Sexual contact is critical to the transmission of all the conditions described in this section, although it is not necessarily the only route of acquisition. There are certain important concepts unique to the management of sexually transmitted diseases.
• sexually transmitted diseases are diseases of lifestyle. The risk of transmission is related primarily to the number of partners, and the same risk factors apply for most sexually transmitted diseases. These include frequency of partner change, lower socio-economic status and non-barrier contraception.
• Patients with one sexually transmitted disease are therefore likely to have others. All patients should be evaluated for other sexually transmitted diseases, including urethritis and syphilis. It may also be appropriate to discuss the need for serological testing for HIV infection.
• Contact tracing is very important. Since many sexually transmitted diseases are asymptomatic and/or difficult to exclude clinically, it is often appropriate to treat asymptomatic contacts presumptively. Referral to a genitourinary medicine clinic is essential for all the conditions described in this chapter.
• Patients attending sexually transmitted disease clinics are drawn predominantly from less advantaged socio-economic groups, and frequently reattend with newly acquired infections. Clinic attendance is an opportunity for discussion and education about risk reduction, contraception and other matters of sexual health, and allows provision of services such as cervical smear testing to groups who are otherwise unlikely to have contact with health services.
• The UK incidence of all sexually transmitted diseases has increased between 1995 and 2000, particularly in teenage females and homosexual men, a trend attributed to increasing practise of unsafe sexual behaviours in these groups.
Detailed and up-to-date UK guidance on management of all sexually transmitted diseases is available at:
Guidelines for managing outbreaks of sexually transmitted infections are at:
Epidemiology: Common worldwide. Risk factors as for other sexually transmitted diseases. 2: ==20000 in 2000, vs. =10000 in 1995. Disproportionately more common among gay men and ethnic minorities. In 2000, 9% of UK isolates were penicillin-resistant, 4% resistant to ciprofloxacin and 40% resistant to tetracycline.
Clinical features: Neisseria gonorrhoeae causes mucosal infection of the urethra, cervix, rectum, conjunctiva and pharynx. Asymptomatic infection is common at all sites. Symptomatic infection in males causes urethritis with copious purulent urethral discharge and dysuria, after an incubation period of 2-5 days. Local complications include epididymitis (>80) and rarely periurethral abscess. Infection in women is usually a cervicitis, which can be asymptomatic or cause discharge, dysuria and itching. Concurrent urethritis and proctitis is usual. Infection of Bartholin and Skene glands may occur (>84). Infection of the vaginal epithelium occurs in prepubertal girls. Anorectal infection occurs in homosexual men, but is unusual in heterosexual males. It is usually asymptomatic, but if not there is discharge, pain and tenesmus. Ophthalmia neonatorum (>107) and disseminated infection both occur in neonates.
Organisms: Neisseria gonorrhoeae (>300)
Microbiological investigations: Gram stain and culture of material from urethra, endocervix, rectum or pharynx. Gram-negative intracellular diplococci may be seen. Antibiotic sensitivity should always be performed. Screening for other sexually transmitted diseases, in particular syphilis, is essential (>86).
Antibiotic management: For infections acquired in UK: ciprofloxacin 500 mg single dose or ofloxacin 400mg single dose or ampicillin 3.5 g plus probenecid 1 g (if local penicillin resistance rate <5%). For known resistance, or in cases acquired outside UK before sensitivity known, consider cefotaxime (500 mg) or ceftriaxone (250 mg) or spectinomycin (2 g), all im single dose. Forpharyngeal gonorrhoea, ciprofloxacin or ceftriaxone should be given. Many physicians treat all patients with gonorrhoea for possible concomitant chlamydial infection (e.g. ceftriaxone, single dose, plus doxycycline for 1 week). Screening/treatment of sexual partners is essential; referral to genitourinary medicine clinic is highly recommended.
Complications: Pelvic inflammatory disease (>92). Disseminated gonococcal infection
(DGI) occurs in 1-2% of untreated cases, causing bacteraemia with a pustular rash and asymmetrical polyarthritis affecting mainly hands, wrists, ankles and knees (>120). Endocarditis and meningitis occur very rarely.
Epidemiology: Very common worldwide. Risk factor as other sexually transmitted diseases (>86). UK incidence continues to increase steadily. 2 =60000 reported cases in 2000 (doubled since 1995).
Clinical features: Infection is very commonly asymptomatic, particularly in women (<70%). Untreated infection can persist for many years. Symptomatic infection in men causes urethritis with dysuria and mucopurulent discharge, usually less copious than in gonorrhoea. Epididymitis may occur. In women, mucopurulent cervicitis with discharge and associated urethritis. Proctitis and pharyngitis occur in either sex. Chlamydial urethritis can be prolonged or present as apparent treatment failure after confirmed gonorrhoea (‘postgonococcal urethritis’). Conjunctivitis (>107, ©) andpneumonia (>142) occur in infants born to infected mothers.
Organisms: Chlamydia trachomatis, trachoma biovar, serovars D-K (>329).
Microbiological investigations: Culture is no longer routinely performed. Antigen detection (e.g. ELISA) has been available since 1984, but has relatively poor sensitivity. Tests for chlamydia DNA (PCR or ligase chain reaction — LCR) are now widely available, with high sensitivity and specificity, and can be performed on endocervical swabs, urine and vulvovaginal swabs. These tests are now the first-line investigation for all specimen types. Best sensitivity is obtained with urine (males) and endocervical swabs (female).
Differential diagnosis: Gonococcal urethritis (>86). Non-specific urethritis may also be caused by Ureaplasma urealyticum (>330). Genital herpes simplex (>88) may cause urethritis, with severe dysuria but little discharge. Trichomonas vaginalis (>92) infection in men may cause urethritis, but is usually asymptomatic.
Antibiotic management: Azithromycin lg single dose or doxycycline 100 mg ql2h for 7 days or erythromycin 500 mg q6h for 7 days or ofloxacin 400mg q24h for 7 days. Referral to genitourinary medicine clinic is highly recommended.
Complications: Pelvic inflammatory disease (>92). Reiter’s disease (>122). Perihepatitis (Fitz-Hugh-Curtis syndrome). Conjunctivitis (>106).
Comments: Recurrent disease is usually due to reinfection, often because of inadequate treatment of sexual partners. Since infection in women is usually asymptomatic, female partners of men with NSU should be treated whether or not there is clinical evidence of infection. The availability of sensitive non-invasive tests for chlamydia introduces the possibility of screening. Criteria for screening programmes vary, but UK Dept of Health has suggested opportunistic screening of women having their first cervical smear.
Primary herpes simplex virus (HSV) infection is followed by latent infection of sacral ganglia, and subsequent reactivation, which may be subclinical or symptomatic.
Epidemiology: Infection is common worldwide. The incidence has increased in recent decades in the UK, as a result of changes in sexual behaviour, and a reduction in childhood infection by HSV-1, but no significant increase since 1995.2 = 18 000. Severity of HSV-2 infection is reduced by prior exposure to HSV-1 and vice versa.
Clinical features: The incubation period is 3-7 days, (range 1- >14 days) although >60% of primary infections are asymptomatic. New diagnoses of genital herpes are equally likely to be caused by HSV-1 or HSV-2, but the recurrence rate is much higher for HSV-2 than HSV-1. Subclinical reactivation and viral shedding occur more frequently than overt recurrent disease. The first clinical attack of genital herpes may therefore be due to primary infection, or may represent a first reactivation episode (‘initial non-primary herpes’). First attacks, whether primary or initial non-primary, are more severe than recurrences. Local burning and tenderness are followed by a vesicular eruption, usually bilateral. In moist areas, the vesicles rupture, leaving shallow, very tender ulcers. In drier areas, vesicles may remain intact to develop into pustules and scabs. New lesions continue to appear for about 1 week. In men, the glans penis, prepuce and shaft of the penis are usually involved. Lesions occur less frequently on the scrotum and thighs. In women, lesions form initially on the external genitalia and vulva, but the cervix is usually subsequently involved and there is usually a wateryvaginal discharge. Urethritis and dysuria occur in both sexes. Constitutional symptoms and local lymphadenopathy are usual. Resolution occurs over 1-3 weeks. Herpetic proctitis, with rectal discharge, pain, tenesmus and sometimes urinary retention, may occur in either sex. One or more recurrent attacks are experienced by 60-80% of patients during the first year after the first episode. Recurrences are less severe and of shorter duration, and constitutional symptoms, lymphadenopathy and urethritis are unusual. Frequent and severe recurrent infection occur in immunocompromised patients (>174). HIV+ patients may develop chronic anal ulceration (>159). Asymptomatic viral shedding occurs most commonly in patients with genital HSV-2 infection, in the first year after infection and in individuals with frequent symptomatic recurrences.
Organisms: Herpes simplex virus types 2 and 1 (>334).
Microbiological investigations: Culture of virus from lesions. Serology is often unhelpful, as it does not reliably distinguish between types 1 and 2. Rapid diagnostic methods for demonstration of viral antigens are available, using type-specific antibodies. PCR is now widely available and is more sensitive than culture, particularly in lesions more than a few days old.
Differential diagnosis: Other causes of genital ulceration, in particular syphilis (>89) and in the tropics, chancroid, lymphogranuloma venereum and granuloma inguinale (>94). Dark ground examination of material from lesions may be indicated. Less common causes of genital ulceration include Behcet’s disease, herpes zoster, candidiasis and impetigo.
Specific management: Aciclovir (ACV), valaciclovir, and famciclovir all reduce the severity and duration of episodes, but do not alter the natural history of the disease. Intravenous therapy is only indicated when the patient cannot swallow or tolerate oral medication because of vomiting. Treatment should commence as soon as possible for maximum benefit. Systemic antivirals are of less benefit in recurrent attacks, which tend to be short and self-limiting. Topical ACV is of marginal benefit only. ACV (400 mg ql2h) is effective prophylaxis for patients with frequent recurrences (e.g. >four attacks per year). Intravenous ACV is indicated for severe, disseminated or neonatal infection (>362).
Complications: Neonatal infection (> 129). Bacterial and candidal superinfection occur rarely. Herpetic whitlow (>338). Viral meningitis may complicate first attacks of genital herpes (>100). Severe disseminated infection occurs rarely in the immunocompetent (>338). If catheterization is required, suprapubic catheterization is preferred to prevent theoretical risk of ascending infection, to reduce the pain associated with the procedure and to allow normal micturition to be restored without multiple removals and recatheterizations.
Clinical features: After an incubation period of about 4-6 weeks, warts (‘condylomata acuminata’) develop as small irregular papules around the external genitalia, in the perianal region and less often in the vagina, urethra and on the cervix. Subclinical infection of surrounding epithelium is the rule. On the cervix, the presence of infected epithelium may be demonstrated by the application of acetic acid, which turns infected areas white. Biopsy of acetowhite areas is indicated to confirm infection and exclude intraepithelial neoplasia.
Organisms: Human papillomavirus. Some types are associated with warts, whereas others are associated with cervical cancer (>342).
Microbiological investigations: Viral culture is not possible. DNA hybridization methods and PCR are available for determining which HPV type is present. These techniques have hitherto been used mainly in epidemiological studies; their value in the management of individual patients is currently being studied.
Differential diagnosis: Moles and skin tags. Syphilis (condylomata lata) (>89), molluscum contagiosum (> 119).
Management: Specific antiviral therapy is not available; therapy is directed towards removal of warts and relief of symptoms. Caustic agents such as podophyllin or trichloracetic acid are effective in =50% of cases, but have a high rate of recurrence. Podophyllin is very irritant, and excess topical application can lead to systemic toxicity with nausea, vomiting, lethargy and neuropathy. It is anti-mitotic and contraindicated in pregnancy and infancy. 5-Fluorouracil has a higher success rate, but can be extremely irritating. Systemic and intralesional interferon is effective, but is not yet in widespread use, not least due to its cost. Recurrence is common when treatment is discontinued. Imiquimod is a recently developed immune response modifier, which acts by local cytokine induction. It is applied topically as a 5% cream and has shown significant effect in clearing warts with few recurrences in limited clinical experience. Cryotherapy is widely used. Laser therapy is particularly useful for cervical lesions. If external warts are very numerous, surgical removal may be necessary.
Complications: Juvenile-onset respiratory papillomata are due to infection with HPVs causing mucosal warts, probably acquired intrapartum from the maternal genital tract.
Transmission occurs by sexual contact. Although Trichomonas vaginalis can survive in urine on towels or clothing for several hours, non-sexual transmission is believed to be very rare. Symptoms are more likely to occur during pregnancy or menstruation when the vaginal pH is highest, as this favours parasite replication. 2 >6000, but rare outside genitourinary medicine clinics.
Clinical features: Infection in men is usually asymptomatic; there may be mild dysuria. Up to 50% of infected women are asymptomatic. Symptoms may develop after an incubation period of 1-4 weeks with yellow vaginal discharge, frequently copious, frothy and offensive. Dysuria, dyspareunia, lower abdominal pain and vulval itching also occur. On examination, there may be erythema of the vaginal walls and cervix, which may be friable with punctate haemorrhages (‘strawberry cervix’).
Organisms: Trichomonas vaginalis.
Microbiological investigations: Microscopy (phase-contrast or dark-ground best) of wet preparation of vaginal discharge usually shows motile flagellated protozoa. Culture is also possible in liquid medium (Feinberg’s). Organisms may also be seen on fixed cervical smears examined cytologically
Antibiotic management: Metronidazole (2g single dose). Sexual partners should be treated. Asymptomatic patients should be treated, except during pregnancy, when metronidazole is relatively contraindicated. It may be given after the first trimester if symptoms are severe.
Differential diagnosis: Candidiasis (>82), bacterial vaginosis (>82), gonorrhoea (>86), non-specific cervicitis (>87).
Pelvic inflammatory disease
pelvic inflammatory disease complicates 10-15% of cases of gonococcal and chlamydial cervicitis. Damage caused by these organisms also facilitates entry of aerobic and anaerobic vaginal flora (>82) into the Fallopian tube, so that many infections are polymicrobial.
Risk factors: Commonest in teenage girls with multiple sexual partners and non-barrier methods of contraception, especially intra-uterine device (IUD). Previous pelvic inflammatory disease predisposes to further episodes.
Clinical features: Fever, pelvic pain, abdominal tenderness, adnexal and cervical tenderness, vaginal discharge. Symptoms do not correlate well with the presence of infection and the likelihood of subsequent complications. Right upper quadrant pain occurs due to peri-hepatitis in =10% (Fitz-Hugh-Curtis syndrome >87).
Organisms: Neisseria gonorrhoeae, Chlamydia trachomatis. Infection is often polymicrobial with mixed aerobic and anaerobic genital flora, including Bacteroides spp., Escherichia colt, Gardnerella vaginalis. Mycoplasma hominis and Ureaplasma urealyticum have also been implicated in pelvic inflammatory disease.
Microbiological investigations: Microscopy and culture of endocervical swab should be done but, with the exception of Neisseria gonorrhoeae, does not accurately reflect contents of Fallopian tube. Material from peritoneal cavity and tube obtained by laparoscopy may be available.
Other investigations: In view of difficulty of diagnosis, leucocytosis and raised ESR may be helpful indicators of ongoing infection. Laparoscopy is frequently done to confirm diagnosis. Ultrasound may be used to examine for tubo-ovarian abscess, but appearances do not otherwise correlate well with clinical symptoms or microbiological results.
Differential diagnosis: Ectopic pregnancy, appendicitis, ruptured or haemorrhagic ovarian cyst, endometriosis.
Antibiotic management: Admission for intravenous therapy will often be required. Cover for aerobic and anaerobic organisms is recommended. Suitable regimens include:
• a single dose of parenteral cephalosporin, then doxycycline plus metronidazole
• or clindamycin plus gentamicin followed by either oral clindamycin or doxycycline plus metronidazole
• or ofloxacin plus metronidazole.
IUD should be removed after antibiotic therapy has commenced.
Complications: Infertility, chronic pelvic pain. Tubo-ovarian abscess (TOA) presents with similar symptoms to uncomplicated pelvic inflammatory disease, and should be excluded by ultrasound (or CT) scan if patient is unwell or if symptoms fail to settle. Early gynaecological referral is essential as a ruptured TOA requires immediate surgery. Intravenous antibiotics should be given. Surgery may be required if there is no response after 72 h or if clinical features suggest rupture. An adnexal mass >8 cm in diameter is unlikely to respond to antibiotic therapy alone. Percutaneous and laparoscopic drainage is sometimes employed as an alternative to laparotomy
Clinical features: Severe pruritis. 1-2 mm grey-brown lice and 0.5 mm ovoid nits attached to hairshafts maybe seen. Tiny red dots on affected skin are louse excreta. Pubic, axillary, chest and abdominal hair may be infested. Eyelashes may also be involved (> 104).
Organisms: Pthirus pubis.
Management: Preparations containing permethrin, phenothrin and malathion are effective. All hairy parts of the body should be treated. Retreatment after 1 week is recommended.
Scabies may be acquired by any close contact, including household contact as well as sexually.
Risk factors: Poor hygiene. Crowded housing. Sexual contact. Prolonged contact (>20min) needed for transmission.
Clinical features: Incubation period is approximately 4 weeks. Severe pruritus. Infestation is usually confined to the interdigital areas and the flexor surfaces of the wrists, where papulovesicular lesions and scaly plaques may be seen. Classical linear burrows are often very difficult to see. Excoriation is usual. Other areas, including the genitalia, buttocks, thighs, breasts, belt line, umbilicus, feet, ankles, elbows and axillae are often infested.
Organisms: Sarcoptes scabiei.
Microbiological investigations: Diagnosis is clinical, and may be confirmed by microscopical demonstration of mites or eggs in skin scrapings.
Management: Malathion or permethrin preparations may be used. The whole body below the chin must be treated, paying particular attention to the finger webs and under the edges of the finger nails. Ivermectin (single dose 200 µg/kg) has been used in combination with topical agents in the treatment of Norwegian scabies that does not respond to topical treatment alone.
Complications: In immunosuppressed patients, Norwegian scabies may develop. This is characterized by very heavy infestation with little or no itching. There is widespread keratosis and erythema, and these patients are highly infectious. Patients with HIV infection develop papulosquamous lesions along lines of skin cleavage (>159).