Sandbox:Infectious Balanitis: Difference between revisions

Jump to navigation Jump to search
No edit summary
Line 9: Line 9:
==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 foreskin
saliva as a lubricant during coitus
sub-optimal hygienic mainta
|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
|-
|-
Line 35: Line 38:
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
|-
|-
Line 45: Line 49:
|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]])
|-
|-
Line 55: Line 59:


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>
Line 70: Line 74:
|-
|-
|
|
====Bacterial====
==== Bacterial ====
|
|
====Anaerobic bacteria====
==== Anaerobic bacteria ====
Gardnerella vaginalis
Gardnerella vaginalis


Line 82: Line 86:


Fusobacterium spp
Fusobacterium spp
====Aerobic bacteria====
 
==== Aerobic bacteria ====
Group B streptococci
Group B streptococci


Line 100: Line 105:
|-
|-
|
|
====Viral====
==== Viral ====
|Human papilloma virus
|Human papilloma virus
Herpes simplex virus
Herpes simplex virus
Line 107: Line 112:
|-
|-
|
|
====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===
Line 128: Line 135:


===Complications===
===Complications===
*Pain
* Pain
*Erosions
* Erosions
*Fissures
* Fissures
 
* Phimosis
* Paraphimosis
* Painful erection
* Reduced urinary flow
* Urinary retention


*Phimosis
*Paraphimosis
*Painful erection
*Reduced urinary flow
*Urinary retention
===Prognosis===
===Prognosis===
Prognosis is good with treatment.
Prognosis is good with treatment.  


==Diagnosis==
==Diagnosis==
Line 284: Line 292:
==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
  • Diabetes
  • Neutropenia
  • 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.[1][2]
  • 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 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
  • Diabetes
  • Neutropenia
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 bacteria

Gardnerella vaginalis

`Bacteroides melaninogenicus

unidentified Bacteroides

Bacteroides fr agilis

Fusobacterium spp

Aerobic bacteria

Group 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
  • Gram stain may show fusiform/mixed bacterial picture
  • Sub-preputial culture wet prep or NAAt(to exclude other causes)
  • G. vaginalis is a facultative anaerobe which may be isolated
  • Swab for HSV infection if ulcerated
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.

Prevention

Primary Prevention

Secondary prevention

References

  1. Taylor PK, Rodin P (1975). "Herpes genitalis and circumcision". Br J Vener Dis. 51 (4): 274–7. PMC 1046564. PMID 1156848.

Template:WikiDoc Sources