THE TR1CHOPHYTONEAE 381 



isolated from lesions on patients, they might have been regarded 

 as distinct species. When subcultures were isolated, using aleuro- 

 spores or fuseaux from these variants, each produced a culture 

 like those from the particular variant from which it originated. 

 Furthermore none of the variants reverted to the parent form. 

 Three different kinds of pleomorphic forms are also known for 

 Micro sporum lanosum, and all are reversible to each other but 

 not to the primary form. The three include a coarse, shaggy, 

 downy form (the most common one), a white, downy form, and 

 an immersed, glabrous, brown form. 



The most remarkable feature of pleomorphism is exhibited by 

 the results of animal inoculations. When used as inoculum, the 

 pleomorphic forms produce lesions that are indistinguishable from 

 those arising from inoculum with the primary or normal form. 

 When the fungus is reisolated from the infected hairs or scales, it 

 invariably grows like the pleomorphic form. Langeron and Talice 

 (1930) used the pleomorphic form of Sabonraudites felinus as 

 inoculum, obtained a typical lesion on guinea pig, and were able 

 to reisolate only pleomorphic mycelium. In its normal parasitic 

 phase this fungus consists of an ectothrix sheath of spores sur- 

 rounding the infected hair and of hyphae internal to the hair. In 

 the pleomorphic form the ectothrix sheath was without spores. 

 If the pleomorphic culture used as inoculum is completely pleo- 

 morphic and quite sterile, the cultures reisolated from scales and 

 hairs are likewise quite sterile. 



Mycides. In 1912 Jadassohn made the interesting observation 

 that primary localized infections (mycoses) by species of Tricho- 

 phytoneae may be accompanied by secondary lesions (mycides) 

 on distant parts of the body in which no fungus can be found. 

 These mycides have come to be designated as trichophytides, epi- 

 dermophytides, microsporides, etc., depending upon the genus 

 responsible for the primary lesions. Jadassohn [Gregory (1935)] 

 explained this phenomenon as an allergic reaction, since he found 

 that secondary lesions could be produced by rubbing the spores 

 into the skin of other children. This external origin of mycides, 

 however, has not been substantiated in subsequent investigations. 

 Instead they have been determined to arise from spores or toxic 

 products of the pathogen liberated in the primary lesions and dis- 

 seminated by the blood stream. The reaction appears, therefore, 

 to result from hypersensitivity to the fungus protein. Evidence 



