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44 Cards in this Set
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Flaviviridae
-Two genus and thier associated disease: |
Flavivirus: WVN
Pestivirus: BVDV1, 2; Border's dz virus; Classic Swine Fever Virus (Hog Cholera) |
SPP affected:
-WNV: Horse and Birds -BVDV: Ox -Borders: Sheep -Swine Fever: Pig |
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Flaviviridae
-size -characteristics |
icosahedral symmetry (spherical)
50 nm (mid size) lipid envelope indistinct peplomers +ssRNA |
Replication:
5' virion protein-ns proteins 3' cotranslational processing as its being made |
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WNV: major spp affected:
Dead end host Reservoir host |
Causes encephalitis in many species: horse, humans, reptiles, and birds
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Horse, human and other mammals= dead end host
Birds= reservoir host high level of viremia, little/no clinical signs; many spp may be infected but not highly susceptible |
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WNV: Pathological signs (bird vs horse)
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Pathologic changes (birds): cerebral & cerebellar hemorrhage, myocardial necrosis, splenomegaly, enterocolitis
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Pathological changes (horses):
Hemorrhage encephalomyelitis (brainstem and spinal cord); many cases subclinical |
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WNV: Clinical Signs (Dog and cat, horse)
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Pathological signs (dog and cat):
Often asymptomatic; rarely may see fever, depression, m weakness, seizures, paralysis, myocarditis |
Clinical signs for horse:
Fever, CNS signs- ataxia, weakness, m fasciculation, behavior changes, recumbency, death (10-50% mortality rate in horses displaying clinical signs; many surviving horses display residual signs 40%) |
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WNV: DDx
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EEEV, WEEV, EHV-1, RABV, EPM
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WNV should be on the ddx list for any horse displaying acute neurological deficits
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WNV: Diagnosis and control
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Diagnostic tests:
IgM: capture ELISA (serum, CSF)- detects IgM Ab to recombinant WNV Ag PCR: -horse- brain -bird- heart, liver, or brain HI: serum Difficult to grow tissue culture |
Control:
Vaccination 1.Killed, Fort Dodge 2.Recombinant, Merial 3.MLV, Intervet Mosquito control |
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Family: Flaviviridae
Genus: Pestivirus Species and host: |
Bovine viral disrrhea virus 1,2
Borders disease virus Classical swine fever virus (hog cholera) |
ox
sheep pig |
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BVDV:
biotype vs genotype variation |
Biotypes:
Cytopathic-pathological changes in the cell Noncytopathic- no pathological changes in the cell |
Genotypes:
Type 1 & 2 based on RNA sequencing |
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BVDV:
Major forms of the disease (4) |
1.Acute BVDV Infection
-mild, role in BRD complex -fever, leukopenia, +/- diarrhea 2.Reproductive disorders -abortion -cerebellar hypoplasia, blindness, PI |
3.Mucosal dz
-severe dz in PI cattle Erosions, ulcerations of GI, diarrhea, lymphopenia -CP AND NCP -acute or chronic 4.Severe acute BVDV -hemorrhagic dz -type 2 BVDV -NCP OR CP (most NCP) |
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BVDV:
PI calves |
-NCP BVDV
-Cow infected 50-125d of gestation -Post 125d calves will mount an immune response in utero so they possess Ab against BVDV but will not be PI calves |
-some in utero and early post natal deaths
-survives continue to shed BVDV and are poor doers, immunocompromised 2ndary infections, stunted, no Ab response to homologous virus |
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BVDV:
Congenital defects (Depend on the stage of development when infection occurred and type of BVDV) |
Cerebellar hypoplasia
Retinal degeneration/ hypoplasia Optic neuritis Cataracts Skeletal malformations Hypotrichosis Growth Retardation |
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BVDV:
Homologous vs. heterologous challenges |
-homologous: If a ncp cow has a mutation inducing cp then she will have mucosal dz since she cannot produce Ab to her own cp since she is immune to bvdv
-Heterologous: If a ncp cow is exposed to cpBVDV from a different cow then she will have an Ab response. |
-Homologous: If a ncp cow has a mutation resulting in cpBVDV and she comes into contact with another ncp cow, both cows will result in mucosal dz
-PI: If a ncp PI cow reproduces all of her offspring will be ncp PI and also yield ncp PI offspring cascade effect- remove ncp from herd |
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BVDV:
Lesions |
1.Mucosal Dz:
-PI with ncp bvdv -Superinfection with ag similar cp due to mutation, vaccination with MLV, experimental infection Result: -Replication of CP BVDV with absence of IR -Peyers patch necrosis -depletion of GALT -GI ulceration, diarrhea -death |
2.Hemorrhagic Dz:
-Severe acute type 2 BVDV -increased severity of acute infections -most are NCP, but can be CP - thrombocytopenia with systemic hemorrhages -hemorrhagic diarrhea -may mimic mucosal dz -usually in younger calves |
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BVDV:
Diagnostic Tests Control |
DX testing:
Virus isolation ELISA-Ag capture (serum, ear notch) IHC-ear notch (MOST COMMON) PCR(lymphatic, blood, milk, ear) SN- types 1, 2 (serum) |
Control:
-Remove PI animals from herd -Vaccination (MLV, killed, type1,2) -Vaccination may not prevent in utero infections |
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Flaviviridae Pestivrius:
Border disease virus "Hairy shaker disease" Clinical signs Pathogenesis |
Clinical sign of borders:
-Abnormal hair coat -Muscle tremors -abortions, stillbirths, congenital abnormalities -subclinical in immunocompetent adults -mucosal like dz with CP and NCP |
Pathogenesis:
-Similar to BVDV (antigenically distinct) -PI (in utero 70-90) -hypomyelination of the CNS* |
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Flaviviridae Pestivirus:
Classical swine fever (Hog cholera) recognition |
-fever, leukopenia, vomitting, diarrhea
-It replicates in the tonsils -2ndary viremia with disseminated infection (endothelial cells) vasculitis, wide spread hemorrhage |
-similar to african swine fever
-systemic hemorrhage*, tonsil swelling*, hepatitis, infarcs, buttons of GI tract |
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Classical Swine fever:
Three forms |
1. Acute form (highly virulent)
-fever, hemorrhage, hyperemia, cyanosis, ataxia, convulsions, death (10-20d) 2. Chronic form -similar but less severe -dullness, diarrhea, erythema, death >30d 3. Mild form -mild dz with relapses stillbirths, reproductive failure, neonatal death, PI |
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Classical Swine fever:
Transmission |
-Secretions, excretions, semen
-Blood, vehicles, clothes, instruments, needles, uncooked waste food fed to pigs -Transplacental infections=PI pigs |
highly contagious systemic dz
reportable dz* |
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Classical Swine fever:
Ddx Controls |
Ddx:
African swine fever*** Salmonellosis, Erysipelas BVDV |
Controls:
-slaughter of affected pigs -burial or incineration of carcasses -vaccination (MLV and subunit vaccines)- not in U.S. |
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Orthomyxoviridae:
symmetry nucleic acid glycoproteins nomenclature |
symmetry: helical
nucleic acid:segmented RNA into 8 parts glycoproteins:HA and NA enveloped with spikes |
nomenclature:
virus type A,B,C/origin/ strain#/yearisolated (virus subtype) A/canine/FL/43/04 (H3N8)- canine influenza |
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Orthomyxoviridae glycoprotein:
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Hemagglutinin (HA): (1-16 diff ag types) binds to sialic acid (sugar molecule on cell membrane of many cells) residues, fusion of membrane with endosome neutralizing epitopes
-flu Abs from here |
Neuramindase (NA): (1-9 diff ag types) cleaves sialic acid residues, major antigenic determinant, liquifaction of mucus, blocked by oseltamivir (tamiflu)
-cuts nucleic acid so once infect cell can get free to infect next cell |
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Orthomyxoviridae:
Reservoir |
Birds: reservoir to all types
Horse: H3*, H7 Swine: H1, H3*, H5 Cat: H1, H5 Canine: H3* Man: H1, 2, 3, 5 |
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Orthomyxoviridae:
Antivirals |
HA: flu abs
M2: blocked by amantadine NA: blocked by oseltamivir (tamiflu) |
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Orthomyxoviridae:
Activation |
1. Cleavage of HA
-low pathogenic avian strains -restricted to respiratory tract (non aquatic birds) 2. HA binds to sialic acid residues; receptor mediacted endocytosis 3. Influx of H+ into endoxome: conformation changes in HA; fusion protein exposed 4. H+ enters M2 ion channel; unoating of nucleocapsid 5. fusion of viral envelope to endosome; release of RNA 6. RNA to nucleus |
-Trypsin is needed for binding and is only available in the respiratory tract
-H+ ions come into HA to acidify; an acidic environment is advantageous to the virus and is needed to uncoat |
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Orthomyxoviridae:
Capping -function -3 methods to cap viral RNA |
Function of 5' cap:
1. protect mRNA from degradation by ribonucleases 2.pre-mRNA splicing; direct mRNA export from nucleus 3. recognition of mRNA for translation |
3 methods of capping viral RNA
1. Use of cellular capping machinery, most DNA viruses except poxviruses, retroviruses 2.Viral coding fo capping machinery, most ssRNA viruses except ortho 3.Cap snatching (stealing of cap from cellular mRNA) ortho*** |
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Orthomyxoviridae:
genetic variation |
1. Point Mutation
-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 2. Genetic reassortment -swapping of entire gene segments -mixed infection necessary 3. Genetic Recombination -swapping of small regions of gene segments |
Genetic reassortment and recombination in influenzavirus infections; can cause a new virus and/or an endemic virus
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Non-avian Influenza spp:
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Equine
Canine Feline Swine |
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Influenza A virus
(Equine Influenza): Recognition |
-young horses (2-8mo)
-mild dz with high morbidity -replication in respiratory epithelial cells, impaired cilia |
Clinical Signs:
-fever, conjunctivitis, nasal discharge, dry cough, laryngitis, tracheitis, bronchitis, bronchiolitis, may develope 2ndary bacterial pneaumonia |
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Influenza A virus
(Equine Influenza): Transmission |
-Highly contagious with rapid spread via aerosol
-Recovery in 7-10d to 2-3wks |
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Influenza A virus
(Equine Influenza): Dx testing Control |
Dx testing:
-history (acute, rapidly spreading respiratory dz) -HI (serum) -ELISA (nasal secreations, lung tissue) -virus isolation (likely negative once it progresses to bacterial infection) -human influenza A test kits used to detect equine influenza PCR |
Control:
-isolation of new horses -Quarantine of infected horses -Vaccination (H3N8, H7N7); killed and intranasal MLV availiable; short term immunity |
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Influenza A virus
(Canine Influenza): Characterisitics Recognition |
-H3N8 subtype
-adaption of H3N8 from equine -first reported case in racing greyhounds -All dogs susceptible, high morbidity(80%), low mortality (1-5%) |
Clinical Signs:
-fever, nasal discharge, mild to severe respiratory dz, maybe mistaken for kennel cough (tracheobronchitis) -mild form: 80%, low grade fever, persistent, soft, moist (productive) to dry cough (10-21d) -severe form: 20%, high grade fever, increased respiration, pneumonia |
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Influenza A virus
(Canine Influenza): Transmission |
aerosols?
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Influenza A virus
(Canine Influenza): Dx testing Control |
Dx testing:
-HI (serum): acute and convalescent serum (2-3 wks apart) -PCR (nasal swab)- may miss other serotypes Virus Isolation (difficult and often negative -Flu ag ELISA kit |
Control:
-cleaning and disinfection -isolation of dogs with respiratory dz -inactivated vaccine: dec severity and duration of dz, dec viral shedding, only recommended for dogs at high risk |
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Feline influenza:
Recognition |
-H1N1 infection
Clinical signs: -diffuse alveolar damage -death |
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Feline influenza:
Transmission |
Horizontal transmission to sentinel cats
Human to cat transmission |
-no dz in H3N2 inoculated cats
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Influenza A virus
(Swine influenza): Characteristics Outbreaks Subtypes |
-acute contagious repiratory dz in pigs
-explosive outbreaks in the fall, winter (esp. young pigs) -subtype H1N1 (N. America) subtype H3N2 (Europe) |
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Influenza A virus
(Swine influenza): Clinical Signs |
fever, nasal discharge, coughing, dyspnea, high morbidity, rapid recovery in 5-7days
-may develope bronchopneumonia -may progress to interstial pneumonia |
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Influenza A virus
(Swine influenza): Transmission |
Pig to human transmission possible
-H1N1 2009 >18000 deaths (250,000-500,000 annual deaths from flu) |
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Influenza A virus
(Swine influenza): Dx testing Control |
Dx testing:
-history -H1N1 and H3N2 Ab ELISA (serum) -VI (nasal secretions, lung) -HI (serum) |
Control:
management, reduce stress, vaccination (killed, contain H1N1 and H3N2) |
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Influenza A virus
(Avian influenza): Characteristics |
-contagious respiratory and systemic dz primarily affecting chickens, turkeys
-*reportable dz* |
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Influenza A virus
(Avian influenza): LPAI HPAI |
LPAI:
-sneezing, coughing, sinusitis, may be subclnical -dec egg production, low morbidity and mortality |
HPAI:
-severe systemic dz, high mortality (90-100%), mutation from LPAI in poultry H5N1:600 human cases 353 deaths (59%) -hemorrhage and edema, cyanosis of combs, wattles, tracheal, subcutaneous, skeletal m and visceral hemorrhage -involvement of respiratory, digestive, and urogenital systems -CNS involvment in severe cases, sudden death |
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Influenza A virus
(Avian influenza): reservoir |
reservoir:
-migratory waterfowl (esp ducks) -infections in reservoir hosts localized to intestinal tracts -no dz or subclinical enteric infections -virus shed via feces of infected birds -virulence in non-resevoir hosts related to ease of cleavage of HA -risk of mutation from LPAI to HPAI |
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Influenza A virus
(Avian influenza): Dx testing Prevention/Control |
Dx testing:
-clinical signs -AGID (serum) -ELISA -HI (serum) -VI -PCR |
Prevention/Control;
-vaccination (killed and recombinant vaccines) state and or USDA approved -routine dz surveillance -quarantine of affected flocks, depopulation -disinfection of premises |
