Orthomyxoviridae (influenza)

Host

Humans, swine

Disease

Respiratory but mostly subclinical

Distribution

Worldwide

Genome

SS negative-sense RNA, 7 segments

Host

Humans, seals

Disease

Respiratory , moderately severe

Distribution

Woldwide

Genome

SS negative-sense RNA, 8 segments

Hosts

Humans, horses, swine, dogs, cats, poultry, waterfowl, whales, seals

Shape?

Icosahedral, helical

Genome

SS RNA, negative sense, 8 segments

Inactivated easily?

Yes by UV light, disinfectants, proteases, RNAses, lipid solvents

Hemagglutin

Glycoprotein in the viral envelope for viral attachment

Neuraminidase

Glycoprotein in the envelope that is involved in the release of the virus

Reservoir

Waterfowl, shorebirds

Species affected

Wide range of avian and mammalian species

Spread between species

"Jumps" from one species to another

Antigenic shift

-sudden appearance of new subtype in humans
-transfer of new subtype from avian to humans
-reassortment of avian virus with human virus
-introduction of new subtype in immunologically naive human pop

Antigenic drift

-point mutations in RNA genome
-selection pressure by immune stimulation
-replication of mutants that can escape immunity of human pops
-accumulation of point mutations in HA gene

Reinfection

Highly mutable and antigenic variation allows for reinfection of individuals and populations

Etiologic agent

Influenza A

HPAI (highly pathogenicity avian influenza)

-"Fowl plague"
-generalized infection
-H5 and 7 subtypes
-polybasic amino acids at HA cleavage site
-high mortality
-necrosis of multiple organs

LPAI (Low pathogenicity)

GI, resp, repro infections. Closely monitor H5 and 7 subtypes for mutations leading to HPAI

Transmission

Ingestion, inhalation, contact with contaminated fomites, human tracking

Shedding

Feces, resp secretions

Geographic distribution LPAI

Worldwide

Geographic distribution HPAI

Occurs sporadically in outbreaks in countries with integrated poultry industries

Etiologic agent

Influenza A

Enzootic subtypes

H1 and 3

Sporadic subtypes

H2,4,5,7,9

Disease

Upper resp, pneumonia

Host range

Suidae, primarily a disease of commercial growers

Clinical signs

-fever
-anorexia
-lethargy
-resp signs
-occassional abortions
-pneumonia

Clincial considerations

-highly contagious, sudden outbreaks
-low mortality, high morbidity
-fall and winter but can cause infection all year
-no carrier state

Etiologic agent

H3N8 (A2)
H7N7 (A1) — not in circulation

Disease

Upper resp, pneumonia

Host range

Equidae

Transmission

Highly contagious, inhalation, contact with fomites, hands, clothing, instruments

Shedding

Aerosolized resp secretions

Geographic distribution

Not found in australia, iceland, new zealand

Immunity

Short lives, specific to type

Risk factors

-young age
-co-mingling
-no previous infections or vax

Clinical signs

-fever
-resp
-conjuctivitis, ocular discharge
-secondary bacterial infections
-4-8 weeks of recovery

Prevention and control

-quarantine for 4 weeks
-sanitary practice
-vax (NOT inactivated)

Etiologic agent

Influenza A (H3N8, H3N2)

Disease

-hemorrhagic pneumonia
-upper resp "kennel cough"

Host range

Canidae

Transmission

Inhalation, contact w fomites

Shedding

aerosolized resp secretions

Clinical signs

-acute onset
-fever
-coughing 4-8 weeks
-resp sigsn

Prevention/control

-isolation 2 weeks
-sanitation
-inactivated whole-virus vax
-bivalent vax