Candida albicans is the major fungus responsible for yeast infections, and it is also a leading cause of hospital-acquired bloodstream infections in the United States. Researchers at The University of Texas (UT) Health Science Center at San Antonio, in collaboration with UT at San Antonio and Spain’s Universidad de Valencia, are learning more about what makes C albicans so deadly. Their paper, which was published in the January 13, 2009 issue of the Proceedings of the National Academy of Sciences, strongly suggests that a particular form of this fungus is especially important for virulence. Further, a master control gene is critical for determining cell shape and virulence of the fungus. Although C albicans is extremely common and is usually harmless to its hosts, the fungus can be deadly for those with immune deficiencies. According to David Kadosh, PhD, assistant professor in the UT Health Science Center Department of Microbiology and Immunology, when the immune defenses are compromised this fungus can infect other parts of the body. “Understanding more about the genes involved in this process will lead us to potential antifungal drug targets,” he says. Ninety percent of AIDS patients have oral C albicans infections with characteristic sores in the mouth. Cancer patients, organ transplant patients, and recipients of artificial joints and devices also are at high risk for C albicans complications, including bloodstream infections. Typical C albicans infections have a mixture of the 3 forms of the fungus, which are yeast (oval, budding cells), pseudohyphae (elliptical and connected), and hyphae (straight with parallel sides and connected). “This study, which documents experiments conducted in a mouse model of C albicans bloodstream infections, shows that, of these 3 forms, the hyphal form is especially important for virulence,” Dr. Kadosh said. Researchers shifted the fungal mixture more toward the hyphal form in one group of mice but not in the control group. Nearly all the mice with the greater proportion of hyphae died within 11 days. By contrast, most of the mice with fewer hyphae were alive after 30 days.
(Source: University of Texas Health Science Center at San Antonio, January 13, 2009)
