Most of a series of 16 conventional rats examined at various ages were found to have and in the nasopharynx and sometimes also in the lungs. Fifteen of the rats had histological evidence of chronic respiratory disease (CRD). Specific-pathogen-free (SPF) rats of the same strain, but kept in isolation, did not appear to carry these infections and had no histological evidence of CRD.

It was not possible to produce CRD in SPF rats by the intranasal inoculation of or a mixture of the two. In contrast with this, lung homogenate from a naturally infected rat readily produced gross lesions of CRD in SPF rats, but the antibody titres to and remained low. The rats that had been given an inoculation of showed little evidence of CRD, but had high antibody titres, and antibodies to the streptobacillus appeared in their progeny, which were in direct contact with their infected parents during a period of 7 mth. Inoculation of failed to produce a significant antibody response.

Cortisone treatment of SPF rats given an inoculation of CRD agent without and promoted goblet-cell proliferation, but otherwise did not activate CRD. As cortisone activates CRD in naturally infected non-SPF rats, these findings suggest that the antibody response mechanism of SPF rats may be different from that of conventional rats.

Our findings suggest that neither nor plays an important part in the causation of CRD; the causal agent in the infective lung homogenate was not identified.


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