Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SS - Exam 1 > EQ SC Disease 2 > Flashcards

EQ SC Disease 2 Flashcards

1
Q

EPM testing

A

Antibodies in serum only indicate exposure - which most horses have been exposed
Antibodies in CSF
- infection of CSF and intrathecal antibody production
Compromised BBB
Contamination of CSF w peripheral blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Effective testing for EPM

A

Check ratio of concentration of antibodies to S. Neruona and N. Hughesi in serum, to CSF (serum/titer ratio)
High titer or low serum/titer ratio in conjunction with clinical signs of EPM is strongly suggestive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Diagnosing EPM

A

Sudden onset of neurological signs consistent w EPM
Possibility of exposure
Presence of antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Treating EPM

A

Sulfadiazine
Pyrimethamine
Duration of treatment is 6-9 months
Drugs have poor CNS penetration ability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Second generation treatment

A

Ponazuril (marquis)
Diclazuril (protazil)
Decoquinate (compounded)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Ponazuril

A

Requires a loading dose and treatment lasts about 27 days
Co-administration w oil raises absorption and CSF concentrations. FDA approved
^^$$ ($800/month)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Diclazuril

A

Food pellet that mixes with food
No loading dose, treatment for 28 days . FDA approved
$$$ (800/month)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Decoquinate

A

Oral admin for 10 days
Not FDA approved
Cheapest form of treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why is co treating with anti-inflammatory drugs a good idea>

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Anti inflammatory drugs

A

Vitamin E - 6-8kIU/day
Immunomodulators: leavmisole, Eq stim, equimune, zylexis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

EPM prognosis

A

Progressive disease and athletic performance is poor with no treatment
50-80% of treated horses improve
10-20% of treated horses recover fully
10-20% of treated horses relapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

EPM differentials

A

Trauma
Equine herpesvirus myeloencephalopathy
Parasitic myeloencephalitis
Polyneuritis equi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

EPM prevention

A

Reducing ingestion by opossum feces
Routine health maintenance of barn cats
Stop feeding barn cats in open area to reduce opossum attraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Equine herpes virus myeloencephalopathy

A

Caused by EHV1
- respiratory disease in young horses
- abortion in mares
- pneumonia in neonatal foals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pathogenesis of EHM

A

Endotheliotropic, immune mediated vasculitis of arterioles of spinal cord/brain
Causes hemorrhage, thrombosis, ischemia of white matter and occasionally the gray matter of the Spinal cord /brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Signalment for EHM

A

Usually adult horses
Pregnant or lactating mares
May effect more than one horses on a premise. Close contact airborne

17
Q

EHV1 transmission

A

Herpes becomes latent in host & becomes activated by stress and then becomes infectious

18
Q

EHM history

A

Sudden onset of in coordination
Starts with one horse then many affected
Reported on breeding farm, race track or training stable
Associated with respiratory disease or abortion
Often late winter or early spring

19
Q

Clinical findings for EHM

A

Biphasic fever - day 1-2, day 6-7 (neuro signs begin)
Nasal discharge
Depression
Hind limb weakness/in coordination
Loss of bladder tone
Dog sitting position
Recumbancy

20
Q

EHM neurological signs

A

Symmetric paresis, ataxia, hypometria in pelvic limbs
Symmetric paresis, ataxia, hypometria in pelvic and thoracic limbs
May exhibit weak, floppy tail, inability to defecate & urinary incontinence
CN deficits & seizures (rare)

21
Q

EHM diagnostic testing

A

CBC - normal
Biochem - CK if recumbent
CSF - xanthochromia & increased protein
Nasal swab & whole blood: PCR test
Virus isolation & serology not clinically useful

22
Q

EHM differentials

A

Trauma
Equine protozoal myeloencephalitis
Polyneuritis equi
Botulism

23
Q

EHM treatment

A

Isolation
Primary supportive care
Anti inflammatory meds
Antiviral meds

24
Q

Anti inflammatory meds

A

Flunixin
DMSO
Dexamethasone

25
Q

Antiviral medications

A

Valacyclovir
Ganciclovir
- heparin

26
Q

EHM clinical course

A

Minority of horses will become recumbent or develop signs of encephalopathy
Majority will stay standing
Control urination
Gait improves gradually

27
Q

EHM prognosis

A

Depends on severity of neurological deficits at onset of treatment
Good prognosis if ambulatory and remains ambulatory
Poor prognosis if recumbent or has signs of encephalopathy

28
Q

EHM gross postmortem

A

Multi focal areas of hemorrhage & degeneration of white /occasionally grey matter of the spinal cord/brain
Multi focal arteritis w hemorrhage & necrosis of adjacent neural tissue

29
Q

EHM histopath

A

Multi focal arteritis with hemorrhage and necrosis of adjacent neural tissue

30
Q

EHM prevention

A

Killed & modified live vaccines = protect against respt disease and abortion NOT EHM
Modified lived may protect against EHM

31
Q

EHM outbreak management

A

Report to state vet immediately
Isolate affected horses to minimize the spread of EHV1 to unaffected horses
Quarantine of premise prevents the transportation of horses on or off the premise for 3 weeks after last case
Vaccination of exposed but unaffected horses is not recommended!!!

32
Q

Equine motor neuron disease

A

Acquired neruodegenerative disorder of ventral horns of gray matter in the spinal cord and selected brain stem nucleii
Occurs sporadically
Diet without grass or green forage = predisposed

33
Q

Pathophys of EMND

A

Vitamin E is an antioxidant
Deficiency of vitamin E = susceptible to oxidative damage of spinal cord and brain
Resembles progressive spinal muscular atrophy in humans

34
Q

EMND presentation

A

WWMM
Weight loss
Weakness
Muscle atrophy
Muscle tremors

35
Q

EMND neuro exam

A

WWMM
Low head carriage
High tail head
Horse on ball stance

36
Q

EMND diagnosis

A

Neurologic sings of weakness /tremors
Prolonged deficiency of vitamin E
Low concentration of serum vitamin E
Atrophy of type 1 muscle fibers (sarco caudalis dorsalis muscle)

37
Q

EMND treatment

A

Fresh forage - pasture
Good quality hay
Vitamin E supplementation 5-7k IU/day

38
Q

EMND clinical course

A

40, 40, 20
40% will improve w treatment, stable, then some release = euthanasia
40% will stabilize but muscle atrophy is irreversible
20% deteriorate = euthanasia

SS - Exam 1 (33 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions