Causes: Contagious Porcine Pleuropneumonia
Previously known as: Haemophilus pleuropneumonia
Introduction
Contagious Porcine Pleuropneumonia is a highly contagious and often fatal respiratory disease, seen in weanlings, growers and finishers ranging from 6 weeks to 6 months. It also causes abortion in sows and will cause milder respiratory signs in pigs of all ages. It is endemic in the UK.
The presence of Actinobacillus in the lungs causes a fibrinous pleurisy and pneumonia.
It is a disease of acute onset in naive/ susceptible herds and can cause high morbidity and mortality (up to 50%). Carrier herds have some immunity, protecting from acute disease, where lesions are often subclinical, and deaths sporadic.
The disease is transmitted by carrier pigs or new pigs brought into the herd and is spread by direct contact or aerosol transmission.
Pathogenesis
There are 12 serotypes causing the same disease. Different serotypes occur in different regions, with serotypes 3,6 and 8 the most common in the UK.
Virulent strains possess capsules which are antiphagocytic and immunogenic. Fimbriae allow the bacteria to attach to cells of the respiratory tract. Damaged neutrophils in the lungs produce lytic enzymes. The sustained inflammatory response causes tissue necrosis. Lungs become consolidated and necrotic with fibrinous pleurisy at post mortem.
The bacteria produce three cytotoxins which belong to the repeats-in-structural-toxin (RTX) cytolysin family. There are several peptide repeats within the molecules. The toxins are produced by various Gram-negative bacteria. There are four contiguous genes, A, B, C and D. A is the structural gene; B and D are required for secretion; C allows post-translational activation of the gene product of A into a functional product.
- ApxI is a strong haemolysin with cytolytic activity
- ApxII is a weak haemolysin
- ApxIII is a cytotoxin
Different Actinobacillus pleuropneumonia serotypes secrete a particular combination of toxins; American serotypes secrete ApxI and II; European serotypes secrete ApxII and III. Toxins introduce pores into cell membranes.
Clinical signs
In acute outbreaks, pigs may be dyspnoeic, pyrexic or anorexic. There will often be presence of blood-stained froth surrounding nose and mouth. Cyanosis follows later along with a sub-normal rectal temperature; death will then ensue. Pregnant sows will abort.
In subacute outbreaks, some pigs will be found dead but others in the group may show varying degrees of exercise intolerance and respiratory distress.
Diagnosis
Clinical signs especially if in the acute form are suggestive of this diagnosis as influenza rarely causes mortality and does not primarily affect young pigs.
The post mortem findings will confirm the diagnosis. The lesions are largely caused by the toxins produced. These will include; haemorrhagic consolidation close to the main bronchi or the diaphragmatic lung lobe, which is usually localised. Necrosis and fibrinous pleuritis may also be visible. Lung scarring and pleural adhesions may have developed in recovered animals.
Samples can be cultured on chocolate agar and diagnosed by immunofluorescent or PCR-based techniques. The bacteria on the palatine tonsil may remain undetected by serological tests and swabbing, and can therefore cause an outbreak in naive pigs.
Treatment and Control
Antibiotics should be administered as soon as clinical signs are suggestive of the disease. Water and feed intake is usually very reduced so in-water or in-feed treatments are of little use and treatment should be administered parenterally. Prophylactic antibiotics may be used for in-contact pigs.
As a control mechanism, killed and polyvalent bacterin vaccines as well as a subunit vaccine are available. They are given as two injections, two weeks apart to pigs no younger than six weeks of age. The sow can also be vaccinated pre and early pregnancy to allow passive immunity to occur.
Isolation on farms using all in all out systems will also dramatically reduce signs of infection, although not prevent it. Hygiene should be improved by improving ventilation and avoiding chilling and overcrowding.
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References
Cowart, R.P. and Casteel, S.W. (2001) An Outline of Swine diseases: a handbook Wiley-Blackwell
Jackson, G.G. and Cockcroft, P.D. (2007) Handbook of Pig Medicine Saunders Elsevier
Shope Richard E, White David C, Leidy Grace. PORCINE CONTAGIOUS PLEUROPNEUMONIA : II. STUDIES OF THE PATHOGENICITY OF THE ETIOLOGICAL AGENT, HEMOPHILUS PLEUROPNEUMONIAE. J Exp Med. 1964 Feb
Straw, B.E. and Taylor, D.J. (2006) Disease of Swine Wiley-Blackwell
Taylor, D.J. (2006) Pig Diseases (Eighth edition) St Edmunsdbury Press ltd
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