glabrata infections and includes specific comparisons to C. This review discusses what is currently known about C. Therefore, studies to understand the pathogenesis of C. glabrata infections (systemic and vaginal) ( 24, 41). There are only two established animal models of experimental C. glabrata, and virtually nothing is known about the host defenses directed against the organism. Very little is known about the virulence of C. glabrata account for only a small percentage of published studies on medically important fungal infections. albicans, difficult to treat, and associated with a high mortality rate, publications to date on C. Although this infection is second or third in frequency after C. glabrata compared to other Candida species. Unfortunately, there have been relatively few investigations of C.
glabrata infections have a high mortality rate in compromised, at-risk hospitalized patients. glabrata infections are difficult to treat and are often resistant to many azole antifungal agents, especially fluconazole ( 65, 90, 167, 179). glabrata is not dimorphic consequently, it is found as blastoconidia both as a commensal and as a pathogen. glabrata infections can be mucosal or systemic and are common in abnormal hosts (e.g., immunocompromised persons or those with diabetes mellitus) ( 53, 148, 149, 182). glabrata is often the second or third most common cause of candidiasis after C. In fact, depending on the site of infection, C. However, following the widespread and increased use of immunosuppressive therapy together with broad-spectrum antimycotic therapy, the frequency of mucosal and systemic infections caused by C. Historically, Candida glabrata has been considered a relatively nonpathogenic saprophyte of the normal flora of healthy individuals, rarely causing serious infection in humans ( 57, 163). albicans as a means of contrasting the two species commonly observed and emphasizing the many recognized differences. glabrata infections with comparisons to C. This review summarizes all known clinical and experimental information about C. glabrata infections can include azoles but often requires amphotericin B or flucytosine. Two established animal models (systemic and vaginal) have been established to study treatment, pathogenesis, and immunity. glabrata and little is known about the host defense mechanisms that protect against infection. Currently, however, there are few recognized virulence factors of C. glabrata currently ranks second or third as the causative agent of superficial (oral, esophageal, vaginal, or urinary) or systemic candidal infections, which are often nosocomial.
Candida glabrata, formerly known as Torulopsis glabrata, contrasts with other Candida species in its nondimorphic blastoconidial morphology and haploid genome. glabrata infections is their innate resistance to azole antimycotic therapy, which is very effective in treating infections caused by other Candida species. glabrata have increased significantly, especially in the human immunodeficiency virus-infected population. However, with the increased use of immunosuppressive agents, mucosal and systemic infections caused by C. Until recently, Candida glabrata was considered a relatively nonpathogenic commensal fungal organism of human mucosal tissues.