Genital Warts | Details on How to Get Rid of Them


What are genital warts?

Anogenital Warts

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.


  1. 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.
  2. Age: The incidence is highest in young adults aged 16-24 years and for this age group is estimated to be 700/100000.
  3. 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.

Genital Wart Symptoms (What do genital warts look like?)

Symptoms are often asymptomatic but may cause discomfort, discharge or bleeding. The typical anogenital wart is soft, pink, elongated and sometimes pedunculated. The lesions are usually multiple especially on moist surfaces, and their growth can be enhanced during pregnancy, or in the presence of other local infections. Large malodorous masses may form on the vulvar and perianal skin. This classical ‘acuminate’ (sometimes called papillomatous, or hyperplastic) form constitutes about two-thirds of anogenital warts. The commonest sites, the area of the frenulum, glans in men, and the posterior wall of the vagina in women, correspond to the likely sites of greatest coital friction. Most other lesions are flat, though more conspicuous than plane warts elsewhere, and some of these, generally on non-mucosal surfaces such as the penile shaft, pubic skin, perianal skin, and groins, may be sufficiently pigmented to resemble seborrheic keratoses. Both acuminate and flat types may coexist. Occasionally, only lesions resembling common warts are seen, in men usually on the penile shaft, and these may be the result of contact with common warts elsewhere on the patient or on the sexual partner.

The duration of anogenital warts varies from a few weeks to many years. Recurrences can be expected in about 25% of cases, the interval varying from 2 months to 23 years. Human papillomavirus DNA can be demonstrated in clinically normal skin adjacent to warts and neoplasia, and this latent infection correlates well with recurrence after clinical cure.

Clinical variants

The low-risk mucosal HPV types responsible for anogenital warts can cause disease at other mucosal surfaces.

  1. Oral warts: Oral warts, including some which appear to have been sexually transmitted, usually contain HPV-6 or -11 and more rarely HPV-2, -57 or -16. They are common in association with HIV disease when a greater variety of HPV types may be found, including HPV-7, more usually associated with butchers’ warts. Antiretroviral treatment may lead to worsening of warts rather than improvement. HPV-13 and -32 seem to be almost specific for lesions of the rare Heck disease. High-risk genital HPVs have been detected in over 80% of cases of oral white patches, and in about 50% of cases of oral carcinoma.
  2. Respiratory papillomatosis: This condition is due most commonly to HPV-11, but also associated with other common genital types such as HPV-6 and very rarely with high-risk HPV-16. Childhood cases are believed to result from maternal infection, probably at birth during vaginal delivery. Latent or subclinical infection in the laryngeal mucosa presumably explains recurrences after successful treatment and might explain adult-onset cases, although some of these may be due to sexual transmission. Treatment usually involves recurrent debulking of lesions. Cancer transformation occurs very rarely and is most commonly associated with HPV-1.
  3. Conjunctival papillomas: Human papillomavirus of the low-risk mucosal type is frequently detected in conjunctival papillomas with rare detection of high-risk types.
  4. Nasal inverting papillomas (synonym: inverted papilloma,Schneiderian papilloma): HPV-6/11, -16/18 and -57 have been detected in nasal inverting papilloma and in an inverting papilloma of the sinuses. Progression to carcinoma is rarely reported.

Complications and co-morbidities

Patients with genital warts frequently have other sexually transmitted genital infections. The presence of any type of anogenital wart should raise the possibility that the patient may also be infected with high-risk HPVs and prompt screening for anogenital neoplasia. Very florid warts warrant consideration of an underlying immune deficiency.



Clinical diagnosis of warts is often sufficient, but atypical, subclinical or dysplastic lesions may need laboratory confirmation of HPV infection. Methods available are as follows:

  • Histology.
  • Immunohistochemistry or immunocytochemistry using type-common or type-specific antibodies.
  • DNA in situ hybridization.
  • PCR for HPV DNA.

Genital Warts Causes

Causative organisms

The low-risk HPVs are most often the cause of anogenital warts, most commonly HPV-6 (in about 45-90%) or HPV-11 and less frequently other types. HPV-1 and HPV-2 may occur in genital warts. In children, warts in the anogenital area are often thicker than in adults and may be caused by HPV types associated with the cutaneous disease as well as HPV-6 and -11. Studies involving HPV typing of childhood anogenital warts have produced somewhat varying conclusions, but overall, approximately 50% have been found to harbor genital HPV with the cutaneous types 2, 27 and 57 also commonly detected.

Genital Warts Treatment - How to get rid of genital warts?

Not all warts need treatment as many give little inconvenience and will resolve spontaneously. In addition, patients may need encouragement to persevere with long-term daily use of simpler preparations and more aggressive therapies, such as cryotherapy or surgery, have potential disadvantages. Gentle reduction of the layer of the thick skin by regular filing or paring down will usually make the lesion more comfortable. Advice on simple measures to limit the spread of the infection will be appreciated. In addition, simple domestic hygiene, such as cleaning of baths after use and avoidance of shared towels, may be advised.

The most commonly used treatments for warts involve the destruction of the area of skin infected with the virus. Such treatments usually initially involve the application of a topical preparation. Other therapies aimed at modifying the growth of the skin or to stimulate an immune response require either a topical or a systemic approach. Combination therapies are often used.

Whatever method is used there will be failures and recurrences. The best clinical guide to cure is the restoration of normal epidermal texture, including the epidermal ridge pattern where appropriate.

First line treatments

  1. Podophyllotoxin: Podophyllotoxin is purified from podophyllin and is the most common treatment used. Podophyllin and purified podophyllotoxin act as growth inhibitors. They are used mainly for the treatment of anogenital warts but can also have an effect in cutaneous warts, although penetration into thick skin may be poor. It is applied as a cream by the patient twice daily for consecutive 3 days in a week for 4 consecutive weeks. They have been used with caution under prolonged occlusion or in a strength of 5% in combination with salicylic acid and cantharidin applied every 2 weeks for up to 10 weeks. Although clearance rates may be as high as 80–95%, acute pain can occur with intense local inflammation. Podophyllin and podophyllotoxin are contraindicated in pregnancy and are not licensed for use in children.
  2. Imiquimod: An alternative home-applied treatment is imiquimod, used as 5% or 3.75% cream. Topical immunomodulation with imiquimod 5% cream is licensed for the treatment of genital warts and superficial skin carcinoma. The 5% cream is applied three times per week for up to 16 weeks but the 3.75% cream applied twice daily for 2 weeks and repeated 2 weeks later seems to be equally effective. The treatment can cause irritation, discomfort and occasionally erosion at the point of application with a small risk of causing vitiligo-like depigmentation.

Second line treatments

  1. Cryotherapy: Dimethyl ether spray, carbon dioxide snow, and liquid nitrogen all produce cold thermal damage to the skin. Liquid nitrogen produces the coldest freeze and is commonly used in hospital practice, applied either by a cotton wool bud or from a cryospray. Both methods are equally effective. The rate of application of freeze is affected by the size of the hole in the spray nozzle or by the size, shape, and density of the cotton wool at the tip of the bud. Any thick skin is pared off, and the surface dried before freezing begins. In a standard treatment, the application is continued until a rim of iced tissue (easily seen as a white discoloration) about 1 mm in width develops in the normal skin surrounding the wart. The freeze is maintained for 5–30 s depending on the size and site of the wart. This may require a continuous or pulsed spray for between 5 and 20 s, depending on the size and thickness of the wart. Longer freezing (over 25 s of continual freeze) is more likely to leave scarring, possibly damage underlying structures and not improve clearance rates. A gentler or ‘traditional’ freeze involves freezing until the 1 mm rim of frozen skin is visible and then stopping. This milder method is less efficacious in clearance. As well as damaging cells, cryotherapy may lead to clearance by stimulating the development of an immune response. Frequent treatments may improve responses although will induce more pain, and longer intervals are less effective. If this fails, or when a wart is particularly painful or deep, or both, more prolonged application, typically up to 30 s, perhaps repeated after thawing, may be used to achieve a greater destructive effect at the cost of significantly greater blistering and pain. For such treatment, local or even general anesthesia may be considered. The main disadvantage of freezing is pain. This is unpredictable and surprisingly variable between patients, but in some cases, especially with longer freezing times, it may be severe and persist for many hours or even a few days. Oral aspirin and strong topical steroids may help. Swelling of the treated area and the surrounding skin begins within minutes. A blister, sometimes hemorrhagic, may ensue within a day or two. After the usual short freezing times, the reaction will be likely to have resolved within 2–3 weeks. Scarring is unlikely with freezing times under 30 s. Occasionally, damage to underlying tissues may result, and excessive freezing times are avoided over nerves. Depigmentation may occur, and can be a significant cosmetic disadvantage in patients with darkly pigmented skin.
  2. Photodynamic therapy: Systemic or topical aminolaevulinic acid can be taken up by dividing cells, metabolized and then photoactivated to produce a damaging effect on the cell. A number of studies have shown clearance rates of 75–90%. Methyl aminolevulinate photodynamic therapy (MAL-PDT with a pulsed dye laser light source is an alternative regime, with a reported clearance rate of 53% of warts. The treatment may need to be repeated two or three times but can be limited by pain.
  3. Surgery: Excision is usually to be avoided since scarring is inevitable and recurrences of the wart in the scar are frequent. Curettage and cautery/electrocoagulation, usually in combination, may be used for painful or resistant warts, but carry a risk of scarring.
  4. Laser: The pulsed dye laser is used to treat warts with cure rates of approximately 32–75%, using a minimum of two treatments. It appears comparable to other treatments such as cryotherapy. Other lasers such as the erbium: yttrium aluminum garnet (Er: YAG) and the neodymium: aluminum garnet (Nd: YAG) can also be used. The carbon dioxide laser has a greater risk of producing scarring but has been used to treat a variety of different forms of warts. It can be effective in eradicating some difficult warts which have been unresponsive to other treatments.  Carbon dioxide laser therapy is well-tolerated but can cause significant postoperative pain, scarring and temporary loss of function.

Third line treatments

In severe cases of extensive or giant warts, often in immunosuppressed patients, more aggressive cytotoxic or antiproliferative treatments are used. Interferon may be considered, administered either systemically or intralesionally, but results are variable. Intralesional IFN alpha or beta as monotherapy gives an overall response rate of 36–63% for genital warts, but oral warts may respond slightly better. Interferon has been used as adjuvant therapy, together with surgery, cryotherapy or topical measures. No augmentation of clearance of HPV infection was observed by the addition of IFN alpha therapy to caustic application or surgery, podophyllin or laser ablation. Used with cryotherapy, IFN alpha and gamma reduced the rate of acquisition of new lesions but none of the interferons when combined with cryotherapy produced any improvement in clearance rate compared with cryotherapy alone.


Genital Warts Prevention - Do genital warts go away?

The risk for acquisition of new genital or cervical HPV infection correlates with the number of sexual partners. The risk of genital infection appears to be lower in circumcised males and in their sexual partners, and there is evidence that regular use of condoms may partially protect against the acquisition of genital HPV infection. Widespread Pap smear screening in the United States and other developed countries has greatly reduced the incidence of invasive cervical cancer.

The prophylactic HPV vaccine represents the newest approach to preventing genital HPV infection. The vaccine, which is noninfectious, is based on self-assembly of the L1 protein into virus-like particles (VLPs). VLP immunization induces high titers of type-specific neutralizing antibodies. In human clinical trials, the L1 VLP vaccine, which is administered intramuscularly, produced response in more than 99% of vaccines and resulted in serum antibody titers 40 times or more than those that develop after natural infection, with nearly 100% protection against the development of cervical infections attributable to the HPV types in the vaccine. A quadrivalent vaccine (Gardasil) composed of L1 VLPs from HPV-6, -11, -16, and -18, is approved by the US Food and Drug Administration for females and males ages 9–26 (in Europe in males only 9–15 years). A bivalent HPV-16 and -18 VLP vaccine (Cervarix) is also marketed as a vaccine to prevent cervical cancer. Both are administered as three intramuscular injections over a 6-month period.

Headache, fever, and pain, itching, redness, swelling, and bruising at the injection site, were the most common side effects observed. Because the quadrivalent vaccine includes HPV-6 and -11 VLP, it offers a reduction in the occurrence of genital warts. Despite nearly 100% efficacy in preventing HPV infection, these vaccines do not have therapeutic activity against established infection. Another limitation is that protection appears to be primarily type-specific, with limited cross-protection against very closely related types, so most infections caused by HPV types other than those in the vaccine will not be prevented. However, HPV-16 and -18 account for approximately 70% of cervical cancer worldwide. Thus, the prophylactic VLP vaccines should protect against the majority of HPV infections that lead to cervical cancer.

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