eMedicine Specialties > Dermatology > Viral Infections

Warts, Genital

Tsu-Yi Chuang, MD, MPH, Clinical Professor, Department of Dermatology, University of Southern California; Staff Dermatologist, Desert Specialty Group, Inc
Ryan Brashear, MD, Staff Physician, Department of Dermatology, Indiana University School of Medicine

Updated: Oct 27, 2009

Introduction

Background

Until the 19th century, genital warts (GWs) were believed to be a form of syphilis or gonorrhea. The viral etiology of warts was established in 1907 by inoculation of wart filtrates into skin, inducing papillomas at the injection site. Today, condyloma acuminatum, or genital warts, generally is recognized as benign proliferations of the anogenital skin and mucosa that result from infection with human papillomavirus (HPV). The HPV family has at least 84 well-documented genotypes. Some believe that the number of HPV types has already approached 130 or more. Despite the generally benign nature of the proliferations, certain types of HPV can place patients at a high risk for anogenital cancer.^1,2,3

The link between cervical cancer and genital warts was first reported in a Rochester, Minnesota population-based cohort study in 1981.² In 1983, HPV type 16 was implicated in the cause of cervical cancer.

Pathophysiology

Genital warts are a result of HPV infection, which is believed to be acquired by inoculation of the virus into the epidermis via defects in the epithelium (eg, maceration of the skin). Autoinoculation of virus into opposed lesions is common. Spread of HPV infection is usually through skin-associated virus and not from blood-borne infection. Probably, cell-mediated immunity (CMI) plays a significant role in wart regression; patients with CMI deficiency are particularly susceptible to HPV infection and are notoriously difficult to treat.⁴

Frequency

United States

Epidemiological studies show genital warts to be one of the most common sexually transmitted diseases (STDs). Annually, 500,000 to 1 million new cases of genital warts occur in the United States. Roughly 10% of the general population, or 24 million people, have been infected by genital HPV at some time in their life. At least 2 studies have documented a 7- to 8-fold increase in the number of patients with genital warts seen at physicians' offices from the 1950s to the mid 1980s; surpassing the number of office visits for genital herpes.⁵ Moreover, it must be emphasized that the prevalence of subclinical HPV infection is likely to be several times higher than the documented prevalence of genital warts.

According to the "National Disease and Therapeutic Index: United States, 1966–2007, the Initial visits to physicians' offices for STD," the increasing trend of HPV infection, after peaking at 351,000 visits in 1987, went down in the following 10 years. Unfortunately, the increasing trend resumed again and reached the highest level ever in 2006 (422,000 visits) before dropping down to 315,000 in 2007.

International

Genital warts have affected as many as 30 million individuals worldwide.

Mortality/Morbidity

Although anogenital warts generally are benign, their significance is drawn from the increased risk of malignancy secondary to HPV infection. Specifically, HPV types 16, 18, 45 , 31, 33, 58, and 52 are associated with the greatest prevalence of anogenital malignancy. Infectivity of anogenital warts may be up to two thirds of sexual contacts. High concordance for the same HPV type has been found among sexual partners.

Race

In the United States, African Americans have a rate of HPV infection that is 1.5 times higher than their white counterparts.

Sex

In a well-defined population study, the female-to-male ratio has been reported to be 1.4:1.⁵ The US Centers for Disease Control and Prevention (CDC) reports have demonstrated that this disease affects females more frequently than males.

Age

The highest incidence of genital warts consistently is found in young adults aged 15-25 years. This observation tends to hold true even after adjustment for lifetime number of sexual partners, which itself is a significant risk factor for HPV infection. In a population study, 80% of the individuals who were affected were aged 17-33 years.

Clinical

History

• Genital warts generally do not become clinically apparent until several months after inoculation with human papillomavirus (HPV).
• Genital warts follow a slow and indolent course and may develop by inoculation from opposing surfaces.

Physical

• Anogenital warts consist of pink-to-brown papillomatous papules or nodules of the genitalia, perineum, crural folds, and anus.

Condyloma acuminatum.

• Warts vary in size and can form large, exophytic, cauliflowerlike masses.

"Cauliflower" condyloma of the penis.

• Discrete papules, 1-3 mm in size can present on the shaft of the penis.

Small papilloma on the shaft of penis.

• The growth can extend into the vagina, urethra, cervix, perirectal epithelium, anus, and rectum.

Small papilloma of the vulva.

Small papilloma of the anus.

Causes

The definitive cause of anogenital warts is HPV infection.^1,2,3,6 See Human Papillomavirus.

• HPV is part of the papovavirus class, which includes SV 40, BK, and JC virus.
• The HPV capsid lacks an envelope, which makes it very stable and resistant to various treatments.
• No serologic typing of HPV is available because of the lack of consistent in vitro culture methods. Typing of HPV is according to genotype, which usually is determined by molecular hybridization techniques using molecularly cloned HPV DNA of known type as the standard. Two HPV are said to be of different types when their DNA hybridize (bind) less than 50% as efficiently to each other as to themselves.
• Nearly 40 types of HPV (of nearly 80 sequenced to date) have been found in genital warts. They are very host specific. These viruses do not infect laboratory animals and are not susceptible to acyclovir.
• As a rule, HPV types causing common warts of the skin do not infect moist epithelium and vice versa.
• Multiple clinical associations with unique genotypes of HPV have been documented. HPV types and their association with the clinical disease are as follows:
  • Plantar warts - Types 1, 2, 4, 60, and 63
  • Common warts - Types 1, 2, 4, 26, 27, 29, 57, 65, and 75-78
  • Meat/poultry/fish handlers - Types 1-4, 7, 10, and 28
  • Flat warts - Types 3, 10, 27, 28, 38, and 49
  • Epidermodysplasia verruciformis - Types 2, 3, 5, 8, 9, 10, 12, 14, 15, 17, 19, 20, 21-25, 28, 36-38, 40, 47, and 50
  • Squamous cell carcinoma or actinic keratosis - Types 14, 16, 18, 36, and 41
  • Squamous cell carcinoma, keratoacanthoma type - Types 7, 9, 16, 29, and 37
  • Squamous cell carcinoma, in immunocompromised - Types 48 and 60
  • Bowen disease (nongenital) - Types 2, 16, 26-29, 31, 33, 34, 54, 56, 58, 61, 62, and 73
  • Melanoma - Types 16, 18, 35, and 38
  • Oral focal epithelial hyperplasia - Types 13 and 32
  • Oral papilloma - Types 11, 7, 32, 57, 72, and 73
  • Laryngeal papilloma (recurrent respiratory papillomatosis)⁷ - Types 2, 6, 11, 16, 30, 40, and 57
  • Laryngeal carcinoma – Types 6, 11
  • Conjunctival papillomas and cancer - Types 6, 11, and 16
  • Epidermal cyst - Types 57, 60
  • Condyloma acuminatum -1-5, 6, 11, 10, 16, 18, 30, 31, 33, 35, 39-45, 51-59, 70, and 83
  • Giant condyloma of Buschke and Löwenstein and other verrucous carcinoma - Types 6, 11, 57, 72, and 73
  • Bowenoid papulosis - Types 16, 34, 39, 40, 42, and 45
  • Vulvar intraepithelial neoplasia - Types 56, 59-64, 67, and 71
  • Anal squamous cell carcinoma and intraepithelial neoplasia⁸ - Types 16, 18, 58, and 83
  • Cervical squamous intraepithelial lesions
    • Low-grade squamous intraepithelial lesions (LGSIL) - Types 6, 11, 16, 18, 26, 27, 30, 31, 33-35, 40, 42-45, 51-58, 61, 62, 67-69, 71-74, 79, and 81-84
    • High-grade squamous intraepithelial lesions (HGSIL) - Types 6, 11, 16, 18, 31, 33, 35, 39, 42, 44, 45, 51, 52, 56, 58, 59, 61, 64, 66, 68, and 82
  • Cervical cancer⁹ - Types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, 68, 70, 73, and 82
  • High-risk HPV types
    • Southeast Asia - Type 18
    • West Africa - Type 45
    • Central/South America - Types 39 and 59

Differential Diagnoses

Other Problems to Be Considered

Anogenital malignancy
Anogenital warts in children
Fordyce spots
Laryngeal papillomatosis of neonates and infants
Syphilis (genital warts sometimes can be confused with syphilitic lesions, condyloma lata)
Verrucous carcinoma of genitalia (giant condyloma of Buschke-Löwenstein)

Workup

Laboratory Studies

• Diagnosis usually is made clinically; it may be helped by the application of acetic acid and biopsy.
• Identification of precise HPV genotypes is available only in research laboratories by using DNA hybridization techniques.¹⁰
  • This technique includes Southern blot (highly sensitive and also most time consuming), dot blot, and in situ hybridization.
  • Others methods include enzyme-linked immunosorbent assay (ELISA) for immunoglobulin G (IgG) antibody (Ab) against HPV 16 capsid.
• Certain screening tests are available with a relatively high sensitivity and specificity; they include the following:
  • ViraPap
  • ThinPrep Pap
  • Hybrid capture II

Other Tests

• Acetic acid test
  • Soaking acetic acid into suspicious lesions can enhance the degree of suspicion in lesions without classic features.
  • The method involves applying a 3-5% acetic acid–moistened gauze pad for 5-10 minutes on suspected lesions of the penis, cervix, labia, or perianal area.
  • Inconspicuous, flat, genital lesions that might be difficult to assess become visible. Dysplastic and neoplastic tissues turn white (acetowhite).
  • False-positive results are common and can result from anything that causes parakeratosis (eg, candidiasis, psoriasis, lichen planus, healing epithelium, sebaceous glands).
  • This technique can be combined with the use of colposcopy to examine cervical lesions.
  • The acetic acid test is reserved only for suspicious lesions and should not be used for routine screening.

Histologic Findings

Histopathology can elucidate diagnosis in most cases.

• Verrucae consist of acanthotic epidermis with papillomatosis, hyperkeratosis, and parakeratosis.
• Elongated rete ridges may point to the center of the wart and dermal capillary vessels may be thrombosed.
• Koilocytes are indicative of HPV infection. These are large keratinocytes with an eccentric, pyknotic nucleus surrounded by a perinuclear halo.
• Anogenital warts lack a granular layer and tend to be more papillomatous and vascular than common warts.
• An electron microscope may show viral particles in nuclei.
• Immunohistochemical staining with the peroxidase-antiperoxidase technique stains cells infected by viral particles.

Treatment

Medical Care

Treatment is aimed at destruction of the warty growths rather than elimination of the virus.

• Subclinical infection probably is lifelong, and no cure is available.
  • Most partners are likely to be subclinically infected with human papillomavirus (HPV), even if they do not have exophytic lesions.
  • Use of condoms may reduce transmission of the virus to uninfected partners.
• Standard therapies for genital warts can remove most warts; however, no ideal treatment is available for all warts and all patients.¹¹
  • Caustics/acids - 80-90% bichloracetic acid (BCA) or trichloroacetic acid (TCA)
  • Podophyllin resin - 10-25% or 0.5% podofilox solution or gel (Condylox)
  • Imiquimod 5% cream (Aldara) - 3 times per week, up to 4 months (A recent article reported that the optimal duration of use for women's genital warts may be 1 month.)¹²
  • Interferon, intramuscular or intralesional injection - 3 million units, 3 times per week for 3 weeks
  • A vaccine against HPV types 6, 11, 16, and 18 (Gardasil, Merck) was approved in June 2006. It is recommended for girls and women aged 9-26 years and is given in a series of 3 shots (day 1, month 2, month 6). The US Food and Drug Administration (FDA) also approved it for boys and men aged 9-26 years. Another vaccine against HPV types 16 and 18 (Cervarix, GlaxoSmithKline) has just been approved for girls and women aged 10-25 years.

Surgical Care

• Cryosurgery is very effective for treating multiple, small, genital warts.
  • Warts on the shaft of the penis and vulva respond very well to cryotherapy.
  • Cryotherapy of the rectum is painful and less successful.
  • Cryotherapy is effective and safe for the mother and fetus when used during the second and third trimesters of pregnancy.
• Electrosurgery is quite effective for a limited number of lesions on the shaft of the penis.
  • Large, unresponsive lesions around the rectum or vulva can be treated with scissor excision of the bulk of the mass followed by electrocautery of the remaining tissue down to the skin surface.
  • Loop electrocautery excisional procedure (LEEP) after colposcopic biopsy has become a standard procedure for cervical lesions particularly for the ones with neoplastic features.
  • Removal of a very large mass of warts is a painful procedure, best performed under either general or spinal anesthesia.
• Carbon dioxide laser is an efficient method of treating primary and recurrent anogenital warts because of its precision and rapid healing without scarring.
  • Primary cure rates as high as 91% have been reported.
  • Carbon dioxide laser is the treatment of choice for pregnant women with extensive lesions or lesions that do not respond to TCA.
• Pulsed-dye laser and other new lasers have been used by some with various successful rates.
• Surgery is indicated particularly for large genital warts or malignant lesions.
• For recurrent carcinoma, Mohs surgery is a good choice.

Consultations

• Dermatologist
• Gynecologist
• Surgeon

Medication

Historically, medical treatments have been destructive in nature, although recently immunomodulators have been introduced.

Keratolytic agents

Cause cornified epithelium to swell, soften, macerate, and then desquamate.

Podofilox (Condylox)

Topical antimitotic that can be chemically synthesized or purified from plant families Coniferae and Berberidaceae (eg, species of Juniperus and Podophyllum). Treatment of anogenital warts results in necrosis of visible wart tissue. Exact mechanism of action is unknown. Genital warts are epidemiologically associated with cervical carcinoma.

Dosing

Adult

Apply 0.5% solution to external genital warts with drug-dampened applicator bid for 3 d, followed by 4 d without treatment; repeat cycle for maximum of 4 wk

Pediatric

Not established

Interactions

Coadministration with other keratolytic agents may cause increased skin irritation

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid >10 cm²/d or 0.5 mL/d of solution; about 15% of patients report severe local reactions to treatment area after first cycle, which reduces to 5% by last treatment cycle; local effects include pain, burning, inflammation, and erosion; avoid contact with eyes (If eye contact, immediately flush eye with copious quantities of water); not for use on mucous membranes of genital area including urethra, rectum, and vagina; do not exceed frequency of application or duration of usage

Podophyllum resin (Podocon-25)

Topical treatment for benign growths, including external genital and perianal warts, papillomas, and fibroids. Arrests mitosis in metaphase; active agent is podophyllotoxin; type of podophyllum resin used determines strength. American podophyllum contains one-fourth the amount of Indian source.
Although procedure is simple, home treatment should be avoided in most cases because patients tend to overtreat and cause excessive inflammation.

Dosing

Adult

20% podophyllin resin in compound tincture of benzoin; apply to lesion and allow to dry, then remove by washing 1 h later; treat again in 1 wk

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; diabetes; impaired peripheral circulation; avoid use on mucous membranes, eyes, bleeding warts, moles, birthmarks, or unusual warts with hair; pregnancy

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Powerful caustic and severe irritant; do not use if surrounding tissue is swollen or irritated; 25% solution should not be applied near mucous membranes; do not use large amounts; avoid contact with cornea; systemic toxicity from absorption of podophyllin; polyneuritis, paralytic ileus, leukopenia, thrombocytopenia, coma, and death have occurred when large quantities absorbed (large surface area and long contact time); can produce bizarre forms of squamous cells, which can be mistaken for SCC; inform pathologist if previously treated wart is sent for biopsy

Trichloroacetic acid (TCA, Tri-Chlor)

Cauterizes skin, keratin, and other tissues. Although caustic, causes less local irritation and systemic toxicity than other drugs in the same class. However, response is often incomplete, and recurrence occurs frequently. Most clinicians use 25-50% TCA, although some use as high as 85% and then neutralize with either water or bicarbonate; tissue sloughs and subsequently heals in 7-10 d. Less destructive than laser surgery, electrocautery, or cryotherapy.

Dosing

Adult

Paint onto lesions, avoid uninvolved skin; can be used in anal areas; repeat q1-2wk prn

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; not for use on premalignant or malignant lesions

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

External use only; restrict use to treatment areas only

Immunomodulators

Stimulate the release of key factors that regulate the immune system.

Imiquimod (Aldara)

Induces secretion of interferon alpha and other cytokines; mechanism of action is unknown. May be more effective in women than in men.

Dosing

Adult

Apply 3 times/wk prior hs; leave on skin for 6-10 h

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Not recommended for treatment of rectal, cervical, intravaginal, urethral, and intra-anal human papilloma infection; following surgery or drug treatment, do not use topical imiquimod until genital/perianal tissue is healed

Interferons

Are naturally produced proteins with antiviral, antitumor, and immunomodulatory actions. Alpha, beta, and gamma interferons may be given topically, systemically, and intralesionally.

Interferon alfa-2b (Intron A)

Protein product manufactured by recombinant DNA technology. Mechanism of antitumor activity is not clearly understood; however, direct antiproliferative effects against malignant cells and modulation of host immune response may play important roles. For patients >18 y with genital warts refractory to other forms of treatment.

Dosing

Adult

Inject 0.1 mL of 10 million IU Intron A in 1 mL of diluent into each lesion 3 times/wk qod for 3 wk

Pediatric

Not established

Interactions

Theophylline may increase interferon alpha toxicity; cimetidine may increase antitumor effects; zidovudine and vinblastine may increase toxicity of interferon alpha

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Influenzalike symptoms usually clear in 24 h; pulmonary infiltrates, elevated liver enzymes, and mild leukopenia (all rare); caution in brain metastases, severe hepatic or renal insufficiencies, seizure disorders, multiple sclerosis, or compromised CNS

Antimetabolites

Inhibit cell growth and proliferation.

5-Fluorouracil or 5-FU (Efudex, Adrucil, Fluoroplex)

For management of superficial basal cell carcinomas. Interferes with DNA synthesis by blocking the methylation of deoxyuridylic acid and inhibits thymidylate synthetase, which subsequently reduces cell proliferation. For use on warts resistant to other forms of treatment.

Dosing

Adult

Alternative for vaginal warts: Insert a special applicator that is one-third full with 5% 5-FU cream deeply into vagina, 1-2 times/wk for up to 10 consecutive wk

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; potentially serious infections

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Protect vulva and urethra with petrolatum and place tampon just inside introitus; if twice a week dosing is used, then protect vulva with either zinc oxide or hydrocortisone ointments (in one study there was no evidence of disease in 85% of cases after 3 mo of treatment); incidence of inflammatory reactions may occur with occlusive dressings; porous gauze dressing may be applied for cosmetic reasons without increase in reaction

Vaccines

An HPV vaccine is now available for prevention of HPV-associated dysplasias and neoplasia, including cervical cancer, genital warts (condyloma acuminata), and precancerous genital lesions. Immunization series should be completed in girls and young women aged 11-26 y. Also indicated for boys and men aged 9-26 years for prevention of condyloma acuminata caused by HPV types 6 and 11.

Papillomavirus vaccine (Gardasil)

Quadrivalent HPV recombinant vaccine.
First vaccine indicated to prevent cervical cancer, genital warts (condyloma acuminata), and precancerous genital lesions (eg, cervical adenocarcinoma in situ; cervical intraepithelial neoplasia grades 1, 2, and 3; vulvar intraepithelial neoplasia grades 2 and 3; vaginal intraepithelial neoplasia grades 2 and 3) due to HPV types 6, 11, 16, and 18. Vaccine efficacy mediated by humoral immune responses following immunization series.
FDA-approved for females aged 9-26 years. Currently under FDA priority review to evaluate efficacy in women aged 27-45 years. Indicated for boys and men aged 9-26 years for prevention of condyloma acuminata caused by HPV types 6 and 11.

Dosing

Adult

<26 years: 0.5 mL IM administered as 3 separate doses; administer second and third doses 2 and 6 mo after first dose, respectively
>26 years: Not established

Pediatric

<9 years: Not established
>9 years: Administer as in adults

Interactions

Immunosuppressive therapies (eg, irradiation, antineoplastic agents, corticosteroids) may decrease immune response to vaccine

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Shake well before administering; administer in deltoid region of upper arm or in higher anterolateral thigh; individuals with impaired immune responsiveness (eg, HIV infection, neoplastic disease, currently taking immunosuppressive drugs) may not elicit antibody response; because of IM administration, do not administer to individuals with bleeding disorders (eg, thrombocytopenia, coagulation disorders, anticoagulant therapy); common adverse effects include pain, swelling, erythema, and/or pruritus at injection site and fever

Miscellaneous topical ointments

Topical product that has gained FDA approval for genital warts.

Sinecatechins (Veregen)

Botanical drug product for topical use consisting of extract from green tea leaves. Mode of action unknown but does elicit antioxidant activity in vitro. Indicated for topical treatment of external genital and perianal warts (condylomata acuminatum) in immunocompetent patients. Ointment containing 15% sinecatechins, available in 15- and 30-g tubes.

Dosing

Adult

Apply tid; use approximately a 0.5-cm strand of ointment topically for each external genital or perianal wart; continue treatment until complete clearance of all warts, but not to exceed 16 wk

Pediatric

<18 years: Not recommended

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Not evaluated for urethral, intravaginal, cervical, rectal, or intra-anal HPV disease and should not be used to treat these conditions; avoid application to open wounds, eyes, and nose; wash hands before and after application; avoid sexual contact while ointment is on skin; may cause application site reactions, phimosis, inguinal lymphadenitis, urethral meatal stenosis, dysuria, genital herpes simplex, vulvitis, hypersensitivity, pruritus, pyodermitis, skin ulcer, erosions in the urethral meatus, and superinfection of warts and ulcers

Follow-up

Further Outpatient Care

• Patients typically are monitored on a periodic basis to assess for efficacy of treatment, unwanted side effects, and the development of complications. Outpatient follow-up care also provides an opportunity to evaluate for other sexually transmitted diseases (STDs) and provides patient education on an ongoing basis.

Deterrence/Prevention

• A vaccine for human papillomavirus (HPV) infection has been approved by the US Food and Drug Administration.

Complications

• Disease complications can include progression to malignancy and transmission to other sexual contacts. In the setting of genital warts active during a pregnancy delivery, there is a small risk of laryngeal papillomatosis.
• Each therapeutic modality carries its own unique set of risks. Risks of individual medical options are enumerated above.
• Expected effects of cryosurgery include pain, edema, vesicles, bullae, weeping, and some necrosis. There is a small risk of infection, bleeding, abnormal scarring, pigment alteration, paresthesias, and alopecia with cryosurgery.
• Similarly, laser surgery of genital warts may result in pigment alteration, abnormal scarring, and infection. Special care must be taken to prevent respiratory infection from the laser plume generated by vaporization of virally infected tissue.

Prognosis

• Prognosis is good, and most cases of genital warts are amenable to treatment.
• Patients who are immunosuppressed with genital warts may represent a special challenge.

Patient Education

• STD counseling and evaluation of partners
  • Patients with genital warts deserve a focused history and physical with appropriate testing to assess for other STDs.
    • In a population study, 7% of men and 31% of women who had genital warts had concurrent STDs. In fact, 28% of these men and 71% of women had other STDs before or after their genital warts.
    • Several consort studies documented that 30% of female consorts and 80% of male consorts had HPV infection. Usually, the same type of HPV involved both parties, and often they were HPV 6, 11, 16, and 18.
  • The benefit of evaluating sex partners of patients with genital warts has been apparent.
• For excellent patient education resources, visit eMedicine's Sexually Transmitted Diseases Center. Also, see eMedicine's patient education article Genital Warts.

Miscellaneous

Medicolegal Pitfalls

• Failure to diagnosis genital warts correctly can result in considerable morbidity. Confusing condyloma lata for genital warts will miss the diagnosis of syphilis and will lead to inappropriate therapy. Confusing pearly penile papules or Fordyce spots with genital warts will result in unnecessary treatment and likely unwarranted psychosocial concern. Missing a diagnosis of verrucous carcinoma or squamous cell carcinoma is likely to delay appropriate therapy and may lead to unneeded morbidity, even mortality.
• Treatment of genital warts can be difficult and lengthy. Patient expectations should be set appropriately. Patients should be counseled on their risk of infectivity to others. They also should be advised of their increased risk of having acquired other STDs.
• Each therapy of genital warts has a unique set of potential adverse effects. Patients should be appropriately aware of potential adverse consequences of therapy.

Special Concerns

• Increased risk of anogenital malignancy
  • Patients with genital warts have an increased risk of anogenital malignancy.
  • Infection with HPV is the primary cause of cervical malignancy, although most patients with HPV-infected cervices have a benign outcome. This mandates that female patients with genital warts should have an annual screening examination and Papanicolaou test. Up to 90% of cervical cancers are caused by HPV infection of the cervix.
  • Strong epidemiologic evidence suggests that 10% of patients who had a high-grade squamous intraepithelial lesion (HGSIL, which includes so-called moderate-to-severe dysplasia, carcinoma in situ, and cervical intraepithelial neoplasia II and III) would have persistence of lesions that eventually would progress to invasive cancer without treatment. Patients with perianal warts, patients who are HIV positive, and those with a history of receptive anal intercourse are at increased risk for anal HGSIL. No direct evidence suggests that this would progress to invasive anal cancer, as lesions of the cervix are capable of doing. Nonetheless, penile, vulvar, vaginal, ovarian, and anal carcinomas have been linked to HPV infection.
• Anogenital warts in children
  • Anogenital warts are rare in the general pediatric population.
  • More than one half of children with anogenital warts have a manifestation either of viral inoculation at birth or of incidental spread of cutaneous warts. Such cases often are caused by nongenital HPV types.
  • Diagnosis of genital warts in a child requires that the clinician report suspected abuse to begin an evaluation process that may or may not confirm sexual abuse.^13,14
• Laryngeal papillomatosis of neonates and infants
  • Although childhood laryngeal papillomas frequently are acquired from condyloma of the mother (HPV types 6 and 11 are frequently cited), most infants of mothers with condyloma do not contract laryngeal papillomas.
  • Accordingly, cesarean delivery should not be performed solely to prevent transmission of HPV infection to the newborn.
  • Route of transmission in pregnancy is not known, and infants born by cesarean delivery have developed laryngeal papillomatosis. However, it is advisable to remove visible lesions during pregnancy.
• Patients who are immunosuppressed: Patients who are immunosuppressed such as those with AIDS and those on immunosuppressive therapy (eg, patients with renal transplants) are more likely to develop persistent HPV infection and subsequent dysplasia and malignancy.
• Verrucous carcinoma of genitalia (giant condyloma of Buschke-Löwenstein): It is a low-grade, locally invasive, squamous cell carcinoma that is associated with HPV types 6 and 11 and should be considered in the differential of lesions measuring greater than 1 cm in diameter. Only radical surgical extirpation is considered appropriate treatment.

Multimedia

Media file 1: Condyloma acuminatum.

Media file 2: Small papilloma of the vulva.

Media file 3: "Cauliflower" condyloma of the penis.

Media file 4: Small papilloma on the shaft of penis.

Media file 5: Small papilloma of the anus.

References

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2. Chuang TY, Perry HO, Kurland LT, Ilstrup DM. Condyloma acuminatum in Rochester, Minn, 1950-1978. II. Anaplasias and unfavorable outcomes. Arch Dermatol. Apr 1984;120(4):476-83. [Medline].

3. Nebesio CL, Mirowski GW, Chuang TY. Human papillomavirus: clinical significance and malignant potential. Int J Dermatol. Jun 2001;40(6):373-9. [Medline].

4. Rhea WG Jr, Bourgeois BM, Sewell DR. Condyloma acuminata: a fatal disease?. Am Surg. Nov 1998;64(11):1082-7. [Medline].

5. Chuang TY, Perry HO, Kurland LT, Ilstrup DM. Condyloma acuminatum in Rochester, Minn., 1950-1978. I. Epidemiology and clinical features. Arch Dermatol. Apr 1984;120(4):469-75. [Medline].

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Keywords

condyloma acuminatum, GW, genital warts, syphilis, gonorrhea, papillomas, benign proliferations of the anogenital skin, benign proliferations of the anogenital mucosa, human papillomavirus, HPV, anogenital cancer, sexually transmitted diseases, STDs, anogenital warts, papillomatous papules, papillomatous nodules, cauliflower like masses

epidermodysplasia verruciformis, squamous cell carcinoma, actinic keratosis, keratoacanthoma, Bowen disease, melanoma, oral focal epithelial hyperplasia, oral papilloma, laryngeal papilloma, recurrent respiratory papillomatosis, conjunctival papillomas, epidermal cyst, giant condyloma of Buschke and Löwenstein, verrucous carcinoma, bowenoid papulosis, vulvar intraepithelial neoplasia

cervical squamous intraepithelial lesions, low-grade squamous intraepithelial lesions, LGSIL, high-grade squamous intraepitheliallesions, HGSIL, cervical cancer

Contributor Information and Disclosures

Author

Tsu-Yi Chuang, MD, MPH, Clinical Professor, Department of Dermatology, University of Southern California; Staff Dermatologist, Desert Specialty Group, Inc
Tsu-Yi Chuang, MD, MPH is a member of the following medical societies: American Academy of Dermatology, American Society for Dermatologic Surgery, and International Society of Dermatology
Disclosure: Nothing to disclose.

Coauthor(s)

Ryan Brashear, MD, Staff Physician, Department of Dermatology, Indiana University School of Medicine
Ryan Brashear, MD is a member of the following medical societies: American Academy of Dermatology and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Mark W Cobb, MD, Consulting Staff, WNC Dermatological Associates
Mark W Cobb, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and American Society of Dermatopathology
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Managing Editor

Edward F Chan, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine
Edward F Chan, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

CME Editor

Catherine M Quirk, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania
Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

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