Swine Influenza

Swine influenza virus (SIV) is an orthomyxovirus of the influenza A group with hemagglutinating antigen H1 and neuraminidase antigen N1 (ie, H1N1). Recently, new subtypes of SIV have been reported (H3N2, H1N2, and H2N3). Influenza B and C viruses have been isolated from pigs but have not caused the classic disease. The classic type A infection with isolates of mild virulence may favor replication of pseudorabies virus (see Pseudorabies), Haemophilus parasuis (Glässer's disease, see Glasser’s Disease), Actinobacillus pleuropneumoniae (see Pleuropneumonia in Pigs), and Mycoplasma hyopneumoniae (see Mycoplasmal Pneumonia in Pigs), any of which may complicate outbreaks. The mixing of carrier and nonimmune pigs is an important predisposing factor. The virus is unlikely to survive outside living cells for >2 wk except in cold conditions. It is readily inactivated by disinfectants.

In North America, outbreaks are most common in fall or winter, often at the onset of particularly cold weather. In warmer areas of the world, infection may occur at any time. Usually, an outbreak is preceded by one or two individual cases and then spreads rapidly within a herd, mainly by aerosolization and pig-to-pig contact. The virus survives in carrier pigs for up to 3 mo and can be recovered from clinically healthy animals between outbreaks. In antibody-positive herds, outbreaks of infection recur as immunity wanes. Up to 40% of herds may contain antibody-positive pigs. Carrier pigs are usually responsible for the introduction of SIV into previously uninfected herds and countries.

The spectrum of infection ranges from subclinical to acute. In the classic acute form, the virus multiplies in bronchial epithelium within 16 hr of infection and causes focal necrosis of the bronchial epithelium, focal atelectasis, and gross hyperemia of the lungs. Bronchial exudates and widespread atelectasis, grossly appearing as plum-colored lesions affecting individual lobules of apical and intermediate lobes, are seen after 24 hr. The lesions continue to develop until 72 hr after infection, after which the virus becomes more difficult to demonstrate. Losses in reproduction associated with primary outbreaks appear to be secondary, because virus has been recovered only rarely from the fetus.

A classic acute outbreak is characterized by sudden onset and rapid spread through the entire herd, often within 1–3 days. The main signs are depression, fever (to 108°F [42°C]), anorexia, coughing, dyspnea, weakness, prostration, and a mucous discharge from the eyes and nose. Mortality is generally 1%–4%. The overt course of the disease is usually 3–7 days in uncomplicated infections, with clinical recovery of the herd almost as sudden as the onset. However, virus may continue to cycle among pigs when clinical signs are suppressed by immune responses. Some pigs may become chronically affected. In herds that are in good condition, the principal economic loss is from stunting and delay in reaching market weight. Some increase in piglet mortality has been reported, and effects on herd fertility, including abortions in late pregnancy, may follow outbreaks in nonimmune herds.

A presumptive diagnosis can be made on clinical and pathologic findings, but confirmation depends on detection of viral RNA via PCR, molecular sequencing, or demonstration of virus-specific antibody. Virus can be isolated from nasal secretions in the febrile phase or from affected lung tissue in the early acute stage. A retrospective diagnosis can be made by demonstrating a rise in virus-specific antibodies in acute and convalescent serum samples using the hemagglutination inhibition test. Both H3 and H1 subtype antigens should be included. This test is also used for herd surveys. To diagnose uncomplicated influenza infection, conditions such as pasteurellosis, pseudorabies, porcine reproductive and respiratory syndrome, and chlamydial and Haemophilus infections must be excluded.

There is no effective treatment, although antimicrobials may reduce secondary bacterial infections. Expectorants may help relieve signs in severely affected herds. Vaccination and strict import controls are the only specific preventive measures. Good management practices and freedom from stress, particularly due to crowding and dust, help reduce losses. Commercially available killed vaccines that contain both H1N2 and H3N2 subtypes appear to induce a strong protective immune response.