Cervical stenotic myelopathy

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43
Q

What is the primary cause of CVM?

A

Compression of the cervical spinal cord due to narrowing of the vertebral canal.

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44
Q

Which horses are most commonly affected by CVM?

A

1- to 2-year-old

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45
Q

What are the key clinical signs of CVM?

A

Symmetric ataxia

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46
Q

Which limbs are usually more affected in CVM?

A

Hindlimbs are more affected than forelimbs.

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47
Q

How is CVM diagnosed?

A

Based on signalment

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48
Q

What is the sagittal ratio in CVM diagnosis?

A

The smallest sagittal diameter of the vertebral canal divided by the width of the cranial aspect of the vertebral body at its widest point.

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49
Q

What are the normal sagittal ratio values in horses?

A

Greater than 52% (C4-6) to 56% (C7).

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50
Q

Why is myelography necessary for CVM diagnosis?

A

It provides a definitive ante-mortem diagnosis by assessing spinal cord compression.

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51
Q

What treatment options are available for CVM?

A

Surgical stabilization or decompression

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52
Q

What is the prognosis for horses with CVM?

A

Poor; conservative therapy may provide transient improvement

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53
Q

Why is surgical treatment for CVM infrequently pursued?

A

Due to the high cost and risk associated with vertebral surgery in horses.

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54
Q

What is colic in horses?

A

A generic term for abdominal pain

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55
Q

What are common clinical signs of colic?

A

Pawing

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56
Q

What are common causes of small intestinal colic?

A

Strangulating lipoma (older horses)

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57
Q

What are key diagnostic signs of small intestinal colic?

A

Severe pain

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58
Q

What is the treatment for small intestinal strangulation?

A

Surgical correction; resection if bowel is devitalized.

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59
Q

What is the prognosis for small intestinal strangulation?

A

Guarded; worse with prolonged duration and extensive bowel necrosis (>15 feet).

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60
Q

What is large intestinal volvulus/torsion?

A

A severe

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61
Q

What are risk factors for large colon torsion?

A

Older broodmares pre/post-parturition

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62
Q

What are key diagnostic signs of large colon torsion?

A

Severe pain

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63
Q

What is the treatment for large colon volvulus?

A

Emergency surgical correction.

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64
Q

What is the prognosis for large colon torsion?

A

Good with early surgery; poor if delayed (>several hours).

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65
Q

What causes colonic impaction?

A

Decreased water intake

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66
Q

What are clinical signs of colonic impaction?

A

Mild to moderate colic

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67
Q

How is colonic impaction treated?

A

Analgesics

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68
Q

What is the prognosis for colonic impaction?

A

Good; surgery rarely needed unless severe or prolonged duration.

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69
Q

What causes gas colic?

A

Diet change

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70
Q

What are key diagnostic signs of gas colic?

A

Mild to severe pain that may be intermittent

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71
Q

How is gas colic treated?

A

Analgesics

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72
Q

What is the prognosis for gas colic?

A

Good

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73
Q

What are common types of colon displacement?

A

Right dorsal displacement

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74
Q

How is nephrosplenic entrapment diagnosed?

A

Rectal palpation (unable to feel left kidney)

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75
Q

How is nephrosplenic entrapment treated?

A

Phenylephrine to shrink spleen

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76
Q

What is the prognosis for colon displacement?

A

Good; high chance of recurrence.

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77
Q

What causes enterolith formation?

A

Precipitation of struvite salts (magnesium ammonium phosphate) around a nidus.

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78
Q

What are risk factors for enteroliths?

A

Feeding alfalfa hay

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79
Q

How is sand colic diagnosed?

A

Positive fecal sand float

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80
Q

How are enteroliths treated?

A

Surgical enterotomy.

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81
Q

How is sand colic treated?

A

Nasogastric tubing with water

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82
Q

What is the prognosis for enteroliths and sand colic?

A

Good if treated early.

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83
Q

What are risk factors for gastric ulcers?

A

Stress

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84
Q

Where do gastric ulcers most commonly occur?

A

Squamous (non-glandular) region of the stomach.

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85
Q

What are clinical signs of gastric ulcers?

A

Mild/moderate pain

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86
Q

How are gastric ulcers diagnosed?

A

Fasted gastroscopy.

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87
Q

What is the treatment for gastric ulcers?

A

Omeprazole (proton pump inhibitor)

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88
Q

How can gastric ulcers be prevented?

A

Feeding alfalfa

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89
Q

What parasites cause colic?

A

Parascaris equorum (ascarid impaction)

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90
Q

What is the pathogenesis of ascarid impaction?

A

Massive die-off of Parascaris equorum following deworming in previously untreated young horses.

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91
Q

What is the treatment for ascarid impaction?

A

Surgery is often required.

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92
Q

What is verminous arteritis?

A

Thromboembolic colic caused by Strongylus vulgaris migration to the cranial mesenteric artery

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93
Q

What is the prognosis for parasite-associated colic?

A

Guarded to poor

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94
Q

What gastrointestinal disease can mimic colic?

A

Acute colitis (Salmonella

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95
Q

What non-GI disease can mimic colic?

A

Urolithiasis (especially in stallions/geldings)

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96
Q

How is uterine torsion diagnosed?

A

Rectal palpation revealing a tight broad ligament over the uterus.

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97
Q

What is the treatment for uterine torsion?

A

Rolling the mare under anesthesia with a plank over the abdomen

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98
Q

What is the prognosis for uterine torsion?

A

Good if treated early for both mare and fetus.

99
Q

What is Exercise-Induced Pulmonary Hemorrhage (EIPH)?

A

A condition in horses characterized by pulmonary hemorrhage during intense exercise.

100
Q

Which horses are most commonly affected by EIPH?

A

Thoroughbred

101
Q

What is the most obvious clinical sign of EIPH?

A

Epistaxis (nosebleed) after exercise.

102
Q

What are some subtle clinical signs of EIPH?

A

Decreased performance

103
Q

What is the most widely accepted theory for the pathophysiology of EIPH?

A

Stress failure of pulmonary capillaries due to high pulmonary arterial pressure during intense exercise.

104
Q

What are other proposed mechanisms for EIPH?

A

Upper airway obstructions

105
Q

Which region of the lung is most commonly affected by EIPH?

A

Caudodorsal lung fields.

106
Q

Does EIPH show any gender predilection?

A

Conflicting reports; some studies show no predilection

107
Q

How does the prevalence of EIPH change with age?

A

The incidence may increase with age.

108
Q

What is the gold standard diagnostic test for EIPH?

A

Endoscopic examination of the airway post-exercise.

109
Q

Why is epistaxis alone not a reliable diagnostic sign of EIPH?

A

Epistaxis is observed in only 0.2% to 13% of racehorses with EIPH

110
Q

What are the findings in bronchoalveolar lavage (BAL) fluid in horses with EIPH?

A

Presence of erythrocytes and hemosiderophages.

111
Q

What is the most commonly used treatment for EIPH?

A

Furosemide (Lasix)

112
Q

How does furosemide help in EIPH?

A

Reduces RBCs in BAL fluid

113
Q

What other treatments have been attempted for EIPH?

A

Pro-coagulants

114
Q

How is the prevalence of EIPH related to exercise?

A

It is more related to the intensity rather than the duration of exercise.

115
Q

Why is EIPH considered a performance-limiting condition?

A

Pulmonary hemorrhage can lead to airway obstruction

116
Q

What percentage of racehorses show evidence of hemorrhage on endoscopic examination post-exercise?

117
Q

What percentage of racehorses show evidence of EIPH when diagnosed using BAL fluid analysis?

A

Nearly 100% of horses involved in intense exercise.

118
Q

Why might nutritional supplements be used for EIPH treatment?

A

Some supplements may help improve capillary integrity and reduce bleeding tendencies.

119
Q

What is the causative organism of Equine Protozoal Myeloencephalitis (EPM)?

A

Sarcocystis neurona.

120
Q

What is the definitive host of Sarcocystis neurona?

A

The opossum.

121
Q

What role does the horse play in the life cycle of Sarcocystis neurona?

A

The horse is an aberrant (dead-end) host.

122
Q

How does the definitive host contribute to EPM transmission?

A

The opossum releases infective sporocysts into the environment

123
Q

What happens when the intermediate host ingests sporocysts?

A

Sporocysts excyst and develop into sarcocysts within skeletal muscle cells.

124
Q

How do horses become infected with EPM?

A

By ingesting sporocysts in contaminated feed or water.

125
Q

Why do only some horses develop neurologic signs of EPM?

A

Many horses are exposed to the organism

126
Q

What are the hallmark clinical signs of EPM?

A

Asymmetric ataxia

127
Q

How can EPM be confused with lameness?

A

Incoordination of one or more limbs may mimic lameness.

128
Q

What are some less common clinical signs of EPM?

129
Q

What distinguishes EPM from cervical vertebral malformation?

A

The asymmetric nature of the neurologic deficits.

130
Q

What is the primary method of diagnosing EPM?

A

Clinical signs such as asymmetric ataxia

131
Q

What diagnostic test can be supportive for EPM diagnosis?

A

Western blot analysis of CSF for S. neurona or immunofluorescent antibody testing.

132
Q

Why can EPM diagnostic tests be difficult to interpret?

A

Contamination of CSF with peripheral blood can affect test results.

133
Q

What are the three primary treatments for EPM?

A

1) Trimethoprim-sulfonamide & pyrimethamine

134
Q

How does trimethoprim-sulfonamide & pyrimethamine work against EPM?

A

It blocks folate metabolism in protozoa.

135
Q

What is the mechanism of Ponazuril (Marquis®)?

A

It targets a protozoal organelle (plastid).

136
Q

How does Nitazoxinade (Navigator®) work?

A

It inhibits electron transfer reactions essential for energy metabolism in protozoa.

137
Q

What is the prognosis for EPM?

A

Variable; some horses fully recover

138
Q

What is placentitis

A

and why is it significant in mares?

139
Q

What is the most common route of bacterial infection leading to placentitis?

A

Ascending infections through the cervix

140
Q

Which bacteria are most frequently isolated in cases of placentitis?

A

Streptococcus zooepidemicus

141
Q

What fungal organism has been reported in placentitis cases?

A

Aspergillus species.

142
Q

What are the two possible routes by which bacteria can reach the uteroplacental unit?

A

Ascending infection and hematogenous spread.

143
Q

How does placentitis contribute to abortion in mares?

A

Placental thickening and separation from the endometrium cause uteroplacental insufficiency

144
Q

What are the main treatment options for placentitis?

A

Antimicrobial therapy

145
Q

What is the prognosis for mares diagnosed with placentitis?

A

Variable; outcomes range from abortion to a septic foal to a normal

146
Q

Which virus is the most common cause of viral abortion in mares?

A

Equine herpesvirus type 1 (EHV-1).

147
Q

Besides EHV-1

A

which other viral infections can cause equine abortion?

148
Q

How does EHV-1 typically cause abortion in mares?

A

By infecting the placenta and causing rapid placental detachment

149
Q

What are the clinical signs of EHV-1 in mares?

A

Often subclinical or mild respiratory signs; abortion may be the only noticeable clinical outcome.

150
Q

At what gestational stages should mares be vaccinated against EHV-1 to prevent abortion?

151
Q

How does the fetus become infected with EHV-1?

A

Via the chorionic vasculature or by inhalation of infected amniotic fluid.

152
Q

What histopathologic findings are characteristic of EHV-1 infection in an aborted fetus?

A

Necrotic foci on the liver

153
Q

What are the diagnostic methods for confirming EHV-1 infection in an aborted fetus?

A

Virus neutralization tests

154
Q

What are the clinical signs of neonatal herpesvirus infection in foals?

A

Respiratory distress

155
Q

Is there an effective treatment for EHV-1 infection in mares or infected neonatal foals?

A

No direct treatment

156
Q

What is the primary approach to managing EHV-1 abortion outbreaks?

A

Prevention through vaccination and biosecurity measures.

157
Q

What is the most common non-infectious cause of abortion in mares?

A

Twin pregnancy.

158
Q

Why is twin pregnancy rarely viable in horses?

A

The mare’s placenta does not support two fetuses

159
Q

What commonly happens if twin fetuses survive until late gestation?

A

One or both may die from malnutrition

160
Q

If twin fetuses are carried to term

A

what are the potential outcomes?

161
Q

What is umbilical torsion

A

and how does it cause abortion?

162
Q

What factors increase the risk of umbilical torsion in equine fetuses?

A

Excessive fetal movement and an unusually long umbilical cord.

163
Q

What are the guttural pouches (GP)?

A

Diverticula of the eustachian tubes

164
Q

What is the suspected function of the guttural pouches?

A

Function is not fully understood

165
Q

What are the major neural structures associated with the GP?

A

Cranial nerves VII

166
Q

What are the major vascular structures associated with the GP?

A

Internal carotid

167
Q

What are the three major disorders affecting the guttural pouch?

A

Guttural pouch tympany

168
Q

What is guttural pouch tympany?

A

A congenital condition causing air distension of the guttural pouch.

169
Q

What is the suspected pathogenesis of GP tympany?

A

Possible abnormal/excessive mucosal flap at the pharyngeal orifice acting as a one-way valve.

170
Q

What are the clinical signs of GP tympany?

A

Non-painful swelling in the throat-latch region

171
Q

How is GP tympany diagnosed?

A

Based on signalment

172
Q

What is the treatment for GP tympany?

A

Surgical correction

173
Q

What is the prognosis for GP tympany?

A

Good for uncomplicated cases; fair to guarded if dysphagia or aspiration pneumonia is present.

174
Q

What is guttural pouch empyema?

A

Accumulation of purulent exudate within the guttural pouch

175
Q

What is the pathogenesis of GP empyema?

A

Secondary to upper respiratory infections or rupture of a retropharyngeal lymph node into the GP.

176
Q

What are the clinical signs of GP empyema?

A

Nasal discharge

177
Q

What is a chondroid in GP empyema?

A

A firm mass of inspissated exudate formed in chronic cases.

178
Q

How is GP empyema diagnosed?

A

History of upper respiratory infection

179
Q

What is the treatment for GP empyema?

A

Aggressive lavage

180
Q

What is the prognosis for GP empyema?

A

Good to excellent.

181
Q

What is guttural pouch mycosis?

A

A fungal infection of the guttural pouch

182
Q

What is the most commonly associated pathogen with GP mycosis?

A

Aspergillus species.

183
Q

What is the pathogenesis of GP mycosis?

A

Fungal plaques erode arterial walls

184
Q

What are the clinical signs of GP mycosis?

A

Epistaxis (sometimes fatal)

185
Q

How is GP mycosis diagnosed?

A

Clinical signs

186
Q

Why is caution needed when performing endoscopy in a horse with epistaxis due to GP mycosis?

A

Disrupting a clot in the GP may cause severe hemorrhage.

187
Q

What is the treatment for GP mycosis?

A

Surgical occlusion of the affected arteries; antifungal therapy may be attempted but is less effective.

188
Q

What is the prognosis for GP mycosis?

A

Guarded to fair; dysphagia worsens prognosis as neural recovery may take a long time.

189
Q

What species are affected by West Nile Virus (WNV)?

190
Q

How is WNV transmitted?

A

Via mosquitoes from infected wild birds; horses are dead-end hosts.

191
Q

What are key clinical signs of WNV?

192
Q

How is WNV diagnosed?

A

IgM-ELISA serology.

193
Q

What is the treatment for WNV?

A

Supportive care.

194
Q

How can WNV be prevented?

A

Vaccination

195
Q

What is a distinguishing feature of Venezuelan Equine Encephalitis (VEE)?

A

VEE can be zoonotic from horse to human; EEE and WEE are dead-end hosts.

196
Q

What are the clinical signs of EEE

197
Q

What is the prognosis for EEE

198
Q

How is EEE

199
Q

What is the causative agent of EHM?

A

Neurogenic variant of Equine Herpesvirus-1 (EHV-1).

200
Q

What are key clinical signs of EHM?

201
Q

How is EHM diagnosed?

A

Nasal swab PCR.

202
Q

What is the treatment for EHM?

A

Supportive care and antiviral drugs.

203
Q

What is the prevention strategy for EHM?

A

Biosecurity and quarantine; current EHV vaccines do not protect against EHM.

204
Q

What is the primary causative agent of EPM?

A

Sarcocystis neurona; Neospora hughesi is also implicated.

205
Q

How is EPM transmitted?

A

Opossums shed sporocysts into the horse’s environment

206
Q

What are key clinical signs of EPM?

A

Unilateral hindlimb muscle atrophy

207
Q

How is EPM diagnosed?

A

CSF and serum antibody titers (cerebral spinal fluid titers are more accurate).

208
Q

What is the treatment for EPM?

A

Ponazuril (Marquis®)

209
Q

What is the prognosis for EPM?

A

Variable; some horses improve

210
Q

What is the causative agent of tetanus?

A

Clostridium tetani.

211
Q

What is the incubation period for tetanus?

A

1-3 weeks.

212
Q

What are key clinical signs of tetanus?

A

Stiff gait

213
Q

How is tetanus diagnosed?

A

Clinical signs and history of a wound.

214
Q

How is tetanus treated?

A

Penicillin

215
Q

What is the prognosis for tetanus?

A

Guarded to poor.

216
Q

How is tetanus prevented?

A

Annual vaccination and tetanus antitoxin for unvaccinated horses with wounds.

217
Q

What are the three clinical forms of rabies in horses?

A

Furious (aggressive

218
Q

How is rabies diagnosed?

A

Post-mortem detection of Negri bodies in brain tissue.

219
Q

What is the prognosis for rabies?

A

Fatal; zoonotic risk.

220
Q

How is rabies prevented?

A

AAEP core vaccine annually.

221
Q

What is the causative agent of botulism?

A

Clostridium botulinum.

222
Q

What is the pathophysiology of botulism?

A

Toxin blocks acetylcholine release at neuromuscular junctions

223
Q

What are key clinical signs of botulism?

A

Flaccid paralysis

224
Q

How is botulism diagnosed?

A

Clinical signs; spores may be difficult to detect in feed.

225
Q

What is the treatment for botulism?

A

Botulinum antitoxin

226
Q

What is the prognosis for botulism?

A

Guarded to poor.

227
Q

How is botulism prevented?

A

Vaccination and proper feed storage.

228
Q

What is the suspected cause of Polyneuritis Equi?

A

Immune-mediated granulomatous inflammation of peripheral and cranial nerves.

229
Q

What are key clinical signs of Polyneuritis Equi?

A

Urinary and fecal incontinence

230
Q

What is the prognosis for Polyneuritis Equi?

231
Q

What causes NAD/EDM?

A

Vitamin E deficiency and genetic factors.

232
Q

What are key clinical signs of NAD/EDM?

A

Symmetric ataxia

233
Q

How is NAD/EDM treated?

A

Vitamin E supplementation

234
Q

What is the pathogenesis of EMND?

A

Chronic Vitamin E deficiency leading to motor neuron degeneration.

235
Q

What are key clinical signs of EMND?

A

Muscle atrophy

236
Q

How is EMND diagnosed?

A

Biopsy and history of Vitamin E deficiency.

237
Q

What is the treatment for EMND?

A

Vitamin E supplementation

238
Q

What is the primary cause of Wobbler Syndrome?

A

Spinal cord compression

239
Q

What are key clinical signs of Wobbler Syndrome?

A

Ataxia worse in hindlimbs

240
Q

How is Wobbler Syndrome diagnosed?

A

Radiographs

241
Q

What is the treatment for Wobbler Syndrome?

A

Ventral cervical stabilization surgery (basket surgery).

242
Q

What is a common cause of sleep deprivation in horses?

A

Behavioral issues or lameness preventing REM sleep.

243
Q

What are clinical signs of narcolepsy/sleep deprivation?

A

Knuckling onto fetlocks

244
Q

How is sleep deprivation managed?

A

Correcting the underlying cause and preventing injury.

Vetprep (7 decks)

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