Also known as Actinobacillus pleuropneumoniae
Actinobacillus pleuropneumoniae occurs worldwide (many free herds) in weaners, growers / finishers.
The effects are Pleurisy, pneumonia, cough, breathing difficulties, poor growth, sudden death.
- Causes of Actinobacillus pleuropneumoniae >
- Effects of Actinobacillus pleuropneumoniae >
- Diagnosis of Actinobacillus pleuropneumoniae >
- Treatment & Control of Actinobacillus pleuropneumoniae >
Causes of Actinobacillus pleuropneumoniae
Pleuropneumonia is caused by Actinobacillus pleuropneumoniae, a Gram negative rod-shaped bacterium which produces fimbriae (filaments), a protective capsule and at least four toxins (Apx11, Apx2, which are haemolytic and destroy red blood cells, which kills cells and APX Apx3 IV , produced only in vivo). At least 12 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 defense cells). They can not kill it because of the capsule and are killed within an hour by the toxins. The organism multiplies in the lung undefended 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 is irreversible.
If the pig recovers, it develops protective immunity to infection, particularly to infecting serotype.
Effects of Actinobacillus pleuropneumoniae
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 or after disturbance within hours of infection.
Cyanosis (a Tinge of the purple 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 animals. 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 pigs may die. Recovering animals cough, respiratory distress and show, 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 gilt or sows.
Where infection is present in a herd, Pleuropneumonia is most common amongst pigs or 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.
Diagnosis of Actinobacillus pleuropneumoniae
The clinical signs are 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 chronic disease mortality may suggest. The diagnosis can be confirmed in most cases by post-mortem examination.
The presence of Pleurisy and firm areas or severe, even blackish, pneumonic lung are characteristic of this disease. The changes may still be seen at slaughter as Fibrous Pleurisy 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 using slide agglutination antibody to capsules, by ELISA, coagulation, latex particle agglutination, and using labeled DNA probes, ribotype, PCR and restriction endonuclease analysis. Extracts of lung may be tested for the organism using similar methods. The Tonsils and 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.
Treatment & Control of Actinobacillus pleuropneumoniae
Clinically-affected animals are treated by injection as they do not eat or drink much, making medication or feed and water Largely ineffective. Penicillin, cephalexin, ampicillin, amoxicillin, oxytetracycline, doxycycline, trimethoprim sulphonamide, tiamulin, florfenicol, enrofloxacin, ceftiofur and lincospectine can all be used.
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 control disease, particularly if all-inclusive, all-out stocking or 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.
