Candida albicans / Candida albicans infection

Concerning Candida albicans / Candida albicans infection, Candida albicans is a commensal fungus and, in >80% of the population, a part of the normal gut microbiota (1, 2). It is normally contained by epithelial barrier immunity (3, 4, 5).

70% - 80% of healthy patients experienced S. aureus, C. albicans, and cytomegalovirus infections (6, 7). Candida albicans can act as both a commensal organism and an opportunistic pathogen. It causes various diseases, from superficial infections to severe invasive diseases in immunocompromised people. The most common infection is Vulvovaginal candidiasis (VVC) / Vaginal yeast infection, affecting about 75% of women during their reproductive years. Approximately 5%–10% of these women experience recurrent Vulvovaginal candidiasis (RVVC), defined by four or more infections annually. RVVC affects around 350 million women globally, posing significant mental health and economic challenges (8, 9, 10).

A bloom of C. albicans during antibiotic therapy is common. It often leads to invasive disease, known as candidemia. This is frequent in patients with blood cancers (11). Disruption of the gut microbiota can occur. Broad-spectrum antibiotics with anaerobic activity cause this. They remove colonization resistance. This leads to intestinal dominance by C. albicans (12, 13).

Colonization resistance is a non-specific defense mechanism. It limits the growth of C. albicans in the large intestine. This keeps the opportunist's abundance low in feces (14).

A single fungal species - Candida albicans - inhibiting multiple dominant genera of gut bacteria (20).

Candidemia is a major cause of hospital infections in the U.S. It has a high mortality rate, up to 49% (15, 16, 17, 18, 19). Candida albicans represents the most common cause of fungal bloodstream infection; and despite adequate antifungal treatment, the overall mortality is 30%–40%, exceeding 60% in critically ill patients (21, 22).

References:

(1) Talapko et al. 2021 J Fungi (Basel) 7: 79
(2) Delavy et al. 2023 Gut Microbes 15: 2287618
(3) Romani 2011 Nat Rev Immunol. 11: 275-88
(4) Netea et al. 2015 Nat. Rev. Immunol. 15: 630–642
(5) Lionakis & Levitz 2018 Annu. Rev. Immunol. 36: 157–191
(6) Sobel 2007 Lancet 369: 1961-1971
(7) Lu et al. 2021d Curr Opin Immunol 72: 1-12
(8) Bauters et al. 2002 Am. J. Obstet. Gynecol. 187: 569-574
(9) Sobel 2016 Am. J. Obstet. Gynecol. 214: 15-21
(10) Denning et al. 2018 Lancet Infect. Dis. 18: e339-e347
(11) Zhai et al. 2020 Nat Med 26: 59-64
(12) Pappas et al. 2018 Nat. Rev. Dis. Primers 4: 18026
(13) Alonso-Monge et al. 2021 PLoS Pathog 17: e1009710
(14) Savage et al. 2024 Cell Host & Microbe 32: 1103-1113
(15) Viscoli et al. 1999 Clin Infect Dis 28: 1071-1079
(16) Wilson et al. 2002 Value Health 5: 26-34
(17) Gudlaugsson et al. 2003 Clin Infect Dis 37: 1172-1177
(18) Morgan et al. 2005 Infect Control Hosp Epidemiol 26: 540-547
(19) Magill et al. 2018 N Engl J Med 379: 1732-1744
(20) Rao et al. 2021
(21) Kullberg & Arendrup 2015 N. Engl. J. Med. 373: 1445–1456
(22) Pappas et al. 2018 Nat. Rev. Dis. Primers 4: 18026

see also:
CD369 (C-Type lectin receptors (CLRs))
Fungal infections
Mycobiota
Septicemia / Sepsis
Vulvovaginal candidiasis (VVC) / Vaginal yeast infection