DISEASE AND EPIDEMIOLOGY

The natural habitat of Bordetella spp., except for the environmental organism B. petri, is the upper respiratory tract of mammals and birds. Bacteria are transmitted from host to host by aerosol. Bordetella bronchiseptica, B. avium, B. pertussis, and B. parapertussis are the primary pathogenic species, and they cause disease worldwide.

Bordetella bronchiseptica was originally named Bacillus bronchicanis because the organism was initially recovered from dogs with respiratory disease. The name was changed when it became evident that this organism infected other animals, and the literal meaning of the specific epithet is “with an infected bronchus.” In addition to canine disease, B. bronchiseptica causes respiratory infections in cats, rodents, horses, pigs, nonhuman primates, sea mammals, koalas, and rarely in humans. Most human cases have been associated with underlying immunosuppression and typically present as respiratory tract infections, ranging from sinusitis to pneumonia. However, more serious conditions, such as endocarditis, meningitis, and peritonitis, have been reported. A non–life-threatening whooping cough–like syndrome has been described in immunocompetent children.

Bordetella bronchiseptica is one of the agents involved in the infectious canine tracheobronchitis or “kennel cough” complex of young dogs. Older naïve animals are also susceptible. The organism is an important secondary invader following dis temper virus infection, where it is often responsible for a fatal bronchopneumonia. The incubation period for kennel cough is 5 to 10 days, followed by acute onset of a harsh, dry, “honking” cough that is aggravated by excitement or activity. Coughing episodes are often followed by gagging and retching, in attempts to clear mucus from the trachea. The cough can be easily elicited by tracheal palpation. The disease spreads rapidly among closely confined animals, as in boarding kennels or animal hospitals, and the primary infection is often self-limiting. Puppies may shed B. bronchiseptica for up to 3 months after infection, and relapses may follow stress and exposure to adverse environmental conditions.

Bordetella bronchiseptica is one of the etiologic agents of atrophic rhinitis and bronchopneumonia in swine, diseases that are associated with intensive rearing conditions. Nearly all herds of swine, including those that are apparently normal, are infected with this organism, and primary introduction is by carrier pigs. The sow is the most common source of infection for piglets, and poor ventilation and overstocking are risk factors. Atrophic rhinitis is characterized by sneezing, nasal discharge, and bony deformity of the nose. Upper respiratory signs may occur in piglets as young as 1 week of age, but more frequently occur at 3 to 4 weeks of age. The characteristic lesion is atrophy of the nasal turbinates, which may be evident only at slaughter, in snouts sectioned at the level of the second premolar tooth. The ventral scroll of the ventral turbinate is the region most commonly affected. Bordetella bronchiseptica by itself is responsible for the less severe, transient, self-limiting form of atrophic rhinitis, usually without significant snout deviations. A more severe, progressive form of the disease is caused by toxigenic strains of Pasteurella multocida in combination with B. bronchiseptica. Histopathologic changes associated with atrophic rhinitis include mucosal infiltration by neutrophils, loss of cilia, metaplasia of the epithelium, and bone resorption with fibrous tissue replacement.

Primary bronchopneumonia in 3- to 4-day-old piglets is a more severe manifestation of infection that usually occurs in the winter months. Coughing is the major clinical sign, and may be accompanied by dyspnea and whooping. Morbidity and mortality may be high.

Tracheobronchitis, conjunctivitis, and pneumonia have been associated with B. bronchiseptica infection in cats. Disease not complicated by infection with other agents (such as feline calicivirus and feline herpesvirus) is mild, and signs disappear within 10 days. However, life-threatening bronchopneumonia may develop, particularly in kittens. Clinical signs in experimental infections include sneezing, nasal discharge, rales, fever, and submandibular lymphadenopathy. Coughing is reported occasionally, but does not seem to be a characteristic feature, as in canine disease. Some cats become long-term carriers on recovery, and shedding for at least 19 weeks postexposure has been documented.

Bordetella bronchiseptica is responsible for outbreaks of pneumonia in laboratory rodents and rabbits. Epizootic respiratory disease can have dis astrous consequences in guinea pig colonies, resulting in high mortality and abortions or stillbirths. Affected animals are anorectic, dyspneic, and exhibit oculonasal discharge. Acute disease has a sudden onset and lasts 2 to 3 days. Many outbreaks are precipitated by stressors, such as improper diet, temperature fluctuations, and overcrowding. Young, old, or pregnant individuals are particularly susceptible. Subclinical infections and carrier animals are common.

Bordetella avium is responsible for a highly contagious upper respiratory disease known as avian bordetellosis or turkey coryza. Clinical disease is of greatest economic importance in young turkeys, but B. avium also infects chickens and several other species of birds. Disease may be exacerbated by environmental stressors and other respiratory pathogens.

The organism exhibits a strong tropism for the ciliated epithelium of the upper respiratory tract. Turkey poults 1 to 6 weeks old experience an acute onset of sneezing, accompanied by open-mouth breathing, conjunctivitis, nasal discharge, moist rales, anorexia, and altered voice. Stunted growth, tracheal collapse (Figure 18-1), and predisposition to other diseases may result. Morbidity may approach 100%, but mortality is usually low in the absence of secondary infections. In older turkeys and chickens, clinical signs are less severe. The most significant necropsy finding in severely affected birds is dorsoventral collapse of tracheal rings with accumulation of a mucopurulent exudate in the tracheal lumen (see Figure 18-1).

FIGURE 18-1 Flattening of tracheal rings, associated with Bordetella avium infection in turkey poults.

(Courtesy J. Glenn Songer.)