Anogenital warts (also known as condylomata acuminata, genital warts, or venereal warts) consist of nodules on the perineum, genitalia, thigh folds, and anus. They vary in size and can form large, cauliflower-like masses, especially in the moist environment of the perineum.
- Incidence and prevalence: In countries with highly developed medical services, referral rates of genital warts have greatly increased in the last 50 years. In the UK, there was a marked increase in the incidence of anogenital warts (condylomata acuminata) from the 1970s to the 1990s, with a continuing rise over the last two decades. The overall population incidence worldwide is approximately 200/100000. There appears to have been a slight decrease in the rate of rise of anogenital warts in developed countries in the last few years and it is speculated that this may be influenced by the introduction of the HPV vaccine, as rates of other sexually transmitted diseases such as chlamydia have continued to rise.
- Age: The incidence is highest in young adults aged 16-24 years and for this age group is estimated to be 700/100000.
- Sex: The incidence and prevalence in males are higher than in females with a male: female ratio of 1: 0.7.
Pathophysiology and Predisposing Factors
Genital warts have high infectivity. The thinner mucosal surface is presumably more susceptible to inoculation of the virus than thicker skin, but in addition, lesions are most common in sites subject to greatest coital friction in both sexes.
Human papillomavirus transmission has been most closely studied in the case of anogenital warts. Acquisition most commonly follows sexual contact but it is generally agreed that anogenital warts are not always transmitted sexually. Perianal warts may accompany genital warts, either due to local spread of infection or to direct contact during anal coitus.
Approximately two-thirds of sexual contacts of patients with genital warts develop lesions themselves within 24 months with infectivity being the highest early in the course of the disease. Close inspection by penoscopy of male sexual contacts of women with genital HPV disease has shown that 88% have at least small lesions. The incubation period between contact and diagnosis of genital warts is 3 weeks to 24 months, with a median of 3–10 months.
Occasional non-sexual acquisition of anogenital warts in adults is assumed to be possible. The sensitivity of PCR analysis has shown that HPV DNA may be present on underwear and the fingers of patients with genital warts, suggesting that transmission could occur by a number of routes.
Transmission of anogenital warts in children
Anogenital warts are uncommon in children, but their occurrence frequently stimulates discussion of the possibility of sexual transmission. With the lack of large-scale prospective studies, the possibility of bias in the referral or in reporting should be considered, and there is insufficient information to offer a reliable estimate of the relative frequency of sexual abuse in such cases.
Infection from the mother’s genital tract at delivery is regarded as a frequent source of childhood anogenital warts, probably including those presenting up to 2 years of age. Genital papillomavirus transmitted from mother to baby at birth may persist in childhood as shown by the retention of the DNA. It is thought that perinatally acquired HPV infection may not manifest as genital warts for some years.
Postnatally, transmission from adults with genital warts may occur non-sexually such as by sharing a bath with an infected adult. In studies of children with anogenital warts assessed for possible sexual abuse, the mode of acquisition was thought to be sexual in no more than 5%.
Thus, on present incomplete information, both sexual and non-sexual routes are significant in the transmission of childhood anogenital warts. The long and variable incubation period, the possibility of latent or subclinical infection in the source and the problems in eliciting an accurate account of sexual contact from the child and of confirming it from the perpetrator, all make it difficult to decide which applies in an individual case. Absence of other physical evidence of molestation, location of warts on external skin as opposed to genital or anal mucosa, a clinical resemblance to common warts and the young age of the child, perhaps up to 1-2 years at the onset of warts, would tend to support non-sexual transmission. Where sexual abuse is suspected, the case is referred to a pediatrician or child abuse specialist. In addition, HPV typing is not routinely of use but might be forensically useful; the same type in child and in suspected abuser would be consistent with but not proof of sexual transmission, while different types would be strong evidence against the possibility.
The infectivity of maternal genital HPV as regards laryngeal (voice box) papilloma in the child seems low; from 51 cases of pregnancy in women with genital warts, no cases of childhood laryngeal papilloma were seen. The risk of transmission from mother to child with subsequent development of disease in the child has been estimated to be between 1/80 and 1/1500 but only 57% of cases of laryngeal papilloma in children are diagnosed by 2 years of age.