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Original Article

Experimental Microsporum canis infection in cats: correlation between immunological and clinical observations

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Pages 177-184 | Accepted 18 Jan 1995, Published online: 09 Jul 2009
 

Abstract

Microsporum canis infection was induced in five of six adult cats by the application of mycelium to shaved and mildly abraided skin. The clinical course of the disease was monitored over 16 weeks by physical examination and Wood's lamp illumination. The inclubation period (time from inoculation to first appearance of infected hairs) varied between 8 and 13 days and was followed by a progressive phase of slow peripheral expansion of lesions accompanied by scaling, alopecia and skin thickening that lasted for approximately 2 weeks. In four of the five cats the lesions then remained stable for between 1 and 6 weeks before regression occurred, with clinical resolution evident in these cats by 11–14 weeks post-infection. In one cat disease was more prolonged, with regression only beginning at the end of the study, and this cat also developed a satellite lesion. Immunological responses during infection were monitored every 2 weeks and consisted of ELISA to measure serum M. canis-specific IgG, IgM and IgA antibody concentrations, M. canis antigen-specific lymphocyte proliferation assay, and mitogen-induced (ConA) lymphocyte proliferation assay. In all three immunoglobulin classes evaluated, a significant (P ≤ 0·020) rise in antibody concentration was seen in response to infection, and occurred earliest with the IgM class (2 weeks post-infection). Overall, a heterogeneous antibody response was found, and changes in antibody concentration showed no clear temporal relationship to recovery from disease. Small increases (P ≤ 0·015) in lymphocyte proliferative responses to M. canis antigen were evident in all cats by 2 to 4 weeks post-infection, but in contrast to the humoral immune response, a close temporal relationship was observed between the occurrence of substantially elevated lymphocyte proliferative responses and the onset of regression of disease. There was no evidence of non-specific suppression of cellular responses (as assessed by ConA-induced lymphocyte proliferation) during the course of disease.

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