Bordetella bronchiseptica infections

M-L PENRITH AND M M HENTON

GENERAL INTRODUCTION: GRAM-NEGATIVE AEROBIC OR CAPNOPHILIC RODS AND COCCI

Introduction

Infection with Bordetella bronchiseptica has been associated with disease in a number of species, but the most important animal diseases caused by this bacterium are non-progressive atrophic rhinitis in pigs and kennel cough in dogs.⁴⁷ Bordetella bronchiseptica has also been implicated in lower respiratory tract disease²⁹ and haematogenous septic arthritis⁴⁸ in foals, as well as in respiratory disease in horses, especially following surgery.⁷²

The first isolates of B. bronchiseptica obtained from pigs emanated from cases of bronchopneumonia.^{25, 46, 68} The organism is relatively unimportant as an agent of pneumonia in pigs, although it has occasionally been recorded as the primary pathogen in bronchopneumonia in young piglets and more often as a secondary pathogen.²⁵ Experimental infection resulted in pneumonia in five-day-old piglets in the absence of any other agents,⁴¹ as well as in nine-day-old caesarean-derived piglets.³⁷ It was first isolated from the nasal cavity of pigs with atrophic turbinates in 1956,⁶⁵ and its ability to produce turbinate atrophy was demonstrated. As a result, it was considered to be the primary agent of atrophic rhinitis in pigs by some authors.⁶⁶ Severe atrophic rhinitis, however, was produced only by combined infection with toxigenic strains of Pasteurella multocida and B. bronchiseptica. ^{57, 58} It is currently accepted that progressive atrophic rhinitis (PAR) is caused by toxigenic strains of P. multocida, but that colonization of the nasal mucosa by B. bronchiseptica is the most important predisposing factor for the development of PAR.^{19, 25} A complex interaction between B. bronchiseptica and P. multocida may be necessary to cause PAR.²³ However, a field outbreak of severe progressive atrophic rhinitis caused by toxigenic P. multocida in the absence of B. bronchiseptica has been reported.⁵⁹ Infection with B. bronchiseptica alone can cause acute rhinitis in young piglets, accompanied by varying degrees of turbinate hypoplasia, which appears to resolve if not complicated by infection with toxigenic P. multocida.¹⁷

Bordetella bronchiseptica infection of pigs and other species occurs worldwide. During the past decade at the Onderstepoort Veterinary Institute in South Africa, ⁷⁴ per cent of approximately 50 isolates emanated from pigs, 12 per cent from dogs, 6 per cent from rodents, 4 per cent from rabbits, and 2 per cent each from goats and ostriches. Atrophic rhinitis yielded 73 per cent of the pig samples, pneumonia 24 per cent, and nephritis 3 per cent.²⁸

Aetiology

Bordetella bronchiseptica organisms are Gram-positive, motile rods or coccobacilli. Other characteristics are that they are aerobic, urease positive, do not ferment carbohydrates, and use citrate.²⁵ Sixteen ribotypes have been identified in a study using the restriction enzyme PvuII.⁵² In that study, ⁸⁸ per cent of the pig isolates analysed belonged to ribotype ³. Refinement of the technique resulted in the identification of three more ribotypes, designated 17, 18 and 19.^{54, 55} There are four phase variations, I to III and a rough phase. Phase I organisms are encapsulated, capable of attaching to pig nasal epithelial cells, and pathogenic.³⁶ Flagella are characteristic of the avirulent phenotype.⁴⁵ Culture conditions can modify colony morphology and antigenic expression.³³ Capsule formation is inhibited by sulphonamides that contain methoxy groups but not by other sulphonamides.³⁶ A single genetic locus is responsible for the expression of most of the factors considered to be responsible for virulence of Bordetella.^{49, 73} This locus also regulates flagellin gene transcription.²

Epidemiology

Bordetella bronchiseptica is widely prevalent in pigs and may be isolated from nasal swabs of healthy piglets as well as those with clinical rhinitis,²⁵ and its prevalence may not differ between herds with and without clinical signs of atrophic rhinitis.³⁸ According to estimates based on culture of nasal swabs, up to 50 per cent of herds in the USA may be infected, although the number of pigs infected per herd is closer to 10 per cent.²⁵ Serological surveys usually indicate a higher prevalence rate,²⁵ since these include pigs that are no longer positive on culture.

Transmission from pig to pig is usually by aerosol droplets. Sows that carry the organism in their nasal cavities are an important source of infection for their litters. Virulent strains have been isolated from the air of pig houses and have proven capable of colonizing the nasal mucosa and inducing rhinitis and pneumonia in piglets.^{62, 63} Pigs can be infected at any age, but clinical signs commonly develop only in young piglets under six weeks of age, either in suckling piglets infected by their dams or in recently weaned piglets that become infected when litters are mixed. The prevalence of infection generally reaches a peak when piglets are about 12 weeks old, but signs and lesions in the late weaning and fattening periods are few.²⁵

Carrier pigs are presumed to be the source of infection for clean herds. The role played by other species such as cats and rodents, from which strains of B. bronchiseptica may be isolated, is dubious. Only porcine strains have been demonstrated to cause severe damage²⁵ although strains isolated from other species have been used to...