Porcine pleuropneumonia is a severe respiratory infection caused by Actinobacillus pleuropneumoniae. Clinical signs include fever, anorexia, reluctance to move, respiratory distress, and sudden death. Diagnosis is confirmed by bacterial culture. Affected animals may be treated with antimicrobials. Because of elimination programs at the breeding stock level, pleuropneumonia is rarely encountered in today's contemporary confinement swine production systems.
Porcine pleuropneumonia is a severe and contagious respiratory disease in pigs, primarily pigs ≤ 6 months old; in an initial outbreak, however, adults also can be affected. The disease has a sudden onset, short course, and high morbidity and mortality rates.
Etiology of Porcine Pleuropneumonia
The causative organism of porcine pleuropneumonia is Actinobacillus pleuropneumoniae. It is recognized as part of the porcine respiratory disease complex. Concurrent mycoplasma infection, pneumonic pasteurellosis, porcine reproductive and respiratory syndrome (PRRS), or influenza A virus infection is common.
Historically, serotypes 1, 5, and 7 of A pleuropneumoniae have been prevalent in the US. Transmission is mainly by nose-to-nose contact, and many recovered pigs are carriers. Clinical signs develop within 4–12 hours in experimental infections. Aerosol transmission is limited.
Clinical Findings of Porcine Pleuropneumonia
The onset of porcine pleuropneumonia is sudden, and in swine herds that have not been infected previously, spread is rapid. Some pigs are found dead without having shown clinical signs. Respiratory distress is severe; visible, spasmodic, or jerky contractions of the abdominal muscles (“thumps”) are typical. Sometimes, open-mouthed breathing with a blood-stained, frothy nasal and oral discharge is observed. Fever up to 41.5°C (107°F), anorexia, and reluctance to move are typical signs.
Although primarily a disease of growing pigs, pleuropneumonia can be fatal in adults or cause sows to abort. The course of the disease varies from peracute to chronic. The morbidity rate can reach 50%, and in untreated cases, the mortality rate is high. Survivors generally show decreased growth rates and persistent cough.
Once established in a swine herd, pleuropneumonia might be evident only as a cause of decreased growth rate and pleurisy at the abattoir, but acute disease exacerbations can occur. However, severe lesions are not always accompanied by equally severe clinical signs. Deaths in transit and carcass condemnation can result.
Lesions of Porcine Pleuropneumonia
Porcine pleuropneumonia is usually bilateral. The characteristic lesion is severe fibrinonecrotic and hemorrhagic pneumonia with accompanying fibrinous pleuritis. Fibrinous pleuritis and pericarditis can be severe (see ).
Necropsy photograph showing severe fibrinous pleuritis and necrotic and hemorrhagic pneumonia in the lung of a pig infected with Actinobacillus pleuropneumoniae.
Courtesy of Dr. Mike Rahe.
In acute cases of pleuropneumonia in pigs, the lungs are dark and swollen, and they ooze bloody fluid from the cut surface (see ); hemorrhagic, even necrotic, bullae of various sizes can be present. The trachea might contain bloodstained froth.
Necropsy photographs of lung tissue from pigs infected with Actinobacillus pleuropneumoniae. A. Seven days after infection, fibrin, adhesions, and abscesses are evident. B. This cut section from a different pig shows signs of severe fibrinonecrotic and hemorrhagic pneumonia, along with fibrinous pleuritis.
A courtesy of Dr. Bruce Lawhorn. B courtesy of Dr. Alyona Michael.
In chronic pleuropneumonia cases, the lesions are more organized and localized. Extrathoracic lesions are uncommon.
Diagnosis of Porcine Pleuropneumonia
Clinical signs
Serological testing
Bacterial culture
PCR assay
A peracute disease onset suggests porcine pleuropneumonia and, when combined with clinical signs and gross lesions, often justifies a tentative diagnosis. Concurrent infections (eg, with pasteurellae) can complicate diagnosis. In swine herds that have been exposed and have developed at least some immunity, the pattern can be less distinctive.
Many serological tests, including complement fixation and ELISA, have been used to confirm a herd diagnosis of pleuropneumonia or to detect carriers; however, the results are not always straightforward. A definitive diagnosis depends on isolation and identification of A pleuropneumoniae, a gram-negative coccobacillus that requires V factor (nicotinamide adenine dinucleotide) supplementation for growth in culture. A Staphylococcus aureus nurse colony can provide the necessary factor.
PCR assay for pleuropneumonia is also available and provides better sensitivity than direct culture.
Treatment and Control of Porcine Pleuropneumonia
Injectable antimicrobials
Good management practices
The rapidity of onset and persistence of porcine pleuropneumonia in infected swine herds make treatment difficult. Ceftiofur, tilmicosin, tetracyclines, synthetic penicillins, tylosin, and sulfonamides have been used. The first treatment should be parenteral, followed by administration in water or feed, which can also protect contact pigs.
Segregated early weaning, all-in all-out management, decreased stocking rates when possible, and improved ventilation are recommended for prevention of porcine pleuropneumonia. In herds free of the disease, replacements should be purchased from herds free of A pleuropneumoniae. If the disease is difficult to control, herd depopulation and repopulation should be considered.
Because of elimination programs at the breeding stock level, pleuropneumonia is rarely encountered in contemporary confinement swine production systems.
Commercial vaccines against A pleuropneumoniae are available, but clinical observations indicate minimal benefit.
Key Points
Actinobacillus pleuropneumoniae causes severe respiratory disease in pigs.
Because vaccination and medication provide little benefit in cases of porcine pleuropneumonia, A pleuropneumoniae should be eliminated from swine herds.
