Age affected: All ages, human risk.
Causes: Swine (SIv), avian and human influenza viruses.
Effects: Fever, inappetence, sneezing, coughing, low mortality with most viruses.
Swine influenza is caused by influenza A virus, an orthomyxovirus with an RNA and protein core and surface spikes bearing haemagglutinating (H) and neuraminidase (N) antigens. It can be grown in embryonated eggs or on a number of porcine cell lines. Influenza viruses are sensitive to heat, drying, detergents and disinfectants. A number of different strains exist and are described by their H and N antigen combinations.
The virus is very variable and is constantly changing its surface proteins. Classical swine influenza is associated with influenza virus A HIN1, and different strains of H1N1 virus occur in Europe and many other parts of the world. Some strains can cause more severe disease in pigs, and some are associated with human infection.
In many European countries, Japan and other South East Asian countries H3N2 also causes disease. Many H3N2 isolates from Europe are closely related antigenically to A/7/Port Chalmers/1/73, a human strain that appears to have persisted in pigs. The virus enters the respiratory tract and multiplies rapidly within cells of the bronchial lining until at 24 hours post-infection most cells are infected and mucoid pus is present in the bronchioles. Infection has largely disappeared by day 9. Infection strips the bronchial lining to stop secretions being cleared, giving rise to pneumonia and allows other respiratory pathogens to invade.
Influenza viruses spread by snout to snout contact, droplet infection and aerosol from pig to pig within a pen or within an airspace, and from contaminated drinkers, feeders and toys. The virus persists longer in cool damp conditions, and longest in cool slurry, but dies out in the environment in warm dry conditions.
Maternal immunity may protect pigs from disease until 4 months of age, but may not prevent colonisation. Recovered pigs may be carriers of the virus and be responsible for spreading the infection to naïve animals. Spread from farm to farm is usually be means of carrier pigs, but aerosol infections occur, particularly in pigs with access to the open air or those housed outside. Influenza viruses can be introduced to pig units by humans and by birds.
The incubation period is 1-2 days and there is rapid, virtually 100% involvement of all susceptible animals in a non-immune herd. Affected animals are apathetic, will not rise, have a reddened skin, inappetence and fever (to 41.8°C, 107°F). Coughing occurs commonly and may be sufficiently severe for pigs to appear to vomit mucus. Sneezing and difficulty in breathing are accompanied by reddened eyes and conjunctival discharge. Loss of condition rapidly becomes apparent. Recovery usually occurs suddenly at 5-7 days after the onset and very few pigs die (usually fewer than 1%).
Growing pigs may reach slaughter up to 14 days later than expected. Piglets may develop disease at 2-5 days of age and adults kept in cold conditions may develop the clinical signs to a greater extent. In some herd infection may be completely sub clinical and only be detected by blood tests for antibody. Outbreaks may end quickly or continue in finishing pigs with new cases for up to 7 months.
In atypical outbreaks only a few animals develop acute signs, others are scarcely affected and the disease spreads slowly. Influenza may be followed 3 days to 3 weeks later by abortions in sows in the second half of pregnancy. Loss of condition may reduce the fertility of sows at the heat following clinical disease and the fertility of boars may be affected by a reduction in sperm numbers caused by fever during the disease.
Clinical signs of a rapidly-spreading respiratory disease affecting all pigs in a non-immune herd suggests that the disease is influenza. The dramatic illness with coughing, sneezing and fever and failure to rise or eat of affected sows is almost unmistakable. The disease is less easily identifiable in herds which are partially immune as coughing, sneezing fever and inappetence may only occur in individuals as their maternal immunity wanes.
Diagnosis is confirmed by a rise in antibody in paired serum samples taken 3-4 weeks apart. Antibodies can be detected using the haemagglutination inhibition (HI) test and ELISA tests. The virus involved in the outbreak gives best results, so new variants may be hard to detect. Virus isolation from nasal or tonisllar swabs is possible if samples are taken within 2-5 days of the onset of clinical signs. Virus may be detected microscopically by the Polymerase Chain Reaction (RTPCR) for viral nucleic acid.
Sharply demarcated purple-red pneumonic lesions are present in the apical and cardiac lobes of the lung in affected pigs and may occur in the other lobes. They become greyish and depressed as they age. Mucus and pus are present in the bronchi and the mucosae (linings) are congested. Necrosis may be seen in some severe infections. Virus may be detected microscopically using fluorescent antibody to N1N1 and H3N2, immunoperoxidase, or by Polymerase Chain Reaction (RTPCR) methods for viral nucleic acid. The lesions are identifiable at slaughter in some cases and are included in lung scoring for disease monitoring.
There is no treatment for swine influenza. Secondary infection with bacteria can be treated by injection with an antimicrobial as food and water intake is erratic during acute disease. Affected animals should have access to water and piglets with affected mothers should be provided with supplementary feeding.
Effects on reproductive performance can be minimised by purchasing semen to supplement boars, which may have had fever, and by serving sows when body condition has improved Spread of the disease may be reduced by preventing contact and by disinfection. Control in infected herds is by vaccination. Adjuvanted, killed vaccines are available to protect against both clinical disease and loss of production. They usually contain H1N1 and H3N2 viruses to protect against the most common strains and are updated with new variants as they appear in a region.
Isolation of seronegative herds and purchase of seronegative stock can protect against introduction of disease; mainly by the introduction of infected pigs which can carry the virus for up to 12 weeks after infection. Wind, birds and infected workers may all introduce the disease, so isolation cannot provide complete protection. Total eradication from enzootically-infected herds must be by depopulation and restocking.
H1N1 strains of pandemic influenza may infect humans in contact with pigs and vice versa, but meat from infected herds does not transmit the disease.