OVERVIEW: What every practitioner needs to know
Are you sure your patient has genital and mucous membranes? What should you expect to find?
Lesions can be multiple and painful, multiple and painless, solitary and painful, or solitary and painless. Some lesions can be indurated or pruritic. Most infectious etiologies do not involve a loss of skin pigment or discoloration. Lesions can be classified by many other characteristics, including duration, size, recurrence, presence of adenopathy, as well as others.
The majority of lesions is considered sexually transmitted diseases (STDs) or requires contact with an infected individual for transmission. Examples of lesions considered STDs are herpes simplex virus, syphilis, chancroid, chlamydia (lymphogranuloma venerium), genital warts (human papilloma virus), pediculosis pubis (phthirus pubis), and granuloma inguinale, as well as others. Some other infectious causes of mucous membrane lesions not related to sexual contact are candidal lesions and tinea cruris.
How did the patient develop genital and mucous membranes? What was the primary source from which the infection spread?
The majority of lesions is considered STDs or requires contact with an infected individual for transmission. Some exceptions are candidal lesions and tinea cruris.
Which individuals are of greater risk of developing genital and mucous membranes?
An important factor to consider when investigating an infectious mucous membrane lesion is the different risk factors that increase the probability that an individual will contract the disease.
The risk factors for infections considered STDs as listed above are having unprotected sex, having multiple sexual partners, using drugs and alcohol, engaging in prostitution, being incarcerated, having limited access to medical care, an early age at first sexual encounter, and having another genital infection. Risk factors for non-STD lesions are different.
Patients are at increased risk for candidal infections of the mucous membranes if they have any of the following risk factors: are HIV positive, elderly or very young, diabetic, recent antibiotic use, and high estrogen oral contraceptives. There is also some evidence to suggest that increasing sexual encounters can increase the incidence of candidal infections.
Beware: there are other diseases that can mimic genital and mucous membranes:
Malignancy and pre-malignant lesions
What laboratory studies should you order and what should you expect to find?
Results consistent with the diagnosis (Table I)
|Organism||Diagnostic Tests||Symptoms consistent with diagnosis|
|Chlamydia Trachomatis||Nucleic acid amplification testsof urine specimen or specimensfrom urethra/cervix||Urethritis;Cervicitis|
|Neisseria Gonorrhoeae||Nucleic acid amplification testsof urine specimen or specimensfrom urethra/cervix||Symptomatic urethritis,cervicitis, epididymitis,or pharyngitis|
|Treponema Pallidum||Darkfield microscopy||Painless clean basedindurated ulcer|
|Herpes Simplex Virus||Tzanck smear looking for multinuceategiant cell PCR is more sensitive in detecting HSV than viral culture 14593592It is important to distinguish between HSV-1 and HSV-2||Often asymptomatic lifelong infection;Group of vesicles that can ulcerate and become painful lesions when active|
|Haemophilus Ducreyi||Often clinical diagnosis but canbe cultured on chocolate agar.No approved polymerase chain reaction (PCR) currently available.||Sharply circumscribed painfululcer with grayish necroticexudate at base;Enlarged suppurative inguinal lymph nodes|
|Human Papilloma Virus (condylomata acuminata)||Often a clinical diagnosis but, if needed, the lesion can be biopsied. HPV 6 and 11 are more often associated with genital warts, whereas HPV 16 and 18 are associated with cervical cancer.||Multiple pink or flesh colored papules or large verrucous papilliform lesion;Lesions can become irritated and symptomatic but are often painless|
|Pediculosis Pubis||Caused by phthirus pubis and is diagnosed with microscopic evaluation looking for lice or nits.||Presence of lice or nits in pubic hair with pruritis;With severe infestation, multiple pruritic pale blue macules can be seen.|
|Granuloma Inguinale(donovanosis)||Caused by gram negative rod Klebsiella granulomatis, which is difficult to culture. Diagnosis is made when dark staining donovan bodies are seen on crush preparation or biopsy.||Rare in the United States but more common in endemic and developing areas;Multiple painless slow growing ulcerative lesions often without lymphadenopathy;Lesions are beefy red and bleed easily on contact.|
|Candida||Pseudohyphae seen on potassium hydroxide microscopy with a vaginal ph of 4.0-4.5.||Pruritis with erythema of vulva or scrotum/penis with a white and clumpy discharge|
|Tinea Cruris||Often caused by T.rubrum or Epidermophyton floccosum. Diagnosis can be made by observing scrapings in potassium hydroxide solution under a microscope.||Often called “jock itch”;Bilateral erythematous pruritic plaques develop over bilateral inner thighs;Often spares scrotum/penis|
What consult service or services would be helpful for making the diagnosis and assisting with treatment?
If you decide the patient has genital and mucous membranes, what therapies should you initiate immediately?
1. Anti-infective agents
Table II provides a list of anti-infective agents.
|Chlamydia Trachomatis||Azithromycin||1G orally in one dose||Doxycycline(100mg orally twice a day for 7 days)Erythromycin(500mg 4 times a day for 7 days)Erythromycin ethylsuccinate(800mg 4 times a day for 7 days)Levofloxacin (500mg once a day for 7 days)Oflaxacin (300 mg twice a day for 7 days)|
|Neisseria Gonorrhoeae||Ceftriaxone||250mg IM in one dose||Cefixime(400mg orally in single dose)Single dose injectable cephalosporin plus either Azithromycin 1g in single dose or doxycycline 100mg twice a day for 7 days|
|Treponema Pallidum||Benzathine Penicillin G||2.4 million units IM in one dose|
|Herpes SimplexVirus||First outbreak:ACYCLOVIR||400mg orally 3 times a day for 7-10 days||Acyclovir(200mg 5 times a day for 7-10 days)Famciclovir(250mg 3 times a day for 7-10 days)Valacyclovir(1g twice a day for 7-10 days)|
|Suppressive therapy:ACYCLOVIR||400mg orally 2 times a day indefinitely||Famiciclovir(250mg 2 times a day)Valacyclovir(500mg once a day or 1g once a day)|
|Haemophilus Ducreyi||AZITHROMYCIN||1gram orally in one dose||Ceftriaxone(250mg 1 dose)Ciprofloxacin(500mg twice a day for 3 days)Erythromycin(500 3 times a day for 7 days)|
|Human Papilloma Virus (condylomata acuminata)||Patient applied:Podofilox 0.5% gel||Apply to visible warts with swab or finger twice a day for 3 days. No therapy for 4 days. Repeat as necessary for four cycles.||Imiquimod 5% cream (apply at bedtime 3 times a week for 16 weeks)Sinecatechins 15% ointment (apply 3 times a day for maximum of 16 days)|
|Provider applied:Cryotherapy with liquid nitrogen or cryoprobe||Repeat every 1 or 2 weeks.||Podophyllin resin 10%-25% in compound tincture of benzoinTrichloroacetic acid or bichloroacetic acid 80%-90%Surgical removal|
|Pediculosis Pubis||Permethrin 1% cream||Apply and wash off after 10 minutes||Pyrethrins with piperonyl butoxide applied and washed after 10 minutesMalathion 0.5% lotion applied for 8-12 hours and washed offIvermectin 200uG/kg orally repeated in 2 weeks|
|Granuloma Inguinale(donovanosis)||Doxycycline||100mg orally twice a day for 3 weeks or until all lesions have resolved||Azithromycin 1g weekly for 3 weeks*Ciprofloxacin 750mg twice a day for 3 weeks*Erythromycin 500mg 4 times a day for 3 weeks*Trimethoprim-sulfamethoxazole one double strength table twice a day for 3 weeks**all therapies continued for at least 3 weeks or until lesions have resolved|
|Candida||Fluconazole||150mg orally one dose||There are multiple topical azole preparations available over the counter and by prescription that are efficacious in treatment.|
|Tinea Cruris||Terbinafine or Naftifine(Allylamines)||1% either cream/gel or spray applied either daily or twice a day||Azoles (Clotrimazole, ketoconazole, miconazole, oxiconazole 1-2% cream/gel applied daily or bid)Griseofulvin 250mg orally 3 times a day for 14 days (often reserved for resistant cases)|
Treatment for different pathogens
2. Next list other key therapeutic modalities.
Patients with any genital lesion need to be concerned about HIV prevention.
Add what-if scenarios here:
Patients in specific populations should be managed differently. This includes pregnancy, immunosuppression, and HIV-infected patients, as well as many others. Specifically, pregnant patients should be well monitored, and the treatment regimen for this patient population must be carefully chosen while considering the specific risks and benefits. HIV and immunosuppressed patients should be closely monitored for resolution or improvement in their symptoms, as treatment failure is more common in this group and they may require a longer course of treatment.
WHAT'S THE EVIDENCE for specific management and treatment recommendations?
Beck-Sague, CM, Cordts, JR, Brown, K. “Laboratory diagnosis of sexually transmitted diseases in facilities within the United States. Results of a national survey”. Sex Transm Dis. vol. 23. 1996. pp. 342-9.
“Sexually transmitted diseases treatment guidelines, 2010”. MMWR. vol. 59. 2010.
Cook, RL, Hutchison, SL, Østergaard, L, Braithwaite, RS, Ness, RB. “Systematic review: noninvasive testing for Chlamydia trachomatis and Neisseria gonorrhoeae”. Ann Intern Med. vol. 142. 2005. pp. 914-25.
Folkers, E, Oranje, AP, Duivenvoorden, JN, van der Veen, JP, Rijlaarsdam, JU, Emsbroek, JA. “Tzanck smear in diagnosing genital herpes”. Genitourin Med. vol. 64. 1988. pp. 249-54.
Gupta, AK, Chaudhry, M, Elewski, BE. “Tinea corporis, tinea cruris, tinea nigra, and piedra”. Dermatol Clin. vol. 21. 2003. pp. 395-400.
Nadalo, D, Montoya, C, Hunter-Smith, D. “What is the best way to treat tinea cruris?”. J Fam Pract. vol. 55. 2006. pp. 256-8.
Quan, M. “Vaginitis: diagnosis and management”. Postgrad Med. vol. 122. 2010. pp. 117-27.
Scoular, A. “Using the evidence base on genital herpes: optimising the use of diagnostic tests and information provision”. Sex Transm Infect. vol. 78. 2002. pp. 160-5.
Sobel, JD. “Vulvovaginal candidosis”. Lancet. vol. 369. 2007. pp. 1961-71.
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- OVERVIEW: What every practitioner needs to know
- Are you sure your patient has genital and mucous membranes? What should you expect to find?
- How did the patient develop genital and mucous membranes? What was the primary source from which the infection spread?
- Which individuals are of greater risk of developing genital and mucous membranes?
- Beware: there are other diseases that can mimic genital and mucous membranes:
- What laboratory studies should you order and what should you expect to find?
- What consult service or services would be helpful for making the diagnosis and assisting with treatment?
- Add what-if scenarios here:
- WHAT'S THE EVIDENCE for specific management and treatment recommendations?