Experimental dermatophilosis in murine models of immunodeficiency

Abstract

Gnotobiotic mice with congenital immune deficiencies were infected with the skin pathogen Dermatophilus congolensis. Athymic (nude) mice with T cell deficiency were less susceptible than nude mice which also carried the beige mutation (beige-nude) with NK cell and granulocyte defects, as part of the murine equivalent of Chediak-Higashi syndrome. The additional presence of the x-linked immuno-deficiency gene in other beige mutant mice, giving reduced B cell responsiveness, did not increase their susceptibility. BALB/c mice with the nude mutation and evidence of macrophage insufficiency, had a moderate level of susceptibility, greater than that of outbred nude mice but less than that of beige, nude mice. The appearance of the lesions on the haired mice was different from that on those with hairless skin (nude and beige-nude). On the haired mice thin crusts developed and healed rapidly, while on the hairless mice the lesions started as nodules and later progressed to crusts. The nude BALB/c mice developed atypical lesions, which resembled ulcers. Germ-free nude and beige-nude mice showed the same types and time course of infection as the gnotobiotic animals, suggesting that bacterial interference, by a limited skin flora, did not play a major role in defence against D. congolensis. However, bacteriological analysis indicated that D. congolensis could survive in the gut of germ-free mice. This work emphasizes the importance of non-specific immune mechanisms, such as epidermal hyperproliferation and the neutrophil, in resistance to D. congolensis.