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Lethal bronchopneumonia caused by Mycoplasma cynos in a litter of golden retriever puppies

MYCOPLASMAS are the smallest and simplest free-living organisms known; they are widespread in the animal kingdom (Waites and others 2005). It is generally accepted that the upper respiratory tract of dogs is frequently colonised by mycoplasmas, where they seem to form a part of the normal bacterial flora (Rosendal 1982, Randolph and others 1993). There are conflicting reports about infections of the lower respiratory tract (Rosendal 1972, Randolph and others 1993). Mycoplasmas have been isolated alone or in combination with other bacteria from the lungs of dogs with pulmonary disease (Kirchner and others 1990, Randolph and others 1993, Jameson and others 1995, Chandler and Lappin 2002, Chalker and others 2004). Little is known about specific infections caused by canine Mycoplasma species. Rosendal (1978) isolated various mycoplasmas, but only Mycoplasma cynos was able to induce an inflammatory response after endobronchial inoculation of one-week-old puppies. This short communication describes a case of M cynos pneumonia in a litter of golden retriever puppies. The litter originally comprised 11 puppies, of which four with a low birthweight (approximately 280 g compared with 400 to 450 g for the other puppies) had faded and died within the first two weeks of life. The breeder had noticed milk running out of the nostrils of two puppies after feeding, but cleft palates were excluded as the cause. Postmortem examinations were not performed. The litter, the seven-year-old dam (whose average litter size over the previous six years was 11 puppies) and the eight other dogs (one golden retriever, three dachshunds and four pugs) belonging to the breeder were examined by the breeder’s private veterinarian, but did not show any signs of disease. No infertility, abortions, stillbirths, illnesses or deaths had been observed within the past two years. The kennels were clean, and no obvious problems in breeding management were observed. At three weeks of age, the remaining seven puppies developed upper respiratory signs with rhinorrhoea, followed by fever (up to 41°C) and a productive cough within a few days. The dogs tested negative for canine adenovirus (CAV) types 1 (CAV-1) and 2 (CAV-2) by PCR on swabs from the nose and mouth and serum, and canine distemper virus (CDV) by PCR on conjunctival swabs and whole blood. Three puppies died despite treatment including amoxicillin (Roxilin; Norbrook Laboratories). A macroscopic postmortem examination of one of these puppies revealed pale organs and tissues, suggesting severe anaemia, a histologically confirmed low-grade serofibrinous pleurisy, and profoundly consolidated and blotchy lungs without significant adhesions. Furthermore, a heavy ascarid infection of the stomach and small intestine, without obstruction, was demonstrated. No pathological alterations were observed in the remaining organs. Histopathology of the lungs showed a severe acute generalised catarrhal-suppurative, partly haemorrhagic fibrinous necrotising bronchopneumonia. Immunohistochemical (IHC) examination of formalin-fixed, paraffin-embedded lung tissue using a polyclonal antibody to M cynos revealed Veterinary Record (2007) 161, 626-628