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Veterinary Virology DMP851 > Swine Influenza: Orthomyxoviruses > Flashcards

Swine Influenza: Orthomyxoviruses Flashcards

1
Q

Orthomyxovirses

A

Swine Influenza Virus

Avian influenza virus

Equine influenza virus

Canine influenza virus

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2
Q

Orthomyxoviridae

A
  • 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
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3
Q

Influenza Virus Genome

A

Segmented genome:

8 segments

ssRNA: 14kb

Classified based on hemagglutinin and neuraminidase:

Spike-like proteins that project from the surface, important in pathogenesis

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4
Q

Influenza Virus:

Standardized Nomenclature

A
  • 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)
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5
Q

Influenza Virus:

Clade system

A

clade = group of viruses with common ancestor

Based on genomic sequences

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6
Q

Influenza Virus:

Hemagglutinin

A

Binds to sialic acid recepots on host cells

Virus entry into cells

18 subtypes

Hight rates of mutation

Target of vaccines

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7
Q

Influenza virus:

Neuraminidase

A

Cleaves sialic acid on host cells

Virus release form host cells and penetrateion of mucus

11 subtypes

Oseltamivir (tamiflu): neuraminidase inhibitor

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8
Q

Understanding Influenza infection:

A

Hemagglutinin is the dominant antigen recognized by the immune system:

Antibodies to hemagglutinin will neutralize the virus

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9
Q
A

Hemagglutinin needed for cell entry

Neuraminidase needed for cell release

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10
Q

Genetic Reassortment

A

If two strains of the virus simultaneously infect the same cell

Progeny viruses can be “er-assortants” of the parental viruses genome segments

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11
Q

Genetic Reassortment vs. Subtle point mutations

A

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)

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12
Q

Swine Influenza Virus

A
  • 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
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13
Q

SIV:

Key concepst

A
  • 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
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14
Q

SIV:

Epidemiology

A
  • 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
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15
Q

SIV

Trnsmission

A

primarily by aerosolization and pig-to-pig contact

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16
Q

SIV

Infection

A

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

17
Q

SIV pathogenesis

A

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

18
Q

SIV

Clinical Disease

A
  • 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
19
Q

SIV:

Gross lesions

Lung

A

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

20
Q

SIV:

Gross lesions

Airways

A

necrotizing bronchitis. bronchiolotis

Airways may contain mucopurulent of blood-tinged exudate

21
Q

SIV:

Gross lesions:

Lymph Nodes

A

vairably enlarged and congested

22
Q

SIV:

Microscopic lesions

A

necrotizing bronchiolitis

Bronchiointerstitial pneumonia

23
Q

When to suspect SIV in a herd

A

History of sudden onset severe respiratory illness affecting most animlas, along with typical signs and lesions

24
Q

SIV:

Diagnosis

A
  • Nucleic acid or antigen detection
    • acute phase:
      • nasal swabs, lung tissues
    • VIrus isolation, PCR< sequencing, FA, IHC, ELISA
  • 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
25
Q

SIV:

Treatment and Prevention

A
  • 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
  • Autogenous killed vaccines:
    • commercial PNA vaccine, commercial intranasal live attenuated influenza vaccine
26
Q

SIV:

Immunity

A

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

27
Q

SIV:

Vaccination

A

Cross-protection between subtypes should not be expected with whole-inactivated vaccines

28
Q

SIV:

Control

A
  • 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

Veterinary Virology DMP851 (12 decks)

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