Expression of the 43 kDa glycoprotein (gp43) was analysed in several Paracoccidioides brasiliensis isolates. Using one- and two-dimensional analysis of crude cellular extracts, it was shown that protein expression in yeast and mycelium was dependent on the isolate analysed. In two strains, in both yeast and mycelium cells. gp43 was present, whereas expression was restricted to the yeast phase of two other strains. The clinical implications of this phase-specific gp43 expression are uncertain.
(1 --> 3)-beta-D-glucan, a characteristic fungal molecule, is known to increase in blood in invasive candidiasis, aspergillosis and cryptococcosis. This report shows that the plasma glucan concentration was also elevated in four patients infected with Fusarium, Trichosporon beigelii, Saccharomyces cerevisiae and Acremonium. In three of the patients, the elevation preceded positive blood cultures by 5-17 days, and in one of them it even preceded the onset of fever by 6 days. In a fourth patient, the glucan level decreased with clinical improvement. Plasma (1 --> 3)-beta-D-glucan determination appears to be useful also for diagnosis and follow-up of these unusual deep mycoses.
This paper deals with the discovery of the teleomorph of a Fonsecaea-like pathogen causing chromoblastomycosis in India. A new genus, Ascosubramania, is proposed to accommodate it.
Experimental Penicillium marneffei infection in mice was investigated histopathologically and by electron microscopy. Viable conidia (5 x 10(6) cells) of P. marneffei were inoculated into each mouse of group A (BALB/c mice) and group B (BALB/c-nu/nu-SIc mice) through the tail vein. All the mice were sacrificed at intervals and the livers were examined. In group A, the conidia were phagocytosed by Kupffer cells soon after inoculation, and proliferated by fission in the cytoplasm. Marked proliferation of yeast cells was observed 7 and 14 days after inoculation. With proliferation of the fungus, the number of lysosomes in Kupffer cells increased, and numerous granulomas were formed in the liver. These granulomas consisted mainly of macrophages with yeast cells, together with a few polymorphonuclear leukocytes, lymphocytes and giant cells. From 28 days on yeast cells were gradually cleared from the granulomas, and 56 days after inoculation almost all the granulomas disappeared. In group B, at an early stage of infection, similar pathological changes to those seen in mice of group A were observed. However, as the infection progressed, the number of granulomas continued to increase and yeast cells continued to proliferate although lymphocytes did not infiltrate these granulomas. With proliferation of yeast cells the liver tissue was replaced with both yeast cells engulfed by macrophages and extracellular yeasts, and dissemination occurred.
In 1991, 1208 cases of coccidioidomycosis were reported to the California Department of Health Services, compared with an annual average of 450 during 1986-90. We conducted a study in Tulare County to define the epidemiology of the disease and identify risk factors for severe disease, focusing on the epidemic period September 1991-December 1991. To identify cases, we used data from the Coccidioidomycosis Serology Laboratory at the University of California, Davis, other laboratories, and the Tulare County Health Department's coccidioidomycosis reporting system. We compared patients who were hospitalized with those who were not to determine risk factors for severe disease. We identified 128 cases of acute coccidioidomycosis diagnosed between 1 September and 31 December 1991 (attack rate 41/100,000); south central Tulare County had the highest attack rate. Thirty-five (27%) case-patients were hospitalized. Male sex (relative risk (RR) 2.5, 95% confidence interval (CI) 1.2-5.0), black people and Asian races (RR 4.8, 95% CI 2.4-9.6), and age > or = 20 years (RR 8.3, 95% CI 1.2-57.4) were univariately significant and remained independently associated with hospitalization in multivariate analysis. The 1991 Tulare County outbreak of coccidioidomycosis was part of a much larger outbreak that began in California during 1991 and continued through 1993. The outbreak was preceded by an unusually rainy spring. Although dust reduction measures during times of increased coccidioidomycosis incidence can help reduce exposure, definitive control awaits the development of a safe, effective vaccine.