Candida glabrata: review of epidemiology, pathogenesis, and clinical disease with comparison to C. albicans

Abstract

Until recently, Candida glabrata was considered a relatively nonpathogenic commensal fungal organism of human mucosal tissues. However, with the increased use of immunosuppressive agents, mucosal and systemic infections caused by C. glabrata have increased significantly, especially in the human immunodeficiency virus-infected population. A major obstacle in C. glabrata infections is their innate resistance to azole antimycotic therapy, which is very effective in treating infections caused by other Candida species. Candida glabrata, formerly known as Torulopsis glabrata, contrasts with other Candida species in its nondimorphic blastoconidial morphology and haploid genome. 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. Currently, however, there are few recognized virulence factors of C. glabrata and little is known about the host defense mechanisms that protect against infection. Two established animal models (systemic and vaginal) have been established to study treatment, pathogenesis, and immunity. Treatment of C. glabrata infections can include azoles but often requires amphotericin B or flucytosine. This review summarizes all known clinical and experimental information about C. glabrata infections with comparisons to C. albicans as a means of contrasting the two species commonly observed and emphasizing the many recognized differences.

FIG. 1

Size differential of C. glabrata and C. albicans. Shown are wet-mount slide preparations of C. glabrata (A) and C. albicans (B) on a hemocytometer. Magnification, ×400.

FIG. 2

CHEF of genomic DNA from representative isolates of C. albicans and C. glabrata. Lanes 1 to 3 and 5 are similar strains of C. albicans; lanes 4 and 6 are strains of C. glabrata.

FIG. 3

Experimental C. glabrata infections in mice with intermediate (CBA/J) and high (DBA/2) susceptibilities to C. albicans systemic infection and in NOD/Lt mice. Data points represent mean CFU ± standard errors of the mean (SEM) in animals with positive cultures only (the percentage of animals with positive cultures is shown). Reprinted from reference with permission of the publisher.

FIG. 4

Comparative analysis of C. glabrata, C. albicans, and S. cerevisiae vaginal fungal burden in NOD mice. Data points represent mean CFU ± SEM for animals with positive cultures (the percentage of animals with positive cultures is shown) following intravaginal inoculation with 1 × 10⁷ blastoconidia of C. glabrata or S. cerevisiae or 5 × 10⁵ blastoconidia of C. albicans. Reprinted from reference with permission of the publisher.

FIG. 5

Histopathology of vaginal tissue from estrogen-treated NOD mice inoculated with C. glabrata (A) and C. albicans (B). Arrows represent blastoconidia or hyphae. Magnification, ×100. Reprinted from reference with permission of the publisher.