Pneumonic Pasteurellosis (Pasteurellosis; Pasteurella multocida; also see Atrophic Rhinitis)
This disease of swine is usually seen in association with other infectious diseases or environmental factors that impair pulmonary function. There are both primary and secondary forms of the disease.
Pneumonic pasteurellosis (PP) occurs throughout the world. Secondary PP is seen in association with several other diseases, especially mycoplasmal pneumonia, viral infections of lung, and Actinobacillus pleuropneumoniae. It often accompanies or follows unusual environmental or other stresses. Similar forms of pasteurellosis occur in many other species, including cattle (genus renamed Mannheimia), rabbits, fowl, sheep and rodents.
Primary pasteurellosis occurs occasionally as a septicemic disease with meningitis in piglets. A septicemic form also occurs rarely in older or adult swine. Secondary pasteurellosis is seen much more frequently than primary pasteurellosis.
In the early days of bacteriology, Pasteur experimented with a disease of poultry now believed to have been fowl cholera caused by Pasteurella multocida; the genus, Pasteurella, was named after him. Subsequent research implicated Pasteurella multocida as an important primary and secondary pathogen in many species, including swine.
The etiologic agent is Pasteurella multocida, a Gram-negative coccobacillus easily grown in the laboratory. There are both toxigenic and non-toxigenic strains. The organism is a common inhabitant of the pig’s nasal passages and can be isolated from most swine herds. There are five capsular serotypes (A, B, D, E, and F) and 16 somatic serotypes. In the United States, pneumonic pasteurellosis of swine is caused by serotypes A and D.
Carrier swine probably introduce P. multocida into most herds, with subsequent vertical and lateral transmission. Transmission is suspected of being via nose-to-nose contact. Although many other species harbor P. multocida; there is little evidence of interspecies transfer of strains pathogenic for swine.
Healthy swine are highly resistant to experimental infection by P. multocida and many normal swine are carriers of P. multocida in their nasopharynx. Chronic, progressive pneumonia occurs when resistance has been lowered and the organism colonizes deeper portions of the lung.
Pathogenic strains appear to produce their effect largely through damage to microvasculature in the lung. This leads to the formation of fibrinous thrombi in alveolar capillaries and escape of fibrinogen into alveoli where it is converted to fibrin. The fibrin then can be slowly organized into fibrous connective tissue. Abscesses that may develop in the pneumonic lung may be a consequence of infarction of localized areas or the result of a necrotizing effect of toxic products produced by P. multocida and other secondary bacteria.
The severe inflammatory reaction that accompanies the process sometimes involves pleura and occasionally the pericardial sac. Fibrin on the pleura overlying pneumonic lesions may organize to form fibrous adhesions that attach the lung to the rib cage, but this finding is more often due to prior effects of Actinobacillus, Haemophilus, or Streptococcus infection. Since the agent is common, easily isolated, and persists in lesions, P. multocida is frequently isolated from lungs in which there are other primary agents of pneumonia (Actinobacillus sp., swine influenza, Mycoplasma hyopneumoniae). In acute cases, bacteremia and septicemia can occur and deaths are believed to be caused by endotoxic shock and respiratory failure.
Signs vary in severity and are those often seen with other types of pneumonia: coughing, dyspnea, fever and prostration. Chronic cases tend to have less fever, a persistent cough and a more marked dyspnea. Swine with well-developed pneumonia or extensive adhesions between lungs and rib cage often have a marked expiratory lift (“thump”).
Pneumonic areas involve the cranioventral lobes of the lungs and often extend to adjacent parts of the diaphragmatic lobes. Pneumonic areas are remarkable for their firmness and density. The pleura over lesion areas may be granular and scant fibrin may be visible on the surface. Regional lymph nodes usually are enlarged. Microscopic lesions are those of a suppurative bronchopneumonia. Fibrin and bacteria often are prominent in affected alveoli and, sometimes, in interalveolar capillaries. Occasionally, acute necrotizing pharyngitis and fibrinous polyarthritis without joint swelling are present. Less often, there is meningitis or meningoencephalitis.
History, signs and the remarkable pulmonary lesions may be suggestive of pneumonic pasteurellosis but culture of lung lesions from a nonmedicated pig is required for confirmation. Pneumonic pasteurellosis is often secondary to one or more of a host of primary diseases that should not be overlooked. Environmental factors such as dusty or overcrowded conditions, excessive ammonia gas or poor ventilation may be important predisposing factors. Only when all other possible causes have been eliminated should there be a diagnosis of primary PP.
Serology and mere isolation of P. multocida from nasal swabs is of little value without being able to predict pathogenicity. The application of the polymerase chain reaction (PCR) to detect and differentiate toxin producing and nontoxin producing P. multocida may prove to be a useful technique for control of both pneumonic pasteurellosis and atrophic rhinitis.
Control methods include all the measures that might prevent introduction of a new strain ofP. multocida into a herd. Herd additions should be quarantined for at least a few weeks. Use of the all in/all out system of raising swine will reduce the likelihood of PP. Mixing and sorting of pigs should be minimized. Implementing control of other respiratory pathogens (e.g. M. hyopneumoniae, porcine reproductive and respiratory syndrome virus (PRRSV), swine influenza, A. pleuropneumoniae) or any other disease, environmental or stress factor that might lower resistance should be addressed.
Bacterins against P. multocida are available but their efficacy in preventing or minimizing the severity of respiratory disease is questionable.
Pneumonic pasteurellosis is difficult to treat effectively. Basic therapeutic caveats of early diagnosis, appropriate choice of antimicrobial, and appropriate dose with sufficient duration of therapy are particularly important for success. Many different antibiotics (tiamulin, tulathromycin, lincomycin with chlortetracycline, penicillins, tilmicosin, tetracyclines, etc) have been recommended for injection or oral medication. In selecting an antimicrobial, it may be useful to run sensitivity tests on the organism isolated from a typical non-treated sick pig in the herd.