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VTPB 911 Vir test 2

questions for exam 2

what genus & family is west nile virus? genus: flavivirus; family: flavivirus
what genus & family is BVDV? genus: pestivirus; family: flavivirus
what genus & family is border disease virus? genus: pestivirus; family: flavivirus
what genus & family is classical swine fever virus? genus: pestivirus; family: flavivirus
flavivirus: enveloped or not? enveloped
flavivirus: symmetry icosahedral
flavivirus: size 50 nm
flavivirus: structure? tightly adherend lipid envelope; indistinct peplomers
flavivirus: group? (+)ssRNA
flavivirus: transcription/translation? cotranslational processing (cleavage as it is being made); make virion (structural proteins) first!
west nile virus: genus flavivirus
west nile virus: basic disease? encephalitis
west nile virus: disease cycle? mosquito-bird (birds can be reservoirs); dead-end hosts: horse, human, other mammals; similar to togavirus
west nile virus: what species of birds are highly susceptible? crows, raptors; house sparrow is important in disseminating the virus & has a low incidence of disease (is a carrier)
west nile virus: pathologic changes in birds cerebral & cerebellar hemorrhage; myocardial necrosis; splenomegaly; enterocolitis
west nile virus: pathologic changes in horses hemorrhagic encephalomyelitis (brainstem, spinal cord); many cases are subclinical
west nile virus: clinical signs in horses fever; non-specific CNS sings (ataxia, weakness, muscle fasciculations, behavior changes, recumbent, death); 10-50% mortality rate among horses with clinical signs, avg 30%; 40% of survivors have residual clinical signs
west nile virus: clinical signs in dogs/cats often asymptomatic; low incidence; fever, depression; muscle weakness, spasms; seizures, paralysis (CNS signs); myocarditis
what disease should you suspect if an animal has neurologic & cardiac signs? west nile virus
what species are susceptible to natural/experimental infection with west nile virus? cattle, goat, sheep; dog, cat; alpaca, llama; rabbit, deer, wolf, mountain goat, alligator, gray squirrel, chipmunk, bat, skunk, black bear, crocodile, seal
how many cases of human WNV were in texas in 2011? 26 cases, 2 deaths
only state with no reported human WNV in 2011? maine
west nile virus: differential diagnoses in a horse? EEEV, WEEV, EHV-1, RABV, EPM (neurologic signs point to these diseases)
west nile virus: diagnosis? IgM capture ELISA (serum, CSF) - detects IgM Ab to recombinant WNV Ag (standard); also: PCR (horse - brain, bird - heart, liver, brain) or HI (serum); difficult to grow virus in tissue culture
west nile virus: control vaccination (killed, recombinant, or modified live); mosquito control
bovine viral diarrhea virus: genus? pestivirus
bovine viral diarrhea virus: tissue culture properties? cytopathic & noncytopathic biotypes
bovine viral diarrhea virus: persistent infections? follows in utero infection at 50-125 days
bovine viral diarrhea virus: acute BVDV infection generally mild disease; role in bovine resp disease complex; fever (decreased immune system), leukopenia, diarrhea; noncytopathic or cytopathic virus (most NCP)
bovine viral diarrhea virus: reproductive disorders, congenital defects abortions, cerebellar hypoplasia, blindness (retinal degeneration/hypoplasia; optic neuritis; cataracts), skeletal malformation; hypotrichosis; growth retardation; incoordination; keratitis; persis. infec; outcome dependent on time of in utero infection
bovine viral diarrhea virus: mucosal disease severe disease in PI cattle; erosions, ulcerations in GI tract, diarrhea, lymphopenia; NCP & CP virus! peyer's patch necrosis, depletion of gut-assoc lymphoid tissue; GI ulcers, diarrhea, death; acute (die 1-2 days) or chronic (months); similar to MCF
bovine viral diarrhea virus: severe acute BVD hemorrhagic disease; Type 2 BVDV; NCP or CP (mostly NCP); young animals; increased severity of acute infections; thrombocytopenia w/systemic hemorrhages; hemorrhagic diarrhea; may mimic mucosal disease
4 types of BVDV acute BVDV infection; reproductive disorders/congenital defects; mucosal disease (acute or chronic); severe acute BVD / hemorrhagic disease
bovine viral diarrhea virus: healthy calves? if infected after 150 days of pregnancy
bovine viral diarrhea virus: homologous/heterologous challenges? homologous: ncp + cp (same strain) = death; heterologous: ncp + cp (different strain) = Ab response & recovery
bovine viral diarrhea virus: persistent infections continually shed BVDV; poor dooers, secondary infections (immunosuppression); stunted growth; may appear completely normal; no Ab response to homologous virus; PI dams will always produce PI calves
bovine viral diarrhea virus: how does mucosal disease happen? PI with NCP, superinfection with antigenically similar CP (mutation, vaccination w/MLV vaccine, experimental infection) = replication of CP with absence of immune response
bovine viral diarrhea virus: diagnosis virus isolation (whole blood; mucosal/nasal swab); ELISA Ag capture (serum, ear notch); immunohistochem (ear notch); PCR (lymph tissue, blood, milk, ear notch); SN types 1, 2 (serum)
bovine viral diarrhea virus: control removal of PI animals; vaccination (MLV, killed, type 1, 2); vaccination may not prevent in utero infections
Border disease virus similar to BVDV (antigenically distinct); persistent infections (in utero @ 70-90 days); abnormal hair coat, m tremors (hypomyelination of CNS), abortion/stillbirth/congenital abnormalities; subclin infections in immunocompotent adults
border disease virus: genus genus: pestivirus
border disease virus: alternative name hairy shaker disease
classical swine fever virus: alternate name hog cholera
classical swine fever virus: genus pestivirus
classical swine fever virus: basic pathogenicity highly contagious systemic disease of pigs; reportable; fever, leukemia, vomiting, diarrhea; replicate in tonsils, LNN; secondary viremia with disseminated infection (endothelial cells, MN cells), vasculitis, hemorrhage
classical swine fever virus: acute form highly virulent; fever, hemorrhage, hyperemia, cyanosis, ataxia, convulsions, death (10-20 days)
classical swine fever virus: chronic form similar to acute form, but less severe; dullness, diarrhea, erythema, death (>30 days)
classical swine fever virus: mild form mild disease with relapses; stillbirths, reproductive failure, neonatal death; persistent infections
classical swine fever virus: endemic? asia, central/south america; parts of europe, africa
classical swine fever virus: transmission secretions, excretions, semen, blood; vehicles, clothes, instruments, needles, uncooked waste food fed to pigs; transplacental infections -> persistent infections
classical swine fever virus: Ddx african swine fever; salmonellosis, erysipelas; BVD
classical swine fever virus: diagnosis PCR (NVSL), immunofluorescence, virus isolation; lymphoid tissue or kidney
classical swine fever virus: control slaughter affected pigs; burial/incineration of carcasses; vaccination (MLV & subunit vaccines) - not in US
cross-species transmission of pestiviruses BVDV-1, BVDV-2 cattle, sheep; BDV-1,2,3 sheep, cattle, goats, pigs; CSFV pigs only, not in US; sheep spread to cattle; wildlife spread to domestics
seroprevalence of BDV in sheep 63% of herds; 30% of sheep; rare but endemic in US - may infect pigs, may be mistaken for CSFV - some PCR tests may not differentiate
coronaviridae: symmetry helical
coronaviridae: envelope? enveloped
arteriviridae? symmetry icosahedral
arteriviridae: enveloped? enveloped
coronaviridae: group (+)ssRNA
coronaviridae: transcription nested set of subgenomic mRNAs (discontinuous transcription); genomic RNA -> complementary RNA (-) -> genomic RNA (+) -> subgenomic mRNAs -> viral proteins; stop transcription where the next starts (no duplicates)
coronaviridae: size 80-220 nm (big)
coronaviridae: shape helical nucleocapsid
coronaviridae: peplomers? large (20 nm) (glycoproteins)
transmissible gastroenteritis virus: who is affected? young pigs <3 weeks
transmissible gastroenteritis virus: general signs vomiting, diarrhea, dehydration; bowel distended with yellow undigested milk
transmissible gastroenteritis virus: transmission fecal-oral
transmissible gastroenteritis virus: pathogenesis infection of enterocytes: short blunted villi (villous atrophy), fusion of villi, altered Na+ transport; malabsorption/maldigestion; loss of lactse & disaccharidases; watery diarrhea, dehydration, death
transmissible gastroenteritis virus: diagnosis sudden onset of severe diarrhea in suckling pigs; severe villous atrophy of small intestine
transmissible gastroenteritis virus: Ddx E. coli; coccidiosis; rotavirus (porcine epidemic diarrhea virus; not in US)
transmissible gastroenteritis virus: treatment supportive care; prevent dehydration, starvation, acidosis
transmissible gastroenteritis virus: control vaccination results variable (pregnant sows); planned infections of pregnant sows (ground intestine, feces)
Porcine respiratory coronavirus: similar to what? mimics TGEV (transmissible gastroenteritis virus) by serology; nonenteropathogenic deletion mutant of TGEV
Porcine respiratory coronavirus: tropism for what cells? respiratory epithelium; alveolar macrophages
Porcine respiratory coronavirus: clinical signs mild; most infections are subclinical; transient cough (young pigs); interstital pneumonia in association with other viruses (ie PRRSV) (like porcine circovirus, etc)
Porcine respiratory coronavirus: diagnosis high Ab titers to coronavirus in absence of enteric disease; coronavirus FA+ lungs, FA- intestine; competitive ELISA (differentiate PRCoV & TGEV); cross-reacts with serology tests for TGEV
TGEV abroad reduced incidence of TGEV in EUrope following outbreaks of PRCoV; PRCoV provides immunization against TGEV - Ab's against TGEV without getting the disease; TGEV-free countries require TGEV & PRCoV negative imports
canine coronavirus: clinical signs mild enteritis, most severe in young puppes, asymptomatic in older dogs; vomiting, diarrhea, dehydration; transmissible to cats (asymptomatic); not lethal
canine coronavirus: pathological changes fusion, atrophy of intestinal villi
canine coronavirus: diagnosis immunofluorescence, EM
canine coronavirus: prevention sanitation, vaccination (inactivated)
Feline enteric coronavirus: clinical signs mild enteritis, diarrhea, vomiting in kittens 6-12wks; subclin infections in older cats; infection limited to GI tract, shed in feces; antigenically similar to FIPV; source of FIPV (deletion mutant)
Feline enteric coronavirus: occurence ubiquitous in environment
Feline enteric coronavirus: diagnosis serologic tests do not differentiate between previous exposure & disease, don't differentiate between FIPV & feline enteric coronavirus; serologic screening useful for catteries, multi-cat households (ELISA, IFA)
Feline enteric coronavirus: pathologic changes fusion, atrophy of intestinal villi
Feline enteric coronavirus: prevention sanitation, minimize exposure to infected cats & feces
feline infectious peritonitis virus: occurence domestic & wild cats affected (lion, cheetah, serval); higher incidence in young cats (6mo-2yr), multi-cat households
feline infectious peritonitis virus: transmission fecal-oral
feline infectious peritonitis virus: morbidity/mortality <5% morbidity; >95% mortality
feline infectious peritonitis virus: cause of disease deletion mutation of enteric FCoV; high level monocyte-associated viremia; activation of monocytes/macrophages; replicate in macrophages, which carries it to other parts of body
feline infectious peritonitis virus: clinical signs fever, depression, emaciation; ascites, dyspnea; *anterior uveitis (inflamm of choroid & iris), *CNS signs; hyperproteinemia; fluid buildup anywhere in body - fluid is thick & viscous
feline infectious peritonitis virus: pathologic changes pyogranulomatous inflammation (neutrophils & macrophages); vasculitis, perivasculitis; dry (noneffusive) or wet (effusive) form - straw-red fluid, fibrin, protein; related to CMI response (partial CMI - dry; weak CMI - wet, more severe vasculitis)
feline infectious peritonitis virus: Ab-dependent enhancement of disease low CMI & good humoral immune response = worse disease; virus is pulled into macrophages & survive, cell can't get rid of it
feline infectious peritonitis virus: diagnosis clinical signs, necropsy; serologic testing of limited value (cross-reactive with enteric coronaviruses); unable to differentiate between previous exposure & disease; useful for catteries, multi-cat households (ELISA, IFA)
feline infectious peritonitis virus: vaccination intranasal MLV vaccine, temperature sensitive; consider risk of Ab-dependent enhancement
feline infectious peritonitis virus: control early weaning & isolation in endemic households; disinfection, isolation of seropositive cats, admission of seronegative cats
What does the H in H#N# regarding influenza refer to? HA; hemagglutinin (1-16); binds to sialic acid residues; fusion of membrane with endosome; neutralizing epitopes; 2 parts: HA1 & HA2, combine into HA0, but must be cleaved to cause infection
What does the N in H#N# regarding influenza refer to? NA; neuroaminidase (1-9); cleaves sialic acid residues (sialic acid = sugar on cell membranes) so it can invade another cell; major antigenic determinant; liquefaction of mucous; blocked by oseltamivir (tamiflu)
Influenza reservoir? migratory waterfowl (ducks, geese) ;infections in GI tract, virus shed in feces; lots of seasonal outbreaks because of recombination
what HA subtypes of influenza A are humans susceptible to? H1, H2, H3, H5
what HA subtypes of influenza A are pigs susceptible to? H1, H3, H5
what HA subtypes of influenza A are dogs susceptible to? H3
what HA subtypes of influenza A are catssusceptible to? H1, H5
what HA subtypes of influenza A are horses susceptible to? H3, H7
what HA subtypes of influenza A are birds susceptible to? H1-H16
what is the nomenclature of influenza? virus type (A, B, or C) / origin / strain number / year isolated (virus subtype)
influenza: shape nucleic acid is spherical or filamentous
influenza: size 80-120 nm
influenza: envelope? enveloped wtih spikes (HA, NA)
influenza: genome segmented (8)
influenza: symmetry helical: elongated; not icosahedral
influenza: function of matrix increases stability; gives envelope shape
influenza: function of M2 ion channel takes up H ions to acidify & uncoat virus
influenza: : cleavage of HA extracellular low pathogenic avian strains, mammalian strains: cleavage site has changed; restricted to respiratory tract (mammals, non-aquatic birds); instead of trypsin can be cleaved by other proteases
Avian influenza virus: low pathogenic strains HA cleaved by trypsin-like proteases; located in upper & lower respiratory tract; viral replication localized to resp tract; if it can be cleaved by diff't protease than trypsin it can affect other body systems (trypsin is restricted to resp tract)
avian influenza virus: high pathogenic strains altered HA (insertions, alterations at cleavage site); cleavage by systemic proteases (plasmin); systemic replication of virus; damage to vital organs (spleen, liver, lung, kidney)
influenza: cellular invasion process cleave HA, HA binds to sialic acid residue, receptot-med endocyt; H+ influx into endosome, HA conformational change, fusion protein exposed; H+ enters M2 ion channel, uncoat nucleocapsid; fusion of viral envelope to endosome, release mRNA; RNA to nucleus
function of 5' cap on eukaryotic mRNA protect mRNA from degradation by ribonucleases; pre-mRNA splicing, direct mRNA export from nucleus; recognition of mRNA for translation; uncapped mRNA is detected as non-self & triggers antiviral immune response (interferons)
capping of viral mRNA use cellular machinery (DNA viruses minus poxvirus; retrovirus); viral coding of capping machinery (ssRNA, minus orthomyxo); cap snatching (stealing cap from cellular mRNA) (orthomyxo)
mechanism for cap snatching cleave cellular capped mRNA, capped frag serves as primer for viral mRNA synth; polymerase binds to cap from host mRNA, cuts it off & attaches it to viral RNA
point mutations random change in single nucleotide; due to lack of proofreading of RNA polymerase; multiple point mutations needed for new strain; passage through multiple hosts necessary
genetic reassortment swapping of entire gene segements; mixed infectoin necessary; classic example: pig that gets human & avian flu at the same time
genetic recombination swappign of small regions of gene segments; most important in pandemics
mechanisms of genetic variation of influenza virus point mutations, genetic reassortment, genetic recombination
equine influenza: who is affected young horses 2-6 months
equine influenza: replication is where respiratory epithelial cells, impaired cilia
equine influenza: clinical signs mild disease, high morbidity; fever, conjunctivitis, nasal discharge, dry cough; laryngitis, tracheitis, bronchitis, bronchiolitis; may develop secondary bacterial pneumonia
equine influenza: transmission? highly contagious with rapid spread via aerosol
equine influenza: length of infection recovery in 7-10 days to 2-3 weeks
equine influenza: diagnosis history (acute, rapidly spreading respiratory disease); HI (serum); ELISA (nasal secretions, lung tissue); virus isolation (likely negative once progresses to bacterial infection); human influenza A test kits used to detect equine influenza; PCR
equine influenza: treatment rest (3 weeks minimum); supportive care
equine influenza: control isolation of new horses, quarantine of infected horses; vaccination (H3N8 & H7N7) - killed & intranasal MLV (temp. sensitive), short-term immunity
canine influenza: subtype? H3N8; adaptation of H3N8 equine influenza to dogs
canine influenza: first cases? racing greyhounds; hemorrhagic pneumonia, acute death
canine influenza: morbidity/mortality all dogs susceptible; high morbidity (80%), low mortality (1-5%)
canine influenza: clinical signs fever, nasal d/c; mild to severe resp disease; mistaken for infectious tracheobronch (kennel cough); mild form (80%) low grade fever, persistent/moist/productive to dry cough (10-21 days); severe form (20%) high-grade fever, increased resp, pneumonia
canine influenza: diagnosis *HI (serum) acute & convalescent serum (2-3 weeks apart); PCR (nasal swab) - may miss other serotypes; virus isolation (difficult, often negative); flu antigen ELISA kit
canine influenza: treatment supportive care
canine influenza: control cleaning & disinfection; isolate dogs with respiratory disease; inactivated vaccine - decreased severity/duration, decreased viral shedding, only recommended for dogs at high risk
feline influenza fatal H5N1 infections in domestic cats & zoo felids fed virus-infected chickens; diffuse alveolar damage, death, horizontal transmission to sentinel cats, human to cat transmission; opportunity for adaptation to mammals? role of cats in spread of H5N1?
swine influenza: when are there outbreaks fall, winter; especially in young pigs
swine influenza: subtype H1N1 (n america), H3N2 (europe)
swine influenza: clinical signs acute, contaigous, respiratory disease of pigs; fever, nasal d/c, cough, dyspnea; high morbidity, recovery in 5-7 days, may develop bronchopneumonia, may progress to interstitial pneumonia
swine influenza: diagnosis history; H1N1 & H3N2 Ab ELISA (serum); virus isolation (nasal secretions, lung); HI (serum)
swine influenza: treatment supportive care
swine influenza: control management, reduce stress; vaccination (killed, contain H1N1 & H3N2)
avian influenza: who does it affect contagious respiratory & systemic disease primarily affecting chickens, turkeys
avian influenza: low pathogenic (LPAI) clinical signs sneezing, coughing, sinusitis, may be subclinical; decreased egg production, low morbidity & mortality; endemic?
avian influenza: high pathogenic (HPAI) clinical signs severe systemic disease, high mortality (90-100%); mutation from LPAI in poultry; hemorrhage, edema, cyanosis of combs, wattles; tracheal, SQ, skeletal m & visceral hemorrhage; respiratory, digestive & urogenital systems; CNS involvement, sudden death
H5N1 and humans H5N1 (asia, europe, near east, africa): human cases/deaths (600 human cases, 353 deaths - 59%)
avian influenza: LPAI & HPAI ducks & geese are main carriers because of migration; ducks & geese bring in LPAI & mutates to HPAI in chickens
avian influenza: Ddx infectious laryngeal tracheitis; herpes (- comb/wattle symptoms)
avian influenza: reservoir migratory waterfowl (esp ducks); infections in reservoir hosts localized to intestinal tract; no disease or subclinical enteric infections; virus shed in feces
avian influenza: virulence in non-reservoir hosts related to ease of cleavage of HA
avian influenza: diagnosis clinical signs; AGID (serum) basic screening test; ELISA (serum); HI (serum); virus isolation (embryonated chicken eggs); PCR; reportable!!
avian influenza: prevention/control vaccination (killed & recombinant vaccines) (state/USDA approval to use); routine disease surveillance; quarantine affected flocks, depopulation; disinfect premises; get rid of low path so it doesn't mutate; US prb because of high density
influenza & pigs pigs serve as mixing vessel
why does flu like asia? pigs, humans, birds in close proximity
Paramyxoviridae: genome? monopartitie
paramyxoviridae: group (-)ssRNA
paramyxoviridae: envelope? enveloped
paramyxoviridae: symmetry helical
filoviridae: genome monopartite
filoviridae: group (-)ssRNA
filoviridae: envelope? enveloped
filoviridae: symmetry helical
bornaviridae: genome monopartite
bornaviridae: group (-)ssRNA
bornaviridae: envelope enveloped
bornaviridae: symmetry icosahedral
rhabdoviridae: genome monopartite
rhabdoviridae: group (-)ssRNA
rhabdoviridae: envelope enveloped
rhabdoviridae: symmetry helical
genus & family of canine distemper virus? genus: morbillivirus; family: paramyxoviridae
paramyxoviridae: size 150-300 nm (big)
paramyxoviridae: shape spherical, large peplomers (8-12 nm)
paramyxoviridae: components of envelopell membrane hemagglutinin, hemagglutinin-neuraminidase,(some species only have N, both H & N or neither) glycoprotein, fusion protein (so membranes can fuse), matrix, phosphoprotein (on nucleocapside, not envelope)
paramyxoviridae: steps in membrane fusion H protein binds to cell receptor; conformational activation of F protein; insert fusion peptide into target cell membrane; infected cell fuses with uninfected cells->decrease form group-> syncytium cell; fusion used in viral penetration, cell-cellfusion
membrane fusion & pH paramyxoviridae: neutral pH; influenza: needs H+ ions
paramyxoviridae: replication in cytoplasm; attachment via H, HN, or G; cleavage of F-> fusion with cell membrane (neutral pH); viral transcription, replication; glycoprotein patches in membrane; exit via budding; uses stop-start transcription (poly-A tail at end of each segment)
canine distemper virus: who is affected acute, highly contagious disease of dogs, ferrets, skunk, raccoon, bears, lions, etc
canine distemper virus: what cell types does it like tropism for epithelium & lymphoid tissue
canine distemper virus: most common systems affected respiratory & CNS signs typical
canine distemper virus: pathogenesis resp epith-> local lymphoid tiss(1wkPI)->systemic lymph(1-2wksPI)-> [humoral/cellular immune response(2-3wks)-> recovery] OR [resp, alimentary, urogen tracts(2-3wksPI) -> clinical signs -> (recovery OR subacute encephalitis OR death)] (2-12wks)
canine distemper virus: clinical signs diphasic fever; ocular & nasal discharge, leukopenia, vomiting, diarrhea, pneumonia, CNS signs (encephalitis, demyelination following initial recovery; paresis, paralysis, convulsions, twitching, chewing-gum fits, paddling); hemorr, inflamm
canine distemper virus: secondary infections? yes, due to immunosuppression
canine distemper virus: old dog encephalitis years after initial infection; persistence of defective virus
canine distemper virus: effects on footpads foodpad hyperkeratosis (hardpad disease); nasal hyperkeratosis; vesicular & pustular dermatitis (abdomen); delayed response due to viral persistence in skin
canine distemper virus: in utero infection enamel hypoplasia & loss; destruction of ameloblasts during gestation;
canine distemper virus: diagnosis history: unvaccinated dog with fever, respiratory disease, CNS signs; *immunofluorescence (conjunctival scrapings, buffy coat, affected lung tissue), serology (IgM (IFA), ELISA), PCR (CSF, swab, tissue, blood), histopath (interstitial pneumonia, syncytia)
canine distemper virus: long-term recovery of infected dogs with GI or respiratory signs fair prognosis with good supportive care; may have permanent damage to mucociliary apparatus; increased susceptibility to respiratory infections; neurological signs may develop up to 3 months after infection
canine distemper virus: long-term recovery of infected dogs with neurological signs poor prognosis; neurological damage often permanent
canine distemper virus: shedding virus shedding may persist up to 3 months in recovered dogs; separate from other dogs for a minimum of 4 weeks; puppies, unvaccinated, or immunosuppressed dogs: 3 months
canine distemper virus: vaccination no evidence for or against use of new caste disease virus vaccine
canine parainfluenza virus 2: clinical signs subclinical or mild infection, self-limiting; fever, nasal & ocular discharge; harsh nonproductive cough; sneezing; tonsilitis, pharyngitis; tracheobronchitis
infectious tracheobronchitis - pathogens canine parainfluenza virus 2; canine adenovirus 2; bordetella bronchiseptica; "kennel cough"
canine parainfluenza virus 2: transmission airborne secretions; nose-to-nose contact; fomites (dishes, hands, etc)
canine parainfluenza virus 2: vaccination combination vaccines available; <6 months prior to boarding, showing
avian paramyxovirus 1: other name newcastle disease virus
avian paramyxovirus 1: systems affected respiratory, CNS, GI
avian paramyxovirus 1: species affected chickens, turkeys, some pet & zoo birds
avian paramyxovirus 1: 3 strains lentogenic (mild); mesogenic (moderate); velogenic (high virulence); most will be lentogenic or velogenic
avian paramyxovirus 1: lentogenic strains low virulence, subclinical or mild respiratory disease; endemic in US; used in MLV vaccines
avian paramyxovirus 1: mesogenic strains moderately virulent; <25% mortality
avian paramyxovirus 1: velogenic strains reportable! high virulence, severe disease; exotic, periodic outbreaks; 90-100% mortality (viscerotropic velogenic - GI hemorrhage; neurotropic velogenic: resp & CNS disease)
avian paramyxovirus 1: what is virulence dependent on? activation of fusion protein by cellular proteases
avian paramyxovirus 1: clinical diagnosis respiratory and/or nervous signs; drop in egg production; diarrhea, hemorrhage; periorbital & neck edema, conjunctivitis
avian paramyxovirus 1: zoonotic? zoonotic risk for poultry workers (transitory conjunctivitis, flu-like symptoms)
avian diseases causing tracheal hemorrhages all are reportable! avian influenza, infectious laryngotracheitis, newcastle
causes of bovine respiratory disease complex (shipping fever, enzootic pneumonia) stress: shipping, sale barn, feedlot, crowding, nutrition; bacteria: m haemolytica, p multocida, h somni; viruses: BHV-1, BRSV (bovine resp syncytial virus), BVDV, BCoV, BPIV-3 (bovine parainfluenza virus 3)
bovine parainfluenza virus 3: uncomplicated infections result in...? subclinical or mild respiratory disease
bovine parainfluenza virus 3: pathogenesis viral replication in alveolar macrophages, respiratory epith; decreased local immunity; damage to mucociliary apparatus; secondary bacterial pneumonia (what kills animal); neutrophils in airways
bovine parainfluenza virus 3: vaccination combination vaccines (BPIV-3, BHV-1, BVDV, BRSV)
Bovine respiratory syncytial virus: who is affected? respiratory disease of cattle, sheep, goats; subclinical or mild in adults; severe interstitial pneumonia in calves <6 mo's; contributes to bovine respiratory disease complex
Bovine respiratory syncytial virus: clinical signs fever, dyspnea, cough, open-mouth breathing; recovery 1-2 weeks (most cases); severe disease, death if secondary bacterial pneumonia; related to high % of calf pneumonias; most severe disease following initial exposure
Bovine respiratory syncytial virus: pathological changes pneumonia, bronchiolitis; emphysema; secondary bacterial infection; allows air to escape from alveoli
Bovine respiratory syncytial virus: characteristic features syncytial cells (bronchiolar epithelium); cytoplasmic inclusions
Bovine respiratory syncytial virus: treatment/control antibiotics to control secondary bacterial infections; MLV & killed vaccines available
avian bornavirus: who does it affect? psittacine birds
avian bornavirus: size 100-130 nm diameter
avian bornavirus: symmetry icosahedral symmetry; spherical
avian bornavirus: envelope? enveloped, with surface glycoprotein spikes (attachment, fusion)
avian bornavirus: group (-)ssRNA
avian bornavirus: where does virus replicate? nucleus
Proventricular dilatation disease: other name? macaw wasting disease
Proventricular dilatation disease: clinical signs depression, weight loss; crop stasis, regurgitation, passage of undigested seeds; proventricular dilatation or dysfunction; CNS signs (ataxia, seizures); Death (6-12 months)
Proventricular dilatation disease: effect on upper GI tract inflammation of myenteric ganglia & nerves of upper GI tract: esophagus, crop, proventriculus, ventriculus, duodenum
Proventricular dilatation disease: organs affected upper GI tract; brain, spinal cord, peripheral nerves; heart; smooth muscle; adrenal glands
rhabdoviridae: size 180 X 180 nm
rhabdoviridae: shape bullet-shaped; cylindrical (very different)
rhabdoviridae: envelope? yes, with peplomers
rhabdoviridae: symmetry helical nucleocapsid
rhabdoviridae: group (-)ssRNA
rhabdoviridae: what are negri bodies? intracytoplasmic inclusions
rhabdoviridae: transcription/translation stop-start transcription; poly-A tail at the end of each segment
rabies virus: escape from host cell? buds from cell membranes; intracytoplasmic membranes (neurons): little cell destruction (noncytopathic), little immune response, production of negri bodies in neurons; plasma membranes (salivary glands): release of virions into saliva
rabies virus: where are raccoons a problem/ eastern US
rabies virus: where are skunks a problem? midwest, texas, north US, pennsylvania, california
rabies virus: where are foxes a problem? texas, alaska, new mexico
rabies virus: time span incubation period (3-8 weeks, but >6 months possible); prodromal phase: change in temperament (2-3 days); furious phase (2-4 days); paralytic (dumb) phase (2-4 days)
rabies virus: furious phase aggressive behavior; restlesness, hypersensitivity to stimuli; hypersalivation, paralysis of hypoglossal nerve, pharyngeal muscles; muscle spasms, inability to drink; possible to skip furious phase & go straight to paralytic
rabies virus: paralytic (dumb) phase seizures, coma, death
rabies virus: pathologic changes encephalitis, perivascular (most severe in dog, mild in ruminants); myelitis, hemorrhage (brainstem & cervical spinal cord; horse, ox); presence of negri bodies in neurons (intracytoplasmic inclusions); hyperesthesia is another clinical sign
rabies virus: diagnosis direct immunofluorescence assay of whole brain tissue (ship on ice, don't freeze, send whole brain, negative test may be reported inconclusive/unsatisfactory); monoclonal Ab & PCR analysis of + isolates; texas department of state health services
Vesicular stomatitis virus: who is affected? cattle, horses, pigs (sheep, goats)
Vesicular stomatitis virus: escape from cell? buds from plasma membrane -> cell lysis (inhibition of RNA transcription)
Vesicular stomatitis virus: clinical signs blisters/ulcers - mouth, lips, teats, feet; pain, salivation, slobbering, lameness (2 weeks); tends to show up in just 1 organ system (FMD is in multiple)
Vesicular stomatitis virus: reinfection? susceptible to reinfection OR secondary bacterial infections
Vesicular stomatitis virus: transmission arthropods (sandflies, blackflies), fomites, direct contact
Vesicular stomatitis virus: relation to FMDV? reportable! can mimic FMDV, but is milder, deaths rare in cattle & horses
Vesicular stomatitis virus: zoonotic? transmissible to humans (flu-like symptoms)
vesicular diseases & species they infect FMD: ox, sheep, pig; VS: ox, sheep, pig, horse; SVD: pig; VE: pig (from eating sea lions)
differences between VS and FMD VS: horses affected, sporadic in herd, morbidity lower; small % of animals with lesions at more than one site; no heart lesions; less severe in yougn animals, most cases in adults; stabled animals usually not affected
Vesicular stomatitis virus: treatment, control separate infected & healthy animals; stable animals; no movement from infected premises until 30 days after last lesion healed; control insects; disinfection of premises; vaccination (efficacy unknown); don't slaughter like you do with FMD
Vesicular stomatitis virus: serotypes multiple serotypes; no cross-immunity; NJ & indiana serotypes predominate
Vesicular stomatitis virus: when do infections occur most? late summer, early fall
Vesicular stomatitis virus: where is it endemic? central america, northern south america; outbreaks every 10 years in US (begin in early spring along US-Mexico border & spread along riverways - insects possibly responsible)
Created by: shelbell8389



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