Porcine pasteurellosis

S S BASTIANELLO AND J W NESBIT

GENERAL INTRODUCTION: FACULTATIVELY ANAEROBIC GRAM-NEGATIVE RODS Pasteurella and Mannheimia spp. infections

Introduction

Porcine pasteurellosis may manifest as septicaemic or pneumonic forms.^{5–7, 11, 12} Septicaemic pasteurellosis occurs in both neonatal and juvenile pigs while pneumonic pasteurellosis is a disease of predominantly juvenile animals. The infection, in conjunction with other infectious agents, Bordetella bronchiseptica in particular, is also implicated in the aetiology of atrophic rhinitis (see Bordetella bronchiseptica infections); a syndrome peculiar to pigs.^{2, 3, 5, 8, 13}

Aetiology

In pigs, infection by Pasteurella multocida is more prevalent than that by Mannheimia (Pasteurella) haemolytica. Of the isolations made from the specimens submitted to the Onderstepoort Veterinary Research Institute, about 92 per cent were P. multocida, ⁶ per cent M. haemolytica and 2 per cent comprised P. pneumotropica or untypable species of Pasteurella. ⁹ Pasteurella multocida serotypes A and D predominate in isolates from specimens obtained from pigs that suffered from septicaemia or pneumonia in South Africa.⁹ Haemorrhagic septicaemia caused by P. multocida serotype B has not been recorded in pigs in the region. It has, however, been implicated in an outbreak of the disease in India.¹¹ Whilst of rare occurrence in pigs, M. haemolytica (biotype and serotype undetermined) has been isolated from aborted foetuses and neonatal piglets suffering from septicaemia^{5, 6} and from pneumonic lesions in juvenile pigs.^{8, 15}

Toxigenic strains of P. multocida serotype D are also associated with atrophic rhinitis in pigs.^{2–5, 8, 13}

Septicaemic pasteurellosis in pigs

Septicaemic pasteurellosis caused by P. multocida has been reported in juvenile and adult pigs.^{5, 11} Although specific pathogen-free animals are apparently at greatest risk,⁵ the prevalence of this form of the malady, irrespective of whether caused by P. multocida or M. haemolytica, is higher in neonatal pigs.^{5–7, 15} The mode of transmission is unknown although infection via the umbilicus and/or the respiratory tract have been mooted.^{7, 10}

The course of the disease is peracute, death supervening after a period of illness that lasts no more than 12 hours in most cases, but rarely 24 to 48 hours.^{5, 6, 11} Clinical signs usually include bluish-red discoloration of the skin of the snout, ears and ventral regions of the neck, flanks and abdomen,lowered habitus, fever, dyspnoea and reluctance to move.^{6, 11} Generalized congestion, cutaneous lividity, subcutaneous oedema and petechiation, serosanguineous effusions in the body cavities and extensive ecchymotic haemorrhages in the lungs and epicardium are often present at necropsy.^{5, 6, 11} Acute catarrhal to fibrinous pharyngitis accompanied by peripharyngeal oedema, severe congestion of the cranial cervical lymph nodes,¹¹ and rarely, also acute fibrinous meningitis, particularly in neonatal pigs, may be encountered.⁵

The diagnosis is confirmed on the basis of isolation of the bacterium in pure culture from specimens of blood, brain, or other suitable tissues (spleen, lymph nodes and liver). The differential diagnosis should include other diseases associated with sudden death, such as African swine fever, colibacillosis, salmonellosis, erysipelas, Haemophilus septicaemia, streptococcal septicaemia, porcine pleuropneumonia and leptospirosis.

Specific antibacterial therapy is hampered by the sporadic nature and acute course of the disease. Control may be best achieved by separating diseased animals from healthy susceptible pigs and improving in the standards of housing, nutrition and hygiene.

Pneumonic pasteurellosis in pigs

Epidemiology

Pneumonic pasteurellosis is the most prevalent form of Pasteurella spp. infection in pigs.^{2, 5, 7, 12, 15} Fattening pigs in overcrowded conditions are at greatest risk.^{7, 15}

As in other species, the causative organism is a normal constituent of the flora of the upper respiratory tract, and stress factors (such as overcrowding, transportation, commingling, handling, exposure to excessive amounts of environmental or feed dust, and poor hygienic conditions), sometimes in association with concomitant pulmonic infection, probably trigger dissemination of P. multocida to the lung parenchyma. Intercurrent viral and bacterial infections, such as hog cholera, Aujesky’s disease and swine influenza,andinfections with Bordetella bronchiseptica, Actinobacillus pleuropneumoniae and Salmonella Choleraesuis have been implicated as predisposing factors in pig-producing countries elsewhere in the world.^{2, 5, 7} However, enzootic mycoplasmal pneumonia is the most important predisposing infectious condition on a worldwide basis, including South Africa.^{5, 7, 12, 15} In South Africa pneumonic pasteurellosis occurs very rarely, except as a complication of mycoplasmal pneumonia.¹⁴

Pathogenesis

The available information on the pathogenesis of pneumonic pasteurellosis in pigs is incomplete and refers mostly to the infection as a complication of mycoplasmal pneumonia.^{5, 7} The infection is acquired through aerosol transmission.^{7, 15} Injury to the lungs that has been induced by prior infection by Mycoplasma hyopneumoniae presumably provides not only a portal of entry for P. multocida but also the environment for local proliferation of the bacteria. Adherence to ciliated epithelial cells and evasion of phagocytosis by alveolar macrophages in the porcine respiratory tract are presumed to be functions of the capsule of P. multocida.² The extent of the inflammatory reaction in the lungs is dependent upon the severity of the preceding injury and the quantum of bacteria that colonizes the lungs.^{7, 12}

Clinical signs

Clinical signs vary in intensity according to the severity and extent of the pneumonic process.⁷ Infections may be inapparent or associated with a dry, non-productive cough that may persist for weeks or months in mildly affected animals. More severely affected cases usually initially show a non-productive cough which becomes productive, and depression, inappetence, fever, dyspnoea, and mucopurulent discharges from the nostrils. Auscultation reveals harsh pulmonary sounds. After a period of five to ten days pigs that suffer from severe disease almost inevitably die in the absence of effective antibacterial therapy. Recovery may be incomplete and characterized by persistent coughing that lasts for up to five weeks, emaciation and eventual death.² Relapses may occur in fully recovered animals.

Pathology

Acute, fibrinous pleuropneumonia succeeded by chronic, suppurative pneumonia is the usual course of events.^{5, 7, 12} The cranioventral areas of the lungs are most commonly affected although the caudal lobes may also be involved. In acute disease, the affected lungs are consolidated, reddish-purple in colour and frequently attached to the pleura and pericardium by fibrinous adhesions. The subpleural and interlobular tissues are distended by inflammatory oedema. The regional lymph nodes are enlarged. The histological features include all the hallmarks of acute fibrinous bronchopneumonia, multifocal necrosis, and the presence of ‘oat cells’ or ‘streaming macrophages’.¹ Gram-negative bacteria are present throughout the affected lungs.^{5, 7}

This reaction is frequently superimposed upon broncho-interstitial or ‘cuffing’ pneumonia indicative of a preceding mycoplasmal infection.⁵ Extrathoracic lesions may include generalized congestion, some degree of icterus, fibrinous or ulcerative pharyngitis and pronounced peripharyngeal oedema, fibrinous pericarditis and polyarthritis.^{5, 7}

Emaciation, chronic suppurative pneumonia, bronchiectasis and extensive fibrosis are common sequelae of the acute disease^{5, 7, 12} and may be complicated by chronic adhesive pleuritis and pericarditis, and chronic polyarthritis.⁵

Diagnosis and differential diagnosis

A definitive diagnosis of pneumonic pasteurellosis is based on isolation of the causative organism from mucus nasal secretions and blood of clinically affected animals, or pneumonic tissues, blood, and pleural and pericardial exudates collected at necropsy.

Porcine pleuropneumonia caused by Actinobacillus pleuropneumoniae should be considered as a possible differential diagnosis.

Control

Parenteral administration of antimicrobial agents (sulphonamides or antibiotics) to affected pigs may be beneficial.^{7, 15} This procedure should be supplemented by the provision of medicated feed or water for the entire group of pigs for three to five days. Certain strains of P. multocida are, however, resistant to some of the antibacterial agents in common usage and it is preferable to treat according to the results obtained from an antibiogram.

Although there is no specific vaccine available against pneumonic pasteurellosis in pigs in South Africa, autogenous bacterins or live attenuated vaccines have been utilized with some success in other parts of the world.⁷ In addition, protection against the disease may be afforded by correcting husbandry procedures that are likely to predispose to the infection. These may include ensuring adequate housing, nutrition and hygiene, reducing commingling, handling and exposure to dusty conditions, ^{7, 15} and preventing the primary infections which predispose to secondary P. multocida infection of the porcine lung.²

References

1. BASTIANELLO, S.S., 1989. Personal communication. Onderstepoort Veterinary Institute, Onderstepoort, 0110.
2. CHANTER, N. & RUTTER, R.M., 1989. Pasteurellosis in pigs. In: adlam, c. & rutter, r.m., (eds). Pasteurella and Pasteurellosis. London: Academic Press.
3. DOMINICK, M.A. & RIMLER, R.B., 1986. Turbinate atrophy in gnotobiotic pigs intranasally inoculated with protein toxin isolated from Type D Pasteurella multocida. American Journal of Veterinary Research, 47, 1532–1536.
4. DOMINICK, M.A. & RIMLER, R.B., 1988. Turbinate osteoporosis in pigs following intranasal inoculation of purified Pasteurella toxin: Histomorphometric and ultrastructural studies. Veterinary Pathology, 25, 17–27.
5. DUNGWORTH, D.L., 1985. The respiratory system. In: jubb, k.v.f., kennedy, p.c. & palmer, n., (eds). Pathology of Domestic Animals. 3rd edn. New York: Academic Press.
6. EDWARDS, B.L., 1959. A note on haemorrhagic septicaemia in neonatal pigs. The Veterinary Record, 71, 208.
7. FARRINGTON, D.O., 1986. Pneumonic pasteurellosis. In: leman, a.d., straw, b., glock, r.d., mengeling, w.l., penny, r.h.c. & scholl, e., (eds). Diseases of Swine. 6th edn. Ames: Iowa State University Press.
8. GILES, C.J., 1986. Atrophic rhinitis. In: leman, a.d., straw, b., glock, r.d., mengeling, w.l., penny, r.h.c. & scholl, e., (eds). Diseases of Swine. 6th edn. Ames: Iowa State University Press.
9. HENTON, M.M., 1989. Personal communication. Onderstepoort Veterinary Institute, Onderstepoort, 0110.
10. JUBB, K.V.F. & KENNEDY, P.C., 1970. Pathology of Domestic Animals. 2nd edn. New York: Academic Press.
11. MURTY, D.K. & KAUSHIK, R.K., 1965. Studies on an outbreak of acute swine pasteurellosis due to Pasteurella multocida type B (Carter, 1955). The Veterinary Record, 77, 411–416.
12. PIJOAN, C. & FUENTES, M., 1987. Severe pleuritis associated with certain strains of Pasteurella multocida in swine. Journal of the American Veterinary Medical Association, 191, 823–826.
13. RUTTER, J.M. & ROJAS, X., 1982. Atrophic rhinitis in gnotobiotic piglets: Differences in the pathogenicity of Pasteurella multocida in combined infections with Bordetella bronchiseptica. The Veterinary Record, 110, 531–535.
14. SPENCER, B.T., 1989. Personal communication. National Pig Health Scheme, Meat Board, 556 Vermeulen St, Arcadia, Pretoria 0083.
15. TAYLOR, D.J., 1986. Pig Diseases. 4th edn. Cambridge: Burlington Press.