Mycoplasmal and Rickettsial Diseases - dogs Canine Infectious Tracheobronchitis

Mycoplasmal and Rickettsial Diseases - dogs Canine Infectious Tracheobronchitis;considered. Canine distemper virus infection, pneumonia, heartworm disease, tracheal collapse, and mycotic;bronchiseptica
Diseases - dogs 

Etiology. Infectious tracheobronchitis (ITB) is a highly contagious illness of the canine respiratory tract that usually manifests as acute but self-limiting disease. Several organisms have been incriminated as causative for this condition:
Bordetella bronchiseptica; canine parainfluenza virus (CPIV); canine adenovirus types 1 and 2 (CAV-1, CAV-2); canine herpesvirus; canine reovirus types 1, 2, and 3; and mycoplasms and

Clinical signs. Clinical infectious tracheobronchitis can be subdivided into mild or severe forms.

 The mild form is the more common presentation and is characterized by an acute onset of a loud, dry, hacking cough. Increased formation of mucus
sometimes results in a productive cough, followed by gagging or retching motions. A cough is easily elicited by tracheal palpation and may be more frequent with excitement or exercise.

Otherwise, the dog is typically asymptomatic, with normal body temperature, attitude, and appetite. Mild tracheobronchitis usually lasts 7-14 days, even if left untreated.

The severe form of tracheobronchitis generally results from mixed infections complicated by poor general health, immunosuppression, or lack of vaccination. Secondary bronchopneumonia can occur and may be the determinant of severity
(Sherding, 1994). Animals are clinically ill and may be febrile, anorexia, and depressed. A productive cough and mucopurulent naso-ocular discharge are more common than in the mild form.

These cases require more aggressive treatment and may be fatal.

Epizootiology and transmission. The natural reservoir for Bordetella bronchiseptica is considered to be the respiratory a tract of infected animals (Bemis, 1992). This bacterium is very
easily spread by aerosol and direct contact, and fomite transmission is also possible (Bemis, 1992). Transmission is favored by confined housing of multiple animals. In experimental studies, B. bronchiseptica transmission to susceptible individuals was 100% (Thompson et al., 1976; McCandlish et al., 1978).

The incubation period is 3-10 days. CPIV and CAV-2 are also spread by aerosols. Of these two viruses, CAV-2 is the most persistent, lasting for up to several months in the environment, whereas CPIV is fairly labile (Hoskins, 2000a). Both viruses can be destroyed by quaternary ammonium disinfectants.

Pathogenesis. The most common clinical isolates are CPIV and Bordetella bronchiseptica. However, B. bronchiseptica may be a commensal organism, and it is often recovered from asymptomatic animals. In cases of clinical infection, B. bronchiseptica attaches to the cilia on the mucosal surface of the upper airway epithelium, causing suppurative tracheobronchitis

and bronchiolitis. Infections with CPIV or CAV-2 alone are usually subclinical; coinfections with B. bronchiseptica or other microbes may result in clinical ITB (Keil and Fenwick, 1998; Wagener et al., 1994). The characteristic lesion from CPIV
or CAV-2 infection is necrotizing tracheobronchitis (Dungworth, 1985). Pathogenic infection of the upper airways typically results in inflammation and ciliary dysfunction.

Diagnosis and differential diagnosis. Diagnosis of infectious tracheobronchitis is often based on clinical signs. Isolation of Bordetella bronchiseptica or mycoplasma by nasal swabs allows only a presumptive diagnosis. Viral isolation or paired serology can be done but is often impractical and expensive. If a cough persists for more than 14 days, other disease conditions should be considered. Canine distemper virus infection, pneumonia, heartworm disease, tracheal collapse, and mycotic infections are differential diagnoses for dogs with similar signs.

Bronchial compression as a result of left atrial enlargement, hilar lymphadenopathy or neoplasia may also elicit a nonproductive cough (Johnson, 2000) and should be considered as a the differential for ITB.

Prevention. Prevention is best achieved by avoiding exposure to infected animals, but this is oftentimes not practical. Dogs should be vaccinated prior to, or at the time of, admission to the animal research facility. Intranasal vaccine combinations for

Bordetella bronchiseptica and CPIV are preferred. Intranasal vaccines protect against both infection and disease, can be given to dogs as young as 2 weeks of age, and can produce immunity within 4 days.

Control. Sanitation and ventilation are critical for control. The animal care staff must practice proper hygiene to prevent fomite transmission. Symptomatic animals should be isolated, and
animal-to-animal contact avoided. Kennels should be disinfected with agents such as bleach, chlorhexidine (Nolvasan) or quaternary ammonium chloride (Roccal-D). Proper ventilation and humidity are important in controlling the spread of these infectious agents; 15-20 air changes per hour at 50% relative humidity are recommended (Sherding, 1994).

Treatment: No specific treatment is available for viral infections. Bordetella bronchiseptica is typically sensitive to potentiated sulfas, chloramphenicol, quinolones, tetracyclines, gentamicin, and kanamycin. Use of antibiotics is indicated when severe or persistent clinical signs occur, and it should be continued for 14 days. Use of empirical antibiotic treatment in mild cases may hasten the resolution of clinical signs. For severe or unresponsive infection, treatment should be based on bacterial culture sensitivity patterns; nebulized gentamicin may be helpful. Cough suppressants (e.g., dextromethorphan) should be

avoided if a cough is bringing up mucus (productive); however, their use is indicated if coughing is causing discomfort or interfering with sleep. Bronchodilators such as aminophylline,
theophylline or terbutaline can be helpful in reducing reflex bronchoconstriction and minimizing discomfort.

Research complications. Because infectious tracheobronchitis results in altered respiratory tract histology and impaired

mucociliary clearance, infected animals should not be used for pulmonary studies. Animals with clinical disease would also be poor surgical candidates.

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