Crossed immunoelectrophoresis with absorption in situ was used to distinguish the cytoplasmic antigens unique to the mycelial or yeast phase of Candida albicans from cytoplasmic antigens shared by both phases. The soluble cytoplasmic extracts of each growth phase had at least six distinct antigenic constituents not shared by the other phase. This technique is recommended for the analysis of closely related antigenic complexes. Candida albicans is a commensal of the mucous membranes and the gastrointestinal tract of humans. This same organism may cause intractable disseminated disease in the compromised patient. The clinical differentiation of colonization from disseminated disease is often difficult. The presence of the organism in blood smears, blood cultures, or urine may indicate active infection, transient candidemia, or candiduria (3, 8, 12). Present serological diagnosis of systemic candidiasis is plagued by the difficulty ofdistinguishing systemic infections from saprobic colonization (16, 20). Agglutinating antibodies to formalin-killed whole yeast cells are found in the sera of most healthy adults (22). The demonstration of serum antibodies to cytoplasmic antigens may indicate active infection (21), but it does not distinguish between local, transient, or systemic invasion (10, 11, 15, 17). Most of the antigens currently used in serological testing for candidiasis are prepared from blastospores, yet invasive candidiasis is usually accompanied by the growth of C. albicans in its mycelial form. Blastospores are most often associated with limited or resolving infection; mycelial elements are associated with spreading or invasive candidiasis. Mycelial elements may facilitate invasion or simply reflect the inability of the host to curtail the organism efficiently (14, 18). In vitro studies have shown that the chemical composition of the mycelial elements differs from that of the yeasts (5, 6, 7, 19)-this difference is reflected in the antigenic composition of yeast and mycelial phases (9). In the present study, the cytoplasmic antigenic composition ofthe two distinct morphological phases of C. albicans is compared by means of two-dimensional crossed line electrophoresis with absorption in situ (2, 4).
Menstrual toxic shock syndrome is a rare but potentially life-threatening illness manifest through the actions of Staphylococcus aureus toxic shock syndrome toxin 1 (TSST-1). Previous studies have shown that tampon additives can influence staphylococcal TSST-1 production. We report here on the TSST-1-suppressing activity of 34 compounds that are commonly used additives in the pharmaceutical, food, and perfume industries. Many of the tested chemicals had a minimal impact on the growth of S. aureus and yet were potent inhibitors of TSST-1 production. The TSST-1-reducing compounds included surfactants with an ether, amide, or amine linkage to their fatty acid moiety (e.g., myreth-3-myristate, Laureth-3, disodium lauroamphodiacetate, disodium lauramido monoethanolamido, sodium lauriminodipropionic acid, and triethanolamine laureth sulfate); aromatic compounds (e.g. phenylethyl and benzyl alcohols); and several isoprenoids and related compounds (e.g., terpineol and menthol). The membrane-targeting and -altering effects of the TSST-1-suppressing compounds led us to assess the activity of molecules that are known to inhibit fatty acid biosynthesis (e.g., cerulenin, triclosan, and hexachlorophene). These compounds also reduced S. aureus TSST-1 production. This study suggests that more additives than previously recognized inhibit the production of TSST-1.
Three hundred fifty human sera were tested by double immunodiffusion, crossed-line electrophoresis, and crossed immuno-affinoelectrophoresis with a concanavalin A intermediate gel for precipitating antibodies to antigens present in cytoplasmic extracts of Candida albicans. Sera from 48 of 287 hospitalized patients at risk of invasive candidiasis contained precipitating antibodies to Candida antigens. Of these 48 sera, 27 had precipitating antibodies only to cell-wall antigens present in the cytoplasmic extract, and 21 sera had precipitating antibodies to both cytoplasmic and cell-wall antigens. The latter sera came from patients who were 2.5 times as likely to have deep-seated candidiasis as those patients with precipitins exclusively to cell-wall antigens. Sera from seven of 22 patients with vaginal candidiasis and 10 of 41 patients with other fungal infections had precipitating antibodies to C. albicans cell-wall antigens; only two of these sera also contained precipitating antibodies to the cytoplasmic antigens. Crossed immunoaffinoelectrophoresis with concanavalin A reduced the number of false-positive results and increased the predictive value positive of the precipitin test for deep-seated candidiasis from 31% to 71%.
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