Reading...
Play button
Play button
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;
7 Cards in this Set
- Front
- Back
|
Describe the genera features of orthomyxoviridae & nomenclature
|
-16 HA subtypes (H1-H16) and 9 NA subtypes (N1-N9)
-nomenclature for naturally occurring strains which arise by antigenic drift are coded as follows: Type/animal species (omitted if human)/place of isolation/number of isolate/year of isolation (H & N subtype) e.g. A/equi/Prague/1/56 (H7N7) |
|
|
Describe the pathogenesis of influenza
|
-small particle aerosols containing virus generated by coughing, sneezing (& talking)
-virus attaches to cilia of nose, trachea, and bronchi, or direct to alveoli -spread through respiratory tract in 1-3 days -fever and pneumonia coincide with necrosis of epithelial cells -secondary bacterial infection may cause bronchopneumonia |
|
|
Describe the genome of influenza viruses
|
Consists of single stranded negative sense RNA in 8 segments in influen A
-the 8 segments encode the envelope glyproteins HA and NA, two matrix proteins, 2 nonstructural proteins (NS1 and NS2), the nucleoproteins (NP) and components of the RNA transcriptase and replication complex PA, PB1, and PB2 |
|
|
Describe the virion structure
|
-highly pleomorphic, mostly spherical/ovoid
-outer surface consists of a lipid envelope derived from host cells, from which project prominent glycoprotein spikes of 2 types: haemagglutinin (HA) and neuraminidase (NA) -lipid envelope makes the virus liable in environmental conditions -they are sensitive to heat (56 oC for 30 mins) and acid (pH3) and lipid solvents |
|
|
Swine Influenza
-clinical signs -epidemiology -pathology -occurrence in Australia -control |
-causes epidemics of acute respiratory disease in pigs with high morbidity but low mortality
-virus persists and becomes endemic -interspecies transmission of influenza between pigs and people has been continually detected since 1930, occurs quite frequenly ✰CLINICAL SIGNS -if an outbreak occurs, most pigs in a herd succumb simultaneously -animals present with inactivity depression, huddling & are anorexic -respiratory distress, mouth breathing & labored breathing -rhinitis with nasal discharge -fever -mortality is low and <1% -recovery after 5-7 days after first clinical signs -reproductive losses with some H3 viruses -considerable economic losses from weight loss or reduced weight gain ✰EPIDEMIOLOGY -transmitted from pig to pig through droplets and small particle aerosols -outbreaks occur from late autumn to winter, or after the introduction of new swine into susceptible herds ✰PATHOLOGY -lesions are confined to the respiratory tract and are not very specific -mucosa of the respiratory tract is hyperemic and there is excess mucus production -trachea can be filled with froth and some atelectasis and emphysema of cardiac and apical lobes of lungs can be seen -in fatal cases there may be lumbar pneumonia ✰OCCURRENCE IN AUSTRALIA -no cases ✰CONTROL -by strict biosecurity and sometimes vaccination -biosecurity measures such as the "all in- all out" production system -vaccines can be used when exclusion is not possible, but do not prevent infection or shedding -instead their aim is to reduce clinical disease and associated production losses |
|
|
Equine Influenza
-occurrence in Australia -epidemiology -clinical signs -transmission |
-the currently circulating H3N8 virus, was first isolated in 1963 and has largely replaced H7N7
-the H3N8 subtype has undergone some antigenic drift and is endemic in North America and Europe with sporadic outbreaks being reported ✰OCCURRENCE IN AUSTRALIA -only once in NSW & Queensland -EIV outbreak resulted in movement control and suspension of race meeting and had a significan financial impact on the industry -came in because of a breakdown in quarantine and infection procedures at a quarantine facility -AUSVETPLAN was activated which enacted: i) quarantine and movement controls of horses, horse products, and potentially contaminated items to prevent spread of infection ii) decontamination of facilities, equipment and other items to eliminate the spread of the virus from infected animals and premises iii) tracing and surveillance to determine the source and extent of infection iv) an awareness campaign to encourage cooperation by the industry and community and v) vaccination since the disease became widespread after detection -live-vectored canary pox equine influenza vaccine was used to "ring" vaccinate affected areas to prevent spread ✰EPIDEMIOLOGY -highly contagious and spread rapidly throughout studs and stables where horses are congregated together -infected horses excrete the virus in their expired air for up to 8 days after initial infection -no long term carrier state -coughing horses project aerosolised and virus laden droplets -influenze virus can retain infectivity for up to 36 hours and so can be spread on horse floats, grooming equipment and veterinary instruments ✰CLINICAL SIGNS -morbidity rate is very high -incubation of 1-5 days followed by fever to 41 oC -coughing is the most pronounced clinical sign -nasal discharge that is initially serous and later mucous or mucopurulent -affected horses are apathetic, easily fatigued, and lose their appetite -full recovery in 3 weeks if well rested -secondary bacterial infection may occur -weak response to vaccination or vaccination with a poor match to circulating strains can result in subclinical infections with significant virus shedding ✰TRANSMISSION -it is believed non-Thoroughbred horses serve as a major source of transmission, esp in Europe -these horses are less likely to be vaccinated and travel freely around Europe |
|
|
Avian Influenza
-occurrence in Australia -epidemiology -clinical signs -control -vaccination |
-highly lethal disease of poultry
-outbreaks occur most commonly in domestic fowl and turkey -waterbirds and seabirds are also susceptible but infection is subclinical in some cases and can be highly pathogenic in others (eg. HP H5N1) -avian influenza is ubiquitous in wild waterbirds and these are believed to provide a reservoir for emerging pathogenic strains ✩OCCURRENCE IN AUSTRALIA -4 outbreaks -in none of these cases was the source confirmed but it was thought to be wild waterbirds -a "stamping out" policy based on slaughter, disinfection, and movement controls was applied and all outbreaks were eradicated before much spread occurred -eradication was confirmed by serological survey ✩EPIDEMIOLOGY -avian influenza viruses representative of most HA and NA subtypes have been isolated from a wide range of wild waterbird species in well separated locations throughout Australia -several of the species involved have been migratory birds -the potential exists for an avian influenza that is virulent for domestic poultry to emerge at any time -the threat can be minimized by preventing access of wild birds to poultry flocks and preventing faecal contamination by wild birds of poultry feed and water supplies -once it is established, wild birds are no longer needed for spread -infected birds excrete virus in high concentration in their faeces and also in nasal and ocular discharges -the disease generally spreads rapidly in a flock by direct contact, but on occasion spread is erratic -most important means of spread is mechanical by persons with contaminated footwear or clothing, or by dirty poultry crates, utensils, feed trucks, or other fomites ✩CLINICAL SIGNS -hemorrhagic lesions in visceral organs, combs, wattles -highly pathogenic isolates usually H5 and H7 subtypes *Highly pathogenic avian influenza (HPAI) -disease occurs suddenly without any premonitory signs -sudden death -watery diarrhea, excessive thirst |
