Sandbox:Infectious Balanitis: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Pathophysiology of Infectious balanitis varies from pathogen to pathogen:<ref name="pmid1156848">{{cite journal| author=Taylor PK, Rodin P| title=Herpes genitalis and circumcision. | journal=Br J Vener Dis | year= 1975 | volume= 51 | issue= 4 | pages= 274-7 | pmid=1156848 | doi= | pmc=1046564 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1156848 }}</ref> | Pathophysiology of Infectious balanitis varies from pathogen to pathogen:<ref name="pmid1156848">{{cite journal| author=Taylor PK, Rodin P| title=Herpes genitalis and circumcision. | journal=Br J Vener Dis | year= 1975 | volume= 51 | issue= 4 | pages= 274-7 | pmid=1156848 | doi= | pmc=1046564 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1156848 }}</ref> | ||
{| class="wikitable" | {| class="wikitable" | ||
!Pathogen | !Pathogen | ||
!Route of transmission | !Route of transmission | ||
!Risk factors | !Risk factors | ||
!virulence factors | !virulence factors | ||
|- | |- | ||
|Candidal Balanitis | |Candidal Balanitis | ||
|Sexual acquired | |Sexual acquired | ||
| | | | ||
*Diabetes | * Diabetes | ||
*Neutropenia | * Neutropenia | ||
*Age>60 yrs | * Age>60 yrs | ||
| | | | ||
*All strains of ''[[C. albicans]]'' possess a yeast surface mannoprotein. This allows the various strains to adhere to both the exfoliated and buccal epithelial cells of the vagina.<sup>[[Candidiasis pathophysiology|[1][2]]]</sup> | * All strains of ''[[C. albicans]]'' possess a yeast surface mannoprotein. This allows the various strains to adhere to both the exfoliated and buccal epithelial cells of the vagina.<sup>[[Candidiasis pathophysiology|[1][2]]]</sup> | ||
*Several virulence factors of [[Candida]] are implicated in Balanitis. These include proteolytic enzymes, toxins and phospholipase. Proteolytic enzymes destroy the proteins that normally impair fungal invasion | * Several virulence factors of [[Candida]] are implicated in Balanitis. These include proteolytic enzymes, toxins and phospholipase. Proteolytic enzymes destroy the proteins that normally impair fungal invasion | ||
|- | |- | ||
|Anaerobic Infection | |Anaerobic Infection | ||
|Possible modes of transmission include contact with infected mucosal surfaces, such as during sexual intercourse, contamination by colonized saliva, or extension from the perirectal area. | |Possible modes of transmission include contact with infected mucosal surfaces, such as during sexual intercourse, contamination by colonized saliva, or extension from the perirectal area. | ||
orogenital sex saliva as a lubricant during coitus | orogenital sex | ||
|Tight | saliva as a lubricant during coitus | ||
sub-optimal hygienic | |Tight foreskin | ||
sub-optimal hygienic mainta | |||
|Anaerobic Gram-negative rods produce various toxins, proteases, elastase, and other virulence factors | |Anaerobic Gram-negative rods produce various toxins, proteases, elastase, and other virulence factors | ||
|- | |- | ||
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Infections | Infections | ||
|Sexually acquired and partners of women with ''Gardnerella vaginalis'' have high isolation rates from the urethra<sup>24</sup> or urine.autoinoculation | |Sexually acquired and partners of women with ''Gardnerella vaginalis'' have high isolation rates from the urethra<sup>24</sup> or urine.autoinoculation | ||
Autoinoculation from other sites | |||
|uncircumcised ch | |uncircumcised ch | ||
*Diabetes | * Diabetes | ||
*Neutropenia | * Neutropenia | ||
|Adherence to epithelial cells, biofilm production, surface hydrophobicity, phospholipase C and protease activity | |Adherence to epithelial cells, biofilm production, surface hydrophobicity, phospholipase C and protease activity | ||
|- | |- | ||
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|Virulence factors such as adherence, contact-independent factors, hemolysis and acquisition of host macromolecules have been shown to play a role in the pathogenesis of this infection | |Virulence factors such as adherence, contact-independent factors, hemolysis and acquisition of host macromolecules have been shown to play a role in the pathogenesis of this infection | ||
|- | |- | ||
|Treponema | |Treponema | ||
pallidum | pallidum | ||
|Transmitted via direct contact with the infected lesion (sexual contact) | |Transmitted via direct contact with the infected lesion (sexual contact) | ||
|Multiple sexual partners | |Multiple sexual partners | ||
|Treponema Pallidum uses [[fibronectin]] molecules to attach to the [[endothelial]] surface of the vessels in organs resulting in inflammation and obliteration of the small blood vessels causing [[vasculitis]] ([[endarteritis obliterans]]) | |Treponema Pallidum uses [[fibronectin]] molecules to attach to the [[endothelial]] surface of the vessels in organs resulting in inflammation and obliteration of the small blood vessels causing [[vasculitis]] ([[endarteritis obliterans]]) | ||
|- | |- | ||
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direct contact with, or droplets from, infected secretions entering via skin or mucous membrane, where primary infection may become evident | direct contact with, or droplets from, infected secretions entering via skin or mucous membrane, where primary infection may become evident | ||
|Multiple sexual partners | |Multiple sexual partners | ||
Low socio-economic status | Low socio-economic status | ||
|Inhibition of MHC Class I, Impairing funtion of dentric cells | |Inhibition of MHC Class I, Impairing funtion of dentric cells | ||
|- | |- | ||
|Human papilloma virus | |Human papilloma virus | ||
|usually transmitted via the sexual route to the human host.<sup>[[Human papillomavirus pathophysiology|[1]]]</sup> | |usually transmitted via the sexual route to the human host.<sup>[[Human papillomavirus pathophysiology|[1]]]</sup> | ||
| | | | ||
|linked to epithelial [[differentiation]] and maturation of host keratinocytes, with [[transcription]] of specific gene products at every level.<sup>[[Human papillomavirus pathophysiology|[2][3]]]</sup> | |linked to epithelial [[differentiation]] and maturation of host keratinocytes, with [[transcription]] of specific gene products at every level.<sup>[[Human papillomavirus pathophysiology|[2][3]]]</sup> | ||
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|- | |- | ||
| | | | ||
====Bacterial==== | ==== Bacterial ==== | ||
| | | | ||
====Anaerobic bacteria==== | ==== Anaerobic bacteria ==== | ||
Gardnerella vaginalis | Gardnerella vaginalis | ||
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Fusobacterium spp | Fusobacterium spp | ||
====Aerobic bacteria==== | |||
==== Aerobic bacteria ==== | |||
Group B streptococci | Group B streptococci | ||
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|- | |- | ||
| | | | ||
====Viral==== | ==== Viral ==== | ||
|Human papilloma virus | |Human papilloma virus | ||
Herpes simplex virus | Herpes simplex virus | ||
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|- | |- | ||
| | | | ||
====Fungal==== | ==== Fungal ==== | ||
|Candida | |Candida | ||
''Malassezia furfur'', | ''Malassezia furfur'', | ||
|- | |- | ||
| | | | ||
====Parasitic==== | ==== Parasitic ==== | ||
|Entamoeba histolytica | |Entamoeba histolytica | ||
''Trichomonas'' | ''Trichomonas'' | ||
|} | |} | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
Epidemiology | Epidemiology | ||
There are no comprehensive studies | There are no comprehensive studies | ||
==Screening== | ==Screening== | ||
There is no established screening guidelines for Infectious Balanitis | There is no established screening guidelines for Infectious Balanitis | ||
==Natural History, Complications, and Prognosis== | ==Natural History, Complications, and Prognosis== | ||
===Natural history=== | ===Natural history=== | ||
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===Complications=== | ===Complications=== | ||
*Pain | * Pain | ||
*Erosions | * Erosions | ||
*Fissures | * Fissures | ||
* Phimosis | |||
* Paraphimosis | |||
* Painful erection | |||
* Reduced urinary flow | |||
* Urinary retention | |||
===Prognosis=== | ===Prognosis=== | ||
Prognosis is good with treatment. | Prognosis is good with treatment. | ||
==Diagnosis== | ==Diagnosis== | ||
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==Prevention== | ==Prevention== | ||
===Primary Prevention=== | ===Primary Prevention=== | ||
===Secondary prevention=== | ===Secondary prevention=== | ||
==References== | ==References== | ||
{{Reflist|2}}{{WikiDoc Help Menu}} {{WikiDoc Sources}} | {{Reflist|2}}{{WikiDoc Help Menu}} {{WikiDoc Sources}} |
Revision as of 17:19, 25 January 2017
Associate Editor(s)-in-Chief: Vishal Devarkonda, M.B.B.S[1]
Synonyms and keywords:Candida balanitis, Candidal balanitis
Overview
Historical Perspective
Classification
Pathophysiology
Pathophysiology of Infectious balanitis varies from pathogen to pathogen:[1]
Pathogen | Route of transmission | Risk factors | virulence factors |
---|---|---|---|
Candidal Balanitis | Sexual acquired |
|
|
Anaerobic Infection | Possible modes of transmission include contact with infected mucosal surfaces, such as during sexual intercourse, contamination by colonized saliva, or extension from the perirectal area.
orogenital sex saliva as a lubricant during coitus |
Tight foreskin
sub-optimal hygienic mainta |
Anaerobic Gram-negative rods produce various toxins, proteases, elastase, and other virulence factors |
Aerobic
Infections |
Sexually acquired and partners of women with Gardnerella vaginalis have high isolation rates from the urethra24 or urine.autoinoculation
Autoinoculation from other sites |
uncircumcised ch
|
Adherence to epithelial cells, biofilm production, surface hydrophobicity, phospholipase C and protease activity |
Trichomonas vaginalis | Sexually | presence of other infections | Virulence factors such as adherence, contact-independent factors, hemolysis and acquisition of host macromolecules have been shown to play a role in the pathogenesis of this infection |
Treponema
pallidum |
Transmitted via direct contact with the infected lesion (sexual contact) | Multiple sexual partners | Treponema Pallidum uses fibronectin molecules to attach to the endothelial surface of the vessels in organs resulting in inflammation and obliteration of the small blood vessels causing vasculitis (endarteritis obliterans) |
Herpes simplex | often transmitted sexually
direct contact with, or droplets from, infected secretions entering via skin or mucous membrane, where primary infection may become evident |
Multiple sexual partners
Low socio-economic status |
Inhibition of MHC Class I, Impairing funtion of dentric cells |
Human papilloma virus | usually transmitted via the sexual route to the human host.[1] | linked to epithelial differentiation and maturation of host keratinocytes, with transcription of specific gene products at every level.[2][3] |
Causes
Infectious causes of Balanitis | |
---|---|
Bacterial |
Anaerobic bacteriaGardnerella vaginalis `Bacteroides melaninogenicus unidentified Bacteroides Bacteroides fr agilis Fusobacterium spp Aerobic bacteriaGroup B streptococci Group A haemolytic streptococci Staphyloccocus aureus Mycobacterium tuberculosis Mycobacterium leprae Borrelia burgdorferi Borrelia vincenti Neisseria gonorrhea |
Viral |
Human papilloma virus
Herpes simplex virus Human immunodeficiency virus |
Fungal |
Candida
Malassezia furfur, |
Parasitic |
Entamoeba histolytica
Trichomonas |
Epidemiology and Demographics
Epidemiology
There are no comprehensive studies
Screening
There is no established screening guidelines for Infectious Balanitis
Natural History, Complications, and Prognosis
Natural history
If left untreated, Infection balanitis may result in complications.
Complications
- Pain
- Erosions
- Fissures
- Phimosis
- Paraphimosis
- Painful erection
- Reduced urinary flow
- Urinary retention
Prognosis
Prognosis is good with treatment.
Diagnosis
Clinical features of Infectious balanitis | |
---|---|
Candidal Balanitis | Erythematous rash with soreness and/or itch, blotchy erythema with small papules which may be eroded, or dry dull red areas with a glazed appearance |
Anaerobic Infection | Foul smelling sub-preputial inflammation and discharg: in severe cases associated with swelling and inflamed inguinal lymph nodes
Preputial edema, superficial erosions: milder forms also occur |
Aerobic
Infections |
Variable inflmmatory changes including uniform erythema and edema |
T. vaginalis | Superficial erosive balanitis which may lead to phimosis |
TP | Multiple circinate lesions which erode to cause irregular ulcers have been described in the late primary or early secondary stage. A primary chancre may also be present |
Herpes simplex | Grouped vesicles on erythematous base over glans, prepuce and shaft which rupture to form shallow erosins. In rare cases primary herpes can cause a necrotic balanitis, with necrotic areas on the glans accompained by vesicles elsewhere and associated with headache and malaise. |
Human papilloma virus | Papilloma virus may be associated with patchy or chronic balanitis, which becomes acetowhite after the application of 5% acetic acid |
Laboratory findings
Laboratory findings | |
---|---|
Candidal Balanitis | Urinalysis for glucose
Sub-preputial culture/swab for primary candidasis/candidal superinfection-to be done in all cases Investigation for HIV or other causes of immunosuppression |
Anaerobic Infection |
|
Aerobic
Infections |
Sub-preputial culture
Streptococci spp. and S. aureus have both been reported as causing balanitis |
T. vaginalis | Wet preparation from the subpreputial sac demonstrates the organism
Culture and NAAT can also be carried out |
TP | Dark field microscopy, TP NAAT and DFA-TP will confirm the diagnosis. This should ideally be done every case.
TPHA coupled with nontreponemal serological tests though of limited value, should be performed since they are useful for follow-up |
Herpes simplex | Tissue scraping from base of erosion subjected to Tzanck smear IgG and IgM for HSV cell culture and PCR-preferred HSV tests for persons who seek medical treatment for gential ulcers or other mucocutaneous lesions |
Human papilloma virus | Diagnosed clinically |
Treatment
Laboratory findings | ||
---|---|---|
Preferred regimen | Alternative regimen | |
Candidal Balanitis | Clotimazole cream 1%
Miconazole cream 2% |
Fluconazole 150 mg stat orally
Nystatin cream-if resistance suspected topical clotrimazole/miconazole with 1% hydrocortisone-if marked inflammation |
Anaerobic Infection | Advice about genital hygiene
metronidazole 400 mg twice daily for 1 week Milder cases- topical metronidazole |
Coamoxiclav(amoxycillin/clavulanic acid) 375 mg 3 times daily for 1 week
Clindamycin cream applied twice daily until resolved |
Aerobic
Infections |
Usually topical
Triple combination (clotrimazole 1%, beclometasone dipropionate 0.025%, gentamicinsilfate 0.3%) applied once daily Severe cases-systemic antibiotics Erythromycin 500 mg QDS for 1 week Co-amoxiclav(amoxycillin/clvulanic acid 375 mg 3 times daily for 1 week |
Alternative regimens depend on the sensitivities of the organisms isolated |
T. vaginalis | Metronidazole 2 g orally single dose
Secidazole 2 g orally single dose |
Metronidazole 400 mg orally twice a day for 7 days |
TP | Single IM administration of 2.4 MU of benzathine penicillin
Doxycycline 100 mg orally BID for 2 weeks or Tetracycline 500 mg orally QID for 2 weeks or Erythromycin 500 mg QID or Ceftriaxone 1 g IM/IV daily for 8-10 days |
|
Herpes simplex | Acyclovir 400 mg orally 3 times a day for 7-10 days or
Acyclovir 200 mg orally 5 times a day for 7-10 days or Famciclovir 250 mg orally 3 times a day for 7-10 days or Valacyclovir 1 g orally twice a day for 7-10 days |
|
Human papilloma virus | Patients applied
Podophyllotoxin(podofilox) 0.5% or gel-twice daily for three consecutive days, but no more than 4 weeks or Imiquimod 5% cream-applied at bedtime 3 times/week for a maximum of 16 weeks, and must be left in place for 6-10 h following application or Sinecatechins 15% ointment Provider-administered Podophyllin resin 20% in a compound tincture of benzoin-once a week for 6-8 week or Cryotherapy with liquid nitrogen ot cryoprobe. Repeat applications every 1-2 weeks or TCA/bichloroacetic acid-80-90% once per week for an average course of 6-10 weeks or Surgical removal either by tangential scissor excision, tangential shave excision, curettage, or electrourgery. |