You have got quite a nerve, Dame Janet!
Genital herpes and warts
Dr Olwen Williams concludes our sexual health series by advising on two of the most common STIs
Genital herpes is the commonest cause of genital ulceration in the UK. The causative virus is herpes simplex type 1 and 2. Interestingly, the prevalence of genital herpes caused by type 1 herpes simplex virus (HSV) commonly associated with the common cold sore has increased. Genitourinary medicine clinics have reported up to 60 per cent of primary or first episode genital herpes being due to HSV 1.
This reflects the decreasing exposure of individuals to the virus as children with improved socio-economic circumstances, subsequent lack of protective antibodies and possibly an increase in individuals having oro-genital contact. Sexual transmission, particularly through oral sex, is becoming an important source.
Attacks are characterised by a prodrome. The individual may experience a tingling sensation in the skin prior to the appearance of vesicles containing clear serum. The vesicles quickly rupture leaving painful, shallow well-defined ulcers, which may coalesce. A vaginal or urethral discharge may occur.
During this period of ulceration, women complain of external dysuria and vulval pain, vulval swelling and inguinal lymphadenopathy. Men are less likely to have dysuria, unless the lesions are on the prepuce or glans. Flu-like symptoms are common during this period.
During the first 72 hours these ulcers excrete herpes simplex virons and this is the optimum time to instigate antiviral medication. The ulcers will crust over and heal without scarring. The primary attack or 'first episode' may last up to three weeks. Recurrences tend to be milder, of shorter duration and with minimal systemic symptoms.
Urinary retention arising from a transient autonomic neuropathy is a recognised complication.
Diagnosis by isolation of herpes simplex virus from the genital lesion is essential for prognosis, counselling and management of the condition. Swabs should be taken from the base of the ulcer and placed in viral transport medium, which needs to be then kept at 4C while transported to the laboratory.
Many practices will not routinely have viral transport medium in stock, so if feasible recommend the patient be seen at a genitourinary or sexual health clinic where testing facilities are available as soon as possible.
In the Friday-night scenario, one should advise the patient that it is preferable to treat 'blind' early than delay therapy until swabbing is available.
Therapy is only effective in the early stages of an attack and delaying it may cause the patient undue suffering. This must be explained to the patient who should be advised that a definitive diagnosis cannot be obtained until the patient re-presents with a recurrence and has viral swabs done.
The current serological tests, which detect HSV antibodies, are not type-specific but newer EIA-type specific tests are becoming available. These have no place in the diagnosis of primary genital herpes as it takes eight to 12 weeks to develop a type-specific immune response.
Clinical use of these tests has not been fully assessed. They may be helpful in recurrent genital ulceration of unknown cause, evaluating genital herpes during pregnancy, or investigating asymptomatic partners of patients with genital herpes. Screening for HSV antibodies does not appear to have any place in the antenatal or genitourinary medicine setting.
Consideration should be given to other causes of genital ulceration, especially as syphilis is re-emerging in the UK. Syphilis, chancroid, lymphogranuloma venerium are the other sexually acquired ulcerative diseases, with Bechets, aphthous ulcers, trauma and bacterial infection being the other common causes. Pain tends to be the distinguishing factor that sets herpes apart from the others.
Management of a first episode should focus on early instigation of oral antiviral therapy. Topical therapy has no place in genital herpes therapy. Valaciclovir 500mg twice daily and famciclovir 250mg three times daily, both pro-drugs of acicolvir, allow for less frequent daily dosing as opposed to five times daily dosing of aciclovir for five days.
Therapy will curtail viral shedding and reduce the length and severity of the attack. Ideally it should be started within the first 72 hours of an episode, and up to five days if new lesions are appearing. Adequate analgesia is essential. External dysuria may be managed by advising the patient to drink plenty of water to dilute their urine and micturating while sitting in a warm bath of salty water.
Topical anaesthetic agents such as Emla cream are beneficial but care must be taken as sensitisation may occur. Follow-up within a week is useful to assess response to therapy, further discussion regarding HSV and the offer of screening for other sexually transmitted infections.
Recurrent genital herpes usually presents with less severe attacks, primarily in the first year of infection. Frequency varies and may be triggered by sexual intercourse, menstruation, and general ill-health. Stress is not thought to be a factor but individuals become stressed by recurrent attacks. Type 1 genital herpes tends to give less frequent recurrences than type 2. Severity of attacks is identical in the primary and recurrent episodes.
Recurrences may be managed by either episodic therapy giving patients control over their treatment by supplying five-day courses of valaciclovir or famciclovir which the patient commences in the prodrome or suppressive therapy with twice-daily aciclovir for a three- to six-month period.
The latter will prevent recurrences and is usually offered to individuals having six or more attacks per annum. Both approaches have their pros and cons.
Often patients on long-term suppressive therapy are reluctant to come off medication. This has to be managed in a sensitive manner, exploring why they feel that way. It might transpire that they have not divulged they have HSV to their long-term partner, or their attacks were very severe.
Each case has to be dealt on an individual basis, but ideally on commencing suppressive therapy one should explain that this is for six months with a review and maximum of one-year suppression. At the end of this period, the patient's circumstances may have altered.
It is not uncommon for a patient on stopping their suppression to have a recurrence within the first month. They should be warned about this and given a spare pack of short-course valaciclovir to overcome the attack, and a follow-up at a couple of months to see how they are progressing. There is evidence that despite using a suppressive dose of anti-herpes medication, the patient may still shed HSV and this should be discussed.
Patients should be advised that HSV can be transmitted even when the individual does not have an attack, due to asymptomatic shedding, hence condoms should be used at all times. But studies have shown that the longer a couple are together the less likely the non-infected individual is to acquire genital herpes.
The human papilloma virus (HPV), of which there are 90 site-specific types, is the causative agent of genital warts. Exophytic genital warts in general are type 6 and 11, while type 16, 18, 31 and 45 are considered to be oncogenic, colonise the genital tract but do not give rise to obvious warts.
Both groups of genital HPV can be present together or independently. Confusion arises in the lay public with HPV, genital warts and genital cancers.
Genital warts are benign epithelial skin tumours. It is important to highlight this when discussing a diagnosis of genital warts with a patient. Women with genital warts do not require increased frequency of cervical screening or screening to start at an earlier age than recommended by the national guidelines.
Visual inspection is the only means of making a clinical diagnosis. Genital warts may appear in a variety of morphological forms, which may dictate therapy and usually affect sites of trauma during sexual intercourse. As part of the differential diagnosis one should consider molluscum contagiosum. These lesions tend to have a pearly appearance and are characterised by a central punctum.
Consider biopsy for any lesion that has an atypical appearance to exclude pre-malignant lesions in both men and women. Routine biopsy and HPV typing is not necessary in day-to-day practice but should be considered in medicolegal cases, especially in children if sexual abuse is suspected.
Many patients are concerned about where the warts have come from, especially if their current sexual partner does not have visible warts. Obviously one is unable to answer this question, but it is important to realise that genital warts have a variable incubation time of two weeks to two years. Individuals who are incubating the virus may transmit it unwittingly to their sexual partner.
In cases where vertical transmission of genital warts has occurred, guidelines quote the fact that it may take up to the age of three before the child develops genital warts acquired during passage through the birth canal.
The mode of transmission is most often by sexual contact but may be transmitted from digital lesions a small study that sampled the hands and genitals of a group of 22 individuals with genital warts identified the same HPV type on both sites in a third of men and an eighth of women.
Transmission through contact via formites is not thought to be possible. Although condoms do offer protection from acquisition of genital warts this is dependent on where the wart is situated and if the condom covers it.
Psychological issues anxiety, guilt, distress, loss of self-esteem and breakdown of relationships are common. The warts themselves may become sore, bleed and cause dyspareunia.
Genitourinary physicians in the majority advocate 'home-based' therapy for patients with suitable lesions. Podophyllotoxin products are suitable for soft, non-keratinised multiple warts in the genital area; it is applied twice-daily for three days followed by four days' rest for four cycles. Patients should be advised to discontinue its use if significant soreness occurs. It should be avoided in pregnancy.
Imiquimod is an immune response modifier which when applied to skin infected with HPV induces a cytokine response. It is suitable for all types of ano-genital warts but should be avoided in pregnancy. The cream is applied nightly on alternate nights in 16-week cycles. Initial response may be delayed.
This may lead to despondency but the apparent low relapse rate should counterbalance this. Patients should be given written information about these therapies and reviewed.
Surgery-based therapies include the use of topical podophylline (not as effective as podophyllotoxin), trichloroacetic acid 80-90%, a caustic agent causing cellular necrosis, physical ablation via excision, cryotherapy, electosurgery or laser therapy.
All have their place, especially in the management of solitary warts. Extensive warts, especially in the perianal region, may require surgical excision under general anaesthetic.
·Therapy is only effective in early stages of an attack
·It is better to treat blind than delay therapy until swabs can be taken at a genitourinary clinic
·Diagnosis needs to be supported by viral culture
·Management of a first episode should focus on early instigation of oral antiviral therapy not topical therapy
·Management of recurrences involves episodic or suppressive antiviral therapy
·Advice regarding asymptomatic shedding is essential
·Diagnosis is by naked eye inspection
·Consider biopsy for any lesion that has an atypical appearance to exclude
premalignant lesions in both men and women
·Transmission is usually by sexual contact, but it can also be transmitted by digital lesions
·In cases of vertical transmission it can take up to three years for the child to develop warts
·Initial response to imiquimod may be delayed so reassure patients about its low relapse rate to counteract despondence
(excellent patient leaflets on herpes)
Olwen Williams, genitourinary physician, Wrexham Maelor Hospital, and chair of the British Association for Sexual Health and HIV's adolescent and sexual health special interest group