Infectious Dzs of the CNS

Question 1

What are the possible body systems that can be affected by equine herpesvirus 1?

Answer 1

(Respiratory, neurologic, and reproductive; both identified genotypes can cause any of the three tho D752 is more likely to cause neurological and respiratory whereas N752 is more likely to cause abortion and respiratory)

Question 2

Where does EHV-1 lie dormant in latently infected horses?

Answer 2

(Lnn and trigeminal ganglion)

Question 3

What are the two recognized viral genotypes of EHV-1?

Answer 3

(D752 and N752)

Question 4

How can horses be exposed to EHV-1?

Answer 4

(Direct contact, aerosol, and fomites)

Question 5

What is the incubation time for EHV-1?

Answer 5

(2-10 days)

Question 6

The respiratory tract is the primary site of infection for EHV-1, then it will enter the lymph nodes and then monocytes will disseminate the virus throughout the body, what results from the viremia?

Answer 6

(Vasculitis and ischemic damage to the brain and spinal cord)

Question 7

What are the classic signs of EHM?

Answer 7

(Pelvic limb weakness (leads to dog sitting) and ataxia +/- fecal/urinary incontinence; can also see a fever, obtundation, cranial nerve deficits, recumbency, and seizures)

Question 8

What do you expect to see on CSF cytology of an EHM case?

Answer 8

(Xanthochromia, increased protein, and mild mononuclear pleocytosis)

Question 9

How is EHV-1/EHM diagnosed?

Answer 9

(Quantitative PCR on nasal secretions and whole blood → allows for determination of both viral load and genotype which can impact prognosis)

Question 10

What is the antiviral drug used for treatment of EHV-1?

Answer 10

(Valacyclovir → prevents viral replication)

Question 11

What other drug can be given in addition to NSAIDs or steroids for treatment of the vasculitis subsequent to EHV-1 infections?

Answer 11

(Heparin → prevents virus-induced activation of coag cascade and platelets, limits clotting of small vessels that supply brain and spinal cord with O2)

Question 12

What are some biosecurity protocols that should be in place anywhere to decrease the chances of an EHV-1 outbreak?

Answer 12

(2 week quarantine for new horses, no nose-to-nose contact with unfamiliar horses, do not use public food/water/wash areas)

Question 13

How often should horses with a high risk of exposure to EHV-1 be vaccinated?

Answer 13

(Every 6 months → does not prevent EHM but it does decrease viral shedding and may decrease disease severity)

Question 14

If you’re asked what immune supplements someone should put their horse on, what should you recommend?

Answer 14

(Just make sure the supplement contains zinc)

Question 15

How are the equine encephalomyelitis viruses spread primarily and what are their reservoirs?

Answer 15

(Spread by mosquitoes, birds and small mammals are reservoir hosts; horses are accidental hosts)

Question 16

Of the equine encephalomyelitis viruses, which is truly a concern of zoonosis?

Answer 16

(VEE → horses will have sufficient circulating virus to amplify dz and spread to other horses or humans, EEE/WEE → horses do not amplify virus enough to be infectious)

Question 17

Equine encephalomyelitis viruses are associated with no/low grade/high grade fevers (choose).

Answer 17

(High grade fevers, up to 106 F; other signs are nonspecific (circling, head pressing, hyperesthesia, seizures, obtundation, aggression, somnolence, proprioceptive deficits so need good hx paired with fever to turn you towards EE)

Question 18

What specific serological test is performed to diagnose an equine encephalomyelitis virus?

Answer 18

(IgM capture ELISA → indicate an acute process; can also do acute and convalescent IgG serum titers if the horse survives that long or PCR of CSF but that is less sensitive)

Question 19

What does the vaccination protocol for WEE/EEE and WNV depend on?

Answer 19

(The location of the horse, if they live in an area with mosquitoes active year round they should be vaccinated every 6 months, if not maybe just an annual in the spring when mosquitoes start to pop off)

Question 20

Why will there be a higher incidence of west nile virus infections in late summer/early fall?

Answer 20

(Bc the virus amplifies in both bird and mosquito populations throughout the entirety of mosquito season which means viral load increases in both populations through the season = lots of virus in the late summer/early fall)

Question 21

Some of the clinical signs seen with west nile virus infection of horses are diffuse fine muscle fasciculations (best seen around the muzzle), changes in mentation/consciousness, CN deficits, and spinal ataxia +/- hypermetria; these signs are all associated with which portion of the brain?

Answer 21

(The hindbrain; fasciculations + hypermetria → lack of inhibition from the cerebellum, consciousness + CN deficits → brainstem affected (houses RAS and CN nuclei))

Question 22

What specific serological test is performed to diagnose west nile virus?

Answer 22

(IgM capture ELISA)

Question 23

Treatment of west nile virus includes supportive care, anti-inflammatories, and what other medication?

Answer 23

(Hyperimmune WNV plasma)

Question 24

What is the main prognostic indicator for west nile virus infected horses?

Answer 24

(If they become recumbent or not, their prognosis is good with return to full function as long as they do not become recumbent, most recumbent horses fail to survive)

Question 25

Give the clinical signs associated with the following rabies presentations:

• Cerebral/furious
• Brainstem/dumb
• Spinal/paralytic

Answer 25

• Cerebral/furious (aggression, hyperesthesia, muscle tremors, and hydrophobia)
• Brainstem/dumb (obtundation, head tilt, pharyngeal paralysis)
• Spinal/paralytic (shifting lameness +/- mutilation, ataxia, paralysis)

Question 26

What should be expected to be seen on histopathology of a brain sample in a horse with rabies?

Answer 26

(Negri bodies (eosinophilic inclusions within neurons or ganglion cells), absent in 30% of horses with rabies)

Question 27

What test might be run at the state diagnostic lab on a brain sample from a horse with rabies?

Answer 27

(Fluorescent antibody test, monoclonal antibody test, or mouse inoculation)

Question 28

What are the possible routes of infection for bacterial meningitis?

Answer 28

(Hematogenous, traumatic, and extension of a paranasal sinus infection/mass into the cranium)

Question 29

How will a CSF cytology from a horse with bacterial meningitis differ from that of a horse with an encephalitis virus or EHV-1?

Answer 29

(There will be neutrophilic pleocytosis instead of mononuclear, proteins will still be elevated, glucose will be decreased (lower than peripheral glucose) bc the bacteria and WBCs are using all of it)

Question 30

What are some of the clinical signs associated with confirmed cases of lyme dz in horses?

Answer 30

(Neck and back pain, hyperesthesia, cranial nerve signs, ataxia, obtundation, fever, and uveitis; some of the clinical signs seen in suspect cases were ADR, weight loss, shifting leg lameness, and mild neurologic signs)

Question 31

What is the most comprehensive test for lyme disease in horses and what sample do you need for it?

Answer 31

(Lyme multiplex, needs serum → tells you if the animal has lyme and the chronicity of the infection)

Question 32

What are the clinical signs of otitis media/interna in horses?

Answer 32

(Head shaking, ear rubbing, aural discharge, and CN VII +/- CN VIII deficits)