• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/69

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

69 Cards in this Set

  • Front
  • Back
Orthomyxoviridae genus
Influenza A
Orthomyxoviridae influenzvirus A
H7N7 - horse- noncirc
H3N8 - horse,dog
H1N1, H3N2, H1N2, H3N1, (pig, human)
H5N1 - cat, human
HA =
hemagglutinin
NA -
Neuraminidase
Orthomyxoviridae reservoir
migratory birds
Cats get influenza from
humans
Influenza characteristics
spherical or filamentous
enveloped with spikes
segmented genome
helical symmetry
HA binds to
sialic acid residues causing fusion of membrane with endosome (neutralizing epitopes)
H2 (ion channel)
allows acidification of the neuroprotein to uncoat the RNA. Blocked by amantadine
NA cleaves
sialic acid residues, major antigenic determinant, liquifaction of mucus, blocked by pseltamivir (tamiflu)
Influenza enters the cell via
receptor mediated endocytosis
To be activated, HA must be
cleaved with trypsin and trypsin like proteases in respiratory tract.
Once Ha bind to sialic acid residues, the virus particle is
endocytosed
With influx of H+ via M2 channel,
HA fusion protein exposed
In the nucleus of the cell the viral genome
steal the cap from host RNA, inactivating it and activating viral mRNA.
mechanisms of genetic variation of influenza virus
point mutations
genetic reassortment
genetic recombination
Point mutations are due to
random changes 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 segments
Gentic recombination
swapping of small regions of gene segments, single or mixed infection
Antigenic drift
point mutations, minor changes
antigenic shift
major shift
totally new virus
usually from coinfection by 2 virus' creating new 3 strain
Equine Influenza A diagnosis
History
Hi, ELISA - kit
virus isolation
Test is best 1 - 2 days before sick
Equine Influenza A treatment
rest, minimum of 3 weeks
supportive care
Equine Influenza A control
isolation of new horses
vaccination of H3N8 and H7N7 via killed and intranasal MLV
Influenza A canine subtype
H3N8
H3N8 infected _____ before it infected ______
horses
dogs
Influenza A H3N8 has a high____ and a low ______
morbidity
mortality
fever, nasal discharge, mild to severe respiratory disease in dogs
Influenza A - Canine influenza
H3N8 may be mistaken for
infectious thracheobronchitis ( kennel cough in dogs)
Mild form of H3N8 presents as
low grade fever
persistent soft moist productive to dry cough
Severe form of H3N8
high-grade fever, increased respiration, pneumonia
Canine influenza diagnosis via
HI - serum
PCR - may miss other serot
Virus isolation - difficult
ELISA kit
Canine influenza TX
supportive care
Canine influenza control
cleaning/disinfecting, isolation of dogs with respiratory disease, inactivated vaccine,
Influenza A virus in swine
H1N1 H3N2
Influenza A has explosive outbreaks in the
fall and winter
Influenza A virus in a pig is a ______ disease
acute, contagious, respiratory disease of pigs
Fever, nasal discharge coughing dyspnea, high morbidity, rapid recovery 5 - 7 days in pigs
Influenza A in pigs
Swine influenza may develop
bronchopneumonia
interstitial pneumonia
Diagnosis of Swine flu
History
H1N1, N3N2
virus isolation
HI
Influenza Swine flu Tx
supportive care
Influenza A control
management, reduce stress
vaccination.
Influenza A Avian flu causes
contagious respiratory and systemic disease
Influenza A avian flu infects
chickens and turkey
Influenza A virus avian flu types
Low pathogenic avian flu
High pathogenic avian flu
Low pathogenic avian influenza causes
sneezing, coughing sinusitis, decreased egg production, low morbidity, and mortality
LPAI may be
subclinical
HPAI is also called
fowl plague
HPAI causes
severe systemic disease, high mortality (90 - 100 %). H5N2, H7N1, H5N1 (avian flu)
hemorrhage, and edema, cyanosis of combs and wattles, tracheal subcutaneous skeletal muscle and visceral hemorrhage
HPAI
HPAI involves what body systems?
respiratory, digestive and urogenital systems, CNS
sudden death
Influenza A avian flu reservoir
migratory waterfowl
Influenza A avian flu is shed in
feces
Influenza A reservoir infections in
intestinal tract, no disease or subclinical enteric infections
LPAI may mutate to
HPAI
Influenza A avian virus diagnosis
clinical signs
AGID - govt approved test
ELISA
HI
Influenza A virus avian flu is a
reportable disease
Influenza A virus prevention
vaccination (killed and recombinant vax)
quarantine of affected flocks, depopulation, disinfection of premises
Influenza A is a problem in Asia because of
the close proximity of pigs, poultry and people.
Influenza has its own
Polymerase - 3 different types
Influenza A virus - equine influenza
H3N8
Equine Influenza infects
young horses - 2 - 8 month
Equine Influenza is a
mild disease with high morbidity
Equine Influenza A replication in
respiratory epithelial cells, imparied cilia,
Equine Influenza A clinical signs
fever, conjunctivitis,nasal discharge, dry cough, laryngitis, tracheitis, bronchitits,
Equine Influenza A is highly
contagious with rapid spread via aerosol, recovery in 7 - 10 days to 2 - 3 weeks
Equine Influenza A diagnosis
history, HI
ELISA (Human test)
PCR 1 - 2 days before sick
Equine Influenza A TX
rest, supportive care
Equine Influenza A Control
Isolation of new horses,
VX