Page 415

Chapter 23 Sexually transmissible and reproductive tract infections in pregnancy

Susan Dapaah, Victor E. Dapaah

CHAPTER CONTENTS

Introduction 415
Epidemiological trends 416
Psychosocial aspects of STIs 417
Types of genital infections 418
Trichomoniasis 418
Vulvovaginal candidiasis (thrush) 418
Bacterial infections 419
Bacterial vaginosis 419
Chlamydia 420
Gonorrhoea 421
Group B streptococcus 422
Syphilis 422
Viral infections 424
Genital warts 424
Hepatitis B virus 424
Hepatitis C virus 425
Herpes simplex virus 425
Human cytomegalovirus 426
Human immunodeficiency virus 427
Conclusion 429
REFERENCES 429
FURTHER READING 431

This chapter presents an overview of issues relating to sexual health. The clinical features, diagnosis and management of the common types of sexually transmissible and reproductive tract infections and their relevance in pregnancy are described. Specialist detail on these infections can be obtained from other sources such as Holmes et al (1999). Treatment regimens are stated but drug dosages have intentionally been omitted as these should be obtained from regularly updated pharmaceutical publications.

The chapter aims to

consider the challenges facing health professionals with the rising trends of HIV and sexually transmissible infections (STIs)
discuss the significance and management of STIs in pregnancy
discuss the role of the midwife in caring for women with STIs during pregnancy

Genitourinary medicine (GUM) clinics specialize in the holistic management of individuals with HIV and STIs. Midwives should be aware of sexual health services so that pregnant women are appropriately referred for management and treatment.

Page 416

Introduction

HIV and STIs are associated with considerable levels of morbidity and mortality. They are thus a major public health concern in the UK and present a serious challenge to health professionals and healthcare provision. High priority has been given to the improvement of sexual health services. In 2001, the National Strategy for Sexual Health and HIV was launched in England (DH 2001). Similar strategies have been produced in the rest of the UK. The strategy has been augmented by an action plan (DH 2002) and more recently by the White Paper ‘Making Healthier Choices Easier’ (DH 2004a).

The successful control of STIs requires a range of activities that includes screening programmes, effective treatment regimens, partner notification and referral, health education, and counselling and voluntary testing for HIV. Health professionals have a role in promoting public health and may contribute to the sexual health strategy by raising awareness and helping people to access services and information.

The diagnosis, treatment and care of women with STIs during pregnancy requires health professionals to work collaboratively to meet individual needs and improve pregnancy outcomes and lower maternal and neonatal morbidity and mortality. Joint management between an obstetrician and a GUM physician is essential for women with STIs during pregnancy and a paediatrician is required to care and manage the neonate infected through vertical transmission. The midwife plays a vital role in caring for the mother and her family in the provision of individualized care during childbirth. This is particularly important for women diagnosed with an STI during pregnancy who have the extra burden of worrying about the well-being of their babies.

Epidemiological trends

There have been significant changes in the epidemiology of HIV and other STIs over the last 25 years, in particular during the decade 1996–2005.

The prevalence of HIV continues to increase. At the end of 2005 it was estimated that 63 500 adults in the UK aged between 15 and 59 were suffering from HIV infection, 32% of whom were unaware of their HIV status (Health Protection Agency (HPA) 2006). This contrasts with an estimated 30 000 cases in 2000. The annual number of new diagnoses of HIV rose by 175% from 2707 in 1996 to 7450 in 2005. However, the high number in 2005 is comparable to the numbers diagnosed in 2003 and 2004 suggesting that the incidence may be stabilizing.

The number of new diagnoses of other STIs in UK GUM clinics rose by 60% during the same period. Chlamydia and gonorrhoea, two of the most common STIs showed considerable increases. The number of uncomplicated genital chlamydial infections trebled, rising by 207% from 35 840 cases to 109 958. Gonorrhoea increased by 54% from 12 579 cases to 19 392. The incidence peaked in 2002 at 25 599 cases, but a gradual decline has since been observed. However, the level of antibiotic resistance to gonorrhoea has increased throughout the UK (HPA 2006).

There has been a dramatic rise of 1954% in the incidence of infectious syphilis. Cases increased from 290 in 1996 to 3712 in 2005 with a reported six-fold increase in the diagnosis of early latent syphilis (HPA 2006).

The incidence of viral STIs also increased. The number of first attack genital warts rose by 26% from 64 178 cases in 1996 to 81 137 in 2005. During the same period the number of first attack herpes increased by 18% from 16 811 to 19 837 cases.

The burden of HIV and STIs falls disproportionately on marginalized groups. The highest infection rates are found in women, gay men, teenagers, young adults and black and minority ethnic groups (House of Commons Health Committee 2003). Additionally, direct links between sexual ill-health and poverty, poor housing, unemployment and other forms of social exclusion have been recognized (DH 2003). Statistics show that females account for most cases of uncomplicated chlamydia and first attack herpes, and males account for most cases of primary/secondary syphilis and uncomplicated gonorrhoea. The number of cases of first attack genital warts is higher in males than females (HPA 2006). The highest rates of gonorrhoea, genital warts and chlamydial infections are found in the 16–19 year age group in women, and the 20–24 year age group in women and men.

Page 417

A number of factors are thought to contribute to the increase in the incidence of HIV and STIs. The rise in the number of diagnoses may be due to the increased availability and sensitivity of tests and greater public awareness of the services available. In addition, there is evidence of changes in attitudes and patterns of sexual behaviour. The second ‘National Survey of Sexual Attitudes and Lifestyles’ also known as NATSAL 2000 (Johnson et al 2001) reported a wide range of behaviours associated with increased risk of HIV and STI transmission. The mean number of sexual partners in a lifetime and the proportion of people having concurrent sexual relationships have increased. The average age at first intercourse has fallen from 17 to 16 years. Although the use of condoms has increased, a greater proportion of people with two or more partners reported inconsistent use.

Risky sexual behaviours are probably influenced by several factors including low self esteem, lack of skills and confidence to negotiate safer sex and a lack of knowledge about the risks of different sexual behaviours. Peer pressure, the attitudes and prejudices of society and the availability of sexual health services are also contributory factors (Ellis et al 2003).

GUM clinics provide important surveillance data for STIs and sexual health in the UK. However, family planning, gynaecology and antenatal clinics, general practice, prison health services and schools also contribute to sexual health. In addition, many infections are often asymptomatic and are consequently not diagnosed. The total number of STI diagnoses is therefore likely to be underestimated (PHLS 2000).

Psychosocial aspects of STIs

Health professionals need to be aware of the broad range of psychological and social responses to STIs. Two general themes appear in the literature. The first is the range of psychological responses often manifest by individuals on initial diagnosis. These include shock, embarrassment, disbelief, distress, anxiety, feeling dirty/contaminated and worry about future health. The second relates to specific areas of concern. These include stigma, guilt/blame for the infection, concerns about transmitting the infection to others and anxiety and fear about disclosure to sexual partners, family and friends (Maissi et al 2004, McCaffery et al 2006). Stigma, shame and ostracism have historically been associated with STIs and are still thought to be important barriers that prevent individuals from seeking diagnosis and treatment (Cunningham et al 2002, Scoular et al 2001). Prejudice and discrimination pose real threats to individuals suffering from STIs, in particular, those with HIV (Terence Higgins Trust 2001).

Good communication skills are essential as individuals who have or are at risk of an STI need to be approached in a sensitive, tactful and non-judgemental manner (Peate 2005). A full sexual history is vital for accurate diagnosis, treatment and risk-assessment, but many patients find discussing sexually related matters difficult and embarrassing. Health professionals therefore must establish trust and rapport with patients and provide a comfortable, friendly and relaxed environment in which to discuss these issues (French 2004). The assurance of confidentiality is a vital component in the promotion of mutual trust, respect and effective partnerships. Healthcare professionals have a professional and a legal duty to ensure the confidentiality and security of all information gained in the course of professional practice (Dimond 2002). In relation to individuals with STIs, particularly HIV, the maintenance of confidentiality is a common source of worry. Midwives should therefore assure their clients that sensitive information will not be disclosed to others without their consent or other lawful exception.

Psychosocial responses to STIs may vary according to the type of infection, the circumstances in which it was acquired, associated sequelae and the likely effect on future lives. Whereas many STIs are curable, some such as HIV and genital herpes cannot be eradicated and require long term management. There have been marked improvements in the treatment of HIV and AIDS but they still carry significant morbidity and mortality. Genital herpes is a lifelong chronic infection with the possibility of recurrences. Women with chlamydial infection are fearful of the possible adverse effects on their reproductive capacity. Victims of sexual abuse and/or assault can experience a wide range of psychological and emotional disorders. It is therefore imperative that these groups of patients receive appropriate specialist management. Some patients are likely to suffer psychological maladjustment and will require psychological/psychiatric assessment and treatment. Psychological support and correct information can help people to come to terms with their conditions (Chippindale & French 2001).

Page 418

Types of genital infections

Trichomoniasis

Trichomoniasis is one of the most common sexually transmitted infections. It is caused by Trichomonas vaginalis, a round/oval flagellated protozoal parasite. The World Health Organization (WHO) estimates that about 170 million new cases occur annually (Mabey et al 2006). Although 10–50% of women are asymptomatic, common symptoms include vaginal and urethral discharge, vulval pruritus and inflammation. Vaginal discharge is present in up to 70% of cases and can range from thin and scanty to profuse and thick and may be malodorous. A classic frothy yellow-green discharge occurs in 10–30% of women. Dyspareunia, mild dysuria and lower abdominal pain may also be experienced (Sherrard 2007).

Trichomoniasis in pregnancy

Trichomoniasis has been linked with a small risk of pre-term delivery and low birth weight, and an increase in the risk of HIV via sexual intercourse. Trichomoniasis may be acquired perinatally and occurs in about 5% of babies born to infected mothers (Sherrard 2007).

Page 419

Diagnosis and treatment

In women, 95% of cases can be diagnosed by cultures and 40–80% by microscopy of a high vaginal swab. Other diagnostic tests include a latex agglutination test and polymerase chain reaction (PCR). UK guidelines state that metronidazole and related drugs achieve a 95% cure rate (Sherrard 2007). The recommended treatment is metronidazole daily for 5–7 days or in a single dose. Although contraindicated in pregnancy, meta-analyses have concluded that there is no evidence of teratogenicity from its use during the first trimester. However, it is not known whether this treatment will have any effect on pregnancy outcomes (Gülmezoglu 2002). Clotrimazole pessaries daily for 7 days can be used in early pregnancy. High single dose regimens should be avoided during pregnancy and breastfeeding. It is usual to treat the partner(s) and advise against sexual intercourse until the treatment is completed. In addition, patients should be advised not to consume alcohol during the treatment and for at least 48 hrs afterwards as this may cause nausea and vomiting.

Vulvovaginal candidiasis (thrush)

Candidiasis is a common cause of vaginal discharge, vulvitis and vaginitis and it is responsible for 20–30% of all vaginal infections. The main causative organism is Candida albicans, a fungal parasite, but other candidal species for example Candida glabrata, account for 10% of genital yeast infections (Schwebke & Hillier 2005). Candida albicans is often found as a commensal in the flora of the mouth, gastrointestinal tract and probably the vagina (Hay 2005). It is not thought to be sexually transmitted. During the reproductive years women are prone to develop vulvovaginal candidiasis because oestrogens encourage Candida albicans to flourish. Most women will probably develop candidiasis at some point during their adult life and <5% will experience recurrent vulvovaginal candidiasis defined as four or more episodes a year. Some 10–20% of women harbour Candida species but remain asymptomatic and do not require treatment (Daniels & Forster 2002).

Several factors are thought to predispose to Candida albicans infections. These include:

changes to the vaginal flora (e.g. antibiotics, spermicides)
immunosuppressant disease or treatment (e.g. AIDS, chemotherapy)
poor diabetic control
pregnancy.

The signs and symptoms of candidiasis include intense vulval itching and soreness and usually a non-offensive, thick, white curdy discharge. On examination the vulva, vagina and cervix may be erythematous and oedematous, and white plaques are noted. Superficial dyspareunia and external dysuria may also be experienced.

Diagnosis and treatment

Microscopy and culture of a high vaginal swab are the most sensitive methods currently available for detecting candida cells. However, diagnosis is often based on clinical signs and symptoms. Candidiasis may be treated with topical preparations such as clotrimazole pessaries or nystatin gel, or oral preparations such as fluconazole. All therapies effect high cure rates (Daniels & Forster 2002). Fluconazole (Diflucan) is available over the counter but has not been tested in pregnancy and therefore cannot be assumed to be safe. It should also be used with caution whilst breastfeeding owing to toxic effects in high doses.

A Cochrane systematic review of topical treatments for vaginal candidiasis in pregnancy concluded that topical imidazole drugs are more effective than nystatin; that single dose treatments are less effective than 3–4 day treatments; and that treatment lasting for 4 days is less effective than treatment for 7 days (Young & Jewell 2001).

Treatment failure can occur in up to 20% of women. It may be helpful to advise on general and genital hygiene such as the avoidance of local irritants e.g. perfumed products, the wearing of tight-fitting synthetic clothing and washing and wiping the genitals from front to back. It is not necessary to treat asymptomatic partners (Daniels & Forster 2002).

Bacterial infections

Bacterial vaginosis

Bacterial vaginosis (BV) is the most common cause of vaginal discharge in women of childbearing age. It does not appear to be sexually transmitted but may be associated with sexual activity and often co-exists with other sexually transmitted infections such as gonorrhoea and chlamydia. It can arise and remit spontaneously. It is more common in black than white women, those with an intrauterine contraceptive device and those who smoke (Hay 2006). The incidence of BV is high in women with pelvic inflammatory disease (PID) and some populations of women undergoing elective termination of pregnancy (TOP). It is also associated with post-TOP endometritis.

The aetiology is unknown but BV is associated with a change in vaginal ecology. The normal lactobacilli-predominant vaginal flora is replaced with an overgrowth of predominantly anaerobic bacteria including Gardnerella vaginalis, Prevotella species, Mobiluncus species and Mycoplasma hominis. The vaginal epithelium is not inflamed, hence the term ‘vaginosis’ rather than ‘vaginitis’. The main symptom is a malodorous and greyish watery vaginal discharge, although approximately 50% of women are asymptomatic. The odour is usually more pronounced following sexual intercourse owing to the release of amines by the alkaline semen.

Bacterial vaginosis in pregnancy

BV is present in up to 20% of women during pregnancy, the majority of whom will be asymptomatic (McDonald et al 2007). Flynn et al (1999) found in a review of case-control and cohort studies that women with BV infections were 1.85 times more likely to deliver pre-term than women without BV. Other adverse outcomes of pregnancy include late miscarriage, pre-term premature rupture of membranes and postpartum endometritis (Hay 2006).

Diagnosis and treatment

The two most common approaches used to diagnose BV are the use of Amsel’s criteria or evaluation of a Gram-stained vaginal smear. A diagnosis of BV is confirmed by fulfilling three out of four criteria (Amsel et al 1983):

a thin, white to grey, homogenous discharge
‘clue cells’ on microscopy
a vaginal pH of >4.5
the release of a fishy odour when adding potassium hydroxide to a sample of the discharge.

An alternative test is the evaluation of a Gram-stained vaginal smear using the Ison-Hay scoring system (Ison & Hay 2002). This method grades the vaginal flora and correlates well with Amsel’s criteria, and has been endorsed by the Bacterial Special Interest Group of the British Association for Sexual Health and HIV (BASHH).

Page 420

A Cochrane systematic review assessing the effects of antibiotic therapy on BV in pregnancy concluded that although it was effective at eradicating infection, it did not reduce the number of pre-term births (McDonald et al 2007). The treatment regimen is the same as for trichomoniasis. Alternative treatments include oral clindamycin or tinidazole or intravaginal clindamycin cream or metronidazole gel. All these treatments have been shown in controlled trials to achieve cure rates of 70–80% after 4 weeks, but recurrences of infection are common. Women should be advised to avoid vaginal douching, use of shower gel and antiseptic agents in the bath (Hay 2006). There is insufficient evidence to recommend the routine screening of pregnant women and the treatment of asymptomatic BV (National Institute for Health and Clinical Excellence (NICE) 2003).

Chlamydia

Chlamydia trachomatis is an intracellular bacterium. It is one of the most prevalent STIs worldwide and the most common cause of sexually transmitted bacterial infection in the UK (Fletcher & Ball 2006). Serotypes D to K are sexually transmitted and are important causes of morbidity in both sexes. Serotypes A, B and C cause trachoma and blindness, and serotypes L1 to L3 cause the genital disease lymphogranuloma venereum.

Genital chlamydial infection is asymptomatic in at least 70% of women and 50% of men (HPA 2006). The clinical signs and symptoms include post-coital or intermenstrual bleeding, a purulent vaginal discharge, mucopurulent cervicitis and/or contact bleeding, dyspareunia and lower abdominal pain. Dysuria, bartholinitis and Fitz–Hugh–Curtis syndrome (peri-hepatitis) may also be experienced (Fletcher & Ball 2006, Horner & Boag 2006).

Chlamydial infection of the cervix is found in 15–30% of women attending GUM clinics, and concurrently in 35–40% of women with gonorrhoea (Schachter et al 1998). Significant factors associated with infection include those aged less than 25 years, a new sexual partner or more than one sexual partner in the past year, lack of consistent use of condoms and those attending GUM clinics (Adams et al 2004, Horner & Boag 2006). In untreated cases the complications among women may include PID and its associated sequelae.

Chlamydia in pregnancy

Infection rates in pregnancy range from approximately 2–13% (Adams et al 2004, Shankar et al 2006). C. trachomatis is associated with pre-term delivery, pre-labour rupture of membranes, chorioamnionitis and postpartum endometritis.

Fetal and neonatal infections

The major risk to the infant is from passing through an infected cervix during birth although intrauterine infection may occur. This can lead to neonatal conjunctivitis (ophthalmia neonatorum, a notifiable condition in the UK) and a characteristic pneumonia. Chlamydial ophthalmia neonatorum is more common than that of gonococcal aetiology. In practice, the conditions are indistinguishable and may occur together. The incubation period of chlamydial ophthalmia is 6–21 days, compared with 48 hrs for gonococcal ophthalmia. Chlamydial pneumonia usually occurs between the 4th and 12th week of life. It affects about half the babies who develop conjunctivitis but is not always preceded by it. It is thought that children affected by chlamydial pneumonia are more likely to develop obstructive lung disease and asthma than those who have had pneumonia from other causes. The pharynx, middle ear, rectum and vagina are also targets for infection, with a delay of up to 7 months before cultures become positive.

The routine screening of pregnant women for asymptomatic chlamydia is not currently recommended in the UK (NICE 2003). However, there is growing evidence that the substantial morbidity associated with chlamydial infections can be reduced through the targeted screening of at-risk populations. In 2002 a National Chlamydia Screening Programme was launched in the UK.

Diagnosis and treatment

Nucleic acid amplification tests (NAATs) are recommended as the most reliable means to diagnose chlamydia (Horner & Boag 2006). Three commercial tests are now available:

Polymerase chain reaction (PCR)
Strand displacement amplification (SDA)
Transcription mediated amplification (TMA).

These tests have high rates of sensitivity and specificity. Less sensitive methods of diagnosis include tissue culture, enzyme immunoassays (EIAs) and direct fluorescent antibody (DFA).

Page 421

Genital chlamydial infections are sensitive to three classes of antibiotics. These are the tetracyclines, the macrolides (e.g. erythromycin) and the fluoroquinolones, especially ofloxacin. The tetracyclines and the fluoroquinolones are contraindicated in pregnancy. Despite the side-effects of nausea and vomiting, erythromycin is considered to be the first line treatment in pregnancy. Erythromycin is also used for chlamydial infections in infants, young children and lactating women. Although available data indicate the safety of azithromycin in pregnancy and lactation (Brocklehurst & Rooney 2000), UK guidelines recommend its use only if no alternative exists (Horner & Boag 2006). Women and partners should be advised to abstain from sexual intercourse until treatment is complete. A test of cure is not routinely recommended but should be performed in pregnancy to identify treatment failure or re-infection.

Gonorrhoea

Gonorrhoea is caused by infection with Neisseria gonorrhoeae, a Gram-negative, intracellular diplococcus. The mode of transmission is almost exclusively by sexual contact. This organism adheres primarily to the mucous membranes of the urethra, endocervix, rectum, pharynx and conjunctiva. Gonorrhoea may co-exist with other genital mucosal pathogens, notably C. trachomatis, T. vaginalis and C. albicans. Up to 80% of initial cases of PID are caused by N. gonorrhoeae or C. trachomatis, or both. Although uncommon, gonorrhoea may also cause disseminated systemic disease and arthritis.

The most common symptom is an increased or altered vaginal discharge although up to 50% of women are asymptomatic. Lower abdominal pain, dysuria, intermenstrual bleeding and menorrhagia may also be experienced, ranging in intensity from minimal to severe (Bignell 2005).

Gonorrhoea in pregnancy

Infection with N. gonorrhoeae has been associated with adverse pregnancy outcomes. These include low birthweight, pre-term rupture of membranes, pre-term birth, chorioamnionitis and postpartum endometritis and salpingitis. Other possible complications are spontaneous miscarriage and secondary infertility (Herbert & Impey 2005, Mitchell 2004).

Neonatal infection

N. gonorrhoeae is usually transmitted from the mother’s genital tract to the baby at the time of birth although occasionally it may occur in utero when there is prolonged rupture of the membranes. The risk of transmission from an untreated mother is about 30–50% (Mitchell 2004). Infection usually manifests as ophthalmia neonatorum (see Plate 23) with a purulent discharge usually evident within 2–5 days of birth. It can be diagnosed by microscopy and culture of an eye swab. The eyes may be cleaned with saline but systemic antibiotics are required. If left untreated the condition can lead to corneal ulceration and perforation with permanent loss of vision. Occasionally the neonate may develop gonococcal arthritis and/or disseminated infection.

Diagnosis and treatment

The methods used to diagnose gonorrhoea consist of:

microscopy of a suitably stained specimen
culture for N. gonorrhoeae on a medium with antimicrobial agents
nucleic acid hybridization or amplification tests.

In women, microscopic examination of Gram-stained endocervical smears is the first-line in diagnosis. Specificity is high (>99%) when screened by trained personnel. Microscopy is unsuitable for pharyngeal and rectal specimens because of the presence of other Gram-negative cocci (Bignell et al 2006).

Culture for N. gonorrhoeae can be undertaken with specimens from all sites. This method provides a viable organism for antibiotic sensitivity testing. Culture has been reported to have a sensitivity of 85–95% for urethral and endocervical infection (Bignell et al 2006). Nucleic acid hybridization or amplification tests are not currently recommended for use in GUM clinics because of the inability to assess antibiotic sensitivity.

Page 422

Penicillin has been used as a first-line therapy for gonorrhoea for many years. However, surveillance data in the UK show that N. gonorrhoeae is becoming resistant to penicillin, tetracyclines and ciprofloxacin (a quinolone) (Gonococcal Resistance to Antimicrobials Surveillance Programme (GRASP) 2004). Nevertheless, local patterns of antimicrobial sensitivity should be taken into account when prescribing treatment. If antimicrobial sensitivity to the above antibiotics is known then ciprofloxacin, ofloxacin and ampicillin plus probenecid may be prescribed in oral, single doses. Otherwise, third-generation cephalosporins such as ceftriaxone or cefixime should be prescribed orally or intramuscularly in single doses. Spectinomycin may also be given in a single oral dose. Pregnant women should not be treated with quinolone or tetracycline (Bignell 2005).

Group B streptococcus

Group B streptococcus (GBS) (Streptococcus agalactiae) is a Gram-positive bacterium that naturally colonizes the body. It is harboured in the genital and gastrointestinal tracts and carried asymptomatically in up to 40% of adults. GBS is not considered to be sexually transmitted but infection increases with sexual activity and rates are highest in women attending genitourinary clinics. Approximately 12–26% of pregnant women are colonized with the organism (Herbert & Impey 2005).

Group B streptococcus in pregnancy

In pregnant women colonized with GBS, high risk factors associated with vertical transmission include: pre-term delivery, prolonged rupture of membranes, maternal pyrexia during labour, GBS cultured in a urine sample, known carriage of GBS or a history of a GBS infection in a previous pregnancy (Feldman 2001, Smaill 2001). GBS is able to infiltrate the amniotic cavity, whether or not the membranes are intact, and infect the fetus through the lung epithelium. Postpartum endometritis and post-caesarean wound infection may also occur in the mother.

Fetal and neonatal infections

GBS is the leading cause of serious neonatal infection in the UK (NICE 2003). The prevalence of early onset GBS disease in the UK is estimated to range from 0.5/1000 to 1.15/1000 live births (Oddie & Embleton 2002). Early onset is when symptoms develop within the first 5 days of life (average 20 hrs) suggesting that the infection started in utero. Late onset usually presents between 7 days and 3 months of age in previously healthy babies.

Diagnosis and treatment

The identification of women colonized with GBS can reliably be undertaken with vaginal and rectal swabs. In the USA, pregnant women are screened in the third trimester for GBS and are treated prophylactically with intrapartum penicillin if identified as high risk of transmitting the infection. However, pregnant women in the UK are not routinely screened because evidence of clinical and cost-effectiveness remain uncertain (NICE 2003, Woodgate et al 2004).

Syphilis

Syphilis is an acute and chronic sexually transmitted infection caused by the bacterium Treponema pallidum, a spirochaete. It can also be transmitted transplacentally to the fetus from the 9th week of gestation onwards (Genç & Ledger 2000). It is a common infection worldwide with an estimated 12 million diagnosed new cases each year (Adler & French 2004). Syphilis is a complex systemic disease that can involve virtually any organ in the body. Acquired syphilis is classified into the following stages (Winter 2006):

Early (infectious) syphilis

Primary: 9–90 days after exposure (mean 21 days)
Secondary: 6 weeks-6 months after exposure (4–8 weeks after primary lesion)
Latent (early): <2 years after exposure.

Late (non-infectious) syphilis

Latent (late): > 2 years after exposure with no symptoms or signs
Tertiary, gummatous, cardiovascular, neurosyphilis: 3–20 years after exposure.

Syphilis in pregnancy

WHO figures estimate that maternal syphilis adversely affects 1 million pregnancies each year, with 460 000 resulting in abortion or perinatal death, 270 000 babies being born with congenital syphilis and 270 000 being born premature or with low birthweight (Walker & Walker 2002). In the UK, antenatal screening for syphilis is routine and the incidence of infectious syphilis is low although there is no systematic national surveillance for the number of cases diagnosed during pregnancy (NICE 2003, Simms & Ward 2006). Herbert and Impey (2005) report an incidence of 0.2% in London and 0.02% in the rest of the UK. The prevalence in Northern Europe is between 0.02% and 4.5% (Genç & Ledger 2000).

Page 423

Vertical transmission may occur at any time during pregnancy in untreated early syphilis but the risk of transmission diminishes as maternal syphilis advances. The rate of vertical transmission in untreated women is 70–100% for primary syphilis, 40% for early latent syphilis and an estimated 10% for mothers with late latent syphilis (Doroshenko et al 2006).

Congenital syphilis

The prevalence of congenital syphilis in the UK is estimated as very low. It is classified into early or late congenital syphilis depending on whether it presents before or after 2 years of age. It is associated with serious neurological, developmental and musculoskeletal sequelae and the prognosis is considered poor if symptoms present in the first few weeks of life (French 2007, Saloojee et al 2004). Diagnosis may be complicated because more than half of all infants are asymptomatic at birth, and signs in symptomatic infants may be subtle and non-specific. Characteristically, prematurity, low birthweight, hepatomegaly with or without splenomegaly and failure to thrive are some of the findings of early syphilis, although these signs are also seen in other congenital infections (Saloojee et al 2004). Serological tests should be performed on the baby’s blood not cord blood. A positive anti-treponemal EIA IgM is consistent with a diagnosis of congenital infection although positive tests should be repeated to confirm this. A negative IgM test should be repeated at 4, 8 and 12 weeks as the IgM response could be delayed or suppressed (Goh 2002).

Babies born to mothers treated antenatally for syphilis should be managed jointly with paediatricians and followed up at 3 months, 6 months and 1 year. UK guidelines suggest that older siblings should also be screened for congenital syphilis (Goh 2002). Treatment is usually with penicillin.

Diagnosis and treatment

Women in the UK are screened for syphilis at antenatal booking and treated if needed in the same way as non-pregnant women. However, this does not detect those who acquire the infection during pregnancy, or are incubating syphilis at the time of serological testing. There are two main classifications of serological tests for syphilis (French 2007):

Non-treponemal tests which detect non-specific treponemal antibodies:

Venereal Diseases Research Laboratory (VDRL)
Rapid plasma reagin (RPR) tests.

Treponemal tests which detect specific treponemal antibodies:

Enzyme immunoassays (EIAs)
T pallidum haemagglutination assay (TPHA)
T pallidum particle agglutination assay (TPPA)
Fluorescent treponemal antibody-absorbed test (FTA-abs).

If syphilis is suspected on the basis of clinical findings, dark-field microscopic examination or fluorescent antibody staining of a specimen taken from a lesion should be undertaken (see Plate 4) (Goh 2002). A Cochrane systematic review of antibiotics for syphilis diagnosed during pregnancy concluded that penicillin is effective in the treatment of syphilis and the prevention of congenital syphilis but more research is needed on the best dosage and duration of treatment (Walker 2001). The management of pregnant women with syphilis should be undertaken jointly between a GUM physician and obstetricians and midwives. In the case of penicillin allergy, tetracycline is the second-line treatment but this is contraindicated in pregnancy. Erythromycin or azithromycin are alternatives but these may be ineffective in treating pregnant women (NICE 2003). Desensitization to penicillin should therefore be considered as an option. Breastfeeding is safe unless an infectious lesion is present on the breast (Genç & Ledger 2000).

Patients should be warned of possible reactions to treatment with penicillin. The Jarisch–Herxheimer reaction is an acute febrile illness characterized by fever, chills, myalgia, headache, hypotension and tachycardia that occurs in up to 45% of pregnant women after treatment for early syphilis. The release of pro-inflammatory cytokines in response to dying organisms is thought to induce this reaction. Symptoms may occur within several hours of treatment but resolve within 24–36 hrs. In pregnant women, it can cause uterine contractions, fetal distress and precipitate pre-term labour. For this reason some recommend that the mother is admitted to hospital for the first 24 hrs of treatment (Genç & Ledger 2000).

Page 424

Women who are known to have been treated for syphilis in the past do not require treatment in subsequent pregnancies if there is no clinical or serological evidence of infection but the baby should be tested to exclude congenital syphilis (Goh 2002).

Viral infections

Genital warts

Genital warts (condyloma acuminatum) are caused by the human papillomavirus (HPV). Although there are over 100 subtypes of HPV, several of which can cause genital warts, they are most commonly caused by types 6 and 11. Transmission is primarily by sexual contact but infants and young children may develop laryngeal papillomas after being infected from maternal genital warts at delivery (Adler 2004). The rate of first attack genital warts has been rising since 1996 with the highest rates seen in women in the 16–19 and 20–24 year age-groups. Most genital warts are asymptomatic and painless and many resolve spontaneously in healthy women. They may occasionally cause irritation and soreness, but essentially they are more of a cosmetic problem often causing psychological and psychosexual distress (Maw 2006). In pregnancy they tend to multiply and grow faster as a result of changes in local cellular immunity and may appear like cauliflower-like masses (see Plate 3) (Mitchell 2004).

Viral eradication is not possible; therefore treatment is aimed at removing the warts (Peate 2006). Treatment can be difficult and time consuming and often depends on patient compliance and skilled health professionals. Warts are usually treated with locally applied caustic agents such as podophyllum. However, this is contraindicated in pregnancy because of possible teratogenicity. Treatment is not recommended during pregnancy, but in exceptional circumstances trichloroacetic acid, cryotherapy, diathermy, laser therapy or surgery may be appropriate (Adler 2004; Peate 2006). Women presenting with genital warts should be fully investigated to exclude other sexually transmitted infections. In addition, colposcopy should be performed to exclude flat warts on the cervix. Most genital warts are benign, but cervical intraepithelial neoplasia is strongly associated with HPV types 16, 18, 31, 33 and 35, therefore an annual cervical smear is recommended (Adler 2004).

Prophylactic vaccines to prevent primary infection with HPV and reduce the incidence of related conditions such as cervical cancer and genital warts are being developed. Trial data point towards the potential for protecting young uninfected girls from cervical cancer (Cadman 2006; HPA 2006).

Hepatitis B virus

Hepatitis B virus (HBV) is an hepadnavirus belonging to a family of DNA viruses that cause acute infection of the liver. HBV can be transmitted sexually, parenterally or vertically from mother to fetus (Gilson & Brook 2006). Body fluids such as saliva, menstrual and vaginal fluid, serous exudates, seminal fluid and breastmilk have been implicated in the spread of infection, but infectivity is largely related to blood and body fluids contaminated with blood. Transmission occurs in injecting drug-users sharing needles and syringes, tattooing or acupuncture, or as a consequence of needle-stick injury in healthcare workers (Brook 2005).

Acute infection with HBV is asymptomatic in 10–50% of adults and virtually all infants and children. In typical cases there are two phases of symptoms:

the prodromal phase (3–10 days) characterized by flu-like symptoms of malaise, myalgia and fatigue, often accompanied by pain in the right hypochondrium
the icteric phase (7–21 days) characterized by jaundice, anorexia, nausea and fatigue. In a small number of cases, symptoms can persist for 12 or more weeks (cholestatic symptoms of itching and deep jaundice).

The diagnosis of HBV relies on serological tests. Acute HBV is diagnosed by the presence of IgM antibodies to the HBV core (anti-HBc IgM). Hepatitis B surface antigen (HBsAg) is detectable during the acute phase. Patients who remain HBsAg positive after six months are classified as persistent virus carriers. Another serological marker is the hepatitis Be antigen (HBeAg) which can be detected during the acute phase but disappears quickly unless the individual becomes a carrier. The appearance of anti-HBs in the serum indicates immunity.

Page 425

Chronic infection occurs in 5–10% of symptomatic cases but higher rates are seen in immuno-compromised patients with HIV infection, chronic renal failure and those receiving immunosuppressive therapy (Brook 2005). In the UK about 1 in 1000 of the population carries the hepatitis B virus. HBeAg positive carriers are much more likely to transmit the infection during sexual contact or from mother to baby at birth (Gilson 2004). More than 90% of infants born to HBeAg positive mothers will also become chronic carriers unless immunized.

The prevalence of infection (HBsAg) among pregnant women ranges from 0.5% to 1%. All pregnant women should be offered antenatal screening for HBV and babies born to infected mothers should be vaccinated at birth (NICE 2003). In addition, the babies of mothers who have become infected with HBV during pregnancy and those who do not have anti-HBe antibodies should also receive hepatitis B specific immunoglobulin (HBIg) (Lee et al 2006). This confers immediate immunity and reduces vertical transmission by 90%. Infected mothers should continue to breastfeed as there is no additional risk of transmission (Brook 2005).

Hepatitis C virus

Hepatitis C virus (HCV) infection is a global health problem with a worldwide prevalence of between 0.5% and 15% (Fischler 2007). In the UK it ranges from 0.06% in blood donors to over 60% in intravenous drug users (Brook 2005). Acute HCV infection is usually asymptomatic. Approximately 50–85% of infected individuals will develop a chronic infection leading to severe liver damage, liver cirrhosis, and hepatocellular carcinoma (Thomas 2005). The principal route of transmission is by percutaneous inoculation of blood and/or blood products, intravenous drug use, tattooing, body piercing and mother-to-child transmission (NICE 2003). Vertical transmission rates are low, occurring at <5%, but co-infection with HIV has consistently been associated with a greater likelihood of transmitting HCV to the fetus. Breastfeeding does not pose an important risk of transmission if the nipples are not traumatized and maternal HCV infection is quiescent (Roberts & Yeung 2002). Sexual transmission rates are very low but these are increased in high risk groups such as female sex workers and those with multiple sexual partners (Brook 2005). At present, there is a lack of effective intervention strategies to prevent vertical transmission and the routine screening of pregnant women for HCV is not recommended (Fischler 2007; NICE 2003).

Herpes simplex virus

There are two herpes simplex virus (HSV) subtypes. Type 1 (HSV-1) causes the majority of orolabial infections, and is often acquired during childhood through direct physical contact with oral secretions. Type 2 (HSV-2) is almost entirely associated with genital disease and is acquired through contaminated secretions during sexual contact. Genital HPV-1 can be acquired through orogenital contact and the incidence of genital HSV-1 infection is increasing, especially in young women (Vyse et al 2000). Genital herpes is a lifelong infection. Once acquired, the virus becomes latent in sensory nerve ganglia and reactivates periodically. Infected people shed the virus regardless of whether or not lesions are present. Infections may be primary, when an HSV seronegative person acquires HSV-1 or HSV-2, or initial non-primary when a person with antibody against one virus type acquires the opposite type (Geretti 2006). Previous oral infection with HSV-1 provides a high level of protection against genital HSV-1 infection but not against genital HSV-2 infection. Nevertheless, it usually prevents the severe symptoms associated with primary HSV-2 infections (Vyse et al 2000).

In adults, primary genital HSV infection may be asymptomatic, but painful, vesicular or ulcerative lesions on the vulva, perineum, vagina and cervix frequently occur. Dysuria and vaginal or urethral discharge may also occur (Barton et al 2001). There may be systemic symptoms of fever, headache and myalgia. Symptoms tend to be more severe in women than in men (Sissons 2005).

Page 426

HSV in pregnancy

Neonatal herpes is a severe systemic viral infection with a high morbidity and mortality (RCOG 2002). The incidence in the UK is about 1.65 in 100 000 births and can be caused by either HSV-1 or HSV-2 (Khare 2005). Women who have had herpes prior to pregnancy will have developed antibodies to the virus. The fetus will also develop these antibodies and consequently at birth will have passive immunity. The greatest risk to the fetus is therefore if the mother acquires a primary infection during late pregnancy and the baby is born before the development of maternal antibodies (RCOG 2002). Primary infection in early pregnancy can lead to congenital HSV infection which although rare can cause severe congenital abnormalities. About 70% of cases of neonatal HSV infection are caused by HSV-2 and result from contact with maternal genital secretions during delivery. Neonatal herpes may be acquired from an ascending infection following rupture of the membranes. The risk of neonatal infection is about 50% with symptomatic primary infection and 20% from a woman with clinically evident recurrent HSV-2 infection (Sissons 2005).

Diagnosis

HSV infections are usually diagnosed clinically. HSV DNA detection by PCR is the preferred diagnostic method for genital herpes. Viral cultures from open lesions are used routinely in the UK. Other methods of diagnosis include direct immunofluorescence assay (IFA) or enzyme immunoassay (EIA). Serological tests for HSV specific antibody can be used to diagnose HSV infection in asymptomatic individuals. The presence of HSV-2 antibodies is indicative of genital herpes but HSV-1 antibodies do not provide any distinction between genital and oropharyngeal infection (Geretti 2006).

Management of HSV infection in pregnancy

A referral to a genitourinary physician should be made for any pregnant woman in whom a first-episode herpes infection is suspected. Primary infection acquired during the first or second trimester should be treated with acyclovir. Acyclovir reduces viral shedding, reduces pain and promotes the healing of lesions. Evidence from the Acyclovir Pregnancy Registry has shown there is no clinical or laboratory evidence of maternal or fetal toxicity (RCOG 2002). Caesarean section is recommended for all women presenting with first-episode genital herpes lesions at the time of delivery as the risk of viral shedding and vertical transmission is high. It should also be considered for women with first-episode genital herpes lesions within 6 weeks of the expected date of delivery or onset of pre-term labour (RCOG 2002). For women with recurrent genital herpes lesions at the time of delivery the risks to the baby of neonatal herpes are small therefore they should be weighed against the risks to the mother of caesarean section. Continuous acyclovir in the last 4 weeks of pregnancy may reduce the risk of clinical recurrence at term but there is insufficient evidence to recommend this practice routinely. It has been proposed that specific antibody testing be undertaken in the latter half of pregnancy in order to identify babies at risk of infection. However, it has been concluded that the low incidence of neonatal herpes in the UK would not make this a cost-effective measure.

Human cytomegalovirus

Human cytomegalovirus (HCMV) is a member of the herpes virus family and humans are the only reservoir. It is found universally throughout all geographic locations and in all socioeconomic groups (Ornoy & Diav-Citrin 2006). About 75% of pregnant women in developed countries are immune and about 1–4% of women acquire a primary infection in pregnancy (Herbert & Impey 2005). Most HCMV infections are asymptomatic. Primary infection may cause generally mild mononucleosis-type symptoms such as myalgia and fever in immunocompetent adults, whereas it is particularly pathogenic among immunosuppressed and immunodeficient individuals. Following primary infection HCMV persists for life as a latent infection with periodic viral shedding in saliva, breastmilk, urine, semen and cervical secretions (Sissons 2005). The source of maternal HCMV infection is therefore likely to be close contact with an asymptomatic child or sexual partner (Pass et al 2006).

Page 427

HCMV infection in pregnancy

The most severe congenital infections are associated with a primary maternal infection during pregnancy. If contracted in early gestation, approximately 50% of fetuses will become infected, half of whom will have symptoms at birth. Babies born to mothers who are immune before pregnancy are rarely symptomatic or severely affected. If affected it is likely that a latent infection has been reactivated but it is also possible that the mother has been re-infected with a new virus strain. The congenital infection rate of babies to mothers with prior immunity is between 0.2 and 2% (Adler et al 2007).

The modes of transmission are incompletely understood but it is assumed that the fetus can be infected with HCMV transplacentally or during birth via cervical secretions or blood, and the neonate can be infected postnatally from breastmilk. Between 5% and 20% of babies with congenital HCMV are symptomatic at birth. The higher rates are associated with primary infection, particularly in the first trimester. The prognosis is poor with 80% likely to suffer serious neurological sequelae and psychomotor retardation. The majority of congenital infections are asymptomatic and only 5–15% subsequently develop sequelae on long term follow-up of which the commonest is sensorineural hearing impairment (Sissons 2005).

Diagnosis and treatment

HCMV infections can be diagnosed by a variety of methods. Maternal seroconversion of HCMV-IgG and IgM antibodies is highly accurate in the diagnosis of immunocompetent individuals in pregnancy. Fetal infection can be diagnosed by viral cultures or DNA analysis of amniotic fluid by PCR, or HCMV-IgM antibody activity in cord blood. Congenital infection can be diagnosed through isolation of the virus from urine, DNA analysis by PCR of urine, blood, saliva and CSF. The demonstration of IgM antibodies in the neonate is indicative of congenital infection (Malm & Engman 2007).

There are currently no vaccines available or prophylactic therapies to prevent the transmission of HCMV other than simple hygiene measures such as handwashing. Antenatal screening is thought to be inappropriate. In addition, there is no evidence to recommend the administration of antiviral treatments to neonates with congenital HCMV infection (Malm & Engman 2007, NICE 2003).

Human immunodeficiency virus

There are two types of human immunodeficiency virus (HIV) which belong to the lentivirus subfamily of retroviruses that cause AIDS (acquired immunodeficiency syndrome). HIV-1 is the cause of the world pandemic of AIDS, whereas HIV-2 is largely confined to West Africa. HIV is transmitted sexually, in blood, blood products and perinatally.

Two to six weeks after exposure to HIV, 50–70% of those infected develop a transient non-specific illness (primary infection or seroconversion illness) with fever, myalgia, malaise, lymphadenopathy, pharyngitis and a rash. This coincides with the development of serum antibodies to the core and surface proteins of the virus. The illness begins abruptly and usually lasts for 1–2 weeks but can be more protracted. Without antiretroviral therapy, seroconversion is followed by a clinically latent phase of about 10 years. During this period there is intense viral and lymphocyte turnover with worsening immunodeficiency. Approximately one-third of patients will experience persistent generalized lymphadenopathy. The average time for progression from HIV to AIDS is between 5 and 20 years (Luzzi et al 2005).

Diagnosis

Over 90% of seroconversions occur within 3 months of infection. In a minority of cases seroconversion may be delayed to more than 6 months. Therefore negative diagnostic tests need to be repeated 3 months after possible exposure and at 6–9 months where there has been a high risk of transmission. Following seroconversion, antibody persists indefinitely in the serum and forms a highly specific test for HIV infection (Luzzi et al 2005).

In the UK, several HIV antibody tests with high sensitivities and specificities are available. These include enzyme immunoassays (EIA) for screening, and PCR which can detect the viral RNA/DNA before antibodies become detectable (Smit 2006). Positive screening tests should be repeated before referral to a specialist laboratory for confirmation of the diagnosis.

Routine antenatal testing for HIV was introduced in the UK in 2000. Antenatal HIV antibody testing should be voluntary and subject to explicit informed consent. Evidence suggests that most women are now offered and accept the test (RCPCH 2006).

Page 428

HIV in pregnancy

As the incidence of HIV infection in women increases so does the problem of vertical transmission. Worldwide, millions of children are infected primarily through mother-to-child transmission during pregnancy or breastfeeding (Volmink et al 2007). By the end of 2005, 1765 children aged <16 years when diagnosed with HIV had been reported in the UK, of which 82% were infected from their mother (HPA 2006). In 2004 the prevalence of HIV infection among pregnant women was greatest in London at 0.45% and 0.11% elsewhere in the UK. The rate reported for women born in sub-Saharan Africa was 2.2% compared with 0.07% for women born in the UK (RCPCH 2006).

HIV infection during pregnancy is associated with an increase in the risk of stillbirth, pre-term delivery and intrauterine growth restriction (Brocklehurst & French 1998). A systematic review of the literature suggested that pregnancy might have a small but detrimental effect on the progression of HIV infection (Brocklehurst & French 1998). The immunosuppressant effect of pregnancy may predispose the woman to opportunistic infections and confuse the clinical picture (Herbert & Impey 2005). Non-specific symptoms relatively common in pregnancy such as breathlessness, tiredness and nausea may lead to a delay in the detection and treatment of a serious problem, thus highlighting the importance of knowledge of HIV status in pregnancy.

Management and treatment of HIV in pregnancy

The incidence of vertical transmission can be significantly reduced if the mother is diagnosed antenatally. A systematic review of antiretroviral therapies for reducing the risk of vertical transmission of HIV confirmed that short treatment regimens are effective and that they are not associated with any safety concerns in the short term. Antiviral drugs include zidovudine, lamivudine and nevirapine. Regimens involve different combinations over different periods of time. They may be given to women antepartum, intrapartum and postpartum and prophylactically to babies. Highly active antiretroviral therapy (HAART) has reduced vertical transmission rates to around 1–2% in affluent countries but is not widely available in poorer ones (Volmink et al 2007).

HIV-positive women should be offered an elective caesarean section because it is an effective way of reducing vertical transmission among infected women not taking antiretrovirals or only taking zidovudine (NICE 2004; Read & Newell 2005). In the event of labour and vaginal birth the following high risk activities known to predispose to vertical transmission of HIV should be avoided: CTG monitoring through scalp clips, fetal blood sampling, prolonged membrane-rupture-delivery interval, episiotomy and instrumental delivery. Amniotomy is contraindicated (de Ruiter & Brocklehurst 1998).

In relation to the risk of vertical transmission in a mother with a low viral load, it is unclear whether a caesarean section is more or less effective than a vaginal birth (Read & Newell 2005).

Breastfeeding contributes significantly to vertical transmission of HIV. It is therefore recommended that breastfeeding be avoided if safe and affordable alternatives are available. The midwife has an important duty to provide women with information about the risks of breastfeeding and help them to choose what is appropriate for them (DH 2004b). It is possible that in many developing countries the high expense and rates of infant morbidity and mortality associated with alternative feeding methods outweigh the benefits of reduced vertical transmission. Babies born to infected mothers are likely to have maternal HIV antibody. A specific test such as PCR can confirm HIV infection in 95% of infected infants by 1 month of age (Luzzi et al 2005).

HIV testing and counselling in pregnancy

The provision of pre- and post-test information, counselling and support for pregnant women is vitally important and should be undertaken by specialist counsellors or midwives who have received appropriate training (RCM 1998). Issues for discussion include the client’s risk of HIV infection, the likelihood and meaning of positive, negative and indeterminate results, confidentiality and the difference between HIV (the virus) and AIDS (the clinical condition). The impact that the diagnosis of HIV may have on a pregnant woman must be appreciated. It is important that adequate time is allowed to handle emotional distress and provide an opportunity for questions. Issues for discussion include the natural history of the infection, treatment options and safe sex to avoid transmission to an HIV negative partner(s) and acquisition of other STIs.

Page 429

A pregnant woman who is diagnosed with HIV infection should be managed and treated by the appropriate specialist teams. It is recommended that every maternity unit should have an appropriately trained multidisciplinary team to manage HIV in pregnancy (RCPCH 2006). Women should be encouraged to allow disclosure of their diagnosis to the primary care team in order to avoid conflicting advice and to ensure they receive appropriate information.

Conclusion

The health, social and economic consequences associated with HIV and other STIs are considerable. They constitute a major worldwide public health problem and their control represents a serious challenge for health professionals. The midwife has a particular role to play in the sexual health of pregnant women and the effect on their babies. Health education about the transmission of STIs, sexual behaviour and attitudes, and safe sexual practice is a primary prevention strategy. Screening programmes leading to early diagnosis and treatment of infections, together with the tracing and treatment of sexual contacts, form important aspects of secondary prevention.

REFERENCES

Adams EJ, Charlett A, Edmunds WJ, et al. Chlamydia trachomatis in the United Kingdom: a systematic review and analysis of prevalence studies. Sexually Transmitted Infections. 2004;80:354-362.

Adler M. Genital growths. In: Adler MW, Cowen F, French P, et al, editors. 2004 ABC of sexually transmitted infections. 5th edn. London: BMJ Books; 2004:56-59.

Adler M, French P. Syphilis-clinical features, diagnosis and management. In: Adler MW, Cowen F, French P, et al, editors. 2004 ABC of sexually transmitted infections. 5th edn. London: BMJ Books; 2004:49-55.

Adler SP, Nigro G, Pereira L. Recent advances in the prevention and treatment of congenital cytomegalovirus infections. Seminars in Perinatology. 2007. d.o.i.:10.1053/j.semperi.2007.01.002

Amsel R, Totten PA, Spiegel CA, et al. Diagnostic criteria and microbial and epidemiologic associations. American Journal of Medicine. 1983;74(1):14-22.

Barton S, Brown D, Cowan FM, et al. National guideline for the management of genital herpes. Clinical Effectiveness Group, British Association for Sexual Health and HIV. 2001. Online. Available http://www.bashh.org.

Bignell C. National guideline on the diagnosis and treatment of gonorrhoea in adults. Clinical Effectiveness Group, British Association for Sexual Health and HIV. 2005. Online. Available http://www.bashh.org.

Bignell C, Ison CA, Jungmann E. Gonorrhoea. Sexually Transmitted Infections. 2006;82(Suppl IV):iv6-iv9. doi:10.1136/sti.2006.023036

Brocklehurst P, French R. The association between maternal HIV infection and perinatal outcome: a systematic review of the literature and meta-analysis. British Journal of Obstetrics and Gynaecology. 1998;105:836-848.

Brocklehurst P, Rooney G. Interventions for treating genital chlamydia trachomatis infection in pregnancy. Cochrane Database of Systematic Reviews. 2000(2), 2000. CD000054

Brook G. United Kingdom National guideline on the management of the viral hepatitides A, B & C. Clinical Effectiveness Group, British Association for Sexual Health and HIV. 2005. Online. Available http://www.bashh.org.

Cadman L. Human papillomavirus. Practice Nursing. 2006;17(2):393-395.

Chippindale S, French L. HIV counselling and the psychosocial management of patients with HIV or AIDS. British Medical Journal. 2001;322:1533-1535.

Cunningham SD, Tschann J, Gurvey JE, et al. Attitudes about sexual disclosure and perceptions of stigma and shame. Sexually Transmitted Infections. 2002;78:334-338.

Daniels D, Forster G. National Guideline on the management of vulvovaginal candidiasis. Clinical Effectiveness Group, British Association for Sexual Health and HIV. 2002. Online. Available http://www.bashh.org.

de Ruiter A, Brocklehurst P. HIV infection and pregnancy. International Journal of STD & AIDS. 1998;9:647-655.

Department of Health. The national strategy for sexual health and HIV. London: HMSO, 2001.

Department of Health. The national strategy for sexual health and HIV: Implementation Action Plan. London: DH, 2002.

Department of Health. Effective sexual health: a toolkit for primary care trusts and others working in the field of providing good sexual health and HIV prevention. London: HMSO, 2003.

Department of Health. Choosing health: making healthier choices easier. London: HMSO, 2004.

Department of Health. HIV and infant feeding: Guidance from the UK Chief Medical Officers’ Expert Advisory Group on AIDS. London: HMSO, 2004.

Dimond B. Legal aspects of midwifery, 2nd edn. Books for Midwives, Edinburgh, 2002;139-161.

Doroshenko A, Sherrard J, Pollard AJ. Syphilis in pregnancy and the neonatal period. International Journal of STD & AIDS. 2006;17(4):221-226.

Ellis S, Barnett-Page E, Morgan A, et al. HIV prevention: a review of reviews assessing the effectiveness of interventions to reduce the risk of sexual transmission. London: Health Development Agency, 2003.

Feldman RG. Group B streptococcus prevention of infection in the newborn. Practising Midwife. 2001;4:16-18.

Fischler B. Hepatitis C virus infection. Seminars in Fetal and Neonatal Medicine, 2007. doi:10.1016/j.siny.2007.01.008

Fletcher J, Ball G. Chlamydia screening in pregnancy: A missed opportunity? British Journal of Midwifery. 2006;14(7):390-392.

Flynn CA, Helwig AL, Meurer LN. Bacterial vaginosis in pregnancy and the risk of prematurity: a meta-analysis. Journal of Family Practice. 1999;48:885-892.

Page 430

French P. The clinical process. In: Adler MW, Cowen F, French P, et al, editors. 2004 ABC of sexually transmitted infections. 5th edn. London: BMJ Books; 2004:11-14.

French P. Syphilis. British Medical Journal. 2007;334:143-147.

Genç M, Ledger WJ. Syphilis in pregnancy. Sexually Transmitted Infections. 2000;76:70-73.

Geretti AM. Genital herpes. Sexually Transmitted Infections. 2006;82(Suppl IV):iv31-iv34. doi:10.1136/sti.2006.023200

Gilson R. Viral hepatitis. In: Adler MW, Cowen F, French P, et al, editors. 2004 ABC of sexually transmitted infections. 5th edn. London: BMJ Books; 2004:62-67.

Gilson R, Brook MG. Hepatitis A, B, and C. Sexually Transmitted Infections. 2006;82(Suppl IV):iv35-iv39. d.o.i.:10.1136/sti.2006.023218

Goh B. UK National guidelines on the management of early syphilis, Online. Clinical Effectiveness Group, British Association for Sexual Health and HIV. 2002. Online. Available http://www.bashh.org.

GRASP The Gonococcal Resistance to Antimicrobials Surveillance Programme – Annual Report. Health Protection Agency, London, 2004. Online. Available http://hpa.org.uk.

Gülmezoglu AM. Interventions for trichomoniasis in pregnancy. Cochrane Database of Systematic Reviews 2002, 2002. issue 3. Art. No: CD000220.d.o.i.:10.1002/14651858.Cd000220

Hay P. National guideline for the management of bacterial vaginosis. Clinical Effectiveness Group, British Association for Sexual Health and HIV. 2006. Online. Available http://www.bashh.org.

Hay RJ. Fungal infections, 4th edn. Warrell D, Cox TM, Firth JD, editors. 2005 Oxford textbook of medicine, Vol. 1. Oxford University Press, Oxford, 2005;689-703.

Health Protection Agency. A complex picture: HIV and other sexually transmitted infections in the United Kingdom. London: Health Protection Agency, Centre for Infections, 2006.

Herbert M, Impey L. Infections in pregnancy. In: Warrell D, Cox TM, Firth JD, editors. 2005 Oxford Textbook of Medicine. 4th edn. Oxford: Oxford University Press; 2005:449-455. Vol. 2

Holmes KK, Sparling PF, Mårdh PA, et al. Sexually transmitted diseases, 3rd edn. New York: McGraw-Hill, 1999.

Horner PJ, Boag F. UK National guideline for the management of genital tract infection with chlamydia trachomatis. Clinical Effectiveness Group, British Association for Sexual Health and HIV. 2006. Online. Available http://www.bashh.org.

House of Commons Health Committee. Sexual health. Third Report of Session 2002–3, Vol. 1. HMSO, London, 2003.

Ison CA, Hay PE. Validation of a simplified grading of Gram-stained vaginal smears for use in genitourinary medicine clinics. Sexually Transmitted Infections. 2002;78(6):413-415.

Johnson AM, Mercer DC, Erens B, et al. Sexual behaviour in Britain: partnerships, practices, and HIV risk behaviours. Lancet. 2001;358(9296):1835-1842.

Khare MM. Infectious disease in pregnancy. Current Obstetrics and Gynaecology. 2005;15:149-156.

Lee C, Gong Y, Brok J, et al. Hepatitis B immunization for newborn infants of hepatitis B surface antigen-positive mothers. Cochrane Database of Systematic Reviews 2006, 2006. issue 2, Art. No: CD004790.d.o.i.10.1002/14651858.CD004790.pub2

Luzzi GA, Teto TEA, Weiss R, et al. HIV and AIDS, 4th edn. Cox TM, Firth JD, editors. 2005 Oxford Textbook of Medicine, 1. Oxford University Press, Oxford, 2005:423-442. D

Mabey D, Ackers J, Adu-Sarkodie Y. Trichomonas vaginalis infection. Sexually Transmitted Infections. 2006;82(Suppl IV):iv26-iv27.

Maissi E, Marteau TM, Hankins M, et al. Psychological impact of human papillomavirus testing in women with borderline or mildly dyskaryotic cervical smear test results: cross sectional questionnaire study. British Medical Journal. 2004;328:1293.

Malm G, Engman ML. Congenital cytomegalovirus infections. Seminars in Fetal & Neonatal Medicine. 2007. doi:10.1016/j.siny.2007.01.012

Maw R. Anogenital warts. Sexually Transmitted Infections. 2006;82(Suppl IV):iv40-iv41. d.o.i. 10.1136/sti.2006.023226

McCaffery K, Waller J, Nazroo J, et al. Social and psychological impact of HPV testing in cervical screening: a qualitative study. Sexually Transmitted Infections. 2006;82:169-174.

McDonald HM, Brocklehurst P, Gordon A. Antibiotics for treating bacterial vaginosis in pregnancy. Cochrane Database of Systematic Reviews 2007, 2007. Issue 1. Art. No. CD000262d.o.i.10.1002/14651858.CD000262.pub3

Mitchell H. Sexually transmitted infections in pregnancy. In: Adler MW, Cowen F, French P, et al, editors. 2004 ABC of sexually transmitted infections. 5th edn. London: BMJ Books; 2004:34-38.

National Institute for Health and Clinical Excellence. Antenatal care: Routine care for the healthy pregnant woman. London: NICE, 2003. Clinical Guideline 6

National Institute for Health and Clinical Excellence. Caesarean section. London: RCOG Press, 2004. clinical guideline

Oddie S, Embleton ND. Risk factors for early onset neonatal group B streptococcal sepsis: case-control study. British Medical Journal. 2002;325:308-312.

Ornoy A, Diav-Citrin O. Fetal effects of primary and secondary cytomegalovirus infection in pregnancy. Reproductive Toxicology, 21. 2006, 399-409. Online. Available http://www.sciencedirect.com.

Pass RF, Fowler KB, Boppana S, et al. Congenital cytomegalovirus infection following first trimester maternal infection: Symptoms at birth and outcome. Journal of Clinical Virology. 2006;35:216-220.

Peate I. Nursing care and treatment of the patient with human papillomavirus. British Journal of Nursing. 2006;15(19):1063-1069.

Peate I. Manual of sexually transmitted diseases. London: Whurr Publishers, 2005.

PHLS (Public Health Laboratory Service), DHSS&PS and the Scottish ISD(D)5 Collaborative Group. Trends in sexually transmitted infections in the United Kingdom. London: PHLS, 2000;1990-1999.

Read JS, Newell ML. Efficacy and safety of caesarean delivery for prevention of mother-to-child transmission of HIV-1. Cochrane Database of Systematic Reviews 2005, 2005; (issue 4). Art. No. CD005479.d.o.i.10.10002/14651858.CD005479

Roberts EA, Yeung L. Maternal-infant transmission of hepatitis C virus infection. Hepatology. 2002;36(5):107-113.

Royal College of Midwives. HIV & AIDS. Position paper 16a. London: RCM, 1998.

Page 431

Royal College of Obstetricians and Gynaecologists. Management of genital herpes in pregnancy. London: RCOG, 2002. Clinical guideline No. 30

Royal College of Paediatrics and Child Health (RCPCH). Reducing mother to child transmission of HIV infection in the United Kingdom: Update Report of an Intercollegiate Working Party. London: RCPHC, 2006.

Saloojee H, Velaphi S, Goga Y, et al. The prevention and management of congenital syphilis: an overview and recommendations. Bulletin of the World Health Organization. 2004;82(6):424-432.

Schachter J, Ridgeway GL, Collier L. Chlamydia diseases. In: Hausler WJ, Sussman M, editors. Topley and Wilson’s microbiology and microbial infections, Vol. 3. London: Arnold; 1998:977-994.

Schwebke J, Hillier SL. Vaginal discharge, 4th edn. Warrell D, Cox TM, Firth JD, editors. 2005 Oxford Textbook of Medicine, Vol. 3. Oxford University Press, Oxford, 2005;486-488.

Scoular A, Duncan B, Hart G. ‘That sort of place…where filthy men go…’ a qualitative study of women’s perceptions of genitourinary medicine services. Sexually Transmitted Infections. 2001;77:340-343.

Shankar M, Dutta R, Gkaras A, et al. Prevalence of Chlamydia trachomatis and bacterial vaginosis in women presenting to the early pregnancy unit. Journal of Obstetrics and Gynaecology. 2006;26(1):15-19.

Sherrard J. UK National Guideline on the Management of Trichomonas vaginalis, Clinical Effectiveness Group, British Association for Sexual Health and HIV. 2007. Online. Available http://www.bashh.org.

Simms I, Ward H. Congenital syphilis in the United Kingdom. Sexually Transmitted Infections. 2006;82:1.

Sissons JGP. Herpes viruses, 4th edn. Warrell D, Cox TM, Firth JD, editors. 2005 Oxford Textbook of Medicine, Vol. 1. Oxford University Press, Oxford, 2005;327-341.

Smaill F. 2001 Intrapartum antibiotics for Group B streptococcal colonization. Cochrane Database of Systematic Reviews, 2001. issue 1. Art. No. CD000115.d.o.i.:10.1002/14651858.CD000115

Smit EJ. HIV. Sexually Transmitted Infections. 2006;82(Suppl IV):iv42-iv45. doi:10.1136/sti.2006.023234

Terence Higgins Trust. Prejudice, Discrimination and HIV: A Report. Terence Higgins Trust, 2001.

Thomas DL. Hepatitis C virus, 4th edn. Warrell D, Cox TM, Firth JD, editors. 2005 Oxford Textbook of Medicine, Vol. 1. Oxford University Press, Oxford, 2005;419-423.

Volmink J, Siegfried S, van der Merwe L, et al. Antiretrovirals for reducing the risk of mother-to-child transmission of HIV infection. Cochrane Database of Systematic Reviews 2007, 2007. issue 1. Art. No: CD003510.d.o.i.:10.102/14651858.CD003510.pub2

Vyse AJ, Gay NJ, Slomka MJ, et al. The burden of infection with HSV-1 and HSV-2 in England and Wales: implications for the changing epidemiology of genital herpes. Sexually Transmitted Infections. 2000;76:183-187.

Walker GJA. Antibiotics for syphilis diagnosed during pregnancy Cochrane Database of Systematic Reviews, 2001. issue 3. Art. No: CD001143.d.o.i.:10.1002/14651853. CD001143

Walker DG, Walker GJA. Forgotten but not gone: the continuing scourge of congenital syphilis. The Lancet Infectious Diseases. 2002;2:432-436.

Winter G. Syphilis: ‘Cupid’s disease’ makes a comeback. Practice Nursing. 2006;17(12):611-614.

Woodgate P, Flenady V, Steer P. Intramuscular penicillin for the prevention of early onset group B streptococcal infection in newborn infants. Cochrane Database of Systematic Reviews 2004, 2004. issue 2. Art. No: DC003667.d.o.i.:10.1002/14651858.DC003667.pub2

Young GL, Jewell D. Topical treatment for vaginal candidiasis in pregnancy (Cochrane review). The Cochrane Library. Update Software, Oxford, 2001. issue 3

FURTHER READING

This chapter has concentrated on sexually transmissible infections in pregnancy. The reader is directed to the following texts for more general detail about the presentation, diagnosis, treatment and management of these infections:

Adler MW, Cowen F, French P, Mitchell H, Richens J. ABC of sexually transmitted infections, 5th edn. London: BMJ Books, 2004.

Holmes KK, Sparling PF, Mårdh PA, et al. Sexually transmitted diseases, 3rd edn. New York: McGraw-Hill, 1999.

Page 432