rhabdoviridae Flashcards
rhabdoviridae morphology
visions enveloped with large spikes bullet shaped, helically coiled cylindrical nucleocapsid
rhabdoviridae general proteins
L protein, G protein, N protein, P protein, M protein, single molecule linear - sense ssRNA, cytoplasmic replication, mature through budding of plasma membrane, can be cytopathoic or noncytopathic forms
L protein Large protein
RNA dependent RNA polymerase (transcriptase)
G protein Glycoprotein
envelope spikes
N protein Nucleoprotein
associates with RNA to form the viral nucleocapsid
P protein Phosphoprotein
mediates binding of L to nucleocapsid
M protein Matrix protein
associates with the viral nucleocapsid and lipid envelope
rhabdo classification
genus: ephemerovirus-bovine ephemeral fever
genus: vesiculovirus-vesicular stomatitis
genus: lyssavirus-rabies
lyssavirus- rabies
caused by genotype 1, carribean islands, japan, singapore, new zealand, low risk, but worldwide distribution
host species for rabies
high risk-cats, cattle
moderate risk-dogs, sheep, goats, horses, monkeys, humans
all warm blooded susceptible
rabies transmission
bite or scratch, virus in saliva less often, sometime aerosol, some even from transplants of organs
epidemiology of rabies
sylvatic cycle with vampire bats in central and south america
foxes in europe, coyotes in NA, jackals africa
this cycle most common in NA
urban cycle of rabies
dogs main reservoir africa asia south and central america; many herbivores are dead end hosts -cattle sheep goats and horses
rabies transmission involving bats
many specie harbor it, asymptomatic usually, can develop paresis or paralysis, may sometimes show aggression, insectivore bats common in NA,
vampire bats in mexico and central america, fruit bats in australia
rabies transmission involving skunks
most important in USA, most cases of cattle rabies, along with raccoons on the east coast
rabies path
- intramuscular inoculation, can enter peripheral nerves or in non-nervous tissue until reach high concentration
- the G protein binds to axons terminals of peripheral nerve fibers through lipoprotein receptors like Ach and enter nerves
- shorter incubation for more highly innervated regions
4 bites to face have greatest risk
uncommon routes rabies
intranasal-trigeminal nerves
spread of rabies
furious form replicates in limbic system, dumb or paralytic form is CNS spread, can move to salivary glands (hypersalivation)
pathology and immunology
inflamed brain, functional lesions over structural.
both hum moral and cell mediated immunity undetected during spread of virus, no MHC proteins, noncytopathic infection, little antigen released but CSF has small amount of antibodies
incubation of rabies
depends on strain, site of bite, and degree of innervation, (closer to the brain is shorter), phases include prodromal, acute excitative (furious), and paralytic/endstage ( dumb)
**survival is rare
prodromal period
shedding of virus and change in temperature
furious form
mad dog syndrome, animal nervous, irritable, aggressive movements, posture change, dilated pupils, lose fear of everything, develop hydrophobia
more common in dogs and cats
paralytic form
encephalitis progresses, fury leads to paralysis and ataxia, seizures, death within 2-14 days
characteristic of bovine rabies
bellowing tail (elevated), salivation
characteristic of equine rabies
dysphagia and salivation, posterior paralysis
canine rabies furious form
growling
canine paralytic phase
ptyalism, depression, paralysis, sternal recumbency with torticollis
diagnosis of rabies
direct FAT to look for rabies antigen, recommended by WHO, look for negri bodies in cytology (only 75% show inclusions), RT-PCR, virus isolation in mice intracerebral inncoluation
Direct fluorescent antibody test
negative-shows no fluorescence
positive-shows fluorescence
rabies control
quarantine in rabies free countries for 6 months, in endemic countries-vaccinate dogs and cats.
preexposure- vaccinate at 3mo and once a year after
postexposure-revaccinate immediately and keep under owner’s control for 45 days
wildlife use bait vaccine*
vesicular stomatitis (VS)
caused by group of anti genetically related but distinct viruses
host-cattle pigs and horses, sometimes humans and sheep and goats
serotypes-indiana and new jersey (most virulent)
VS distribution
occurs primarily in the Americas and certain areas of the Carribbean
VS transmission
enters through breaks in the skin, contaminated milking machine, ingestion of fomites, arthropods (black flies, sand flies, leaf hoppers)
VS Path
enters through broken mucosa/ski, common in mucous membrane of the oral cavity and the skin, fluid filled vesicles form, extensive ulceration, entire epithelium of the tongue or teat sloughed, does not usually become systemic and viremic
VS clinical signs
excessive salivation, fever, lameness, vesicles on tongue, ulcers, anorexia, more vesicular lesions in swine, humans have self limiting influenza like symptoms 3-5 days
VS in cows
ruptured tongue vesicles, almost complete detachment of epithelial surface
VS Dx
indistinguishable clinically from other vesicular diseases like foot and mouth, yet horses have only one vesicular Dx (VS)
VS is reportable**
Bovine Ephemeral fever
genus: Ephemerovirus
host-water buffalo, cattle
never reported in NA
arthropod borne Cullicoides and mosquitos
Bovine Ephemeral virus path
3 day sickness, poorly understood, virus in buffy coat of blood, early neutrophilia with high level of immature neutrophils (left shift), there is an increase in plasma fibrinogen and a significant decrease in plasma calcium
Bovine Ephemeral Virus clinical features
polyerositis affecting joints, pleural and peritoneal surfaces, influx of neutrophils
fever, salivation, nasal discharge, lameness, may lay recumbent
bovine ephemeral virus Dx
isolation of virus is difficult, can be attempted by inoculation of infected buffy coat cells into culture from A. albopictus
