Candida parapsilosis: from Genes to the Bedside

Abstract

Patients with suppressed immunity are at the highest risk for hospital-acquired infections. Among these, invasive candidiasis is the most prevalent systemic fungal nosocomial infection. Over recent decades, the combined prevalence of non-albicans Candida species outranked Candida albicans infections in several geographical regions worldwide, highlighting the need to understand their pathobiology in order to develop effective treatment and to prevent future outbreaks. Candida parapsilosis is the second or third most frequently isolated Candida species from patients. Besides being highly prevalent, its biology differs markedly from that of C. albicans, which may be associated with C. parapsilosis' increased incidence. Differences in virulence, regulatory and antifungal drug resistance mechanisms, and the patient groups at risk indicate that conclusions drawn from C. albicans pathobiology cannot be simply extrapolated to C. parapsilosis Such species-specific characteristics may also influence their recognition and elimination by the host and the efficacy of antifungal drugs. Due to the availability of high-throughput, state-of-the-art experimental tools and molecular genetic methods adapted to C. parapsilosis, genome and transcriptome studies are now available that greatly contribute to our understanding of what makes this species a threat. In this review, we summarize 10 years of findings on C. parapsilosis pathogenesis, including the species' genetic properties, transcriptome studies, host responses, and molecular mechanisms of virulence. Antifungal susceptibility studies and clinician perspectives are discussed. We also present regional incidence reports in order to provide an updated worldwide epidemiology summary.

Keywords: Candida parapsilosis; antifungal; epidemiology; experimental tools; genome; host response; pathogenicity; treatment; virulence.

FIG 1

Transmission routes and pathogenesis of C. parapsilosis. (A) Central venous catheter (CVC) colonized by C. parapsilosis cells as the source of infection. Implantation of the contaminated device results in systemic dissemination. (B) Colonization and invasion of host epithelial surfaces. Invasion is supported by various virulence factors, including morphology transition and the release of fungal secretions such as hydrolytic enzymes. (C) Following phagocytosis, fungal cells not only survive but also may induce exocytosis or replicate within host cells. (Microscopic image series were taken by Csaba Papp.)