Sandbox: ay: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
(Blanked the page)
No edit summary
Line 1: Line 1:
==Pathophysiology==
===Vaginal Defensive mechanisms aganist Candida===
====Innate Mechanisms====
{| class="wikitable"
!Defense
!Mechanism of protection
!Evidence of protection
|-
|Vaginal [[epithelial cells]]
|
*[[In vitro]] inhibition of [[Candida]] growth<ref name="pmid16239581">{{cite journal| author=Barousse MM, Espinosa T, Dunlap K, Fidel PL| title=Vaginal epithelial cell anti-Candida albicans activity is associated with protection against symptomatic vaginal candidiasis. | journal=Infect Immun | year= 2005 | volume= 73 | issue= 11 | pages= 7765-7 | pmid=16239581 | doi=10.1128/IAI.73.11.7765-7767.2005 | pmc=1273905 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16239581  }}</ref>
|
*Protective role [[in vivo]] unknown
*Patients with recurrent [[candida]] infections have decreased anti-Candida activity
|-
|Mannose-binding lectin
|
*[[Epithelial cell]] associated [[protein]] which binds to [[Candida]] surface mannan.<ref name="pmid18715406" />
*Inhibits [[Candida]] growth by activating [[complement]]<ref name="pmid15243942">{{cite journal| author=Ip WK, Lau YL| title=Role of mannose-binding lectin in the innate defense against Candida albicans: enhancement of complement activation, but lack of opsonic function, in [[phagocytosis]] by human dendritic cells. | journal=J Infect Dis | year= 2004 | volume= 190 | issue= 3 | pages= 632-40 | pmid=15243942 | doi=10.1086/422397 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15243942  }}</ref>
*Activity is genetically determined
|
*Decreased expression can increase the susceptibility for [[vaginal colonization]] of [[candida]] and leading to [[vaginitis]]
|-
|Activated [[lactoferrin]]<ref name="pmid15603095">{{cite journal| author=Naidu AS, Chen J, Martinez C, Tulpinski J, Pal BK, Fowler RS| title=Activated lactoferrin's ability to inhibit Candida growth and block yeast adhesion to the vaginal epithelial monolayer. | journal=J Reprod Med | year= 2004 | volume= 49 | issue= 11 | pages= 859-66 | pmid=15603095 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15603095  }}</ref>
|
*Fungistatic and fungicidal activity
|
*Role in protection aganist infection is not clear
|-
|Vaginal [[bacterial flora]]
|
*[[Lactobacillus]] species compete for nutrients.
*[[Bacteriocins]] and [[hydrogen peroxide]] inhibit yeast growth/[[germination]]
|
*Role in protection aganist vaginitis still unclear
|-
|Phagocytic systems/polymononuclear [[leukocytes]], [[mononuclear cells]], [[complement]]
|
*Mainly found in [[lamina propria]] in experimental vaginitis, help in reducing the [[yeast]] load and its invasion by [[phagocytosis]] and intracellular killing<ref name="pmid340470">{{cite journal| author=Diamond RD, Krzesicki R, Jao W| title=Damage to pseudohyphal forms of Candida albicans by neutrophils in the absence of serum in vitro. | journal=J Clin Invest | year= 1978 | volume= 61 | issue= 2 | pages= 349-59 | pmid=340470 | doi=10.1172/JCI108945 | pmc=372545 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=340470  }}</ref>
*[[Nitric oxide]] has anti-Candida activity
|
*Role in protection still unclear
|}


====Adaptive Mechanisms====
{| class="wikitable"
!Defense
!Mechanism
!Role in Protection
|-
|[[Immunoglobulin]] mediated [[immunity]]
|Systemic [[IgM]], [[IgG]], and local [[IgA]] antibodies are produced in response to the  infection<ref name="pmid4556009">{{cite journal| author=Waldman RH, Cruz JM, Rowe DS| title=Immunoglobulin levels and antibody to Candida albicans in human cervicovaginal secretions. | journal=Clin Exp Immunol | year= 1972 | volume= 10 | issue= 3 | pages= 427-34 | pmid=4556009 | doi= | pmc=1713147 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4556009  }}</ref>
|
*Protective role not proven.
*Elevated [[titres]] of vaginal anti-Candida [[IgG]], [[IgA]] are detected in women with recurrent vaginitis
*Persistent symptoms could be attributed to anti-Candida [[IgE]]<ref name="pmid8809464">{{cite journal| author=Fidel PL, Sobel JD| title=Immunopathogenesis of recurrent vulvovaginal candidiasis. | journal=Clin Microbiol Rev | year= 1996 | volume= 9 | issue= 3 | pages= 335-48 | pmid=8809464 | doi= | pmc=172897 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8809464  }}</ref>
|-
|[[Cell Mediated Immunity]]
|
[[Interleukin 4]] (Th2) inhibits anti-Candida activity of [[nitric oxide]] and protective pro-inflammatory Th1 [[cytokines]].<ref name="pmid15735412">{{cite journal| author=Fidel PL| title=Immunity in vaginal candidiasis. | journal=Curr Opin Infect Dis | year= 2005 | volume= 18 | issue= 2 | pages= 107-11 | pmid=15735412 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15735412  }}</ref>
|
*Role in protection from [[vulvovaginitis]] is still not clear
*It is still a hypothesis<ref name="pmid15102806">{{cite journal| author=Fidel PL, Barousse M, Espinosa T, Ficarra M, Sturtevant J, Martin DH et al.| title=An intravaginal live Candida challenge in humans leads to new hypotheses for the immunopathogenesis of vulvovaginal candidiasis. | journal=Infect Immun | year= 2004 | volume= 72 | issue= 5 | pages= 2939-46 | pmid=15102806 | doi= | pmc=387876 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15102806  }}</ref>
*Patients with recurrent infection have undetectable Th2 [[cytokines]].
|}
===Candida Virulence Factors===
*[[C. albicans]] exists as [[blastospores]], [[germ tubes]], [[pseudomycelia]], [[true mycelia]] and [[chlamydospores]] on special [[culture]] media. [[C. glabrata]] exists exclusively in [[blastospores]].
*All strains of [[Candida]] species possess a [[yeast]] surface [[mannoprotein]] which helps in adhering to [[epithelial cells]] of the [[vagina]].<ref name="pmid17560449">{{cite journal |vauthors=Sobel JD |title=Vulvovaginal candidosis |journal=Lancet |volume=369 |issue=9577 |pages=1961–71 |year=2007 |pmid=17560449 |doi=10.1016/S0140-6736(07)60917-9 |url=}}</ref><ref name="pmid3895958">{{cite journal |vauthors=Sobel JD |title=Epidemiology and pathogenesis of recurrent vulvovaginal candidiasis |journal=Am. J. Obstet. Gynecol. |volume=152 |issue=7 Pt 2 |pages=924–35 |year=1985 |pmid=3895958 |doi= |url=}}</ref>
*[[Germination]] of the spores helps in colonizing the vagina.<ref name="pmid6327527">{{cite journal| author=Sobel JD, Muller G, Buckley HR| title=Critical role of germ tube formation in the pathogenesis of candidal vaginitis. | journal=Infect Immun | year= 1984 | volume= 44 | issue= 3 | pages= 576-80 | pmid=6327527 | doi= | pmc=263631 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6327527  }} </ref>
*Proteolytic enzymes, toxins and [[phospholipase]] destroy the [[proteins]] that normally impair [[fungal]] invasion, enhancing the ability of [[Candida]] to colonize the [[vagina]].<ref name="pmid17560449">{{cite journal |vauthors=Sobel JD |title=Vulvovaginal candidosis |journal=Lancet |volume=369 |issue=9577 |pages=1961–71 |year=2007 |pmid=17560449 |doi=10.1016/S0140-6736(07)60917-9 |url=}}</ref><ref name="pmid3895958">{{cite journal |vauthors=Sobel JD |title=Epidemiology and pathogenesis of recurrent vulvovaginal candidiasis |journal=Am. J. Obstet. Gynecol. |volume=152 |issue=7 Pt 2 |pages=924–35 |year=1985 |pmid=3895958 |doi= |url=}}</ref><ref name="pmid2688924">{{cite journal |vauthors=Sobel JD |title=Pathogenesis of Candida vulvovaginitis |journal=Curr Top Med Mycol |volume=3 |issue= |pages=86–108 |year=1989 |pmid=2688924 |doi= |url=}}</ref><ref name="pmid12761103">{{cite journal| author=Schaller M, Bein M, Korting HC, Baur S, Hamm G, Monod M et al.| title=The secreted aspartyl proteinases Sap1 and Sap2 cause tissue damage in an in vitro model of vaginal candidiasis based on reconstituted human vaginal epithelium. | journal=Infect Immun | year= 2003 | volume= 71 | issue= 6 | pages= 3227-34 | pmid=12761103 | doi= | pmc=155757 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12761103  }}</ref>
*[[Phenotypic switching]] of [[Candida]] is described in patients with recurrent vaginitis.<ref name="pmid3284370">{{cite journal| author=Soll DR| title=High-frequency switching in Candida albicans and its relations to vaginal candidiasis. | journal=Am J Obstet Gynecol | year= 1988 | volume= 158 | issue= 4 | pages= 997-1001 | pmid=3284370 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3284370  }}</ref>
*[[C. albicans]] can form [[biofilm]]s on the [[intrauterine devices]] or sponges, causing disease recurrence.<ref name="pmid25935553">{{cite journal| author=Muzny CA, Schwebke JR| title=Biofilms: An Underappreciated Mechanism of Treatment Failure and Recurrence in Vaginal Infections. | journal=Clin Infect Dis | year= 2015 | volume= 61 | issue= 4 | pages= 601-6 | pmid=25935553 | doi=10.1093/cid/civ353 | pmc=4607736 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25935553  }}</ref>
===Pathogenesis===
*[[Candida (genus)|Candida]] vulvovaginitis is a microbial disease and not all patients with detectable pathogen are symptomatic. Multiple [[risk factors]] and the imbalance in the protective vaginal defenses predispose patients to develop active disease.
*[[Candida]] vaginal infections are more common in the reproductive age group because of the high concentration of [[estrogen]] as it increases the amount of [[glycogen]] in the [[vagina]] providing a carbon source for [[Candida]] organisms to [[colonize]]. It also increases the adherence of [[Candida]] to the [[vaginal epithelial cells]].<ref name="pmid11592551">{{cite journal| author=Dennerstein GJ, Ellis DH| title=Oestrogen, glycogen and vaginal candidiasis. | journal=Aust N Z J Obstet Gynaecol | year= 2001 | volume= 41 | issue= 3 | pages= 326-8 | pmid=11592551 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11592551  }}</ref>
*The most common source of the infection is from the [[perianal]] area. Other less common source is [[sexual transmission]] and persistence of organisms in the [[vagina]] after treatment which is responsible for recurrence.<ref name="pmid333134">{{cite journal| author=Miles MR, Olsen L, Rogers A| title=Recurrent vaginal candidiasis. Importance of an intestinal reservoir. | journal=JAMA | year= 1977 | volume= 238 | issue= 17 | pages= 1836-7 | pmid=333134 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=333134  }}</ref>
*The initial step of infection is [[colonization]] and symptoms appear with the invasion of the [[blastospores]] or [[pseudohyphae]] of the [[vaginal wall]].<ref name="pmid9880475">{{cite journal| author=Fidel PL, Vazquez JA, Sobel JD| title=Candida glabrata: review of epidemiology, pathogenesis, and clinical disease with comparison to C. albicans. | journal=Clin Microbiol Rev | year= 1999 | volume= 12 | issue= 1 | pages= 80-96 | pmid=9880475 | doi= | pmc=88907 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9880475  }}</ref>
*The understanding of the transition from asymptomatic vaginal colonization with [[Candida]] to symptomatic [[vulvovaginitis]] is not clear.<ref name="pmid3895958">{{cite journal |vauthors=Sobel JD |title=Epidemiology and pathogenesis of recurrent vulvovaginal candidiasis |journal=Am. J. Obstet. Gynecol. |volume=152 |issue=7 Pt 2 |pages=924–35 |year=1985 |pmid=3895958 |doi= |url=}}</ref><ref name="pmid2688924">{{cite journal |vauthors=Sobel JD |title=Pathogenesis of Candida vulvovaginitis |journal=Curr Top Med Mycol |volume=3 |issue= |pages=86–108 |year=1989 |pmid=2688924 |doi= |url=}}</ref>

Revision as of 17:16, 1 May 2017

Pathophysiology

Vaginal Defensive mechanisms aganist Candida

Innate Mechanisms

Defense Mechanism of protection Evidence of protection
Vaginal epithelial cells
  • Protective role in vivo unknown
  • Patients with recurrent candida infections have decreased anti-Candida activity
Mannose-binding lectin
Activated lactoferrin[4]
  • Fungistatic and fungicidal activity
  • Role in protection aganist infection is not clear
Vaginal bacterial flora
  • Role in protection aganist vaginitis still unclear
Phagocytic systems/polymononuclear leukocytes, mononuclear cells, complement
  • Role in protection still unclear

Adaptive Mechanisms

Defense Mechanism Role in Protection
Immunoglobulin mediated immunity Systemic IgM, IgG, and local IgA antibodies are produced in response to the infection[6]
  • Protective role not proven.
  • Elevated titres of vaginal anti-Candida IgG, IgA are detected in women with recurrent vaginitis
  • Persistent symptoms could be attributed to anti-Candida IgE[7]
Cell Mediated Immunity

Interleukin 4 (Th2) inhibits anti-Candida activity of nitric oxide and protective pro-inflammatory Th1 cytokines.[8]

  • Role in protection from vulvovaginitis is still not clear
  • It is still a hypothesis[9]
  • Patients with recurrent infection have undetectable Th2 cytokines.

Candida Virulence Factors

Pathogenesis

  1. ↑ Barousse MM, Espinosa T, Dunlap K, Fidel PL (2005). "Vaginal epithelial cell anti-Candida albicans activity is associated with protection against symptomatic vaginal candidiasis". Infect Immun. 73 (11): 7765–7. doi:10.1128/IAI.73.11.7765-7767.2005. PMC 1273905. PMID 16239581.
  2. ↑
  3. ↑ Ip WK, Lau YL (2004). "Role of mannose-binding lectin in the innate defense against Candida albicans: enhancement of complement activation, but lack of opsonic function, in [[phagocytosis]] by human dendritic cells". J Infect Dis. 190 (3): 632–40. doi:10.1086/422397. PMID 15243942. URL–wikilink conflict (help)
  4. ↑ Naidu AS, Chen J, Martinez C, Tulpinski J, Pal BK, Fowler RS (2004). "Activated lactoferrin's ability to inhibit Candida growth and block yeast adhesion to the vaginal epithelial monolayer". J Reprod Med. 49 (11): 859–66. PMID 15603095.
  5. ↑ Diamond RD, Krzesicki R, Jao W (1978). "Damage to pseudohyphal forms of Candida albicans by neutrophils in the absence of serum in vitro". J Clin Invest. 61 (2): 349–59. doi:10.1172/JCI108945. PMC 372545. PMID 340470.
  6. ↑ Waldman RH, Cruz JM, Rowe DS (1972). "Immunoglobulin levels and antibody to Candida albicans in human cervicovaginal secretions". Clin Exp Immunol. 10 (3): 427–34. PMC 1713147. PMID 4556009.
  7. ↑ Fidel PL, Sobel JD (1996). "Immunopathogenesis of recurrent vulvovaginal candidiasis". Clin Microbiol Rev. 9 (3): 335–48. PMC 172897. PMID 8809464.
  8. ↑ Fidel PL (2005). "Immunity in vaginal candidiasis". Curr Opin Infect Dis. 18 (2): 107–11. PMID 15735412.
  9. ↑ Fidel PL, Barousse M, Espinosa T, Ficarra M, Sturtevant J, Martin DH; et al. (2004). "An intravaginal live Candida challenge in humans leads to new hypotheses for the immunopathogenesis of vulvovaginal candidiasis". Infect Immun. 72 (5): 2939–46. PMC 387876. PMID 15102806.
  10. ↑ 10.0 10.1 Sobel JD (2007). "Vulvovaginal candidosis". Lancet. 369 (9577): 1961–71. doi:10.1016/S0140-6736(07)60917-9. PMID 17560449.
  11. ↑ 11.0 11.1 11.2 Sobel JD (1985). "Epidemiology and pathogenesis of recurrent vulvovaginal candidiasis". Am. J. Obstet. Gynecol. 152 (7 Pt 2): 924–35. PMID 3895958.
  12. ↑ Sobel JD, Muller G, Buckley HR (1984). "Critical role of germ tube formation in the pathogenesis of candidal vaginitis". Infect Immun. 44 (3): 576–80. PMC 263631. PMID 6327527.
  13. ↑ 13.0 13.1 Sobel JD (1989). "Pathogenesis of Candida vulvovaginitis". Curr Top Med Mycol. 3: 86–108. PMID 2688924.
  14. ↑ Schaller M, Bein M, Korting HC, Baur S, Hamm G, Monod M; et al. (2003). "The secreted aspartyl proteinases Sap1 and Sap2 cause tissue damage in an in vitro model of vaginal candidiasis based on reconstituted human vaginal epithelium". Infect Immun. 71 (6): 3227–34. PMC 155757. PMID 12761103.
  15. ↑ Soll DR (1988). "High-frequency switching in Candida albicans and its relations to vaginal candidiasis". Am J Obstet Gynecol. 158 (4): 997–1001. PMID 3284370.
  16. ↑ Muzny CA, Schwebke JR (2015). "Biofilms: An Underappreciated Mechanism of Treatment Failure and Recurrence in Vaginal Infections". Clin Infect Dis. 61 (4): 601–6. doi:10.1093/cid/civ353. PMC 4607736. PMID 25935553.
  17. ↑ Dennerstein GJ, Ellis DH (2001). "Oestrogen, glycogen and vaginal candidiasis". Aust N Z J Obstet Gynaecol. 41 (3): 326–8. PMID 11592551.
  18. ↑ Miles MR, Olsen L, Rogers A (1977). "Recurrent vaginal candidiasis. Importance of an intestinal reservoir". JAMA. 238 (17): 1836–7. PMID 333134.
  19. ↑ Fidel PL, Vazquez JA, Sobel JD (1999). "Candida glabrata: review of epidemiology, pathogenesis, and clinical disease with comparison to C. albicans". Clin Microbiol Rev. 12 (1): 80–96. PMC 88907. PMID 9880475.
Retrieved from "https://www.wikidoc.org/index.php?title=Sandbox:_ay&oldid=1310043"