---start--- c sweeney imd (not medsurg!) 4/15 EIA, EEE, WEE, VEE, EVA these diseases are hard to remember. we will try to emphasize something... there is more known about these diseases than is written in our handouts. these are our main points. EIA: not a lot seen here - thank goodness. we have seen it though. Nickname: Swamp Fever Etiology: EIA Retrovirus - genetically related to HIV and others Who? Equidae - horses, mules, donkeys - any age, any breed Where? most often in Southern and Eastern USA and up the Mississippi When? mostly late summer and fall, due to vector Rates: morbidity < 2.5% here, about 90% in S. and Latin america. mortality under 50% about 2000 new cases/yr, but fewer new cases each year transmission: blood borne -intrauterine is possible but not common -transfer of blood via transfusion - rare -blood transfer in other ways -unsanitary veterinary practice -blood sucking vector (slide of ray sweeney)** vectors: #1 is the horse fly - tabanidae - painful bite causes it to be interrupted frequently so it moves from host to host, and has a large mouthpiece which carries a large volume of blood. one good thing is these flies generally have only a 200 yard range. #2 mosquitoes - but these do little damage, not as much blood slide: tabanid fly. ugly. large mouth. pathogenesis: EIA virus spreads to horse via blood horse becomes viremic for life virus stimulates B and T cell response EIA multiplies in mphages throughout body EIA then localizes in LNs, spleen, liver, and kidney fever 10-29 days post infection, horse already viremic before that though EIA virus damages vasular intima of small vessels EIA virus causes inflammatory changes in organs such as liver EIA virus causes immune mediated hemolytic anemia and thrombocytopenia seroconversion occurs by 16-90 days so, after inoculation, there is a rise in amount of virus, then it drops down to lower level and remains there. fever starts as virus amount rises, then it drops down as immune response kicks in. end results of EIA infection: #1 acute clinical signs --> death - 1 ml of blood can infect a lot of horses #2 subacute or chronic signs -- > possible death - waxing waning, anemia, hepatitis, edema, glomerulonephritis, thrombocytopenia. these horses are less viremic than the #1 horse #3 inapparent disease --> +/- death. only 1 out of 6 million horseflies likely to pickup and spread EIA from these horses - low level viremia signs: depression, weakness, wt loss fever spikes up to 105 F - when evaluating FUO in horse, always rule out EIA tachycardia icterus due to hemolysis edema due to vasculitis petechial hemorrhages possible abortions Dr. S. hasn't seen a classic clinical case of EIA at NBC, but we have some slides from LA - horse loooks sick, thin, bony, some have ventral edema, conjunctivitis. Clinical course - slow recovery over 3 to 21 days or death within 2 weeks. relapses occur during stressful periods postmortem findings: gross lesions: edema, hemorrhage, splenomegaly, hepatitis, lymphadenopathy, emaciation microscopic lesions: lymphoid necrosis, others skipped lab dadta: results vary 1. anemia 2. thrombocytopenia 3. leukopenia 4. increased bilirubin, liver enzymes 5. increased gamma globulins dx: 1. clinical signs 2. lab results 3. Coggins test - AGID to detect antiviral Ab - classic test. this test is very very specific. not the most sensitive test, but the most specific. a Coggins positive test definitely has EIA. yes, there are some false pos and neg. you have a false neg early in infection, during first 35-40 days. false positives are foals with colostral antibody - this isn't really a false reading, it's just antibody presence that isn't due to disease. no false positives in adults. 4. ELISA-Celsia - more sensitive but occasional fase pos - often used to test questionable AGID sera - can detect earlier than AGID. if AGID is questionable, the ELISA will be positive if animal is really positive. Coggins again is really the best test 5. RIA or FA -more sensitive but less specific 6. horse inoculation - most sensitive, really expensive, not nice to the horse. rule outs: other causes of anemia or vasculitis or hepatopathy immune mediated red maple leaf toxicity anemia of chronic disease babesia liver disease leptospirosis do not learn this list for the exam purpura hemorrhagia equine viral arteritis treatment: none. you can't eliminate the virus. a sick horse - give supportive care, nursing, tx symptomatically. rest. suggest euthanasia knowing that the horse must otherwise be isolated forever... prevention: vaccine exists but isn't used b/c it is difficult to differentiate vaccinated horses from infected horses. They are working on an antibody test which can differentiate horse vaccine strain from natural infection mainly disease is prevented by good hygiene and insect control. testing and ID of carriers: federal law says no interstate movement of positive horses "unless reactor officially identified and unless moving directly to slaughter, traveling under a permit and in a sealed conveyance." state laws vary - some require quarantine of positive horses, other states require euthanasia, some require branding and lifelong quarantine at 200 yards. prevention again: this is a reportable disease. all positive cases must be filed with the state vet. a year and a half ago - outbreak in SE PA. 1 had clinical signs. horses potentially exposed to the affected horses were quarantined for a while, and tested 45 days later. horse 1 was sick 2 weeks before testing. 40 horses had contacted him. farm was closed, horses were removed. all horses were traced and quarantined pending negatie test. two other horses from first farm tested positive. one was euthanized. two others - one went to philadelphia park - tested negative. all horses at philadelphia park were now quarantined. this is obviously a very serious problem. PA requires quarantine, not euthanasia. so, most horse events require negative coggins tests, so this is helpful. -- Viral encephalidites - we do see these around here, esp NJ and DE EEE, WEE, and VEE (eastern, western, and venezuelan) Nickname: sleeping sickness Definition: an infectious dz infecting horses characterized by signs of deranged consciousness, motor irritation, and paralysis etiology: RNA alpha virus of family Togaviridae. there are separate EEE, WEE< and VEE viruses which vary in virulence but produce similar syndromes. distribution: seem to be restricted to N and S america. in USA most common in southern coastal states but also we see it here. also ohio, michigan. not just coastal states. VEE is mostly in central and south america, though there was an outbreak in the US in 1971. EEE 1994 173 horse cases in the US, and 4 human cases - 1 fatal WEE 1994 5 horse cases VEE 1995 outbreak in venezuela and colombia - 15000 humans - 42 died. 500 horses affected. VEE 1996 outbreak in mexico - 32 horses, no humans Who gets it? horses and humans (dead end hosts). 152 EEE cases in humans in the past 40 years, 50% fatal. transmission - any bird especially swamp birds are reservoirs of the virus from year to year. birds harbor the virus. Vectors are insects - usually mosquitoes, usually swamp mosquitoes. remember: this is the virus they worry about in Disneyworld, because they are down there in warm weather, with mosquitoes, and people all over - they closed Disneyworld b/c of this once. they also sometimes close schools when they worry about this. occurence in man and horses may be predicated by an unusually high activity of virus in mosquitoes. usually lots of horse deaths occur before the first human case. horses are kind of like sentinels for this virus EEE-WWW - horse is dead end host, non infectious VEE - horse is viremic and infectious to other horses and to humans by way of mosquito vectors. infected mosquito bites horse ->proliferation in LNs->viremia ->then either inapparent infection with mild fever and leukopenia OR generalized febrile illness with anorexia, depression, fever, leukopenia OR encephalomyelitis with signs occuring within 5 days of infection and death usually within a few days. signs of encephalitic form: fever anorexia, behavior changes, head pressing, dullness, somnolence, circling, tooth grinding, hyperexcitable - sudden onset of bizarre behavior (mimics rabies, herpes encephalitis), blindness, pruritis, cranial nerve deficits - sagging lip, nystagmus, dysphagia ataxia, paresis - brainstem and cord signs seizures respiratory arrest - may be terminal event example: dysphagic, trembling horse with chewing, erection, and depression survivors: those that survive may have residual deficits - "dummy horse" mortality rates - EEE horse 75-98%, man 50-75% etc. just know they are different postmortem lesions - histo will reveal brain lesions -see handout dx: clinical signs, presence of vector (location, season), lack of vaccination? (vaccination doesn't rule out the disease), CSF: increased protein ++++, increased WBC + (typical of any encephalitis); serology; viral isolation; postmortem findings rule outs: hard to rule stuff out. could be almost anything hepatoencephalopathy - icterus and increased liver enzymes would be present rabies - tough to rule out EPM - rarely has these signs treatment - if horse is recumbent, prognosis is very poor. odds are he won't get up again supportive tx - fluids, well padded area DMSO should maybe reduce cerebral edema antipyretics dexamethasone is sometimes used...good idea? diazepam for seizure control chloral hydrate for sedation prevention - no eradication program due to reservoir (birds) control mosquitoes vaccination - bivalent/trivalent killed vaccine EEE-WEE-VEE vaccine adults: 2 injections 3-4 wks apart 1 mo prior to mosquito season, yearly boost foals: after 2-4 mos, vaccinate 2-3 times, then yearly booster vaccinate during outbreaks. for humans, wear long sleeves, avoid mosquito habitats/use bug spray, also sometimes change school hours or park hours in endemic areas because mosquitoes are crepuscular. EVA: equine viral arteritis etiology: nonarthropod borne togavirus like BVD and hog cholera first recognized as separate from equine influenza in 1953 after an outbreak of respiratory disease and abortions on a farm in Ohio. serological surveys show us it is pretty much everywhere except britain and japan,but clinical outbreaks are rare. the virus is everywhere and is endemic in standardbreds. many infections are subclinical. prevalence in thoroughbreds is low. there are periodic outbreaks. an outbreak in 1993 of EVA amongg 2000 horses at a track - affected 162 horses - caused outbreaks in nebraska nad kentucky. this was mild but abortigenic potential was present. EVA causes panvasculitis and affects all areas of the cardiovascular system. the virus is picked up by mphages in lung and goes to LNs, spreads to circulatory system, causes necrotizing arteritis and edema. can cross placenta and cause fetal death and abortion. signs: fever, anorexia, depression, lacrimation, coughing, nasal d/c, edema, skin rash, abortions in up to 50% of infected mares. signs are sometimes indistinguishable from those seen with EHV1 or EHV4 lab findings - leukopenia/lymphopenia as in EIA, a 4 fold increase in EVA elisa titer. transmission 1. venereal - up to 50% of infected stallions become carriers. many then infect mares for months and some continue to be infectious for life. mares do not carry the disease - they get it and then get over it. 2. inhalation - aerosol droplets from resp tract - shedding up to 2 wks postinfection 3. indirectly via contact with contaminated food/water buckets, etc 4. urine is a potential source of infection dx: clinical dx not possible, virus can be isolated from nasal swabs or elsewhere. prevention - Ab screening provides initial indication of whether stallion is shedding virus in semen. up to 50% of infected stallions shed. viral isolation on semen will confirm if stallion can infect mares at cover. it is strongly recommended that horses moved to farms from the track be kept totally separate from pregnant mares, foals, and yearlings for at least a month. if breeding is to be attempted with a shedding stallion, the mare must first be vaccinated. the MLV vaccine is safe and provides protection for breeding stock. it's safe and protects them. hmm. why do they not use it more? all stallions should be vaccinated; open mares and nonbreeding males should be vaccinated any time and boostered yearly. breeding mares and stallions should be vaccinated at least 3 wks before breeding. pregnant mares and folas under 6 wks shouldn't be vaccinated. you need to know - vaccinated horses do seroconvert and get an Ab titer. semen will be unacceptable in some countries. the EU however allows vaccinated stallions and their semen to be imported if they were vaccinated under 180 days or had a negative serology prior to vaccination. again, females are not carriers. males are. bottom line - EVA is a disease of high morbidity, low mortality (occasional foal), and usually complete, uneventful recovery (+/- carrier state) abortion is the main problem. ---end---