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Equine > Equine 3 > Flashcards

Equine 3 Flashcards

1
Q

What are the 3 ways a muscle can respond to an injury

A

Necrosis
Atrophy
Hypertrophy

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2
Q

AST is released from muscle and ______

A

Liver

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3
Q

Which half life is longer? AST or CK

A

AST

CK goes up first

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4
Q

Is myglobin harmful to kidneys

A

Yes

If CK above 10k needs fluids

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5
Q

Is CK doubles or goes above 10K after exercise then

A

Muscle dz

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6
Q

Where do we take muscle biopsy

A

Gluteal

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7
Q 
What is not a clinical sign of muscle disease
A. Hind limb cramping
B. Lose gait 
C. Reluctant to move
D. Anxious
E. Sweating 
E. Tachycardia 
F. Painful muscle palpation and firm muscles
G. Myoglobinuria
A

B- stiff gait

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8
Q

Why would increased potassium occur with muscle dz

A

Muscle breakdown

AST LDH also go up with CK

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9
Q

A dark brown urine with no red blood cells indicates

A

Myoglobin

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10
Q

Exertional ehabdomylysis myopathies occur (acutely, chronically)

A

Acutely

Emergency therapy required

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11
Q

A shortened stride may be a sign of

A

Muscle pain

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12
Q

How is ER treated

A 
Rest
NSAID
Fluid
Pain control - flunixin phenylbutazone
Muscle relaxants- methocarbamol dantrolene sodium 
Acepromazine
Vitamin E
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13
Q

Why types of horses do we normally see exhausted horse syndrome

A

Prolonged submaximal exercise
Endurance horses
Race horses

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14
Q 
What is not a sign of exhausted horse syndrome
A. Muscle cramp 
B. High blood pressure
C. Depresses
D. Profuse sweating 
E. Colic
A

B- poor perfusion

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15
Q

How much fluid can be lost from sweating

A

1 gallon/hr
Severe na k cl depletion
Moderate loss of Ca and mg

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16
Q 
What is the acid base status of exhausted horse?
A. Metabolic alkalosis 
B. Metabolic acidosis 
C. Respiratory alkalosis
D. Respiratory acidosis
A

A- decreased Cl decreased binding of Ca

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17
Q

What is the cardiovascular response to exhausted horse

A

Higher HR
Colic in endurance horse
Decreased blood volume

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18
Q

What is the respiratory response of a exhausted horse

A

Panting

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19
Q

What do fluid and electrolyte abnormalities lead to in horses with exhaustion

A

Obtundatiin
Muscle cramps and spasms
Synchronous diaphragmatic flutter- Ca abnormality causes this

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20
Q

T/F metabolic acidosis is often a feature of exercise induced myopathies

A

False. IS NOT

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21
Q

What are risk factors for post anesthetic myopathy

A 
Duration of procedure
Hypotension
Hypoxia
Acidosis
Poor perfusion 
Insufficient padding
Weight
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22
Q

How is post anaesthesia myopathy treated

A 
Fluids. Especially if low Ca
Dilute myoglobin in kidney
Acepromazine
Methocarbamol
Rest
Sling 
High fat low carb diet
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23
Q

What are causes of recurrent rhabdomyolysis

A 
Polysaccharide storage myopathy (type 1 quarter horses) and type 2 (quarter horse warm blood draft Arabians)
Recurrent exertional rhabdomyolysis (RER) ( thoroughbred and standard bred)
Mitochondrial myopathy (Arabians)
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24
Q

What are some blood abnormalities of horses with recurrent rhabdomyolysis

A

CK AST creatinine with myoglobinuria

No inflammation

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25
Q

How is recurrent rhabdomyolysis dx

A

Exercise test

Muscle biopsy

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26
Q

What are presenting signs for PSSM (type 1 and 2)

A

Decreased performance
Mild or none rhabdomyolysis
Muscle wasting

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27
Q

Type 1 PSSM is caused by a mutation in_____

A

Glycogen synthase 1 (GYS1)

PAS positive inclusion on biopsy

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28
Q

In type one PSSM muscles cannot generate adequate energy Which does not occur
A. Enhanced insulin sensitivity and uptake of glucose
B. Enzyme imbalances
C. Decreased synthesis of less branches glycogen

A

C- increased

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29
Q

How is PSSM definitively diagnosed
A. Genetic test from hair or whole blood (75% sensitivity)
B. Muscle biopsy (type 2 only 100% sensitive)

A

A

B

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30
Q

How is PSSM treated and managed

A 
No cure
Acute episodes
Consistent exercise
Decreased soluble carbs 
Grass hay
Add fat
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31
Q

When is recurrent exertional rhabdomyolysis seen

A 
Thoroughbreds
Standardbred
Lameness
In cold weather 
Stressful events
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32
Q

What mineral is changed by recurrent exertional rhabdomyolysis

A

Defect in intracellular Ca regulation in sarcoplasnjx reticulum - no test
Look at CK and AST

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33
Q

RER is managed by

A 
No stress
Regular exercise
Low carb diet
Balances electrolytes
Dantrolene (alters Ca release in muscle) before exercise
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34
Q 
Which is false about shivers
A. Gradually progressive
B. Chronic neuromuscular disease
C. Gait abnormalities when backing up
D. Occurs in front limbs primarily
A

D- pelvic region limbs and rail (jerky and trembling tenseness

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35
Q

What is pathogenomic for shivers

A

Raised tail head

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36
Q 
Stringhalt is
A. Hocks flex violently toward abdomen
B. Medial patellar ligament momentarily caught
C. Scar tissue formation due to injury
D. Symmetrical muscle wasting
A

A

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37
Q

Treatment of shivers includes

A 
No good treatment 
Vitamin e
Selenium
Massage
Consistent exercise
Acupuncture
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38
Q

Mitochondrial myopathy makes it very hard to

A

Exercise longer than 6 minutes

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39
Q

Mitochondrial myopathy occurs when there are spontaneous mutations in _____. This is inherited from the (mother/ father). Defective oxidative phosphorylation results in a rise in _______

A

MtDNA
Mother
Lactate- greater emphasis on anaerobic glycolysis for energy production

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40
Q

How is mitochondrial myopathy

A

Muscle biopsy
Normal CK
marked plasma lactate values
EMG- dive bomber sounds

Poor prognosis (unlikely to be athletic)

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41
Q

_______ is an important energy source for fetus and neonate

A

Glycogen

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42
Q

Glycogen branching enzyme deficiency (GBED) causes there to be no measurable _________ activity

A

GBE- enzyme
Unable to form normally branches glycogen -no glucose homeostasis
Always fatal before 8 weeks old (quarter horses pain Appaloosa)

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43
Q

Hyperkalemia periodic paralysis affects mainly what breed

A

Quarter horses

Mutation in voltage gated Na channels=hyperexcitable muscles

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44
Q

What are the 2 differentials of prolapse of the 3rd eyelid in horses

A

HYPP

Tetanus

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45
Q

What are some clinical signs of HYPP

A 
Weakness muscle fasciulations 
Anxious 
Stridor
Dyspnea. Tachypnea
Recumbancy
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46
Q

How is HYPP diagnosed

A

Plasma K

DNA of blood or hair

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47
Q

How is HYPP treated

A 
Karo syrup 
Grain 
(NOT MOLASSES)
Bicarbonate- severe 
Dextrose- severe
Calcium gluconate 
Insulin- try not to use
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48
Q

What cannot be fed to horses with HYPP

A

Low K
No alfalfa bran or molasses
Avoid rapid feed changes
Acetazolamide reduces K

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49
Q

Immune mediated myositis (non exertional rhabdomyolitis) affects what gene of what breeds

A

E321G myosin heavy chain 1 MYH1 gene in quarter horses

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50
Q

What are clinical signs of immune mediated myositis

A 
Symmetrical muscle atrophy 
Stiff gait
Fever
Concurrent infection or vxn
Increased muscle enzymes, WBC and fibrinogen
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51
Q

What are treatments for immune mediated myositis

A

Corticosteroids. Dexamethasone then prednisolone

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52
Q

Nutritional mouse generation is also known commonly as

A

White muscle disease

Nutrional muscular dystrophy

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53
Q

What is the nutrional deficiency of horses with white muscle disease

A

Selenium and or vitamin e

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54
Q

The cardiac form of WMD affects (very young foals/ weanlings).

A

Very young foals. Weaning is skeletal form (weakness. Stiff gait. Poor suckle. Painful muscles. Limited jaw motion and weight loss). Cardiac (edema. Recumbancy. Heart murmur. Fatal)

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55
Q

How is WMD diagnosed

A 
Increased CK and AST
Myo globinuria 
Selenium concentration in blood 
Glutathione peroxidase activity 
Muscle biopsy
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56
Q

Which is false about WMD’s treatment and prevention
A. Give oral shipments as IM injections can have severe reactions in adults
B. Restrict exercise
C. NSAIDS
D. Give selenium injections at birth
E. None of the above

A

E. It’s all of them

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57
Q

Seasonal pasture associated myopathy occurs in the mid-west in the spring and summer. It’s caused by ingestion of

A

Seed pods from box elder trees

Hypoglycin A causes multiple accounts CoA dehydrogenase deficiency (MADD)

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58
Q

T/F. Seasonal pasture myopathy tends to have a good prognosis when given supportive care

A

False. Up to 90% mortality. Severe rhabdomyolysis of skeletal cardiac and respiratory muscles. Sudden death

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59
Q

Clostridial myonecrosis is caused by what pathogen and usually occurs with what

A

Clostridial perfringes ( Gram + rod)
Follows IM injection or puncture wound
May also invade GIT
Necrotizing and hemolysin toxins cause Cl Signs

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60
Q

What are clinical signs of clostridial myonecrosis

A 
Death
Obtunded 
Pyrexia
Tachypnea 
Swelling pain
Discharge. Odorous 
Rapidly progressive
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61
Q

How is clostridial myonecrosis treated

A 
K penicillin 
Debridement
Metro
Fenestration 
Remove necrotic tissue to disrupt anaerobic environment 
O2
AB min 7 days after wound is resolved
Corticosteroids are controversial
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62
Q

CN1

A

Olfactory

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63
Q

CN2

A 
Optic
Menace
Dazzle
Obstacle course 
PLR
Fundic
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64
Q

CN3

A

Oculomotor
PLR
Eye position

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65
Q

CN 4 and CN6

A

Trochlear and abducens
Eye position
Strabismus if abnormal

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66
Q

CN5

A

Trigeminal
Muscles of mastication
Sensory- skin and MM

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67
Q

CN7

A 
Facial
Motor of muscles of facial expression
Menace blink
Prehension 
Lacrimal gland
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68
Q

CN8

A

Vestibulocochlear
Balance
Hearing

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69
Q

CN 9 10 11

A 
Glossopharyngeal 
Vagus
Accessory
Pharynx and larynx atrophy. Slap test. Endoscopy
Swallowing, aspiration pneumonia
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70
Q

CN12

A

Hypoglosus

Tongue motor

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71
Q

Sacral segments of damaged nerves may show what

A

Atrophy and sweating y

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72
Q

What is the difference between lame and neurological gait

A

Lame- regularly irregular

Neuro- irregularly irregular

73
Q

What is pacing in. A horse

A

Both front and back leg on one side move at the same time with a step forward

74
Q

Gait grading- horse that stumbles and is at risk for falling

A

4/5

75
Q

Gait grading- detectable during maneuvers. Hard to see I straight line

A

2/5

76
Q

Gait grading. Normal gait

A

0/5

77
Q

Gait grading- recumbent

A

5/5

78
Q

How is juvenile epilepsy treated

A

Resolves 6-12 months
Diazepam iv and phenobarbital
Acepromazine. Xylazine and ketamine make it worse

79
Q

A premature foal (premature separation of the placenta) has a nystagmus and seizures

A

Perinatal asphyxia syndrome
Multiple organs affected
Control seizures
Poor prognosis

80
Q

Enrofloxacin given into the carotid would result in what clinical signs

A 
Seizures
Unresponsive
Low HR
No PLR
Hypothermia
Blindness
Necrosis of brain
81
Q

Severity with a carotid injection is dependent on

A

PH
Composition (oil worse)
Volume

82
Q

How is a carotid injection treated

A

Edema- mannitol, hypertonic saline, furosemide
NSAIDS DSMO
Elevate head
Fluids diazepam

83
Q

What is seen in blood work with a horse with hepatic encephalopathy

A 
Neutrophilia
High liver enzymes
Low fibrinogen
High ammonia
Prolonged coagulation
84
Q

Leukoencephalomalacia is caused by what bacteria and where is that bacteria found

A

Fusarium moniliforme and moldy corn disease

In late fall or early spring

85
Q

What are some clinical signs of leukoencephalomalacia

A 
In coordination
Lethargy
Obtundation 
Head pressing 
Liver failure
Seizures
Sweating 
Hyperexcitability
86
Q

How is leukoencephalomalacia treated

A

Not
Euthanasia
Grey/ brown areas of malacia on necropsy in white matter. Unilateral

87
Q

Nigropallidal encephalomalacia is caused by what

A

Yellow star thistle
Russian knapweed
Prolonged ingestion (not palatable)

88
Q

What are clinical signs of nigropallidal encephalomalacia

A 
Sudden onset
Impaired prehension and mastication
Can swallow if food put in back of throat
Tongue paresis 
Lethargy 
Ataxia
Chewing
Hypertonicity of facial muscles
Head droop
Not treatment (bilateral symmetrical malacia necropsy)
89
Q

EEE WEE VEE all cause severe encephalitis. How do the symptoms progress

A

Fever stiffness to
Compulsive walking depression excitability abnormal CN to
Recumbancy and death

EEE is 2-3 days until stage 3

90
Q

EEE VEE AND WEE have what prognosis

A

EEE 90% mortality
VEE 40-80% mortality
WEE 50% (no cases in 50 years)
Supportive treatment

91
Q

T/F vaccinating for EEE is highly effective and is given yearly

A

True. Every 6 months if year round mosquitos

92
Q

What are other ways to prevent EEE

A

Mosquito control
Full body blanket- zebra stripes
Screens

93
Q

How is EEE diagnosed

A

IgM capture Elisa
CSF- increased LT high protein
Necropsy- viral isolation

94
Q

When are peak levels of west bile virus

A

Peak in late summer b/c mosquito

95
Q

What are clinical signs for WNV

A 
Weakness
Ataxia
Altered mentation
Muscle fasciculations
CN deficits 
Recumbency 
30% experience a recrudescence of cl. Signs
96
Q

How is WNV diagnosed

A

IgM capture ELISA
CSF increased LT high protein
Necropsy - polioencephalomalacia tissue PCR
Only symptomatic treatment

97
Q

T/F WNV has a very effective vaccine that needs to be given Q4 months

A

True

98
Q

Rabies have 3 broad categories of clinical signs in horses. What are they

A

Furious (brain)- photophobia and aggressive
Dumb (brainstem) - obtunded anorexia circling
Paralytic (spinal)- paralysis ataxia lameness self mutilation

99
Q

Rabies is diagnosed once euthanized How

A 
Direct fluorescent Ab
Negri body (less used now due to direct fluorescent ab)
100
Q 
A IgM titer of WNV >400 indicates
A. Infection
B. Vaccinated
C. Both 
D. Neither
A

A only

Vaccine doesn’t get that high

101
Q

Cerebellar abiotrophy is the most common cerebellar disease and causes the premature death of what cells

A

Purkinje cells

Arabian foals- genetic

102
Q

At what age is cerebellar abiotrophy typically seen

A

6 weeks - 4 months

Born normal

103
Q

What are clinical signs of a foal with cerebellar abiotrophy

A 
Intention tremor
Symmetric ataxia
Hyper extension of limbs
Wide base stance
No menace
Visual and normal mentation 
No sense of space or distance
Hard to coordinate and balance
104
Q

How is cerebellar abiotrophy diagnosed

A

Test carrier status

Histology- degeneration of purkinje cells

105
Q

What is the prognosis of a foal with cerebellar abiotrophy

A

Good but there is no treatment. It doesn’t get worse but won’t get better
Can’t be safely ridden
Prone to self trauma and can be euthanized

106
Q

A head tilt from a peripheral lesion goes (toward/away) from the lesion

A

Toward

107
Q

A horizontal nystagmus fast phase from a peripheral lesion goes (toward/away) from the lesion

A

Fast phase away from lesion

108
Q

A head tilt from a central lesion goes (toward/away) from the lesion

A

Away?

109
Q

A head tilt from a peripheral lesion goes (toward/away/unknown) from the lesion

A

Unknown. Can go in any direction

110
Q

What are seen in both central and peripheral CN 8 lesions

A

EPM

Trauma

111
Q

What are seen in central CN 8 lesions

A

EEE
WNV
EHM
Mass

112
Q

What are seen in peripheral CN 8 lesions

A

THO
otitis interna
Idiopathic labyrinthitis

113
Q

Are CN7 signs seen before or after CN8 in THO

A

After
7- keratitis and corneal ulceration
Subpalpebral lavage (enucleation?)

114
Q

Where are THO typically seen

A

West side of US for unknown reasons

Fractured hyoid inner ear infection trauma

115
Q

In THO it is usually (unilateral/ bilateral)

A

Bilateral. But 1 usually happens first

116
Q

Cervical vertebral stenotic myelopathy (CVSM) occurs primarily in what types of breeds

A

Large fast growing breeds

Malformed vertebrae

117
Q

What are some components of CVSM

A

Stenosis of vert canal
Compression of the spinal cord
Persistent or dynamic

118
Q

What are the clinical signs of CVSM

A 
Weakness
Symmetrical Ataxia
Spasticity and paresis
All limbs= c1-5 (hind limbs worse)
C6-7 (same or front limb worse)
119
Q

How is CVSM diagnosed

A

Radiographs (looking for any fracture or arthritis site)
Don’t correlate with compression site
Narrow- likelihood of CVSM
Indication for myelogram- ataxia with no neck lesion diagnostic if malformation

120
Q

How should the horse be placed for a myelogram

A

Elevate the head to prevent contrast from getting to the brain (b/c seizure)

121
Q

How is CVSM treated

A

Corticosteroids (intra articular)
NSAIDS (phenylbutazone)
Surgery - cervical stabilization (80% improve 1 degree of ataxia, 40% improve 2) but takes 1 year to recover r

122
Q

Equine degenerative myeloencephalopathy is also known as

A

Equine neuroaxonal dystrophy (NAD)

Is a non-compressive diffuse symmetric degeneration seen 1minth-3 years

123
Q

What can predispose a horse to. EDM

A

Low vitamin E in diet

Dry lot= higher risk

124
Q

What are clinical signs of EDM

A 
Symmetrical ataxia
Weakness
No menace (40%) but visual
Pigment rentinopathy 
Behavioral issues- aggression 
DOES NOT affect CN, anal tone or atrophy!!
125
Q

How is EDM diagnosed

A

Rule out other dz
Plasma/serum alpha-tocopherol levels (not difinitive)
Opththalmic exam
Histo of brain and spinal cord

126
Q

How is EDMA prevented/treated

A

Green pasture with vitamin E in mares and foals
Natural RRR for vitamin E supplement
Poor prognosis- usually stabilize signs but don’t improve. Wasting of muscle

127
Q

EMP 3 A’s are

A

Asymmetric
Ataxia
Atrophy

128
Q

CVSM and EDM both have what type of ataxia

A

Symmetric and less atrophy

129
Q

Equine protozoal myeloencephalopathy is caused by what pathogens

A

Sarcocystis neurona- 1
Neospora caninum/ hughesi
Western Hemisphere
All breeds all ages

130
Q

Ataxia in a horse with EPM will be

A

Asymmetric

Focal muscle atrophy LMN

131
Q

T/F EPM clinical signs tend to be acute

A

F
Onset gradual
Multi focal or diffuse lesions
Gray and white matter- brain brainstem or spinal cord

132
Q

How is EPM diagnosed

A

None are good
Serum/ CSF ratio- <100= dz
Serology - rules it out if negative

133
Q

EPM treatment will allow what percent to improve

A

60-75%

15-30% relapse

134
Q

How is EPM treated

A 
Pyrimethamin and sulfadiazine
4-6months but cheaper than:
Ponazuril 28day
Diclazuril 28day
Supportive- NSAIDS Vitamin E thiamine
135
Q

Equine herpes myeloencephalomalacia causes what in young horses

A

Respiratory dz
Abortion in last 1/3 of pregnancy
Myeloencephalopathy - uncommon (neuropathic strain)

136
Q

What are clinical signs with EHM

A 
Fever
Ataxia
Tetraparesis (weakness, hind limbs are worse)
Hypotonia- anus and tail
Urinary incontinence
137
Q

How is EHM diagnosed

A

Contact state vet
Quarantine
Nasal swab and blood PCR
CSF- Canthochromia and high pt and monocytes

138
Q

How is EHM treated

A 
Heparin
Antiviral (acyclovir valacyclovir)
NSAID
Only 50% survival. If down much less
Vaccine doesn’t work
139
Q

Acquired neuro degenerative disease known as equine motor neuron disease affects the ventral horns of the ____ matter

A

Grey. Spinal cord (brainstem nuclei). Horses are older than 2 and vitamin E deficiency

140
Q 
Which is not a sign of Equine motor neuron disease
A. Sweating 
B. Ataxia
C. Muscle trembling
D. Weight shifting 
E. Weak and muscle wasting 
F. Elevated tailhead and low head
G. Sluggish PLR
H. Honeycomb pattern (non-tapetal)
A

B- no ataxia

141
Q

How is equine motor neuron disease treated

A

Vitamin E (RRR)
20- unchanged
40%- deteriorate (6 weeks)
40%- recover

142
Q

What biopsy is taken for equine motor neuron disease

A

Sacrocaudalis dorsalis (tailhead)

To dx - low serum/ plasma alpha tocopherol, increased CK AST, abnormal EMG or accessory nerve biopsy

143
Q

Suprascapular nerve injury can be caused from trauma of the cranial shoulder What muscles does it innervate

A

Supraspinatus and infraspinatus muscles. See atrophy over a few weeks and outward rotation of the shoulder

144
Q

A horse that is not weight bearing of the front right leg with the dorsum hoof in the ground and a flexed elbow what is a likely cause

A

Radial nerve paralysis. Also can’t flex shoulder or extend limb. Elbow trauma is the cause

145
Q

Bilateral damage of the brachial plexus could result in

A

Inability to stand on front legs. Trying to get up

Can be torn nerve or just swollen

146
Q

Severe pruritus of perineum followed by a lack of tail tone or anal tone may indicate an issue with what nerves

A

Polyneuritus equi

EHV- also differential

147
Q

Polyneuritis equi is a immune mediated disease with no sex, breed or age predisposition that forms what on nerve roots

A

Granulomatous lesions

148
Q

What is the toxin of tetanus

A

Tetanopasmin that inhibits inhibitory neurons of the spine

149
Q

What types of wounds cause tetanus

A

Low o2 (deep. Necrosis)
Impaired blood supply
Puncture would castration metritis abscess
Umbilical infection- foals

150
Q

What is a common clinical sign of both vaccinated and non vaccinated horses that were infected with tetanus

A

Third eyelid prolapse

151
Q

How is tetanus treated

A 
Wound debridement 
AN- penicillin
Tetanus antitoxin (TAT)
Toxoid
Theiler’s dz
152
Q

What usually kills a tetanus horse

A

Paralysis of respiratory muscles

153
Q

T/F the vaccine for tetanus is 100% effective

A

True. According to sanz

154
Q

What type of botulism is most common

A

B. - from wound. Shaker foal

A(west)
C (FI). These are from feed

155
Q

What are clinical signs of botulism

A 
Weak
Dysphasia 
Poor muscle tone
No PLR
Muscle fasciculations
156
Q

What are treatments for botulism

A

Antitoxin (bind to free toxin) not effective if down

Supportive - wait until new receptors are made

157
Q

When should a mare be vaccinated for botulism when bred

A

I month pre foaling

No vxn for A or C (no cross protection)

158
Q

What is the prognosis of botulism

A

Poor if down

Guarded to good if standing with antitoxin

159
Q

Wound for toxin testing for botulism tests for what types

A

PCR for A B C

160
Q

What should be immediately addressed when a outbreak is thought to have occurred

A 
Minimize exposure
Contain spread
Treat affected horses
Stop movement
Isolate
Don’t be a fomite
161
Q

What oxidizing agents are used in foot mats to prevent spread of dz

A

Virkon accel

Broad spectrum and safe but corrosive to metal

162
Q

How long should new arrivals be quarantined

A

28 days/ > 2 weeks

Test for EIA S. equi

163
Q

If a horse has diarrhea leukopenia and fever what should it be tested for

A

Salmonella

Target testing ( no whole herd if they don’t have symptoms)

164
Q

What is the best way to ensure streptococcus free status in an outbreak

A

Nasopharyngeal washes on all horses every other week until 3 negatives consecutively

165
Q

What biosecurity resource helps with vaccination guidelines and infectious dz control guidelines

A

AAEP

166
Q

For a substance to be considered antigenic it’s must have a molecular weight above

A

8000

Also depends on spirited on cell surface

167
Q

T/F Vaccines are considered a passive immunization process

A

False. Is active

Passive- Ab go unimmunized individual

168
Q

Killed vaccines rely on _______ to create an immune response

A

Adjuvants

169
Q

T/F a vaccine must be demonstrated to be safe and effective before marketing

A

False. Only safe

170
Q

What are the core vaccines in horses

A

Tetanus toxoid
EEE WEE Venezuelan EE
WNV
Rabies

171
Q

T/F administration of MLV and killed vaccine is discouraged as adjuvants may inactivate MLV

A

True

172
Q

Horses greater than 3 years old are more susceptible to parasite infection

A

False

Younger than 3

173
Q

Currently _____ are considered the primary equine parasitic pathogen

A

Cyathostomin. Small strongyle

Anaploceohala perfoliata can be a major cause of colic in horses

174
Q 
Which is false regarding cyathostomin
A. In environment 
B. All grazing horses are infected
C. Only disease at very high levels
D. Frequent anthelmintic needed
A

D- not needed

175
Q

What are the main anthelmintics

A

Ivermectin
Moxidectin
Pyrantel
Fenbendazole

Deworming every 2-3 months is not recommended

176
Q

What is the only test currently available for detecting parasite resistance in horses

A

Fecal egg count reduction test

177
Q

Low egg shedders should be dewormed how often

A

2 times a year

178
Q

Resistance is considered to be less than ___% of egg reduction

A

80

Deworm if above 200 (moderate to high shedders)

179
Q

1st deworming is at _____ months of age with fenbendazole/oxibendzole

A

2-3 months

Fecal float then at 5-6 months

Equine (10 decks)

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