Fungal biofilm-associated infections in immunocompromised African populations: A narrative review of Candidozyma auris emergence, antifungal resistance mechanisms, and laboratory detection algorithms.

Abstract

Candidozyma auris the abbreviation C. auris is retained throughout has become one of the most concerning hospital-acquired fungal infections over the past decade, colonizing the environment and skin for extended periods, exhibiting multidrug resistance, and forming biofilms that are resistant to both the host immune response and antifungal treatments. Sub-Saharan and North African medical institutions have a unique set of risks: a significant HIV-positive population, widespread malnutrition, high rates of tuberculosis co-infection, the appearance of critical care units, and diagnostic laboratories that often lack the tools to accurately identify emerging yeast species. This paper aims to analyze the current understanding of the emergence and prevalence of C. auris infections in African healthcare facilities, discuss the properties of biofilm formed by this yeast that facilitate its persistence and resistance to treatment, examine the features of immunosuppressed African patients who are at the highest risk of C. auris colonization and infection, and identify the available laboratory tests that can be used to diagnose this fungus in African hospitals. A narrative review has been performed to gather the evidence on the emergence of C. auris in African healthcare facilities and describe the general trends in its clinical presentation. The data were retrieved from reports and research articles published in peer-reviewed journals, utilizing resources such as national and multinational surveillance records, World Health Organization documents, and scientific publications from regional reference labs that investigate the clinical characteristics and treatment of C. auris infections and report on the local epidemiology of this yeast. Four principal findings emerge. First, documented African activity is concentrated in South Africa, Kenya, Nigeria and Egypt and is dominated by clade III and clade I, but the apparent continental increase conflates genuine transmission with rapidly improving detection capacity and should not be read as an incidence estimate. Second, fluconazole resistance is consistently high across African series (of the order of 85-90%), amphotericin B resistance is elevated relative to global pooled estimates (approximately 15-35%, highest in the clade III-dominated South African series), whereas echinocandin resistance remains below 5% but is no longer negligible. Third, biofilm growth confers a reversible, largely non-genetic tolerance matrix-mediated drug sequestration, biofilm-induced efflux upregulation and persister-cell dormancy that raises effective inhibitory concentrations by one to more than two orders of magnitude above planktonic values, so routine susceptibility reports systematically understate the drug exposure required in device-associated infection. Fourth, the dominant diagnostic constraint across the continent is not the absence of technology as such but systematic misidentification by the conventional biochemical panels that remain the mainstay of African yeast identification; this is addressable through a tiered algorithm anchored on a low threshold of suspicion rather than on universal access to mass spectrometry or sequencing. We conclude that C. auris preparedness in Africa is best pursued not as a vertical, pathogen-specific programme but as an explicit extension of the antimicrobial resistance surveillance, laboratory strengthening and infection prevention frameworks already under construction across the region, with tiered diagnostics, antifungal stewardship, biofilm-aware clinical management and the systematic evaluation of natural product-derived adjunctive agents as the immediate priorities.