|Agar plate culture of Candida albicans|
Candidiasis Main page
Synonyms and Keywords: Candida infection, Candida caused diseases
Candida is a normal commensal of the skin and mucous membranes. The balance between the virulence of the fungus and the host immune defense is responsible avoiding opportunistic infection of candida. Deficiency of cell-mediated immunity or poor general status are the main risk factors for having opportunistic candidiasis. Candidiasis is usually localized to skin and mucous membranes. In rare cases, candidiasis can spread causing candidaemia and distant infection. These cases are usually associated with deficient immunity C. albicans is the main species causing infection in humans more than any other candida species.
Oral and esophageal candidasis:
- Candida albicans accounts for majority of the cases followed by some non albicans species as C. krusei and C. glabrata.
- Candida albicans: These strains are isolated in 85 to 95% patients with yeast infection.
- Candida non albicans: Candida glabrata is the most common isolated pathogen in this group affecting 10 to 20% of women and is associated with recurrent Candida vulvovaginitis.
Chronic mucocutaneous candidiasis:
- C. albicans is the most common isolated organism. However, some non C. albicans species were isolated beside C. albicans.
- In severely immuno-copromised patients, non C. albicans species were isolated alone.
- Among causes of fungal endophthalmitis, Cadida albicans and non candida albicans species are the 2 most common causes. However, Non albicans species are slightly more prevalent.
Candida osteoarticular disease:
Candidiasis can be classified according to the site of infection into:
|Localoized mucocutaneous candidiasis||Invasive Candidiasis|
|Oropharyngeal candidiasis||Esophageal candidiasis||Candida vulvovaginitis||Chronic mucocutaneous candidiasis||Candidaemia||Candida endophthalmitis||Candida endocarditis||Candida osteoarticular disease|
Candida Virulence factors
The main virulence factors that mediate the infection:
- Secreting molecules that mediate adherence into host cells
- Production of hydrolases which has a lytic effect on tissues and facilitate the invasion by the fungus.
- Polymorphism: Candida has the ability to grow either as pseudohyphae (elongated ellipsoid form) or in a yeast form (rounded to oval budding form. While the role of polymorphism is not clearly understood in the virulence of Candida, it’s noted that the species that are capable of producing the most severe form of the disease has this ability.
- Biofilm production: which means the ability to form a thick layer of the organism on the mucosal surfaces or even on catheters and dentures.
Patients with candida vulvovaginitis were found to have decreased levels of mannose binding lectins (MBL) . Further investigations revealed that 2 genetic mutations in genes responsible for MBL and IL4 production increase the host susceptibility of getting recurrent candida vulvovaginitis.
Host immune defects
Any condition that compromises cell mediated immunity, worsens the general status of the patient or provide a favorable medium for Candida to form biofilms put the patient at increased risk for having candidiasis.
Conditions that compromises cell mediated immunity:
- T cell deficiencies as in DiGeorge syndrome, Wiscott-Aldrich syndrome and Ataxia-telangiectasia.
- Bone marrow transplant
- Corticosteroids use or immunosuppresive drugs.
Conditions that worsens the general condition:
- Recent chemotherapy
- Recent surgery
- Prolonged hospitalization
- Broad-spectrum antibiotics
- Renal failure
- Haemodialysis (especially if prolonged)
Dentures that provide a favorable media for forming biofilms:
- Prolonged central venous catheters insertion
- Prolonged foley’s catheter insertion
- Prolonged mechanical ventilation
Candidiasis should be differentiated from other diseases presenting with an erythmatous, scaly, annular and pruritic rash. The differentials include the following:
|Name of superficial infection||Clinical presentation||Extension to hair follicle||Fungus(i)||Systemic disease||KOH preparations||Morphology in tissue sections|
|Tinea or ringworm||Round lesions with scaly border, accompanied by pruritis and burning||Yes; when suppurative known as kerion, when chronic known as Majocchi's granuloma||Dermatophytes (Epidermophyton spp., Trichophyton spp., Microsporum spp.)||Very rare but can invade the dermis and soft tissues, causing mycetomas||Hyphae with or without septations||Hyphae cannot be visualized in the keratin with H&E, special stains are needed|
|Tinea versicolor||Hypo and hyperpigmentation in patients with oily and sweaty skin, fine scales when scratching||Yes, known as Pityrosporum folliculits||Malassezia spp.||Systemic infections may occur in premature neonates receiving parenteral nutrition and in other immunosuppressed hosts||Yeasts and hyphae (“spaghetti and meat balls”)||Faintly basophilic hyphae in the stratum corneum|
|Tinea nigra||Brown to black macule, usually on palms, with some scaling||No||Phaeoannellomyces werneckii||Not described||Darkly pigmented, septated, and branching hyphae||Pigmented hyphae in the stratum corneum|
|White piedra||Creamy-white, small, soft nodules in hair shafts||No||Trichosporon spp.||Immunosuppressed patients may have lung infiltrates, renal involvement, and fungemia||Septate hyphae perpendicular to hair shaft||Not used for diagnosis|
|Black piedra||Hard dark nodules in hair shafts||No||Piedraia hortae||Not described||Collections of crescent ascospores surrounded by pigmented hyphae||Not used for diagnosis|
|Superficial candidiasis||Intertrigo, chronic paronychia, onychodystrophy, cheilitis||Yes||Candida spp.||Yes, particularly in patients with AIDS and depending on the level of immunosuppression||Yeasts, pseudohyphae may be observed||Fungal elements may be seen through the biopsy, vascular invasion must be determined|
- Laurent M, Gogly B, Tahmasebi F, Paillaud E (2011). "[Oropharyngeal candidiasis in elderly patients]". Geriatr Psychol Neuropsychiatr Vieil (in French). 9 (1): 21–8. doi:10.1684/pnv.2011.0259. PMID 21586373. <templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
- "Candidaesophagitis | SpringerLink".<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
- Corsello S, Spinillo A, Osnengo G, Penna C, Guaschino S, Beltrame A; et al. (2003). "An epidemiological survey of vulvovaginal candidiasis in Italy". Eur J Obstet Gynecol Reprod Biol. 110 (1): 66–72. PMID 12932875. <templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
- Okungbowa FI, Isikhuemhen OS, Dede AP (2003). "The distribution frequency of Candida species in the genitourinary tract among symptomatic individuals in Nigerian cities". Rev Iberoam Micol. 20 (2): 60–3. PMID 15456373. <templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
- "Chronic mucocutaneous candidiasis - Journal of the American Academy of Dermatology".<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
- Ostrosky-Zeichner L, Pappas PG (2006). "Invasive candidiasis in the intensive care unit". Crit. Care Med. 34 (3): 857–63. doi:10.1097/01.CCM.0000201897.78123.44. PMID 16505666.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
- Ellis ME, Al-Abdely H, Sandridge A, Greer W, Ventura W (2001). "Fungal endocarditis: evidence in the world literature, 1965-1995". Clin. Infect. Dis. 32 (1): 50–62. doi:10.1086/317550. PMID 11118386.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
- Dupont B, Drouhet E (1985). "Cutaneous, ocular, and osteoarticular candidiasis in heroin addicts: new clinical and therapeutic aspects in 38 patients". J. Infect. Dis. 152 (3): 577–91. PMID 3897399.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
- "Candidiasis | Types of Diseses | Fungal Diseases | CDC".<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
- Mayer FL, Wilson D, Hube B (2013). "Candida albicans pathogenicity mechanisms". Virulence. 4 (2): 119–28. doi:10.4161/viru.22913. PMC 3654610. PMID 23302789.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
- Donders GG, Babula O, Bellen G, Linhares IM, Witkin SS (2008). "Mannose-binding lectin gene polymorphism and resistance to therapy in women with recurrent vulvovaginal candidiasis". BJOG. 115 (10): 1225–31. doi:10.1111/j.1471-0528.2008.01830.x. PMID 18715406.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
- Pappas PG (2006). "Invasive candidiasis". Infect. Dis. Clin. North Am. 20 (3): 485–506. doi:10.1016/j.idc.2006.07.004. PMID 16984866.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>