eMedicine Specialties > Dermatology > Viral Infections

Warts, Genital

Author: Tsu-Yi Chuang, MD, MPH, Clinical Professor, Department of Dermatology, University of Southern California; Staff Dermatologist, Desert Specialty Group, Inc
Coauthor(s): Ryan Brashear, MD, Staff Physician, Department of Dermatology, Indiana University School of Medicine
Contributor Information and Disclosures

Updated: Mar 11, 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

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, 1966–2006, 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).

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.

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

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

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

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

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