Swine Influenza: Orthomyxoviruses Flashcards
Orthomyxovirses
Swine Influenza Virus
Avian influenza virus
Equine influenza virus
Canine influenza virus
Orthomyxoviridae
- Orthomyxo -
- straight mucus
- Single-stranded, negative sense, RNA viruse, enveloped
- Four primary genera
- Influenza A virus
- flu pandemics are influenza A viruses
- Influenza B virus
- Influenza C virus
- Influenza D virus
- Influenza A virus
Influenza Virus Genome
Segmented genome:
8 segments
ssRNA: 14kb
Classified based on hemagglutinin and neuraminidase:
Spike-like proteins that project from the surface, important in pathogenesis
Influenza Virus:
Standardized Nomenclature
- Type / animal of origin / geographic origin / strain number / year of isolation / subtype in parentheses
- Human virus is no animal species given
- Example:
- A/swine/kansas/B4553/2010 (H1N1)
Influenza Virus:
Clade system
clade = group of viruses with common ancestor
Based on genomic sequences
Influenza Virus:
Hemagglutinin
Binds to sialic acid recepots on host cells
Virus entry into cells
18 subtypes
Hight rates of mutation
Target of vaccines
Influenza virus:
Neuraminidase
Cleaves sialic acid on host cells
Virus release form host cells and penetrateion of mucus
11 subtypes
Oseltamivir (tamiflu): neuraminidase inhibitor
Understanding Influenza infection:
Hemagglutinin is the dominant antigen recognized by the immune system:
Antibodies to hemagglutinin will neutralize the virus
Hemagglutinin needed for cell entry
Neuraminidase needed for cell release
Genetic Reassortment
If two strains of the virus simultaneously infect the same cell
Progeny viruses can be “er-assortants” of the parental viruses genome segments
Genetic Reassortment vs. Subtle point mutations
Genetic reassortment allows rapid major changes in the genetic make-up of influenza viruses (Antigenic Shift)
Sublte point mutations and small changes that occur gradually over time (Antigenic drift)
Swine Influenza Virus
- Caused by influenza type A virus
- Classified by 2 proteins:
- hemagglutinin
- Neruaminidase
- Different combinations of H and N proteins create subtypes
- Little or no cross-protection between subtypes
- Pigs are principle hosts
- potential for human infection but relatively rare
- person-to-person transmission typically inefficient
- 2009: pandemic strain of H1N1
- reassortment of NA and Eurasian SIV
- Global spread
- Infected humans, swine, poultry
- Now circulates as seasonal flu virus in humans
- Worldwide distribution
- One of the most importtant causes of acute respiratory disease in pigs
- potential for human infection but relatively rare
SIV:
Key concepst
- SI is an acute, highly contagious, respiratory disease of swine
- SIV is common and widespread in U.S. swine
- Nearly all herds in Midwest seropositive
- Effective vaccination become difficult due to increased viral diversity
- Primary subtypes circulating in swine:
- H1N1
- H1N2
- H3N2
SIV:
Epidemiology
- Outbreaks historically common in fall and winter but can occur year-round and in swine of all ages
- Sudden onset and rapid spread throughout herd
- clinical signs 1-3 days post infection
- Shedding starts 1-2 ddasy post infection and continues f or 5-8 days post infection
- Asymptomatic long-term carrier pigs are rate
- Ab+ herds
- antibody mitigates severity of disease and spread thorughout the herd
- Outbreaks occur when immunity wanes
- Field isolates vary in virulence
- infection ranges form subclinical to acute severe disease
- May depend on co-factors, co-pathogens
SIV
Trnsmission
primarily by aerosolization and pig-to-pig contact
SIV
Infection
SIV gains access by nasopharyngeal route, replicates in the epithelial cells of the nasal mucose, tonsils, trachea and lungs
Epithelium of the bronchi, broncholes and alveoli can be severly compromided due to SIV infection
Influx of neutrophils and other infammatory cells lead ot epithelial cell necrosis and obstruction of airways
Bronchial exudates and widespread atelectasis are seen
SIV pathogenesis
Inflammation and widespread degeneration and necrosis of cells lining the bronchi and bronchioles
Alveolar type 2 pneumocytes can be affected and produce less surfactant
impairs phagocytosis by alveolar macrophages
Inflammatory exudate can block smaller airways, leading to atelectasis, emphysema, and bronchiointerstitail pneumonia
Epithelium usually heals within 5-7 days
SIV
Clinical Disease
- Sudden onset and rapid spread within 1-3 days
- Clinical signs:
- depression, pyrexia, decreased appetitie, deep hacking cough, sneezing, weight loss, huddling, dyspnea, tachypnea, weakness, conjunctivitis, mucoid oculonasal discharge
- Morbidity high: up to 100%
- Mortality low: 1-4%
- Duration short: 3-7 days
- Economic loss:
- reduction growth rates adn increased time to market weight
- Potential for abortions in late pregnancy due to acute infection in sow/gilt
- Severity of infection mitigated by the quantity of hemologous circulating Antibody
- depression, pyrexia, decreased appetitie, deep hacking cough, sneezing, weight loss, huddling, dyspnea, tachypnea, weakness, conjunctivitis, mucoid oculonasal discharge
SIV:
Gross lesions
Lung
cranioventral bronchiointerstital pneumonia
Lobular distribution of congestion, firmness, atelectaiss, emphysema
Lesions typically well-demarcated, consolidatied and purple/red
Lesions tend to be more extensive in apical and cardiac lobes
SIV:
Gross lesions
Airways
necrotizing bronchitis. bronchiolotis
Airways may contain mucopurulent of blood-tinged exudate
SIV:
Gross lesions:
Lymph Nodes
vairably enlarged and congested
SIV:
Microscopic lesions
necrotizing bronchiolitis
Bronchiointerstitial pneumonia
When to suspect SIV in a herd
History of sudden onset severe respiratory illness affecting most animlas, along with typical signs and lesions
SIV:
Diagnosis
- Nucleic acid or antigen detection
- acute phase:
- nasal swabs, lung tissues
- VIrus isolation, PCR< sequencing, FA, IHC, ELISA
- acute phase:
- Antibody
- ELISA
- Hemagglutination inhibition
- paired acute and convalescent titers
- H1 or H3 subtypes antigens
- Virus shedding can be brief: samples should be collected within 24-72 hours of clinical onset
SIV:
Treatment and Prevention
- No effective treatment
- antimicrobials for secondary bacterial infections
- NSAIDs for severly affected pigs
- Vaccination:
- commercial killed vaccines avialable in U.S.
- combinations of H1N1, H1N2, H3N2
- Vaccination of sows/gilts, boars and piglets
- Reduce clinical signs but do not always prevent infection
- commercial killed vaccines avialable in U.S.
- Autogenous killed vaccines:
- commercial PNA vaccine, commercial intranasal live attenuated influenza vaccine
SIV:
Immunity
Maternal Antibodies decrease severity of illness in piglets but can also impair the development of immunity
Colostral antibodies may protect piglets for 5-14 weeks
Potential interference with vaccine efficacy
Vaccines typically given in 2 doses 3-weeks apart
Vaccines give good protection to viruses with homologous Hemagglutinin
SIV:
Vaccination
Cross-protection between subtypes should not be expected with whole-inactivated vaccines
SIV:
Control
- Virus unlikely to survive in environment > 2 weeks
- Readily inactivated by heat/disinfectants
- All in/ all out with cleaning and disinfection facilities
- Strict import controls and biosecurity
- maintain closed herd to avoid introducing infected pigs
- Stabilizing breeding herd by acclimatization or vaccination
- vaccine replacement during isolation
- Isolating clinical animals may reduce transmission among herd
- Management practices and reducing stress
- overcrowding, air quality, reducing dust
- People with influenza-ike illness should avoid contact with pigs
- Determine sequence/subtype of circulating SIV
