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.

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.

Treatment

During an attack a woman should wash her hands after touching the infected area. If she is unable to pass urine because of pain or retention, a suprapubic catheter may need to be inserted. Local applications of ice or anaesthetic jelly provide some relief.

The antiviral drugs aciclovir, famciclovir and valaciclovir reduce the duration and severity of the initial and recurrent attacks, and shorten the time of viral shedding if given early in the attack. If a woman has five or more attacks each year, or the outbreaks are particularly severe, long-lasting or interfere with her psychosocial functioning, the drugs can be given daily as suppressive treatment for 6–12 months or longer.

Women who have recurrent genital herpes are often more concerned about the psychosocial sequelae of the disease, rather than the physical symptoms, and may need to be counselled.

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.

Treatment

Genital warts, if not too exuberant, may be treated with podophyllotoxin (twice daily for 3 days, repeated if needed after 4 days) applied by the woman herself, after trimming away any vulval hair around the wart; or the medical practitioner may apply 20% podophyllin in benzoin tincture to the wart without touching the surrounding skin, to avoid skin burns and ulceration. The mixture is allowed to dry and the woman washes it off 6 hours later. This is repeated once weekly, if necessary. This should not be used in pregnancy. Larger condylomata on the cervix may respond to the application of trichloroacetic acid. Imiquimod cream 5% can be applied before bedtime so that it is left on the skin for 6–10 hours, three times weekly.

Large warts, or warts that fail to respond to medical treatment, are treated by diathermy or by laser. The procedure is painful and anaesthesia is needed. Postoperatively, pain requires analgesics. A problem that has recently been reported is that neither diathermy nor laser may cure the woman, as the virus may have infected neighbouring normal cells and warts commonly recur. Because of the concern that HPV infection with types 16 and 18 may be involved with the development of cervical carcinoma, a woman who has vulval warts should have regular Pap smears.

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.

Diagnosis

The diagnosis is confirmed by examining exudate expressed from the ulcer or mucous patches, through a microscope under dark-ground illumination. To obtain an accurate diagnosis the chancre is first cleaned with a swab, and then, if necessary, its edge and base are scarified with a scalpel so that exudate appears before the specimen is taken. The tests should be interpreted in conjunction with specialist sexual health physician or clinical microbiologist. A full STI screen should be ordered.

Treatment

Treatment consists of antibiotics, procaine benzylpenicillin 1 g daily for 10 days, a long-acting penicillin, benzathine penicillin, 1.8 g as a single dose or, for penicillin-sensitive individuals, doxycycline 100 mg twice daily for 14 days. Meticulous follow-up is essential.

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.

Diagnosis

In acute bartholinitis the woman complains of acute discomfort in the region of the gland, and a reddened, tender swelling appears beneath the posterior part of the labium majus.

Treatment

Treatment consists of excluding sexually transmitted infections (STIs) and prescribing analgesics and a broad-spectrum antibiotic. If an abscess has formed it should be marsupialized. An elliptical piece of the vagina and the abscess wall, just inside the hymen, is removed. The vaginal and abscess walls are sutured to maintain patency and a small drain is inserted.

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.

Leucorrhoea

When a woman presents with leucorrhoea, infection by pathogenic organisms must be excluded by obtaining an endocervical (for potential pathogens Cl. trachomatis, N. gonorrhoeae) or a vaginal smear (Candida, bacterial vaginosis, Trichomonas), which is examined or cultured.

Treatment

Treatment consists of reassuring the woman that the discharge is not pathogenic and exploring reasons for her concern. A few women have recurrent vaginal discharges that show no pathogens on repeated laboratory investigations. Some women have a dermatosis. Often these cases are difficult to treat. Some of these women have abnormal scores on psychometric tests, or have the somatizing syndrome, so the woman’s lifestyle, including her sexuality, should be investigated rather than concentrating on the vaginal discharge. Some women repeatedly douche themselves for ‘vaginal hygiene’, a practice that may increase the chance of vaginal infection by reducing the number of vaginal lactobacilli.

If the woman wants medication, a vaginal acidifying jelly (Aci-Jel) may be prescribed. Antibiotics should be avoided as they may aggravate the discharge rather than relieve it.

Pathological vaginal discharges

The three common irritating pathological vulvovaginal discharges are caused by:

• Trichomoniasis

• Candidiasis

• Bacterial (amine) vaginosis.

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).

Fig. 33.4 Trichomonas vaginalis.

Fig. 33.5 ‘Clue cells’, seen in bacterial vaginitis.

Fig. 33.6 Candida albicans.

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.

Trichomoniasis

The parasite Trichomonas vaginalis is a 20 mm long flagellate. It is a little larger than a leukocyte (see Fig. 33.4). Once introduced into the vagina, it shelters at the bottom of the crypts of the velvet-like vaginal epithelium. It may be symptomless, or may cause vaginitis with discomfort and discharge. It is readily sexually transmitted and infects the man’s urethra, where it is often symptomless.

Clinical aspects

The main complaint is a moderate to profuse vaginal discharge that produces itching and irritation inside the vagina and around the vaginal introitus. In longstanding cases the discharge is greenish and frothy. In pregnant women it is associated with prematurity. There is also an increased risk of HIV transmission.

Treatment

The patient is given a single oral dose of tinidazole 2 g or metronidazole 2 g. Alternatively, oral metronidazole is prescribed in a dose of 400 mg twice a day for 5 days. The woman’s sexual partner should be invited to take the same treatment. These regimens cure 90% of infected women. A vaginal swab is taken 7 days after completing treatment, and if the flagellates are still present a second course of treatment is given. Side-effects of treatment are minimal: a few women feel nauseated and alcohol should be avoided while taking the tablets as it may lead to headaches and flushing.

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:

• First, the vaginal walls lie in apposition and the vaginal secretions are acidic, which inhibits bacterial growth.

• Second, the cervical mucus forms a meshwork, except at the time of ovulation, which limits upward spread.

• Third, the endometrium is shed each month during menstruation. However, if the cervix is infected directly, the above mechanisms are less effective.

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).

Fig. 33.7 Route of spread of non-gonococcal and gonococcal infection.

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

Chlamydial infection

Infection with Cl. trachomatis is commonly symptomless, but a few women (less than 20%) may complain of a mucopurulent discharge from the cervix, dysuria, or intermenstrual bleeding. Community studies have shown that between 15 and 30% of healthy women have circulating antichlamydial antibodies, indicating previous subclinical infection, and that between 4 and 12% have symptomless infection of their cervical cells (as have men who have symptomless infection of the urethral cells). Symptomatic infection affects between 1 and 3% of sexually active women aged 15–50 years (and rather more men) each year. With the availability of polymerase chain reaction (PCR) and ligase chain reaction testing on urine, greater diagnostic accuracy has been obtained. A higher incidence occurs in women under the age of 25, with multiple sexual partners, or whose sexual partners have had several partners.

Gonococcal genital infection

Gonococcal genital infection may be symptomless or may produce early symptoms of dysuria, urinary frequency and a purulent vaginal discharge. The discharge originates from infected endocervical cells and from Bartholin’s gland, but not from the vaginal mucosa, as the gonococcus is unable to penetrate vaginal stratified epithelium. The severity of the initial infection varies, and in 50–80% of infected women the symptoms are so mild that they are ignored. Spread, if it occurs, is upwards to the endometrium and Fallopian tubes, or downwards to infect Bartholin’s gland.

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:

• Severe bilateral lower abdominal tenderness and pain

• Abdominal muscle spasm (guarding)

• Pelvic tenderness and pain on moving the cervix (cervical excitation)

• Fever (>38°C), often with rigors

• Leukocytosis, raised ESR and C-reactive protein (CRP).

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.

Diagnosis

The diagnosis may be established clinically, but confirmation by laparoscopy is required in most cases as the symptoms are non-specific and may occur in tubal pregnancy, accompany a complication of an ovarian cyst, or have a psychosomatic basis. Ideally a definitive diagnosis can be made from an endometrial sample (using a protected triple-lumen sampler) sent to a laboratory to detect plasma cells. Transvaginal pelvic ultrasound scanning is as accurate as laparoscopy and less invasive. The transvaginal ultrasound looks for:

• Multiple ovarian cysts

• Thickened fluid-filled Fallopian tubes

• Free fluid in the pelvis.

Laboratory tests should be made: urethral and endocervical swabs should be taken and sent in appropriate transport media for microscopy and culture for N. gonorrhoeae and potentially pathogenic endogenous flora. Screening for chlamydia is largely by PCR from first-void urine (FVU), endocervical swab or self-collected genital swab.

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.

Prevention

Both chlamydia and gonorrhoea are sexually transmitted. Prevention is therefore best obtained if people are prepared to use ‘safer sex’, that is, limiting the number of sexual partners and insisting on the use of a condom, particularly if either partner cannot be relied on to disclose their previous sexual behaviour. This advice is idealistic and usually ignored. An alternative is to suggest that a person who has had several sexual partners, or whose partner has had several sexual partners, is screened for chlamydia and gonorrhoea every 6 months or so.

Long-term effects of PID

A first chlamydial genital infection, unless treated, causes damage to the Fallopian tubes in 10% of cases. If a second infection occurs the proportion of women who develop tubal damage increases to 25% and, after a third infection, to over 50%. Gonococcal infection, unless treated, is associated with an even higher chance of tubal damage. As many infections, particularly with chlamydia, are symptomless, it is not surprising that evidence of previous tubal infection is often first detected during investigations for infertility. If a previously infected woman who has had tubal damage does succeed in becoming pregnant, she has five to seven times the risk of having an ectopic pregnancy compared with a woman who has not had PID.

Subacute salpingitis

This is often symptomless, but the woman may feel unwell. A vaginal examination may show a tubal mass. This is found in half the number of women infected with gonorrhoea, but in only a quarter of those infected with chlamydia.

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.

Fig. 33.8 Bilateral pyosalpingitis – the appearance at operation.

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.

Fig. 33.9 Bilateral chronic salpingitis.

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.

Hydrosalpinx

Hydrosalpinx (Fig. 33.10) is the end result of burnt-out pyogenic salpingitis, which was of low virulence but highly irritating, producing large quantities of clear exudate within the closed portion of the oviduct. The distended oviduct has a thin wall, which is translucent and usually retort-shaped (Fig. 33.11). Adhesions to contiguous structures may be present.