Pleuropneumonia in Pigs

The causal organism is Actinobacillus pleuropneumoniae. To date, 15 serotypes have been identified; they vary widely in virulence and significance across countries. Historically, serotypes 1, 5, and 7 have been prevalent in the USA. Transmission is mainly by nose-to-nose contact, and many recovered pigs are carriers. Clinical signs develop within 4–12 hr in experimental infections. Aerosol transmission is limited.

Onset is sudden, and in herds that have not been infected previously, spread is rapid. Some pigs may be found dead without having shown clinical signs. Respiratory distress is severe; there are “thumps,” and sometimes open-mouth breathing with a blood-stained, frothy nasal and oral discharge. Fever up to 107°F (41.5°C), anorexia, and reluctance to move are typical signs.

Although primarily a disease of growing pigs, A pleuropneumoniae infection may be fatal in adults or cause sows to abort. The course of the disease varies from peracute to chronic. Morbidity may reach 50%, and in untreated cases, mortality is high. Survivors generally show reduced growth rates and persistent cough.

Once established in a herd, the disease may be evident only as a cause of reduced growth rate and pleurisy at the abattoir, although acute disease exacerbations may occur. However, severe lesions may not always be accompanied by equally severe clinical signs. Deaths in transit and carcass condemnation may result. Concurrent infection with mycoplasma, pasteurellae, porcine reproductive and respiratory syndrome, or swine influenza virus is common.

An explosive disease onset is suggestive and, when combined with clinical signs and gross lesions, often justifies a tentative diagnosis. Concurrent infections, eg, with pasteurellae, may complicate diagnosis. In herds that have been exposed and have developed at least a degree of immunity, the pattern may be less distinctive. Many serologic tests, including complement fixation and ELISA, have been used to confirm a herd diagnosis or detect carriers, but results are not always straightforward. A definitive diagnosis depends on isolation and identification of A pleuropneumoniae, a gram-negative coccobacillus that requires V factor (NAD) supplementation for growth. A Staphylococcus aureus nurse colony can provide the necessary factor. PCR testing is also available and provides better sensitivity than direct culture.

Rapidity of onset and persistence in infected herds make treatment difficult. Ceftiofur, tilmicosin, tetracyclines, synthetic penicillins, tylosin, and sulfonamides have been used. The first treatment should be parenteral, followed by medication given in water or feed, which also may protect contact pigs.

Because survivors frequently remain carriers, control is difficult, although good results are being claimed for some vaccines. Segregated early weaning, “all-in/all-out” management, reduced stocking rates when possible, and improved ventilation are recommended. In herds free of the disease, replacements should be purchased from herds free of A pleuropneumoniae; if the disease proves difficult to control, herd depopulation and repopulation should be considered. Serologic testing effectively detects previously infected herds but may not identify carrier animals.