Infections of the genital tract

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Chapter 33 Infections of the genital tract

VULVOVAGINAL INFECTIONS

The skin of the vulva, in common with other parts of the skin that are liable to friction and chafing, may be infected by common skin pathogens. Boils may occur, particularly when the standard of hygiene is low. Multiple vulval ulcers occur occasionally, particularly in debilitated women, and are due to staphylococcal infection. The ulcers are shallow, with a grey, discharging base and surrounding oedema. The vulva is extremely tender. Treatment consists of antibiotics and 1% chlorhexidine cream if this can be applied without causing much pain.

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.

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.

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.

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

Organism Percentage
Lactobacilli 80–90
Staphylococci, micrococci 50–70
Ureaplasma 40–50
Anaerobes 20–50
Streptococci 20–30
Gardnerella 10–30
E. coli 5–15
Candida spp. 5–15
Bacteroides 5–10
Trichomonas 3–7

The vagina is normally kept moist by transudation of fluid through its walls, which mixes with the exfoliated vaginal cells, aliphatic acids and the microorganisms mentioned earlier. The quantity of vaginal secretions varies throughout the menstrual cycle, peaking at ovulation. The quantity is also increased by emotional stress. If an increased quantity of vaginal secretion is present it may form a white coagulum, which may cause concern to the woman when she notices a whitish discharge that may cause itching. The discharge is termed leucorrhoea, which is defined as a non-infective, non-bloodstained physiological vaginal discharge.

Pathological vaginal discharges

The three common irritating pathological vulvovaginal discharges are caused by:

In many cases they can be differentiated in the doctor’s office or outpatient clinic by taking a sample of the discharge and looking at a ‘wet preparation’ under a microscope. Part of the swab is mixed with a drop of saline and part is mixed on a second slide with two drops of 10% potassium hydroxide (KOH). The saline preparation may reveal trichomonal flagellates, which can be observed moving and thrashing their tails (Fig. 33.4). Alternatively, the wet preparation may also show vaginal epithelial cells with indistinct borders, ‘clue cells’ due to the ‘hundreds and thousands’ effect of the presence of large numbers of Gram-variable coccobacilli (Fig. 33.5), which suggest that the woman has bacterial vaginosis. Clue cells are more readily apparent on a Gram-stained slide. Bacterial vaginosis is also suggested by a strong fishy smell from the KOH preparation (the amine test). The KOH preparation is examined under a microscope, when hyphae of Candida species can be seen, if this is the cause of the discharge (Fig. 33.6).

The alternative is to take the vaginal swab and place it in a transport medium, and send it to a laboratory for microscopy and culture.

Candidiasis (thrush)

Candida spp. infect the vaginal epithelial cells, particularly if in the fungal-germinating stage, when they develop spores and long threads (hyphae) (see Fig. 33.6). Inside the cells they may lie dormant until environmental conditions encourage germination. Candida spp. may also infect the vulval skin, the anogenital region, the mouth and the intestinal tract. For recurrent candidiasis underlying conditions such as diabetes, the recent use of broad-spectrum antibiotics or immunosuppressive therapy, e.g. corticosteroids, and HIV should be considered.

INFECTIONS OF THE INTERNAL GENITAL ORGANS

The fact that, apart from the lowest third, the genital tract derives from the Müllerian duct and has anastomosing systems of arteries, veins and lymphatics, means that infections of individual organs are less frequent than sequential ascending infection of the genital tract.

Ascending vaginal infection is controlled to some extent by the following mechanisms:

Upper genital tract infections may be sexually acquired or result from ascending infection from endogenous vaginal flora, particularly after disruption of the normal cervical barrier following miscarriage, delivery or gynaecological surgery. Infections are usually not due to endogenous flora.

As it may be difficult, clinically, to determine which organ is infected, and as more than one organ is usually infected, the condition is generally diagnosed as acute pelvic infection or pelvic inflammatory disease (PID). Infection of the internal genital organs may also occur following an abortion or after childbirth. In these cases the infective agents (which are usually staphylococci, streptococci, E. coli or anaerobes) enter the tissues through cervical lacerations, or more frequently, through the placental bed. Infections following pregnancy or childbirth are discussed in Chapter 23.

Rarely pelvic infections occur either from haematogenous spread, as in tuberculosis, or from pelvic peritonitis.

STI-related pelvic inflammatory disease (PID)

The microorganisms invade the columnar cells lining the crypts of the cervical canal. They may be eliminated by the body’s immune system, spread rapidly to cause an acute infection, or remain quiescent in the columnar cells, with the potential to spread to other pelvic organs. Spread occurs via the lymphatics, the veins or, possibly, by ‘riding on the back of spermatozoa’. In a few instances the infection is carried into the uterus during the insertion of an intra-uterine device, and it is advisable to screen women for Chlamydia and Neisseria gonorrhoeae prior to insertion (see p. 248).

The endometrium is first infected, causing endometritis. From here the infection may spread to the myometrium, causing myometritis, or through the uterine cavity to the Fallopian tubes, causing acute or subacute salpingitis. In some cases the ovaries and the pelvic peritoneum may be involved (Fig. 33.7).

The two principal infecting agents are Cl. trachomatis and Neisseria gonorrhoeae. They require further discussion.

Clinical presentations of PID

Cervical infection has been discussed and endometritis is usually symptomless except when it follows a bacterial infection after abortion or childbirth.

Salpingitis may be symptomless or symptomatic. In acute symptomatic cases the growth of organisms in the cells lining the oviduct produces the acute phase of primary infection. A large amount of mucus is secreted, together with a fibrinous exudate which produces agglutination of the mucosal folds of the endosalpinx. The Fallopian tubes become inflamed and oedematous, producing recognizable signs and symptoms. These are:

On examination the lower abdomen is tender, and on pelvic examination bimanual palpation of the lateral vaginal fornices is excruciatingly painful.

In particularly virulent infections pus may collect in the Fallopian tube, producing a pyosalpinx, or the infection may spread to the ovaries.

Low-grade infections will either be symptomless or associated with non-specific lower abdominal pain.

Treatment

In most cases treatment should be started before the exact infective agent has been identified. In severely ill patients antibiotics should be started intravenously. In less severe cases intramuscular or oral antibiotics should be given. Because of the frequent association of chlamydia and gonococcal infection, and the increasing prevalence of penicillin-resistant N. gonorrhoeae, the Center for Disease Control in the USA and the Therapeutic Guidelines in Australia recommend that the current treatment of doxycycline and metronidazole should be replaced with a single dose of probenecid 1 g and ceftriaxone 250 mg intramuscularly (one dose), followed by doxycycline 100 mg orally twice daily for 14–21 days. Alternative regimens include clindamycin 450 mg four times a day for 10 days, or gentamicin 4–6 mg/kg IV daily.

In severe infections, including tubo-ovarian abscess, intravenous treatment should be started with cefoxitin 2 g four times daily plus doxycycline 100 mg twice daily. This regimen is continued for 4 days and is followed by doxycycline 100 mg twice daily for a further 10 days. Such cases may require either surgical or radiologically guided drainage.

Oral azithromycin 1 g stat has a major role in combating bacterial sexually transmitted diseases, particularly chlamydia infections, and may be superior to other treatments. As the recommended antibiotic treatment is constantly changing it is important for the doctor to keep up to date and adopt the latest recommendations.

Surgery is indicated if the drug treatment fails in the presence of obvious abscesses that do not respond to antibiotics. The surgery should be as conservative as possible, drainage being preferred. ‘Total clearance’ of the genital organs is rarely indicated.

Chronic genital infection (chronic PID)

Chronic genital infection is a long-term sequela of acute or subacute infection and may follow post-abortion or puerperal infection. It may present as a pyosalpinx, a hydrosalpinx or a chronic tubo-ovarian abscess (Fig. 33.8). In other cases the infection involves the connective tissues of the pelvis, causing chronic pelvic cellulitis.

Pyosalpinx

Pyosalpinx, or ‘chronic pus tube’, forms as a result of blockage of the lumen of the oviduct at the fimbrial end and at one or more points along the Fallopian tube. This occurs in the acute phase of the infection, and exudate accumulates, distending the oviduct to a greater or lesser degree (Fig. 33.9). The distension of the oviduct flattens the endosalpinx and the wall of the oviduct is thickened by the inflammatory process. Because the inflammatory process extends through the wall of the oviduct, adhesions to surrounding structures are common. The ovary may be involved to form a chronic tubo-ovarian abscess.

There may be no symptoms, or vague pelvic pain may occur which is intermittent or constant. It is often worse in the premenstrual phase of the menstrual cycle, and some women complain of deep dyspareunia. These symptoms are not specific for chronic pelvic infection and may be due to psychosomatic conditions. The symptoms may vary in severity, possibly because of an exacerbation of the infective process. This may occur months or years after the first infection. Laparoscopy may be needed to establish the diagnosis. In some cases the woman becomes acutely ill.

Treatment of chronic pyosalpinx which is causing symptoms is surgical. The extent of the surgery depends on the severity of the condition and, in general, requires bilateral salpingectomy and often oophorectomy, although some ovarian tissue may be saved. Hysterectomy is also usually performed in case residual infection is present.