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The production of various eremophilane-type sesquiterpenes by Penicillium roqueforti strains has allowed us to propose a biochemical pathway for PR toxin synthesis. A time-course study of P. roqueforti metabolite production by high-performance liquid chromatography was performed to check this hypothetical pathway. The results obtained suggested that eremofortin C was the direct precursor of PR toxin in the P. roqueforti cell. Attempts to determine the amount of PR toxin in the mycelium failed. It was shown that the absence of PR toxin in mycelium was due to its instability during the extraction procedure.

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Serum samples from patients with candidosis and from rabbits experimentally infected with serotype B C. albicans strains consistently showed higher antibody titers against Candida strains with serotype A antigens than strains with serotype B antigens, in indirect fluorescent antibody tests. When sera from rabbits-infected with C. albicans serotype B strains were absorbed with blastospores of the homologous strain they continued to react against strains of C. albicans serotype A and a C. tropicalis strain with serotype A antigens. Serotype Aspecific antisera reacted against tissue forms of C. albicans serotype B in vivo and against serotype B germ tubes, but not their parent blastospores, in vitro. These findings suggest that C. albicans B serotype cells may sometimes express, in vitro or in vivo, one or several antigens so far considered as specific of serotype A. The results have implications for the classical concept of C. albicans serotypes and for the serological diagnosis of candidosis in relation with the previously described strain P variable antigens.We have previously demonstrated that not all strains of Candida albicans show the same reactivity in the indirect fluorescent antibody (IFA) test against sera from patients with candidosis. In particular, we found that strains isolated from patients reveal more antibodies than strains isolated from healthy subjects [19,22]. Moreover, strains freshly isolated from patients give much stronger reactions than those that have been subcultured for a long time in the laboratory [10]. These observations suggest phenotypic variability in the antigenic structure of C. albicans in vivo and in vitro. For ease of discussion, and in the absence of more precise information about them, we refer to all of the blastospore antigens that-are qualitatively and/or quantitatively variable and responsible for these differences in reactivity as P antigens--for "paretial" and "pathogenicity" [19,20].Our preliminary studies seemed to show that P antigens are not related to the serotypes described by Hasenclever and Mitchell [9]. So, monospore cultures prepared from a given strain and belonging to the same serotype, exhibit different reactivities against patients' sera, as do our reference strains, L and VW32, both of which were serotype A [18][19][20]. However, during a recent routine control experiment we observed that, although the VW32 strain was still of serotype A, the L strain now behaved as a B serotype. Therefore, we felt the relationship between P antigens and serotypes must he elucidated.There is little information available concerning the diagnostic significance of C. albicans antigens and their relationship to serotype-specific antigen, although the latter have been partially characterized [23] and studied by proton magnetic resonance spectra [5], and localized ultramicroscopically [21]. From a practical point of view, published serological studies have logically involved serotype A