Occurrence: Worldwide, many herds free.
Age affected: Weaners, growers / finishers.
Causes: Strains of the bacterium – Actinobacillus pleuropneumoniae; poor ventilation; chilling; stress.
Effects: Pleurisy, pneumonia, cough, breathing difficulties, poor growth, sudden death.
Occurrence: Worldwide, many herds free.
Pleuropneumonia is caused by Actino- bacillus pleuropneu- moniae, a Gram negative rod-shaped bacterium which produces fimbriae (filaments), a protective capsule and at least four toxins (ApxI, ApxII, which are haemolytic and destroy red blood cells, ApxIII which kills cells and Apx IV, produced in vivo and essential for pathogenicity).
At least 15 different capsular types (serotypes) occur, but each serotype may not produce all the toxins. Different combinations of serotypes are found in each country. A pleuropneumoniae grows readily in the laboratory, but most strains require NAD, a growth factor, often supplied by other bacteria or by altered blood.
The organism colonises the tonsils and adheres to them, but in non-immune pigs, or those which are stressed by mixing, it is inhaled into the lungs where it adheres to cells lining the alveoli. There it is taken up by alveolar macrophages (lung defence cells). They cannot kill it because of the capsule and are killed within an hour by the toxins.
The organism multiplies in the undefended lung and produces more toxin which damages the lung, causing inflammation (pneumonia, leakage of capillaries (leading to pleurisy) and destruction of the lung tissue, some of which damage is irreversible. If the pig recovers, it develops protective immunity to infection, particularly to infecting serotype.
Infection is by the respiratory route from contact between pigs, by aerosol, from contaminated drinkers and from contaminated clothing etc. The organism does not survive for long on drying, but can persist in clean water for days. Introduction to a clean farm is usually by means of carrier pigs.
Infection may be inapparent, but 15-30% of pigs may suffer depression, inappetence, high fever (41.5°C, 107°F), or laboured breathing, especially after rising to drink of after disturbance within hours of infection. Cyanosis (a purple tinge of the ears and feet), subnormal rectal temperature and death may follow within 4-6 hours of the onset of clinical signs.
Blood stained froth may be seen at the mouth and such pigs will die. Mortality may reach 30-50% of affected pigs. Less severely affected pigs do not eat, are fevered, and show respiratory distress, coughing and exercise intolerance and do not pull away strongly when restrained. Some of these pigs may also die. Recovering animals cough, and show respiratory distress, particularly when disturbed. Exercise intolerance may continue for days and affected animals may eat less, appear gaunt and hairy, are depressed and show reduced rates of live weight gain.
Non-immune animals of all ages may be affected and abortion may occur in affected gilts or sows. Where infection is present in a herd, pleuropneumonia is most common amongst pigs of 6-12 weeks of age. Treatment can alter the clinical signs and mortality. Some animals may remain chronically affected, in very poor bodily condition with continued exercise intolerance and respiratory distress.
The clinical signs of inappetence, high fever, laboured breathing, cyanosis and death within 4-6 hours of the onset of clinical signs, often with blood-stained froth at the mouth suggest acute pleuropneumonia. The presence of pigs with respiratory distress, coughing and exercise intolerance in very poor condition with some mortality may suggest chronic disease. The diagnosis can be confirmed in most cases by post-mortem examination.
The tonsils of recovered pigs can be swabbed to test for carriage and antibody can be detected in their blood using a number of tests. Some tests will only detect one serotype.
The presence of pleurisy and firm areas of severe, even blackish, pneumonic lung are characteristic of this disease. The changes may still be seen at slaughter as fibrous pleurisy and pericarditis with firm nodules representing partially-healed pneumonia. Confirmation of the diagnosis is by laboratory demonstration of A. pleuropneumoniae or its products. The organism can be cultured and its identity confirmed biochemically. A. pleuropneumoniae isolates may be serotyped by slide agglutination using antibody to capsules, by ELISA, coagulation, latex particle agglutination, and using labelled DNA problems, ribotyping, PCR and restriction endonuclease analysis. Extracts of lung may be tested for the organism using similar methods.
Clinically-affected animals are treated by injection as they do not eat or drink much, making medication of feed and water largely ineffective. Penicillin, cephalexin, ampicillin, amoxicillin, oxytetracycline, doxycycline, trimethoprim sulphonamide, tiamulin, florfenicol, enrofloxacin, ceftiofur and lincospectin can all be used where registered. Treatment may need to be repeated for 3 days.
Affected pigs may have to be given water by stomach tube. The remainder of the group can be treated in water or feed with the antimicrobials listed above. Antibiotic resistance may occur. Lung damage may remain in treated pigs until slaughter, reducing productivity. Treatment with antibiotic in feed or water at entry to a house controls disease by eliminating early infections, particularly if all-in, all-out stocking of airspaces or sites is practised, Vaccination of sows with killed whole cell vaccines protects their piglets against the serotypes present in that vaccine.
Young pigs may be protected against all serotypes by vaccination with inactivated toxins and membrane proteins of A. pleuropneumoniae. The disease can be eradicated by depopulation and farm disinfection and pleuropneumonia-free pigs are available for repopulation and breeding stock replacements. Eradication has also been carried out by identification and removal of carriers. A. pleuropneumoniae does not spread far by aerosol and isolation is usually effective.