Pleuropneumonia is a severe and contagious respiratory disease, primarily of young pigs (≤6 mo old), although in an initial outbreak, adults also may be affected. It has a sudden onset, short course, and high morbidity and mortality. It occurs worldwide and appears to be increasing in incidence, although some reports suggest that severity is declining in countries where it has been long established.
The causal organism is Actinobacillus pleuropneumoniae. 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.
The pneumonia is usually bilateral. The characteristic lesion is a severe fibrinonecrotic and hemorrhagic pneumonia with accompanying fibrinous pleuritis. Fibrinous pleuritis and pericarditis may be severe. In acute cases, the lungs are dark and swollen and ooze bloody fluid from the cut surface; hemorrhagic, even necrotic, bullae of various sizes may be present. The trachea may contain bloodstained froth. In chronic cases, the lesions are more organized and localized. Extrathoracic lesions are uncommon.
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 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.
Treatment and Control
Rapidity of onset and persistence in infected herds make treatment difficult. Ceftiofur, 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 is an effective means of detecting previously infected herds but may not identify carrier animals.
Last full review/revision March 2012 by Scott A. Dee, DVM, MS, PhD, DACVM