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Respiratory disease in a colony of rats. II. Isolation of Mycoplasma pulmonis from the natural disease, and the experimental disease induced with a cloned culture of this organism

  • P. Whittlestone (a1), Ruth M. Lemcke (a2) and R. J. Olds (a3)
Abstract
SUMMARY

Mycoplasma pulmonis was isolated from the pneumonic lung of a rat. Two groups of mycoplasma-free rats were inoculated, one with a culture of the M. pulmonis strain winch had been cloned four times (group A) and the other with a lung homogenate of the rat from which the strain had been isolated (group B). A third group (C) consisted of uninoculated control animals. Each group was kept in strict isolation and allowed to breed so that the progeny was naturally exposed to any pathogens present in the inoculated animals. After different periods of exposure, rats were autopsied, respiratory tracts and inner ears were cultured for mycoplasmas and bacteria, and sera were tested for complement-fixing antibodies to murine mycoplasmas.

In group-A rats, M. pulmonis was consistently isolated from the inner ears or lungs from 50 to 715 days after exposure. Complement-fixing antibody to M. pulmonis was detected 20 days after inoculation, but in the naturally exposed progeny antibody took longer than 50 days to develop. Antibodies to the other known mycoplasmas of murino origin, M. arthritidis and M. neurolylicum, were never found. Purulent otitis interna was consistently found from day 55 onwards, while lung lesions were first observed at 85 days and persisted to 715 days. Pulmonary lesions developed more slowly in inoculated parents than in exposed progeny. Similar results were found in group-B rats, which were examined up to 441 days after inoculation. Uninoculated group-C rats were examined up to 768 days of ago, but M. pulmonis was not recovered; of tho 54 animals whose serum was tested all wore negativo to tho three species of mycoplasmas, except one which had a titre of 16 with M. pulmonis. Pneumonia, bronchiectasis or lymphoroticular hyperplasia wore not seen in any of these control rats. Bacterial respiratory pathogens were not isolated from rats in any of the groups, nor was antibody to Sendai virus detected.

Tho results suggest that M. pulmonis alono can cause pneumonia and bronchiee-tasis in rats since mechanical carry-over of another pathogen with the initial cloned inoculum is very unlikely and there was no evidence for the participation of any other rat pathogen. The respiratory disease induced by the cloned culture was comparable with that induced by the lung homogenate, and with the well-known syndrome of chronic respiratory disease and bronchiectasis in the rat.

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D. P. Bell (1967). Chronic respiratory disense in a caesarian-derived and a conventional rat colony. Laboratory Animals 1, 159.

R. M. Lemcke (1965). A serological comparison of various species of mycoplasma by an agar gel double-diffusion technique. Journal of General Microbiology 38, 91.

J. B. Nelson (1940). Infectious catarrh of the albino rat. II. Tho causal relation of coccobacilliform bodies. Journal of Experimental Medicine 72, 655.

D. A. J. Tyrrell & C. R. Coid (1970). Sendai virus infection of rats as a convenient model of acute respiratory infection. Veterinary Record 86, 164.

H. Vrolijk , J. D. Verlinde & W. G. Braams (1957). Virus pneumonia (snuffling disease) in laboratory rats and wild rats due to an agent probably related to grey lung virus of mice. Antonie van Leeuwenhoek Journal of Microbiology 23, 173.

P. Whittlestone (1907). Mycoplasma in enzootic pneumonia of pigs. Annals of the New York Academy of Sciences 143, 271.

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Epidemiology & Infection
  • ISSN: 0950-2688
  • EISSN: 1469-4409
  • URL: /core/journals/epidemiology-and-infection
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