Candidiasis
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Candidiasis Main page |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]
Overview
Causes
Candida Albicans is responsible for the majority of Candidal infections.
Localized candidiasis
Oral and esophageal candidasis:
- Candida albicans accounts for majority of the cases followed by some non Albicans species as C. krusei and C. glabrata.[1][2]
Candida vulvovaginitis:
- Candida albicans: These strains are isolated in 85 to 95% patients with yeast infection.[3]
- 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.[4]
Chronic mucocutaneous candidiasis:
- C. albicans are the most isolated species.[5]
Invasive candidasis
Candidaemia:
- C. albicans is the most common isolated organism. However, some non C. albicans species were isolated beside C. albicans.[6]
- In severely immunocomoromised patients, non C. Albicans species were isolaetd alone.
Candida endocarditis:
Among causes of fungal endophthalmitis, Cadida and non candida species are the 2 most common causes. However, Non candida species are slightly more prevalent.[7]
Candida osteoarticular disease:
C. albicans is the most common cause. However, C. glabrata and C. tropicalis are also involved.[8]
Classification:
Candidiasis can be classified according to the site of infection into:[9]
Localoized mucocutaneous candidiasis:
- Oropharyngeal candidiasis
- Esophageal candidiasis
- Candida vulvovaginitis
- Chronic mucocutaneous candidiasis.
Invasive Candidiasis:
More serious and usually presenting in an immunocompromised host.
- Candidaemia
- Candida endophthalmitis
- Candida endocarditis
- Candida osteoarticular disease
Pathophysiology
Candida is a normal commensal of skin and mucous membranes. A competent immune system and an intact regenerating healthy skin prevent the virulence of Candida.
Candida Virulence factors
The main virulence factors that mediate the infection:[10]
- Secreting molecules that mediate adherence into host cells
- Production of hydrolases which has a lytic effect on tissues and facilitate the invasion by the bacteria.
- Polymorphism: Candida has the ability to grow either as pseudohyphae (elongated elipsoid 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 species 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 was 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 susceotibility of getting recurrent candidal vulvovaginitis.[11]
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.[12]
Conditions that compromises cell mediated immunity:
- T cell deficiencies as in DiGeorge syndrome, Wiscot-Aldrich syndrome and ataxia-telengictasia.
- Bone marrow transplant
- Leukaemias
- Corticosteroids use or immunosuppresive drugs.
Conditions that worsens the general condition:
- Malignancies
- Recent chemotherapy
- Trauma
- 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
References
- ↑ 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.
- ↑ "Candidaesophagitis | SpringerLink".
- ↑ 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.
- ↑ 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.
- ↑ "Chronic mucocutaneous candidiasis - Journal of the American Academy of Dermatology".
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ "Candidiasis | Types of Diseses | Fungal Diseases | CDC".
- ↑ 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.
- ↑ 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.
- ↑ Pappas PG (2006). "Invasive candidiasis". Infect. Dis. Clin. North Am. 20 (3): 485–506. doi:10.1016/j.idc.2006.07.004. PMID 16984866.