Genital herpes

Herpetic infection of the genital tract is becoming increasingly common. The virus, herpes simplex virus (HSV), exists in two forms, HSV1 and HSV2. Type specific HSV1 usually causes oral cold sores, but in up to 40% of cases is the cause of genital herpes. In the remainder HSV2 causes genital herpes. Serological testing shows that between 10 and 40% of adults have been infected at some time, but the infection was symptomatic in less than a quarter.

The first clinical attack of genital herpes is usually worse than the recurrences. It follows sexual contact with an infected person who was either symptomatically or asymptomatically shedding the virus. The inner surfaces of the labia majora are most likely to be infected. After a short period of itching or burning, small crops of painful, reddish lumps appear which become blisters within 24 hours. The blisters ulcerate rapidly to form multiple shallow, painful ulcers (Fig. 33.1). The surrounding tissues become oedematous and secondary bacterial infection may occur, aggravating the oedema and pain. Micturition may be very painful. Over 5 days the ulcers crust over and heal slowly, the healing being complete in 7–12 days after the appearance of the blisters for a primary infection, and less for recurrences. During this time, and intermittently, the virus is shed from the infected area and in vaginal secretions. The virus also enters the sensory nerves supplying the affected area, and tracks to lie in the dorsal root ganglion. It may lie dormant for the rest of the person’s life, or may be reactivated and track back along the nerves to cause a new attack of herpes. Second and subsequent attacks are less severe, but can cause considerable discomfort and affect relationships.

Fig. 33.1 Genital herpes – lesions are visible on the labia and the inner aspect of the left thigh.

In 30% of infected women a single recurrence occurs, and between 2 and 5% have recurrent attacks, sometimes more than six times a year. As time passes the attacks (clinical and asymptomatic) become less frequent and may cease. In most cases the cause of the recurrence is not known, but recurrences are more common in the luteal phase of the menstrual cycle, if the woman has other sexually transmitted infections, or if she is emotionally stressed.

Intermittent asymptomatic shedding and atypical unrecognized lesions explain the unrecognized transmission to sexual partners. As HSV2 has a tropism for the genital area (HSV1 for the oral area) clinical recurrences are more frequent if the genital infection is HSV2 rather than HSV1.

Genital warts (condylomata acuminata)

Genital warts are caused by types 6 and 11 of the human papilloma virus (HPV), usually transmitted sexually. Vulval infections are the most common, although the virus may spread to infect the vagina, the perineum (Fig. 33.2) and occasionally the cervix.

Fig. 33.2 Multiple genital warts on the introitus and surrounding the anus.

Vulval warts usually present as cauliflower growths of varying sizes, but may be clinically undetectable. It has been estimated that 5–10% of sexually active adults are infected annually, and that 30% have evidence of previous infection with other HPV genotypes.

In most cases the warts are symptomless, but some women complain of vulval discomfort, including itching. If the warts involve the vaginal entrance or the vagina, the woman may complain of dyspareunia.

The importance of HPV infections is that they are surrogates for the exposure to and carriage of the oncogenic HPV types 16 and 18, which are the cause of cervical carcinoma. The risk of this occurring from vulval warts is small. This is discussed further in Chapter 37.

Syphilitic vulval ulcer

Syphilis is caused by invasion of the tissues by Treponema pallidum and is sexually transmitted. The primary lesion, which is often unrecognized, is a small papule that appears at the site of inoculation, usually 14–28 days after the person is infected. In women, the usual site of infection is one of the labia majora, but the cervix may be infected instead. The papule rapidly enlarges to form an oval lesion of variable size, the centre of which becomes eroded and granulomatous. The edges of the eroded area are sharp, and outside this a thickened, indurated zone occurs, hence the name for the lesion – hard chancre. The chancre is painless and may be ignored by the woman or considered a small sore of no consequence, but as it is teeming with treponemas it is highly infectious. The primary lesion disappears in 21 days or so. Secondary lesions, which include mucous patches and condylomata lata (Fig. 33.3), appear 5–6 weeks later.

Fig. 33.3 Secondary syphilis – condylomata lata on labia and perianally.

Infection of Bartholin’s gland (Bartholinitis)

The infection is usually due to Escherichia coli or staphylococci, but may follow Neisseria gonorrhoeae or Clostridium trachomatis infection. In the acute stage both the duct and the gland are involved. If it is not treated the infection may subside or a Bartholin’s abscess may form. Occasionally the gland becomes chronically enlarged following an inflammatory conglutination of the duct epithelium, to form a Bartholin’s cyst.

Vaginal discharges and infections

The vagina of a woman in the reproductive years is lined by a layer of stratified epithelium, 10–30 cells thick. As is described on page 333, the superficial cells of the vagina are shed constantly into the vaginal cavity and release glycogen, which is acted on by Döderlein’s bacilli (lactobacilli) to produce lactic acid and hydrogen peroxide (natural defences against vaginal infection) and to maintain the vaginal pH between 3.5 and 4.5.

The vagina harbours large numbers of bacteria, which constitute its normal flora (Table 33.1). However, a significant number of women harbour potential pathogens such as E. coli, anaerobes, Candida spp., and Gardnerella vaginalis (bacterial vaginosis). They produce symptoms in only a few women.

Table 33.1 Normal vaginal flora

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