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J Med Microbiol 56 (2007), 1377-1385; DOI: 10.1099/jmm.0.47136-0
© 2007 Society for General Microbiology
ISSN 1473-5644

A virulent genotype of Microsporum canis is responsible for the majority of human infections

Rahul Sharma1,2, S. de Hoog3, Wolfgang Presber1 and Yvonne Gräser1

1 Institute of Microbiology and Hygiene (Charité), Humboldt University, Dorotheenstr. 96, D-10117, Berlin, Germany

2 Mycological Research Laboratory, Department of Bioscience, Rani Durgavati University, Jabalpur 482001, MP, India

3 Centraalbureau voor Schimmelcultures, Utrecht, The Netherlands

Correspondence
Yvonne Gräser
yvonne.graeser{at}charite.de

Received 22 December 2006
Accepted 1 June 2007

The zoophilic dermatophyte species Microsporum canis belongs to the Arthroderma otae complex and is known to mate with tester strains of that teleomorph species, at least in the laboratory. Human infections are likely to be acquired from the fur of cats, dogs and horses. Epidemiological studies to reveal sources and routes of infection have been hampered by a lack of polymorphic molecular markers. Human cases mainly concern moderately inflammatory tinea corporis and tinea capitis, but, as cases of highly inflammatory ringworm are also observed, the question arises as to whether all lineages of M. canis are equally virulent to humans. In this study, two microsatellite markers were developed and used to analyse a global set of 101 M. canis strains to reveal patterns of genetic variation and dispersal. Using a Bayesian and a distance approach for structuring the M. canis samples, three populations could be distinguished, with evidence of recombination in one of them (III). This population contained 44 % of the animal isolates and only 9 % of the human strains. Population I, with strictly clonal reproduction (comprising a single multilocus genotype), contained 74 % of the global collection of strains from humans, but only 23 % of the animal strains. From these findings, it was concluded that population differentiation in M. canis is not allopatric, but rather is due to the emergence of a (virulent) genotype that has a high potential to infect the human host. Adaptation of genotypes resulting in a particular clinical manifestation was not evident. Furthermore, isolates from horses did not show a monophyletic clustering.

Abbreviations: IA, index of association.




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