Candidiasis: Difference between revisions

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===Localized candidiasis===
===Localized candidiasis===
====Oral and esophageal candidasis:====  
====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 accounts for majority of the cases followed by some non Albicans species as C. krusei and C. glabrata.  
   
   
====Candida vulvovaginitis:====  
====Candida vulvovaginitis:====  

Revision as of 14:35, 3 May 2017

Candidiasis Main page

Patient Information

Overview

Causes

Classification

Pathophysiology

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.

Candida vulvovaginitis:

Chronic mucocutaneous candidiasis:

C. albicans are the most isolated species.

Invasive candidasis

Candidaemia:

C. albicans is the most common isolated organism. However, some non C. albicans species were isolated beside C. albicans. In severely immunocomoromised patients, non C. Albicans species were isolaetd alone.

Candida Ophthalmitis:

Among causes of fungal endophthalmitis, Cadida and non candida species are the 2 most common causes. However, Non candida species are slightly more prevalent.

Candida osteoarticular disease:

C. albicans is the most common cause. However, C. glabrata and C. tropicalis are also involved.

Classification:

Candidiasis can be classified according to the site of infection into:[3]

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:[4]

  1. Secreting molecules that mediate adherence into host cells
  2. Production of hydrolases which has a lytic effect on tissues and facilitate the invasion by the bacteria.
  3. 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.
  4. 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.[5]

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.[6]

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

  1. 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.
  2. 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.
  3. "Candidiasis | Types of Diseses | Fungal Diseases | CDC".
  4. 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.
  5. 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.
  6. Pappas PG (2006). "Invasive candidiasis". Infect. Dis. Clin. North Am. 20 (3): 485–506. doi:10.1016/j.idc.2006.07.004. PMID 16984866.