Swine influenza is an acute, highly contagious, respiratory disease that results from infection with type A influenza virus. Field isolates of variable virulence exist, and clinical manifestation may be determined by secondary organisms. Pigs are the principal hosts of classic swine influenza virus. (Human infections have been reported, but porcine strains of influenza A do not appear to easily spread in the human population. However, deaths have occurred in immunocompromised people.) In 2009 a pandemic strain of H1N1 influenza A virus spread globally. It infected people, swine, and poultry, as well as a small number of dogs, cats, and other animals. The disease in swine occurs commonly in the midwestern USA (and occasionally in other states), Mexico, Canada, South America, Europe (including the UK, Sweden, and Italy), Kenya, China, Japan, Taiwan, and other parts of eastern Asia.
Swine influenze virus (SIV) is an orthomyxovirus of the influenza A group with hemagglutinating antigen H1 and neura-minidase 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 (see
glässer's disease, see Glässer's Disease), Actinobacillus pleuropneumoniae (see Respiratory Diseases of Pigs: Pleuropneumonia in Pigs), and Mycoplasma hyopneumoniae (see Respiratory Diseases of Pigs: 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.
Transmission and Epidemiology
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 1 or 2 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 normal 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, seen grossly as plum-colored lesions affecting individual lobules of apical and intermediate lobes, occur 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.
In uncomplicated infections, the lesions usually are confined to the chest cavity. The pneumonic areas are clearly demarcated, collapsed, and purplish red. They may be distributed throughout the lungs but tend to be more extensive and confluent ventrally. Nonpneumonic areas are pale and emphysematous. The airways contain a copious mucopurulent exudate, and the bronchial and mediastinal lymph nodes are edematous but rarely congested. There may be severe pulmonary edema, especially of interlobular septae, or a serous or serofibrinous pleuritis. Histologically, the lesions, when fully developed, are primarily those of an exudative bronchiolitis with some interstitial pneumonia.
A presumptive diagnosis can be made on clinical and pathologic findings, but confirmation depends on isolation of the virus 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 eliminated.
Treatment and Control
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.
Last full review/revision March 2012 by Scott A. Dee, DVM, MS, PhD, DACVM