EXPERIMENTAL MICROSPORUM-CANIS INFECTION IN CATS - CORRELATION BETWEEN IMMUNOLOGICAL AND CLINICAL OBSERVATIONS

Microsporum canis infection was induced in five of six adult cats by t he application of mycelium to shaved and mildly abraided skin. The cli nical course of the disease was monitored over 16 weeks by physical ex amination and Wood's lamp illumination. The incubation period (time fr om inoculation to first appearance of infected hairs) varied between 8 and 13 days and was followed by a progressive phase of slow periphera l expansion of lesions accompanied by scaling, alopecia and skin thick ening that lasted for approximately 2 weeks. In four of the five cats the lesions then remained stable for between 1 and 6 weeks before regr ession occurred, with clinical resolution evident in these cats by 11- 14 weeks post-infection. In one cat disease was more prolonged, with r egression only beginning at the end of the study, and this cat also de veloped a satellite lesion. Immunological responses during infection w ere monitored every 2 weeks and consisted of ELISA to measure serum M. canis-specific IgG, IgM and IgA antibody concentrations, M. canis ant igen-specific lymphocyte proliferation assay, and mitogen-induced (Con A) lymphocyte proliferation assay. In all three immunoglobulin classes evaluated, a significant (P less than or equal to 0.020) rise in anti body concentration was seen in response to infection, and occurred ear liest with the IgM class (2 weeks post-infection). Overall, a heteroge neous antibody response was found, and changes in antibody concentrati on showed no clear temporal relationship to recovery from disease. Sma ll increases (P less than or equal to 0.015) in lymphocyte proliferati ve responses to M. canis antigen were evident in all cats by 2 to 4 we eks post-infection, but in contrast to the humoral immune response, a close temporal relationship was observed between the occurrence of sub stantially elevated lymphocyte proliferative responses and the onset o f regression of disease. There was no evidence of non-specific suppres sion of cellular responses (as assessed by ConA-induced lymphocyte pro liferation) during the course of disease.