Porcine pleuropneumonia

Pleuropneumonia in pigs is spread rapidly by airborne route or by direct contact. Considerable economic losses are seen due to mortality, growth retardation and the increased need for medication with antibiotics.

About Actinobacillus Pleuropneumoniae

• Etiology
• Clinical Signs
• Post Mortem Lesions
• Treatment and Prevention

Etiology
Actinobacillus pleuropneumonia is a facultative anaerobic Gram-negative rod. It belongs to the family Pasteurellaceae, which contains the genera Haemophilus, Actinobacillus and Pasteurella.

The serotypes
13 serotypes have been described. Serotyping is based on capsular polysaccharides (CP’s) and lipopolysaccharides (LP’s). Some serotypes show structural similarities between the LP chains. This explains the cross reactions seen between certain serotypes.
Each geographical area or country has its own predominant serotype(s). See Table 1.

Table 1: Each geographical area or country has its own predominant serotype(s)

The prevalence of the predominant serotype(s) may change with time.

The virulence factors
Differences in virulence between the serotypes or even within the same serotype have often been observed. In general, strains of serovars 1, 5, 9, 10 and 11 are thought to be more virulent than those from other serovars.

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Clinical signs
Clinical signs vary with:

• the state of immunity of the animals
• the stress of adverse environmental conditions
• the degree of exposure to the infectious agent
• the virulence of the strain(s) involved

The course of the disease may be peracute, acute or chronic.

Acute form:

• The sudden appearance of severely ill animals in one or more pens
• High fever (41,5°C)
• Distinct respiratory symptoms; severe dyspnoea, mouth breathing, sitting position, foamy bloodtinged discharge through mouth and nostrils
• Cyanotic skin

Pigs showing peracute symptoms of APP infection - open mouth breathing, frothing at the mouth, neck extension and sitting.

Chronic form:
The chronic form develops after the disappearance of acute symptoms

• Coughing
• Loss of appetite
• Growth retardation

In chronically infected herds there are often many subclinically diseased animals.

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Post mortem lesions
(Per)acute stage

• Well demarcated, severe uni- or bilateral necrotizing haemorrhagic pneumonia is found at post mortem.
• Bronchi and trachea are filled with a foamy, blood-tinged mucous exudate.
• Fibrinous pleurisy is seens and the thoracic cavity contains a blood-tinged fluid.

Chronic cases

• Nodules of different sizes are found mainly in the diaphragmatic lobes. These nodules are surrounded by a thick capsule of connective tissue.
• Some areas of adhesive pleurisy are seen. In many cases the lung lesions resolve and only a residual, focal adhesive pleurisy is present. A high incidence of chronic pleurisy at slaughter is highly suggestive of pleuropneumonia.

Firm grey coloured lungs typical of chronic APP

Abscess in a lung caused by chronic APP infection

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Treatment and Prevention

Parenteral antibiotic treatment in the initial phases of the disease, will help to reduce mortality.

Effective antimicrobials include penicillins, cephalosporins, chloramphenicol, cotrimoxazole, oxytetracyclines

APP Prevention

1. Farms free of the pathogen should only introduce stock from APP free herds. New stock should be quarantined.
2. Determine periods of risk from post mortem examinations, serological testing and clinical examinations and consider strategic medication.
3. General management principles for controlling respiratory disease are effective
4. Vaccination with with multivalent inactivated vaccines protect against different serotypes. See Vaccines.

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Fibrous pleural adhesions in chronic APP disease