CHAPTER 63 Non-HIV sexually transmitted infections
Introduction
Sexually transmitted infections (STIs) are infections whose primary route of transmission is through sexual contact. They are common, often occult in nature, have serious sequelae and are synergistic with human immunodeficiency virus (HIV). In developing countries, they are the second most common cause of death amongst women aged 15–44 years, after maternal mortality. The serious nature of many of these conditions and the fact that the presence of one STI suggests the possibility of others is a caution to the gynaecologist to manage such patients with appropriate input from others, notably genitourinary physicians and microbiologists.
More than 20 pathogens are transmissible through sexual intercourse. Many are curable but, in spite of the availability of effective treatment, they remain a major public health concern in both industrialized and developing countries.
Globally, the exact prevalence of STIs is largely unknown. Surveillance systems exist in some countries but the data rendered are not always reliable or complete. The quality and completeness of the available data and estimates depend on the quality of STI services, the extent to which patients seek health care, the intensity of case finding and diagnosis, and the quality of reporting.
The completeness is further affected by the natural history of STIs, since a large number of infections are asymptomatic. Moreover, only part of the symptomatic population seeks health care and an even smaller number of cases are reported. The social stigma that is usually associated with STIs may result in people seeking care from alternative providers or not seeking care at all. As a result, report-based STI surveillance systems tend to underestimate the total number of new cases substantially.
World Health Organization (WHO) estimates suggest that more than 12 million new cases of syphilis, 62 million new cases of gonorrhoea, 92 million new cases of chlamydial infection and 174 million new cases of trichomoniasis occurred throughout the world in 1999 (World Health Organization 2001). Congenital syphilis, prevention of which is relatively easy and cost-effective, may still be responsible for as many as 14% of neonatal deaths. Up to 10% of women who are untreated, or inadequately treated, for chlamydial and gonococcal infections may become infertile as a consequence. On a global scale, up to 4000 newborn babies each year may become blind because of gonococcal and chlamydial ophthalmia neonatorum (note: ophthalmia neonatorum is a notifiable disease).
STIs also enhance the sexual transmission of HIV infection. The presence of an untreated STI can increase the risk of both acquisition and transmission of HIV by a factor of up to 10. Ulcerative STIs disrupt the integrity of the protective tegument and increase the presence of HIV-susceptible cells (e.g. CD4 lymphocytes). Non-ulcerative STIs similarly increase HIV-susceptible cells in the area. Moreover, improvement in the management of STIs can reduce the incidence of HIV-1 infection in the general population by approximately 40%. STI prevention and treatment are, therefore, important components in HIV prevention.
Guidelines covering the majority of STIs exist within the UK. They discuss aspects relating to screening, diagnostic criteria, management and prevention. Crucially, they also set standards for audit, providing a tool for improvement in all these aspects in all units across the UK. They will be quoted from heavily in this chapter in condensed form. The guidelines are not primarily directed per se at gynaecologists, but it is of vital importance that specialists in this area are aware of them.
Epidemiology
WHO estimated that 340 million new cases of STIs occurred worldwide in 1999. The largest number of new infections occurred in South and South-east Asia, followed by sub-Saharan Africa, Latin America and the Caribbean. However, the highest rate of new cases per 1000 population occurred in sub-Saharan Africa (World Health Organization 2001).
Globally, the highest rates of STIs are generally found in urban men and women aged 15–35 years. On average, women become infected at a younger age than men.
In the UK, peaks in STI diagnoses occurred in the mid-to-late 1940s (post World War II) and from the mid 1960s through to the early 1980s [from the age of sexual liberation to the advent of acquired immunodeficiency syndrome (AIDS)]. From 1998 to 2007, there was a substantial increase in diagnoses of most STIs (overall 6%). Cases of uncomplicated gonorrhoea increased by 42%, while chlamydia increased by 150%. Chlamydia has been the most commonly reported STI since 2001, overtaking genital warts (see Figure 63.1).
Figure 63.1 All new episodes of sexually transmitted infections seen in genitourinary medicine clinics 1998–2007.
Source: Health Protection Agency 2008 All new episodes seen at GUM clinics: 1998–2007. United Kingdom and country specific tables.
The rapid increase in reports of STIs is probably, in part, due to a general deterioration in sexual health amongst young people and men who have sex with men. However, the greater acceptability of using genitourinary medicine (GUM) services and new campaigns to encourage testing have also made a contribution. In 2000, the UK survey of sexual attitudes and lifestyle over 10 years reported that 30% of 15-year-old girls were sexually active and half of all UK teenagers were sexually active before 17 years of age. Consistent condom usage decreased by 3% over the period of study. Male homosexual activity increased, as did the prevalence of unsafe sex in this group, especially in London. The number of heterosexual partners also increased, and more people were engaging in concurrent relationships.
Certain ethnic minority groups are disproportionately affected by some STIs. In 2005, the GRASP (Gonococcal Resistance to Antimicrobials Surveillance Programme) survey found that Black Caribbeans accounted for 18% of gonorrhoea diagnoses at the clinics studied.
The UK population is mobile and certain groups are at particular risk, including tourists, professional travellers, immigrants and members of the armed forces. In addition, poverty, urbanization, social migration and war often increase levels of prostitution.
The important features in maintaining an STI in a community have been factored into the following formula:
where Ro is the average number of new infections that result from one infection, β is transmissibility, c is the average rate of acquiring partners, and d is the duration of infection.
If Ro >1, the rate of spread in a community will rise; if Ro <1, the rate of spread will fall. This gives the principles behind effective STI control. β can be reduced by promoting condom use and vaccination, c can be reduced by encouraging behavioural change, and d can be reduced by encouraging diagnosis, treatment and contact tracing. These principles then translate into effective health education. d can also be reduced by screening.
Screening
There are guidelines for routine screening in pregnancy in the UK, and the current programme screens all pregnant women at booking for syphilis, hepatitis B and HIV after a pretest discussion. In addition, screening for hepatitis C should be undertaken in intravenous drug users. There is also a national screening programme for Chlamydia trachomatis.
In the UK, the National Institute for Health and Clinical Excellence (NICE) issued guidelines entitled ‘Prevention of sexually transmitted infections and under 18 conceptions’ in 2007. These guidelines were not specifically aimed at gynaecologists but more at primary care agencies. In summary, these guidelines set recommendations as follows.
Recommendations 1 and 2: for key groups at risk of STIs
Recommendation 3: patients with an STI
Information given to patients for any condition should be supported by written evidence-based information, in a clear, jargon-free format, to reinforce the message.
Principles of Management of Sexually Transmitted Infections
History
Whilst in the UK, STIs are principally managed by specialist clinics (GUM), STIs also commonly present to the gynaecologist. The threshold at which the gynaecologist should take a sexual history is correspondingly low. The essentials are establishment of a rapport, privacy and confidence in the manner of questioning. Embarrassment on the part of the patient is quite understandable and should be dealt with empathetically. Phrases can be couched in terms such as ‘I am sorry to have to ask you this, please don’t be offended, it is important’. Essential elements of the sexual history, taken in combination with a general gynaecological and medical history, are shown in Box 63.1.
One of the markers for women at risk of STIs is the age range (15–34 years). This takes the age range down to childhood, and these patients frequently present with a parent. It is highly unlikely that a girl will reveal all matters regarding her sexual activity in front of her mother. Such questions relating to this may be more profitably asked in the examination room with the mother back in the waiting room. In such cases, confidentiality should be emphasized and reassurance given that the information will not get back to her parents.
Examination
It is essential that a chaperone is present (irrespective of the gender of the examining doctor) and that consent has been obtained for intimate examination. Ideally, examination should be performed in lithotomy; in any case, there should be adequate exposure to allow thorough examination in good light of the external genitalia, mons pubis, perineum and perianal area. One should observe for Pediculosis pubis (crabs), scabies, molluscum contagiosum, warts, ulceration, excoriation, scars and any discharge from the introitus; and palpate for inguinal lymphadenopathy and tenderness. A bivalve speculum should be passed, gently, as the patient may find this uncomfortable. The cervix should be examined, looking for ectropion, warts, cervicitis and mucopurulent discharge. The vaginal walls should be observed for inflammation or warts. At this time, ‘triple swabs’ should be taken.
The first swab is taken from the posterior fornix and is placed into Stuart’s transport medium (agar and charcoal). This swab essentially screens for Trichomonas vaginalis, bacterial vaginosis and Candida spp. The second swab is taken from the endocervix and is a screen for Neisseria gonorrhoeae; this is also placed into Stuart’s transport medium. The third swab is also taken from the endocervix and is a screen for C. trachomatis. This last swab needs to be taken in a particular way as C. trachomatis is an obligate intracellular organism. Thus, to be sampled, the swab needs to pick up some cells from the sampled area. The swab should be rotated in the endocervix for at least a count of 10 and placed into chlamydia transport medium.
The speculum should then be removed and a digital examination performed. The patient should be examined for cervical excitation, uterine and adnexal tenderness, and adnexal masses.
Specialist clinic tests
In a GUM clinic, further refinements to this examination include a test of vaginal pH using narrow-range pH paper. The normal vaginal pH is 3.8–4.5. Bacterial vaginosis, trichomoniasis and atrophic vaginitis often cause a vaginal pH higher than 4.5. For a ‘whiff test’, several drops of a potassium hydroxide solution are added to a sample of the vaginal discharge. A strong fishy odour (ammonia) from the mix means that bacterial vaginosis is present. For a wet mount, a sample of the vaginal discharge is placed on a glass slide and mixed with a salt solution. The slide is looked at under a microscope (under dark ground illumination) for yeast cells, trichomoniasis and treponemes. A Gram stain is made of any discharge and examined for N. gonorrhoeae (Gram-negative diplococci) and the clue cells of bacterial vaginosis. Further swabs are frequently taken from the urethra, anus and throat, and sent in Stuart’s transport medium for culture (looking for N. gonorrhoeae). Any woman reporting anal intercourse will also undergo proctoscopy looking for warts.
If one STI is present, there may be others. In practice, a patient with an STI will be referred to a GUM clinic, counselled and offered a full screen including serological tests for syphilis, hepatitis B, HIV and hepatitis C, if indicated. The GUM clinic will also arrange for contact tracing to break the chain of infection. They may also arrange for a follow-up test of cure.
If drug treatment is given, it is better to use simple, if possible, single-dose regimes and advise the woman to abstain from intercourse during treatment to prevent reinfection until her partner is also treated. In practice, regimens are given that will cover N. gonorrhoea, C. trachomatis, T. vaginalis and bacterial vaginosis.
In the spirit of the NICE guidelines, time should be allocated to discuss modification of any high-risk activity to prevent reinfection (National Institute for Health and Clinical Excellence 2007). This should be non-judgmental and should be accompanied by written information on the subject to reinforce the message.
Clinical Presentations
Patients present with clinical syndromes rather than microbiological presentations. In fact, the most common presentation is none whatsoever! The patient is picked up on opportunistic screening, by partner notification or by chance when presenting with another condition. This emphasizes the importance of the NICE guidelines, especially in the light of increasing prevalences of STIs in the UK.
Vaginal infection and/or cervicitis may present with a discharge, and cervicitis may also present as postcoital bleeding. Endometritis may cause erratic bleeding and pelvic pain. Adnexitis is synonymous with acute PID and may produce dyspareunia and pelvic pain. Fitz–Hugh–Curtis syndrome consists of right upper quadrant pain resulting from ascending pelvic infection and inflammation of the liver capsule or diaphragm.
Genital Herpes
Genital ulcers have a broad differential diagnosis, but the most common cause of de-novo and recurring multiple painful ulceration is herpes simplex virus (HSV). The infection is lifelong and has the potential for recurrence. It can be managed but not eradicated. It is a disease that has long been in the public domain with varying levels of informed and misinformed knowledge. A patient with this diagnosis needs careful counselling, explanation and support. Between 1998 and 2007, diagnoses of genital herpes rose by 51% in the UK.
Aetiology
Herpes simplex virus 1 and 2 (HSV-1 and HSV-2) are species of Herpesviridae, which cause genital herpes. Herpes viruses are composed of relatively large double-stranded, linear DNA genomes encoding 100–200 genes encased within an icosahedral proteinaceous capsid which is wrapped in a lipid bilayer envelope. They are nuclear, replicating the viral DNA being transcribed to RNA within the infected cell’s nucleus. HSV enters a latent phase within the neurones (local sensory ganglia) between active symptomatic episodes. Reactivation leads to production of virions, which may then be passed to a new host by sexual contact (in the case of genital herpes). Genital HSV-2 recurs and sheds more often than genital HSV-1; the converse is true for oral herpes.
Clinical features
Only about half those infected will get symptoms at the time of infection. Some may become symptomatic at a later date and some not at all. The seropositivity rates are 7% in the UK, 22% in the USA and 40% in 19-year-old females in Tanzania. In those cases that become symptomatic, the incubation period is 7–14 days.
The first episode presents with multiple painful genital ulcers (see Figure 63.2). It is less severe in those with a history of oral herpes. Typical lesions begin as vesicles, at any or all sites from the introitus to the cervix, which become superficial tender ulcers with an erythematous halo and a yellow or grey base (Figure 63.3). Immunocompromised patients may have an atypical appearance which is an elongated ‘knife cut’ ulcer. There may be bilateral inguinal lymphadenopathy. Viral shedding continues until the lesions crust over. One-third of patients have systemic symptoms of fever and general malaise. Ten percent will experience viral meningitis with photophobia and headache. A few patients experience retention of urine, either because of pain due to passing urine over the lesions (in which case, micturating in a bath may help) or because of a viral autonomic neuritis. Involvement of other nerves may lead to hyperaesthetic buttocks, thighs or perineum for a time. Severe encephalitis is rare but may be seen more frequently in immunocompromised patients. Without treatment, the first episode lasts for 3–4 weeks.
Figure 63.2 Primary genital herpes: multiple painful ulcers are present.
From Bolognia J et al, Dermatology 2e, with permission of Elsevier.
Complications of the first episode are common. There may be secondary bacterial infection of lesions. Autoinoculation may occur, often to fingers and eyes.
Recurrent episodes occur in approximately half of patients, tend to be less severe and are relatively less common after the first year. HSV-2 is more likely to become recurrent than HSV-1. There does not necessarily have to be a precipitating event, although stress, menstruation, trauma (sexual intercourse) and ultraviolet light are implicated. Immunosuppression increases the frequency and duration of episodes; herpetic ulceration persisting for over 1 month in a patient with HIV is AIDS defining.
Diagnosis
In the UK, guidelines for diagnostic criteria for herpes were drawn up by the British Association for Sexual Health and HIV (BASHH) in 2006. These are summarized below.
Screening of asymptomatic GUM clinic attendees by either HSV antibody testing or HSV detection in genital specimens is not recommended at present, although this area is under active review.
Virus detection and characterization
The confirmation and characterization of the infection and its type, by direct detection of HSV in genital lesions, are essential for diagnosis, prognosis, counselling and management. Methods should be used that directly demonstrate HSV in swabs taken from the base of the genital lesion. Virus typing to differentiate between HSV-1 and HSV-2 should be performed in all patients with newly diagnosed genital herpes. HSV isolation in cell culture is the current routine diagnostic method in the UK. Virus culture is slow, labour-intensive and expensive. Specificity is virtually 100%, but levels of virus shedding, quality of specimens, and sample storage and transport conditions influence sensitivity. Delayed sample processing and lack of specimen refrigeration after collection and during transport significantly reduce the yield of virus culture at all stages of infection.
HSV DNA detection by polymerase chain reaction (PCR) increases HSV detection rates by 11–71% compared with virus culture. PCR-based methods allow less stringent conditions for sample storage and transport than virus culture, and new real-time PCR assays are rapid and highly specific. Real-time PCR is recommended as the preferred diagnostic method for genital herpes.
Serology
Testing for HSV type-specific antibodies can be used to diagnose HSV infection by the detection of HSV-1 IgG or HSV-2 IgG or both. It is difficult to say whether the infection is recent, as immunoglobulin M (IgM) detection is unreliable. Collection of serum samples a few weeks apart can be used to show seroconversion. HSV-2 antibodies are indicative of genital herpes, whereas HSV-1 antibodies do not differentiate between genital and oropharyngeal infection.
Western blot is the diagnostic gold-standard, but it is not commercially available. Several commercial assays, as well as validated in-house methods, are available which show 91–99% sensitivity and 92–98% specificity relative to Western blot in sexually active adults.
Caution is needed in interpreting serology results because even highly sensitive and specific assays have poor predictive values in low-prevalence populations. Local epidemiological data and patient demographic characteristics should guide testing and interpretation of results. In patients with a low likelihood of genital herpes, a positive HSV-2 antibody result should be confirmed in a repeat sample or by a different assay.
The differential diagnosis of vulval ulcers is shown in Table 63.1.
Table 63.1 The differential diagnosis of genital ulcers
| Infective | Non-infective |
|---|---|
| Herpes simplex virus | Aphthous ulcers |
| Primary syphilis | Trauma |
| Lymphogranuloma venereum | Skin disease (e.g. lichen sclerosis et atrophicus) Chancroid |
| Donovanosis | Behçet’s syndrome |
| Human immunodeficiency virus | Other multisystem disorder (e.g. sarcoidosis) |
| Dermatitis artefacta |
Treatment
First episode of genital herpes
Saline bathing should be advised and oral analgesia provided. Topical anaesthetic agents, such as 5% lidocaine (lignocaine) ointment, may be useful to apply, especially prior to micturition, but should be used with caution because of the risk of potential sensitization.
Oral antiviral drugs are indicated within 5 days of the start of the episode and while new lesions are still forming.
Aciclovir, valaciclovir and famciclovir all reduce the severity and duration of episodes. Antiviral therapy does not alter the natural history of the disease. Topical agents are less effective than oral agents. Combined oral and topical treatment is of no benefit. Intravenous therapy is only indicated when the patient cannot swallow or tolerate oral medication because of vomiting. There is no evidence for benefit from courses longer than 5 days. However, it may be prudent to review the patient after 5 days and continue therapy if new lesions are still appearing at this time.
Recommended regimens (all for 5 days)
Hospitalization may be required for urinary retention, meningism and severe constitutional symptoms. If catheterization is required, suprapubic catheterization is preferred to prevent the 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.
Recurrent genital herpes
Recurrences are self-limiting and generally cause minor symptoms. Management decisions should be made in partnership with the patient. Strategies include supportive therapy alone, episodic antiviral treatments and suppressive antiviral therapy. The best strategy for managing an individual patient may change over time according to recurrence frequency, symptom severity and relationship status.
General advice includes saline bathing, Vaseline, analgesia and 5% lidocaine (lignocaine) ointment.
Episodic antiviral treatment (oral aciclovir, valaciclovir and famciclovir) reduces the duration (by median of 1–2 days) and severity of recurrent genital herpes. Patient-initiated treatment started early in an episode is most likely to be effective.
Suppressive antiviral therapy
Patients who have taken part in trials of suppressive therapy have had at least six recurrences per annum. Such patients have fewer or no episodes on suppressive therapy. Patients with lower rates of recurrence will probably also have fewer recurrences with treatment.
Patient safety and resistance data for long-term suppressive therapy with aciclovir now extends to over 18 years of continuous surveillance.
Recommended regimens
If breakthrough recurrences occur on standard treatment, the daily dosage should be increased (e.g. aciclovir 400 mg three times daily). Suppressive therapy should be discontinued after a maximum of 1 year to reassess recurrence frequency. The minimum period of assessment should include two recurrences. Patients who continue to have unacceptably high rates of recurrence may restart treatment.
Condoms may be partially effective in preventing acquisition of HSV, especially in preventing transmission from infected males to their female sexual partners. The efficacy of male condoms in preventing transmission from infected females to uninfected male partners has not been demonstrated, and the efficacy of female condoms to reduce HSV transmission during intercourse has not been assessed.
Suppressive antiviral therapy with valaciclovir 500 mg once daily reduces the rate of acquisition of HSV-2 infection and clinically symptomatic genital herpes in serodiscordant couples. In a randomized trial involving 1484 patients treated for 8 months, 0.5% valaciclovir recipients developed symptomatic infection compared with 2.2% of placebo recipients (75% reduction); however, 60 people needed to be treated to prevent one transmission. Other antivirals may be effective but efficacy has not been proven in clinical trials.
Diagnosis often causes considerable distress. Counselling should be as practical as possible and should address particular personal situations. The Family Planning Association (FPA) produces a range of leaflets on sexual health for the UK National Health Service (NHS). Their leaflet on genital herpes provides comprehensive patient information based on the BASHH guidelines, and can be purchased or viewed as a non-printable PDF file on the FPA website.
No vaccines have been approved for prevention of genital herpes, although trials are ongoing. Published studies using the HSV-2 glycoprotein-D adjuvant vaccine have shown limited efficacy in preventing clinical disease, and only in women who were seronegative for both HSV-1 and HSV-2 at baseline. The guideline authors do not support the use of unauthorized or unlicensed vaccines outside of clinical trials.
Management of herpes in pregnancy and neonatal herpes prevention
Guidelines for genital herpes in pregnancy are categorized into management of first episodes and recurrent episodes. Accurate clinical classification is difficult. Viral isolation and typing and the testing of paired sera (if a booking specimen is available) may be helpful. Referral to a genitourinary physician for advice on management of women with suspected genital herpes is recommended.
First-episode genital herpes
First-episode genital herpes has been associated with first-trimester miscarriage; however, there is no conclusive evidence that it causes developmental abnormality if the pregnancy continues. The occurrence of first-episode genital herpes is not considered an indication for termination of pregnancy (TOP). An anomaly scan may be considered at 20–22 weeks of gestation where this is not routine. Management should be in line with the clinical condition, with the use of either oral or intravenous aciclovir. Although aciclovir is not licensed for use in pregnancy, there is substantial clinical experience supporting its safety. Vaginal delivery should be anticipated.
Daily suppressive aciclovir from 36 weeks of gestation may be considered for women who experience first-episode genital herpes in order to reduce the likelihood of HSV lesions at term, and negate an offer of caesarean section (CS) delivery. There are sound arguments for using aciclovir 400 mg three times daily because of the altered pharmacokinetics of the drug in late pregnancy.
Third-trimester acquisition
CS for the prevention of neonatal herpes has not been evaluated in randomized controlled trials. CS should be offered to all women presenting with first-episode genital herpes lesions at the time of delivery, or within 6 weeks of the expected date of delivery or onset of labour. However, CS may not be of benefit in reducing transmission for women presenting with ruptured membranes for greater than 4 h. In all these cases, the paediatricians should be informed. Continuous aciclovir in the last 4 weeks of pregnancy reduces the risk of both clinical recurrence at term and delivery by CS.
Recurrent genital herpes
Antiviral treatment is rarely indicated for treatment of recurrent episodes of genital herpes during pregnancy. Symptomatic recurrences during the third trimester are likely to be brief, and vaginal delivery is appropriate if no lesions are present at delivery.
CS should be considered for women with recurrent genital herpes lesions at the onset of labour. Recurrent genital herpes at any other time during pregnancy is not an indication for delivery by CS. The risks of vaginal delivery for the fetus are small and must be set against risks to the mother of CS.
Syphilis
There was a post World War II peak in the incidence of syphilis, but with the advent of penicillin, it became one of the less common STIs in the UK. However, infectious syphilis is reported to have increased by a factor of 19 between 1998 and 2007 (2680 new diagnoses in that year). To a large extent, this rise has been fuelled by syphilis outbreaks among male homosexuals.
Nevertheless, the most dramatic recent increases in syphilis cases have been among women and heterosexual men. Although the numbers involved are considerably lower than those for chlamydia, this is still a worrying trend as syphilis can have serious health implications (left untreated, syphilis can damage the heart, aorta, brain, eyes and bones, and can be fatal) and had been thought for years to be under control in the UK.
Globally, WHO estimates that there are 12 million new cases of syphilis each year, most of which occur in South and South-east Asia, and sub-Saharan Africa. Infectious syphilis is reaching epidemic proportions in states of the former Soviet Union, and is increasingly substantially in the USA, especially in the African-American population.
Aetiology
Treponema pallidum venereum or Treponema pallidum pallidum is a motile spirochaete, entering the host via breaches in epithelium. The organism can also be transmitted vertically to a fetus in the later stages of pregnancy, giving rise to congenital syphilis.
The subspecies of T. pallidum causing yaws (pertenue), pinta (carateum) and bejel or endemic syphilis (endemicum) are morphologically and serologically indistinguishable from T. pallidum pallidum (syphilis); however, their transmission is not venereal in nature and the course of each disease is significantly different. They are worthy of mention as they can cause diagnostic confusion. Yaws occurs in sub-Saharan Africa, the Caribbean and most of the humid tropics. Bejel occurs in desert regions, and pinta occurs in parts of Central and South America. If venereal syphilis cannot be excluded in someone originating from one of these areas, it is safest to treat.
Clinical features
Primary syphilis
The incubation period after inoculation is 9–90 days (mean 21 days). The lesions may be extragenital and may be multiple. Chancres are usually painless, raised, well-circumscribed ulcers (Figure 63.4). There is a non-tender regional lymphadenopathy. The lesion may well go unnoticed, especially if it is intravaginal or rectal. It will heal spontaneously in 3–10 weeks.
Full access? Get Clinical Tree
