Equine Med- Infectious and Neuro Diseases 2

wilsbach's version from 2016-04-30 23:10

Neuro Diseases

Question Answer
Zoonoticrabies, encephalitis (EEE/WEE), WNV
CORE VXsRabies, EEE/WEE, WNV, tetanus
etiological agent of rabies? How is it spread?Lyssavirus of rhabdoviridae, RNA. Bullet shaped. Transmission via bite w/ infected saliva. Neurotropic. ZOONOTIC
CSs of rabies?Dumb vs Furious- horse get dumb form: ataxia, paralysis of masseter mm and pharynx, inability to swallow, ptyalism, paralysis throughout body, colic-coma, death.
dx of rabiesNo def testing antemortem. PM: direct fluorescent ab testing of brain tissue, negri IBs in nerve cells, CSF may have pleiocytosis, ↑ protein, xanthochromia
what are negri bodies/what dz?rabies, cytoplasmic IBs
Tx of rabies?Tx depends on vx status: Unvx: euthanasia or 6mos quarantine and vx for rabies 1 mo prior to release. Vx: rabies booster and observe for 45 days for CS. Diff protocols depending on their moms vx status
prog of rabies?Prognosis: If get rabies will die. VACCINATE!! Annually or 4-6 wks prior to breeding or prior to partus
Equine Protozoal Myeloencephalitis(EPM) etiology? how do they get it?Sarcocystis neurona. Opossum is definitive host. Other mammals can be incidental hosts but horses and ponies considered abberant (dead end) hosts. Horse ingest sporocyst in contaminated feed or water from opossum feces. Protozoan migrates to CNS causing lesions.
lifecycle of sarcocystis neurona? what dz does this cause?EPM: DH: opossum, poops eggs. horse is aberrant host, eats feed contaminated with possum poop. (IH are cat, skunk, raccoon, otters, armadillo- sarcocysts in their mm)
CSs of EPM? who is most affected?YOUNG most affected, avg age <4y (mules/donkeys/other equids NOT affected).- see: Asymmetrical ataxia and weakness, incoordination, gait abnormalities, leaning to one side. Weight loss bc quidding, behavior changes. Asymmetrical gluteal atrophy, CN deficits depending on localization of lesions. Cauda equine syndrome. (basically not right neuro, mm melting off them) (*IF FEVER, PROLLY NOT EPM)
how do you dx EPM?Dx based on exclusion of ALL other dzs! Serum:CSF Ab titer < 1:100- means more Ab production in CSF indicates S. neurona inf highly possible. Western blot, IFAT (IFAT best test, use CSF), PCR. ELISA test for surface antigens 1-4. PM: multifocal hemorrhage and necrosis, malacia, schizonts present....(*if take blood sample, if Abs, doesnt tell you much because many are Ab postiive without CSs)
Tx for EPM?FDA approved tx: Ponazuril or Diclazuril for about 30 days. Or combo of sulfadiazine and pyrimethamine. NSAIDs or immunmodulators like Levamisole. Decoquinate not FDA approved yet
prog of EPM?60% horses improve but most will not recover completely and have some CNS damage still. Some horses can relapse. Not really any proven prevention- keep water and food from contamination. Keep wildlife and opossums away.
Equine encephalitis: WEE, EEE, VEE. Etiology, how do they get it?Togaviridae, Alphavirus. Transmission via biting insects. Birds are reservoir hosts and amplifiers. Horses and Humans are dead end hosts-- ZOONOTIC (The alpha makes me go EEE with excitement)
birds are reservoir hosts for?encephalitis
which encephalitis has the worst signs?EEE
CSs of the encephalitises?EEE CS more severe and progress more rapidly. All have fever, tachycardia, obtunded, Neuro signs- depression, wide base stance, lowered head, CN deficits, lack of menace, abnormal PLRs, head tilt, paralysis, nystagmus, facial and tongue paralysis. Encephalitis, circling, head pressing, ataxia, seizures. Anorexia, diarrhea. Recumbency and death.
what will CBC/CSF be like with encephalitis?EEE might be suggested with a lymphopenia. CSF will show pleocytosis and inc protein.
how do you dx encephalitis?Antemortem testing is difficult: ELISA IgM*. Do paired titers to DDX exposure vs vaccine. Virus neutralization to confirm w/ high IgM.PM: RT-PCR from brain tissue for def dx
definitive dx for encephalitis?POST MORTEM RT-PCR of brain tissue
prog of encephalitis? which is the best prog?Prognosis is Poor. EEE > VEE > WEE for mortality rates (EEE IS THE WORST). If survive will have lifelong immunity but can have residual CNS signs. Prevention via vaccines!! VEE is not core but used in high risk areas. Need to give 2 boosters 10 days apart and then annually. Or booster mare 4-6 before partus. Mosquito control.
birds AND alligators reservoir hosts?WNV
west nile virus- etiological agent? how do horses get it?Flaviviridae virus and arbovirus (culex mosquito). Birds and alligators are reservoir hosts and mosquitoes transmit dz. Horses and humans are dead end hosts. ZOONOTIC. Assoc flaviviruses: Murray Valley, Japanese, St. Louis encephalitises (nile water is flavi-full)
CS of WNV?CS are varied: not all horses develop CS, and some can die w/o CS. Fever, lameness, ataxia of hindlimbs, paresis, mm tremors, muzzle twitching, impaired vision, wandering, head pressing, circling, recumbency, death. Majority are asymptomatic!
dx WNV?IgM* ELISA- serum or CSF. Can ddx from exposure or vaccine. RT-PCR and then IHC. Neg IgM does not r/o infection though
tx of WNV?No specific tx: supportive care: IV fluids, NSAIDs, prevent pressure sores and support limbs
prog of WNV?Prognosis depends on severity of CS and vx status. If recumbent- poor prognosis. Relapses can occur. Prevent w/ Vaccines! 4 USDA approved vx. Do NOT vx preg mares. Vector control and ecological stewardship
Equine Herpes Myeloencephalopathy- etiological agent? how do they get it?neuropathic form of EHV1*. Happens because of ischemic damage of SC or brain during herpes infection (from vasculitis). Transmitted via direct contact (usually resp tract secretions).
CSs of Equine herpes myeloencephalopathy?white matter neuro damage. Can be slight changes to total recumb. CN nerve deficits. incontinence. nasal discharge, edema, colic. Also can see resp and abortions since the EHV-1 could just be doing what it normally does.
white or grey matter affected with equine herpes myeloencephalopathy?WHITE
Dx of equine herpes myeloencephalopathy?CSF (inc protein, xanthochromic, inc cells)...virus neutralizing ab titers >4x inc between paired samples= active. virus isolation. PCR
they can't pee with this dzequine herpes myeloencephalopathy
tx equine herpes myeloencephalopathy?supportive care. and make sure bladder manually expressed. rectal decompression. fluids, nutrition, abx if 2* infxn
prog of equine herpes myeloencephalopathy?CSs stabilize within 48 hrs but can get worse too. Most improve within 5-7 days, can recover completely in time. Recumbency - worse prognosis. Guarded= partial/full recovery.
can you prevent equine herpes myeloencephalopathy?vaccination may not be effective against EHM, but might reduce EHV-1 prevalence - decrease risk of exposure. but neuro form might be linked to frequency of vx tho.