Candidiasis: Difference between revisions
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===Candida Virulence factors=== | ===Candida Virulence factors=== | ||
The main virulence factors that mediate the infection:<ref name="pmid23302789">{{cite journal |vauthors=Mayer FL, Wilson D, Hube B |title=Candida albicans pathogenicity mechanisms |journal=Virulence |volume=4 |issue=2 |pages=119–28 |year=2013 |pmid=23302789 |pmc=3654610 |doi=10.4161/viru.22913 |url=}}</ref> | The main virulence factors that mediate the infection:<ref name="pmid23302789">{{cite journal |vauthors=Mayer FL, Wilson D, Hube B |title=Candida albicans pathogenicity mechanisms |journal=Virulence |volume=4 |issue=2 |pages=119–28 |year=2013 |pmid=23302789 |pmc=3654610 |doi=10.4161/viru.22913 |url=}}</ref> | ||
#Secreting '''molecules that mediate adherence''' into host cells | |||
#Production of '''[[hydrolases]]''' which has a [[Lytic|lytic effect]] on tissues and facilitate the invasion by the fungus. | |||
#'''[[Polymorphism]]:''' [[Candida]] has the ability to grow either as [[Hyphae|pseudohyphae]] (elongated ellipsoid form) or in a [[Yeast|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|Biofilm production]]:''' which means the ability to form a thick layer of the [[organism]] on the [[Mucosal|mucosal surfaces]] or even on [[catheters]] and [[dentures]]. | |||
Patients with [[candida vulvovaginitis]] were found to have decreased levels of [[Lectins|mannose binding lectins (MBL)]] . Further investigations revealed that 2 [[genetic mutations]] in [[genes]] responsible for [[Lectins|MBL]] and [[Interleukin 4|IL4]] production increase the host susceptibility of getting recurrent [[candida vulvovaginitis]].<ref name="pmid18715406">{{cite journal |vauthors=Donders GG, Babula O, Bellen G, Linhares IM, Witkin SS |title=Mannose-binding lectin gene polymorphism and resistance to therapy in women with recurrent vulvovaginal candidiasis |journal=BJOG |volume=115 |issue=10 |pages=1225–31 |year=2008 |pmid=18715406 |doi=10.1111/j.1471-0528.2008.01830.x |url=}}</ref> | Patients with [[candida vulvovaginitis]] were found to have decreased levels of [[Lectins|mannose binding lectins (MBL)]] . Further investigations revealed that 2 [[genetic mutations]] in [[genes]] responsible for [[Lectins|MBL]] and [[Interleukin 4|IL4]] production increase the host susceptibility of getting recurrent [[candida vulvovaginitis]].<ref name="pmid18715406">{{cite journal |vauthors=Donders GG, Babula O, Bellen G, Linhares IM, Witkin SS |title=Mannose-binding lectin gene polymorphism and resistance to therapy in women with recurrent vulvovaginal candidiasis |journal=BJOG |volume=115 |issue=10 |pages=1225–31 |year=2008 |pmid=18715406 |doi=10.1111/j.1471-0528.2008.01830.x |url=}}</ref> | ||
Revision as of 18:07, 3 May 2017
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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
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.
Causes
Candida Albicans is responsible for the majority of Candida 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 immuno-copromised patients, non C. albicans species were isolated alone.
Candida endocarditis:
- 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.[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.
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 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.[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, Wiscott-Aldrich syndrome and Ataxia-telangiectasia.
- 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.