Infectious Dzs of the CNS Flashcards
What are the possible body systems that can be affected by equine herpesvirus 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)
Where does EHV-1 lie dormant in latently infected horses?
(Lnn and trigeminal ganglion)
What are the two recognized viral genotypes of EHV-1?
(D752 and N752)
How can horses be exposed to EHV-1?
(Direct contact, aerosol, and fomites)
What is the incubation time for EHV-1?
(2-10 days)
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?
(Vasculitis and ischemic damage to the brain and spinal cord)
What are the classic signs of EHM?
(Pelvic limb weakness (leads to dog sitting) and ataxia +/- fecal/urinary incontinence; can also see a fever, obtundation, cranial nerve deficits, recumbency, and seizures)
What do you expect to see on CSF cytology of an EHM case?
(Xanthochromia, increased protein, and mild mononuclear pleocytosis)
How is EHV-1/EHM diagnosed?
(Quantitative PCR on nasal secretions and whole blood → allows for determination of both viral load and genotype which can impact prognosis)
What is the antiviral drug used for treatment of EHV-1?
(Valacyclovir → prevents viral replication)
What other drug can be given in addition to NSAIDs or steroids for treatment of the vasculitis subsequent to EHV-1 infections?
(Heparin → prevents virus-induced activation of coag cascade and platelets, limits clotting of small vessels that supply brain and spinal cord with O2)
What are some biosecurity protocols that should be in place anywhere to decrease the chances of an EHV-1 outbreak?
(2 week quarantine for new horses, no nose-to-nose contact with unfamiliar horses, do not use public food/water/wash areas)
How often should horses with a high risk of exposure to EHV-1 be vaccinated?
(Every 6 months → does not prevent EHM but it does decrease viral shedding and may decrease disease severity)
If you’re asked what immune supplements someone should put their horse on, what should you recommend?
(Just make sure the supplement contains zinc)
How are the equine encephalomyelitis viruses spread primarily and what are their reservoirs?
(Spread by mosquitoes, birds and small mammals are reservoir hosts; horses are accidental hosts)
Of the equine encephalomyelitis viruses, which is truly a concern of zoonosis?
(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)
Equine encephalomyelitis viruses are associated with no/low grade/high grade fevers (choose).
(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)
What specific serological test is performed to diagnose an equine encephalomyelitis virus?
(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)
What does the vaccination protocol for WEE/EEE and WNV depend on?
(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)
Why will there be a higher incidence of west nile virus infections in late summer/early fall?
(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)
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?
(The hindbrain; fasciculations + hypermetria → lack of inhibition from the cerebellum, consciousness + CN deficits → brainstem affected (houses RAS and CN nuclei))
What specific serological test is performed to diagnose west nile virus?
(IgM capture ELISA)
Treatment of west nile virus includes supportive care, anti-inflammatories, and what other medication?
(Hyperimmune WNV plasma)
What is the main prognostic indicator for west nile virus infected horses?
(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)
