Rhabdovirus, reovirus, birnavirus Flashcards
rhabdoviruses of interest
- rabies
- vesicular stomatitis virus
reoviruses of interest
- blue tongue virus
- African horse sickness virus
- rotavirus
birnaviruses of intrest
- infectious bursal dx virus
rhabdoviridae general characteristics
- neg sense RNA
- enveloped
- distance bullet shape
rhabdoviridae life cycle
- entry = membrane fusion, take up by endocytosis and that acid of endoscope -> triggers fusions
- raps rna in nuceloprotein; can’t produce any protein until transcribe genome -> mrna which can turn into varied of different proteins
- exit= via budding
rabies distribution
- worldwide distribution
rabies transmission
- biting, primarily by bat bite
rabies presenations
- urban: dogs
- syllabic rabies: wildlife (primarily what we see in us)
sylvatic rabies effects who
- bats
- racoons
- foxes
- skunks
- woodchucks
raccoon out during the day
- rv and distemper
rabies pathogenesis
inoculation from bite of rabid animal -> local replicaiton -> attachment and infection or peripheral nerves at motor end plate -> retrograde spread w/ in axoplasm of peripheral nerves -> spread to spinal cord and brain -> replicate in brain -> centrifugal spread from brain to salivary glands and other tissues -> secretion into saliva and transmission via biting
how does rabies gain access to cns
neurons endocytosis through cell body then gain access to cns then spreads neuron to neuron;
what happens if rabies infects through sensory nerve endings
gets stuck in dorsal root ganglion
rabies gross id
normal appearance brain and spinal cord
rabies histopathology
- mild changes
- cytoplasmic eosinophilic inclusion bodies in neurons of hippocampus and cerebellum- negri
rabies pathology
- mild perivascular cuffing and mononuclear cell infiltrates
- no neuronal loss, see disorganization axon and dendritic connections
- no gross changes
- no histopath
incubation period of rabies
- 14-90 days
- up to 2 years
length incubation period depends on where bitten
phases of rabies
- prodromal phase
- one of two forms (furious rabies or dumb/ paralytic rabies)
prodromal phase
change in temperament (normally friendly animal -> dnt recognize owner, aggressive, normally fearful animal seems friendly)
two forms of second phase or rabies
- furious rabies
- dumb or paralytic rabies
furious rabies signs
- restlessness, nervousness, aggression
- loss fear humans
- hypersalviarion
- hypersensitivity to sound/ light
- hyperesthesia
dumb or paralytic rabies
- depression
- paralysis
- seizures
- coma, resp arrest, and death
- harder to pin this down as rabies, tend to see this is larger animals ie cows and horses
laboratory diagnosis of rabies where require what
- approved labs
- require whole brain
lab diagnostics of rabies tests
- direct immunofluorescence (detect rabies antigen)
- RT-PCR (detect viral rna in brain)
prevention and control of rabies
- animal control programs (cat, dog, ferret)
- vaccination (mandatory dogs, cats, domestic ferrets in nys)
post exposure rabies
- for vac animals need rabies booster w/ in 5 days
- un vac animals: euthanasia or quarantine (6 months at owners expense)
protocol animal bite human
- 10 day mandatory confinement/ observation of animal that bites human
prevention of rabies
- avoid handling wild animals
- screen windows to prevent bat access
- vac at risk individuals
- post exposure prophylaxis
post-exposure prophylaxis rabies
- clean wound w/ soap/ water or iodine solution
- seek medical attention
- post exposure immune globulin
- series of vac over course month
rabies virus type
rhabdoviruses
vesicular stomatitis virus virus type
rhabdoviruses
vesicular stomatitis virus causes what in who
- vesicular dx
- cow, horse, pig
- rarely also in sheep and goats
vesicular stomatitis virus horse significance
- if vesicular dx in horse its not foot and mouth its vsv
vesicular stomatitis virus serotypes
2
- new jersey
- indiana
vesicular stomatitis virus vs foot-and-mouth dx
- clinically indistiguishable
vesicular stomatitis virus transmission
- biting insects
- fomites (via breaks in mucosa)
- doesn’t transmit animal to animal
- no viremia in domestic animals, dx not contagious
- ZOONOTIC
vesicular stomatitis virus seen when
seasonal (bc insect vecor0
vesicular stomatitis virus in us
- endemic in pt of southeaster US occasional outbreaks in south west
- REPORTABLE
vesicular stomatitis virus economic impact
- losses bc culling, dec milk, costs
clinical signs vesicular stomatitis virus
- transient fever
- lameness
- vesicles and erosions (usually in mouth can -> inc salivation, teats, coronary band lesions)
- horses: most severely affected, oral lesions, coronary band lesions
diagnosis vesicular stomatitis virus clinically
- can’t distinguish from other vesicular dxs unless in horses bc the dnt get foot and mouth
- lesions generally restricted to one area of body
lab diagnostics vesicular stomatitis virus
- viral antigen (elisa)
- virus neutralization
- antibody (elisa, paired serum sample)
differential diagnoses vesicular stomatitis virus
- vesicular stomatitis virus
- foot and mouth dx
- swine vesicular dx
- Seneca valley virus
control vesicular stomatitis virus
- control movement of animals
- quarantine infected faciliies
- separate healthy/ died animals
- disinfect milking machines
- milk affected animals last
- control insects
- vac available but not really used
- REPORTABLE
Rabies virus index of suspicion
- maintain high index of suspicion bc you see rarely but its v bad to miss
reoviridea general characteristics
- nonenveloped
- double or tripple layered capsid
- segmented dsRNA genome
- 5 genera of vet importance
transmission orthoreoviruses and rotaviruses
fecal oral
transmission oribiviruses (blue tongue and African horse sickness virus) and coltiviruses
biting insects
transmission aquareoviruses
water
orbiviruses include
blue tongue
African horse sickness virus
orbivirus replciation
replicate in insects and mammals
- this means can overcome mammalian innate and adaptive immune system and insect innate immune system
orbivirus transmission
- blood eating insects
- non-contagious
orbivirus infect what
- prolonged cell associated viremia
- infect and damage endothelial cells -> damage
blue tongue dx spread
- spread by biting midges (no seeums)
blue tongue virus affects who and infects who
- infects ruminants but clinical dx = severe in sheep
blue tongue dx control
- hard to control bc variety of serotypes around
- serotype in Europe = more severe dx than serotype currently in us
economic importance blue tongue us and europe
- us: low virulence serotype blue tongue, greatest impact on cattle industry -> lost money bc loss trade and cost animal testing
- europe- sigificant emergence blue tongue virus -8 in Northern Europe
sheep susceptibility to blue tongue virus + morbidity and mortality
- dx severity varies with serotype and strain of virus
- morbidity = up to 100%
- mortality = up to 50%
cattle and goats blue tongue virus morbidity/ mortality/ dx
- low morbidity - 5%
- clinical dx = rare
deer, antelope, pronghorn blue tongue virus morbidity/ mortality/ dx
- severe dx
- morbidity up to 100%
- mortality 90-100%
Blue tongue virus transmission
- midges (gnats)
- ticks, sheep keds (mechanical)
- mechanical
- general (in semen but unlikely route of transmission)
blue tongue virus lifecycle
- adult female feeds, virus replicates inside insect 4-20 days, then infected adult bites again and if bites susceptible host infects suceptible host, susceptible hosts viremic 2-4 days
- other modes transmission possible but this one via biting midge = most common
blue tongue virus epidemiology
- dx occurs late summer when vector = most numerous
- geo distribution mirror that of insect vector (tropical, subtropical, and temperate zones across the world; if in tropics virus persists year round if there is winter dx disappears in winter then reappears)
blue tongue virus overwintering theories
- prolonged viremia (viremia late fall to spring so infectious for insects in spring)
- transplacental transmission
- persistent infeciton ys T cells
blue tongue virus pathogeneiss
- saliva of biting midge
- local spred
- viral réplication in regional lns
- viremia
- virus réplication in hematopoietic cells and endothelial cells (endothelial ell infection -> clinical signs) ->
1. endothelial damage ->
1a. vascular occlusion -> tissue edema or epithelial sloughing bc loss microvasculature
1b. hemorrhage
2. cell associated viremia (prolonged) -> new vectors become infected by feeding on viremic animal
blue tongue clinical signs
- fever, face, feet
- weight loss
- edema*****
- hyperemia muzzle, face, neck
- rarely cyanotic mucosa (ie blue tongue)
- salivation
- resp (heavy breathing / panting)
- sores tongue, mouth, nostrils
- lamness (if on hard surface)
- aborption, congenital abnormalities (repro)
blue tongue pathology
- edema and hyperemia of mucosa
- petechial hemorrhages
- abrasions or ulcers lips, dental pad, tongue, cheeks
- hemorrhage tunica bee of luminary artery
- pathoneumonoc for blue tongue but see this rarely
blue tongue in us
REPORTABLE
blue tongue immunity
- systemic antibody response -> lifelong protection against infectiong serotype
- lambs born to immun ewes= partially protect by colostral immunoglobulins
- vac (use in rare cases when outbreak hard to keep up bc virus evolves quickly and mult serotypes)
blue tongue control
- vectors control (get rid of place insects breed)
- housing (covered buildings
- > dec insects)
- move to higher altitudes during insect season
blue tongue virus type
reoviruses
African horse sickness virus virus type
reoviruses
African horse sickness virus affects who where
- serious dx horses
- affects donkeys and mules but not as much as horses
- zebras = natural resrvious but are asymptomatic carriers
- not in us
- sub-saharan, central, east, south, africa
African horse sickness transmisison
- very high mortality
African hrose sickness concern
- that dx will spread with inc range vector
african horse sickness forms
- peracute dx
- subacute edematous form
African horse sickness peracute dx signs
- acute fever
- sudden onset resp distress
- terminally spasmodic c+and frothy nasal exudate
- rapid death (30 min - 1-2 hrs)
African horse sickness subacute edematous form
- fever 3-6 days
- edema (supraorbital fossa and eyelids)
- colic
- petechiae under tongue and on conjunctivae
African horse sickness diagnosis
- clinical signs and hx
- lab tests: viral isolation and id, serology, necropsy
- REPORTABLE
- no tx
rotavirus virus type
reoviruses
rotavirus affects who and causes what
- infects all domestic animals
- d+ in intensively reared young animals (neonatal scours)
rotavirus transmission and stablity
- fecal oral transmission
- v stable in environment
rotavirus pathogenesis
- infects mature enterocytes and enteroendocrine cells in proximal ileum, crypt cells = spared
- mature enterocytes = infected at tip; kill apical enterocyte villi which become blunted and loose ability to absorb and get inc fluid and electrolyte loss
- enteroendocrine cells = infected (along with enterocytes) then produce serotonin -> inc mobility and peristalsis of gut
- virus release its own toxin -> secretion cl- ions -> water loss
- epithelial cells stop secreting disaccharide like lactase -> change osmotic conditions -> bacteria overgrowth
- NOT leakage dx bc gut enterocyte tigh junctions remain tight
rota virus clinical features
- affects young animals (1-8 weeks)
- recover rapidly
- stress can worsen dx
rotavirus clinical signs
- white scours or milk scours
- feces may be mucoid
- depression but eating
rota virus tx
- supportive tx
rota virus immunity
- mucosal immunity = protective- IgA
- colostrum = protective for short time
- vac: give to preg cows (modified live) or vac new calf give to unvaccinated dam or that didn’t get colostrum
rota virus control
- housing
- separate dxed and healthy
- hygiene
birnaviridae general characteristics
- non enveloped
- ds rna
- two segments
infectious bursal dx virus what type of virus
birnaviridae
infectious bursal dx virus alt name
gumboro dx
infectious bursal dx virus affects who where
- chickens
- worldwide
infectious bursal dx virus important
- economically important
infectious bursal dx virus infects what
- primarily bursa of Fabricius (pre-b lymphocytes -> acquired B lymphocyte deficiency)
infectious bursal dx virus isolates
- isolates in us = low virulence
- v virulent isolates can -> mortality rates > 50%
infectious bursal dx virus transmission
- fecal oral
- v stable and highly contagious also spread by fomites and insects
- hard to disinfect
infectious bursal dx virus pathogenesis
- infects pre-b cells in bursa of rabricius
- clinical d in chicks 2-6 weeks
- loss b-lymphocytes -> permanent immunosuppression
- most severe immunosuprsson in chicks infected closer to hatch
clinical signs infectious bursal dx virus
- feather ruffling
- trembling/ dehydration
- watery d+
- recovered birds = permeant immunosuppression (inc susceptibility to other viral infections and poor response to vac)
infectious bursal dx virus control
- difficult
- can give oral live attenuated vac to breeders; passive transfer immunity to hatching chick; not fully affective plus possibility of vaccine reversion
- newer vac antibody-coupled ibdv give at 1 day
- once chicks > 8 weeks virus not that big a deal
