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38 Cards in this Set
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Paramyxoviridae:
Morbillivirus genus |
Subfamily Paramyxovirinae
Morbillivirus- Canine Distemper virus Host- dog |
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Paramyxoviridae:
size symmetry fusion protein |
paramyxoviridae:
size- 150-300nm enveloped, spherical helical symmetry -ssRNA |
fusion protein:
-binding of H protein to cellular receptor inducing confirmation activation of F protein -Insertion of fusion peptide into target cell membrane Membrane fusion utilizes: -viral penetration (neutral pH) -cell to cell fusion (synctia formation) |
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Canine Distemer Virus
(genus: morbillivirus): characteristics pathogenesis |
-acute, highly contagious disease of dogs, ferrets, skunk, raccoon
-tropism for epithelium and lymphoid tissue -respiratory and CNS signs typical |
If it becomes systemic can affect: respiratory, ailmentary, or urogenital tracts
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Canine Distemper virus:
clinical signs |
diphasic fever
ocular/ nasal dishcarge leukopenia vomiting, diarrhea pneumonia (bronchointerstitial pneomonia) CNS signs (seizure, chewing gum fits, salivation) Secondary infection due to immunosuppression |
Canine Distemper virus CNS signs:encephalitis, demylination (follows initial recovery), paresis, paralysis, convulsions, twitching, chewing gum fits, addling
old dog encephalitis -years after initial infection, persistence of defective virus |
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Canine Distemper virus:
clinical signs contd footpad in utero |
Clinical signs CDV:
footpad hyperkeratosis, nasal hyperkeratosis, vesicular and pustular dermatitis, delayed response due to viral persistence in skin |
CDV in utero:
enamel hypoplasia and loss, destruction of ameloblast during gestation |
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Canine Distemper virus:
Prognosis Long- term recovery of CDV infected dogs |
1. dogs with GI or respiratory signs: Fiar prognosis with good supportive care may have permanent damage to mucociliary apparatus, secondary infections (neuro signs deveoloope 3 mo after infection)
2. dogs with neuro signs: poor prognosis, neuro damage often permanent |
3.virus shedding may persist up to 3 mo in recovered dogs separate from other dogs for minimum of 4 weeks; puppies, unvaccinated, or imunosuppressed dogs- 3 mo
4.no scientifically documented evidence (for or against) use of NDV vaccine |
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Paramyxoviridae paramyxovirinae
Canine Parainfluenza virus 2: disease (3 causes) clinical signs |
disease:
Contributor to infection tracheobronchitis (kennel cough) canine parainfluenza virus 2 canine adenovirus 2 Bordetella bronchoseptica |
Clinical signs:
-subclinical or mild infection, self limiting -fever, nasal and ocular discharge -harsh nonproductive cough sneezing tonsilitis, pharyngitis trachobronchitis |
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Paramyxoviridae
paramyxovirinae Newcastle disease virus: species affected forms of dz |
species affected: chickens, turkeys, some pet and zoo birds
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Forms of the dz: mild to severe
1. lentogenic strains: low virulence, subclinical or mild respiratory dz, endemic in US, used in MLV vaccines 2. mesogenic strains: moderately virulent <25%mortality 3. velogenic strains: high virulence, severe dz exotic, periodic outbreaks, 90-100% mortality a. viscerotropic-GI hemorrhage b. neurotropic-respiratory and CNS signs -virulence depends on activation of fusion protein by cellular proteases |
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Newcastle disease virus:
clinical signs lesions control |
Lesions: respiratory, GI and CNS signs
clinical signs: respiratory &/or nervous signs drop in egg production diarrhea, hemorrhage periorbital and neck edema, conjunctivitis |
Control: reportable dz
zoonotic for poultry wokers (transitory conjunctivitis, flu-like symptoms) |
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Paramyxoviridae:
paramyxovirinae Bovine parainfluenza virus 3: clnical signs role in BRD complex |
Clinical signs for BPIV3:
uncomplicated infections-> subclinical or mild respiratory dz pathogenesis: viral replication in MPs, respiratory epi, dec local immunity, damage to mucociliary apparatus susceptible to secondary bact pneumonia |
Role in BRD complex:
stress: shipping, sale barn, feedlot, crowding, nutrition bacteria: M. haemolytica, P. multocida, H. somni viruses: BHV-1, BRSV, BVDV, BCoV, BPIV-3 |
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Paramyxoviridae
pneumoviriae Bovine respiratory syncytial virus: Clinical signs |
-subclinical or mild respiratory dz (adult cattle)
-severe interstitial pneumonia (calves <6mo) -contributes to the bovine respiratory disease complex |
Clinical sings:
-fever, dyspnea, cough, open mouth breathing -recovery in 1-2 weeks (most) sever dz, death (2ndary bacterial pneumonia) -related to high percentage of calf pneumonias, most severe dz following initial exposure; may cause severe dz on its own in calves less than 6 mo of age |
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BRSV
(Bovine respiratory synctial virus): lung pathology |
pathological changes: pneumonia, bronchiolitis, emphysema, 2ndary bacterial infection
Characterisitc features: -syncytial cells (bronchiolar epi) -cytoplasmic inclusions |
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Bornaviridae
Bornavirus Avian bornavirus: Proventricular Dilatation Dz Lesion |
Lesion:
Replication in the nucleus*** Intranuclear inclusion in cell culture |
inflammation of myenteric ganglia of upper GI tract
-esophagus, crop, proventriculus, ventriculus, duodenum |
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Avian bornavirus
Proventricular Dilatation Dz: Clinical Signs organs affected |
Clinical signs:
depression, weight loss, crop stasis, regurgitiation, passage of undigested seed, proventricular dilatation or dysfunction CNS signs (ataxia, seizures) death (6-12 mo) |
organs affected:
upper gi tract brain, spinal cord, peripheral n heart smooth m adrenal glands |
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Rhabdoviridae:
2 virion morphology size symmetry |
size: large 180x80 nm
morphology: bullet-shaped, cylindrical; enveloped with peplomers symmetry: helical nucleocapsid -ss RNA intracytoplasmic inclusions *** "Negri bodies"*** |
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Rhabdoviridae:
Rabies virus: Replication |
From virion RNA to *Stop-start codon transcription* translation to viral protein
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Rhabdovirus
Lyssavirus Rabies virus: cytoplasmic budding immune response |
Virus buds from cell membranes:
a. intracytoplasmic membranes (neurons)-little cell desruction (NCP); little immune response; production of Negri bodies in neuron b. plasma membrane (saliva gland) release of virions into saliva |
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Rhabdovirus
Lyssavirus Rabies virus: Most common spp infected -US -TX |
US:
1. racoon 2. skunk 3. bat 4. fox |
TX:
1. Skunk 2. Bat 3. Racoon 4. Fox |
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Rabies virus:
pathogenesis-rabies cycle |
virus replication in neurons of spinal cord>trans synpatic spread to brain (incubate for up to six mo)>viral rep in brain encephalitis>orthograde transport to salivary gland> shed in salivary gland> death within ten days for dog cat or ferret OR viral entry via bite wound> viral replication into nerve ending of next animal and cycle continues
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Rabies virus:incubation period
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typically 3-8 wks, but can be up six months
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Rabies virus:
phases and associated clinical signs |
*Prodromal phase- change in temperament (2-3d)
*Furious phase (2-4d)- aggressive behavior, restlessness, hypersensitivity to stimuli, hypersalivation, paralysis of hypoglossal n, pharyngeal m, m spasms, inability to drink *Paraltic (dumb) phase (2-4d)- seizures, coma, death |
clinical dz: furious and paralytic phases
-Also seen with rabies: hyperesthetic, over sensative to stimulus |
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Rabies virus:
pathological changes/ lesions |
encephalitis, perivascular- most severe in dogs, mild in ruminants
myelitis, hemorrhage- brainstem and cervical spinal cord, horse, ox presence of negri bodies in neurons (cytoplamsmic inclusions) |
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Rabies virus:
Diagnosis |
1. Direct IFA of whole brain tissue, ship on ice dont freeze, negative test may report unsatisfactory or inconclusive
2. monoclonal Ab or PCR analysis of positive isolates -TX dept of state health services -Laboratory services section austin tx |
-testing for Ag
-test brainstem because rabies tends to harbor there, texas wants both sides of brain |
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Rhabdoviridae
Vesiculovirus: Vesicular stomatitis virus: spp affected |
spp affected:
-cattle, horse, pig (sheep, goats) |
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Vesicualr stomatitis virus:
lesion clinical signs |
lesion: buds from plasma membrane-> cell lysis (inhibition of RNA transcription)
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clinical signs:
-blisters/ ulcers-mouth, lips, teat, feet -pain, salivation, slobbering, lameness (~2wks) -susceptible to secondary bacterial infections *reportable dz* |
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VSV
(Vesicular Stomatitis Virus): source |
source: tends to occur along riverways; endemic in central america and northern s. america; begin in spring along US Mexico border, spread north along river ways
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VSV:
transmission |
arthropods (sandflies, blackflies), fomites, direct contact
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VSV vs FMD
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-FMD did not infect horses whereas VSV does
-VSV more mild, death is rare in cattle and horses -sporadic in herd, morbidity lower -small percentage of animals with lesion at more than one site -no heart lesions -less severe in young animals, most cases in adults -stabled animals usually no affected, less flies |
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VSV:
immunity control |
TX and CTRL:
-seperate infected animals and healthy animals -stable animals -no mvmt from infected premise until 30d after last lesion healed -control insects -disinfection of premises -vaccination (efficacy known) multiple serotypes, no cross immunity |
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Coronaviridae:
replication size symmetry virion morphology |
Replication of coronaviridae:
Nidovirales (corona, arteri) +ssRNA enveloped nested set of subgenomic mRNA (*discontinuous transcription*) |
symmetry: helical w/ nucleocapsid
80-120nm large large peplomers (20nm) Morphology: crown |
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Coronaviridae
Coronavirus: TGEV (Transmissible gastroenteritis virus): (host=pig) age affected, clinical signs lesion, ddx |
Age affected: piglets <3wks
Clinical signs: vomiting, diarrhea, dehydration, bowl distension w/ yellow undigested milk) |
lesion: infection of enterocyes
-short blunted villi, fusion of villi, altered Na+ transport, malabsorption, maldigestion, loss of lactase and disaccharidases-> watery diarrhea, dehydration, death Ddx:E. coli, coccidiosis, rotavirus, porcine epidemic diarrhea virus |
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PRCoV (Porcine Respiratory Coronavirus):
origin of virus, lesion clinical signs |
origin of virus: Nonenteropathogenic deletion mutant of TGEV
lesion:tropism for repiratory epi, alveolar MPs *** |
clinical signs:
-most infections are subclinical -transient cough (young pigs), interstitial pneumonia in assocation with other viruses (PRRSV) |
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PRCoV (Porcine respiratory coronavirus):
difference with TGEV diagnosis and cross reactivity |
PRCoV vs TGEV and DX:
-high Ab titers to coronavirus with absence of enteric dz -coronavirus FA pos in lungs and neg in intestines -competitive ELISA (differentiates b/w the two) |
cross reactivity:
-cross reacts with serology tests for TGEV -reduced incidence of TGEV in Europe following outbreaks of PRCoV provides immunization against TGEV |
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Canine Coronavirus:
clinical signs lesion |
Clinical signs:
-mild enteritis -most severe in young puppies, asymptomatic in older dogs -vomiting, diarrhea, dehydration -transmissible to cats (asymptomatic) Lesion: fusion, atrophy of intestinal wall -not a severe dz but can cause diarrhea |
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FECV
(Feline Enteric Coronavirus): clinical signs lesions serologic testing |
clinical signs:
-ubiquitous -mild enteritis, diarrhea, vomitting in kittens (6-12wks) -subclinical infections in older cats -infection limited to GI, shed in feces -Ag similar to FIPV source of FIPV deletion mutation Lesion: fusion, atrophy of intestinal villi |
serologic testing:
-serologic tests do not differentiate b/w FECV and FIPV) -dont differentiate b/w exposure and dz -useful for catteries, multi cat households ( ELISA, IFA) |
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FIPV
(Feline Infectious Peritonitis Virus): origin, morbidity vs mortality clinical signs |
origin: dz results from deletion mutation from FECV
morbidity=5% mortality=95% |
clinical signs:
fever, depression, emaciation, ascites, dyspnea, anterior uveitis, CNS signs, hyperproteinemia |
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FIPV:
lesions organs infected |
lesions (pathological changes):
pyogranulomatous inflammation, vasculitis, perivasculitis, dry or wet form- straw red fluid, fibrin, protein; related to CMI (weak CMI=wet, partial CMI=dry) -may develope CNS and ocular dz |
organs infected: GI, heart more rare, lungs, lymph organs
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FIPV:
Dx Ab-dependent enhancement vaccination control |
Dx: clinical signs, necropsy, serologic testing of limited value (cross reactivity with FECV), unable to differ b/w previous exposure and dz, usefull for catteries ELISA, IFA
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Vaccination: intranasal MLV vaccine, temp sensative
Ab-dependent: since infect MP Ab bring dz to MP where they can live so act as a vehicle for the virus so vaccination(Ab) can acutally help the virus replicate and survive control: -early weaning and isolation of endemic households, disinfection, isolation of sero+ cats, admission of sero- cats |
