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Infections in pregnancy 

Infections in pregnancy
Infections in pregnancy

Lawrence Impey



HIV—expanded discussion of approaches to reduce the risk of mother-to-child transmission.

Streptococci—comments on recent increase in maternal deaths in the United Kingdom due to group A streptococci.

Updated on 28 Nov 2012. The previous version of this content can be found here.
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The mother

Maternal illness is often more severe in pregnancy, e.g. varicella, malaria, and the treatment of infections in pregnancy is complicated by potential effects of drugs on the fetus. Peri- and postpartum maternal infection is a major cause of maternal mortality.

The fetus

The effects of infection in pregnancy can be broadly categorized as follows (these are not mutually exclusive): (1) transplacental infection causing fetal malformation, e.g. treponema pallidum, rubella; (2) transplacental infection causing severe in utero illness, e.g. parvovirus; (3) neonatal infection / carrier status as a result of transplacental or intrapartum infection, e.g. HIV, herpes zoster; such neonatal infection may be severe; (4) preterm delivery, late miscarriage, perinatal death and cerebral palsy at term delivery are more common in the presence of in utero and placental infection (chorioamnionitis), e.g. Group B streptococcus.

The baby

Viral—(1) HIV—vertical transmission occurs most frequently during delivery and breastfeeding. Prevention is achieved by the use of antiretrovirals, mode of delivery planned according to the viral load at 36 weeks, and the avoidance of breastfeeding. (2) Parvovirus—transplacental infection can cause fetal anaemia and cardiac failure. (3) CMV—transplacental infection is variable, but severe neurological damage, impaired growth, and deafness may follow. (4) Herpes simplex—intrapartum infection can cause severe neonatal illness following a primary attack. (5) Herpes zoster—chickenpox in early pregnancy is occasionally teratogenic, but severe neonatal illness can follow late pregnancy disease; maternal disease is often severe. (6) Hepatitis B—vertical transmission usually causes chronic carrier status and is reduced by neonatal immunization.

Other—(1) Bacterial vaginosis—associated with preterm delivery. (2) Streptococcal infection—Group A causes puerperal sepsis, a major cause of maternal mortality worldwide, and is also responsible for much of the recent increase in the rare antepartum deaths from sepsis in the United Kingdom; group B can cause severe neonatal illness following intrapartum infection. (3) Chlamydia—associated with preterm delivery and neonatal conjunctivitis. (4) Syphilis—although rare in the West, syphilis is endemic in many countries, with transplacental infection causing congenital syphilis and perinatal death. (5) Toxoplasmosis—transplacental infection can cause severe fetal disease; treatment may prevent transmission and reduce disease severity. (6) Malaria—a major cause of neonatal mortality in parts of Africa; prevention is with nets and chemoprophylaxis.


Immunity is mildly suppressed in pregnancy and the fetal immune system is developmentally immature. Infections in pregnancy can therefore be devastating both for the mother, as is occasionally seen with varicella, and for the fetus, as exemplified by congenital infections such as those caused by rubella, cytomegalovirus (CMV), syphilis, and toxoplasmosis.

Preterm delivery accounts for 80% of neonatal unit cot days, is the single most important contributor to long-term handicap, and is a major cause of perinatal mortality. In addition to the specific effects of individual infections, infection in pregnancy is an important risk factor for these adverse outcomes. Infection is implicated in over 50% of preterm deliveries and considerably worsens the prognosis for the neonate at any given preterm gestation.

The vaginal pathogens, including bacterial vaginosis and Group B streptococcus, (GBS) are varied and only intermittently associated with adverse outcomes: it is likely that cervical integrity is both affected by bacteria and affects the access of bacteria to the uterus. Non-‘ascending’ infection may also be important, with periodontal disease recently associated with an increased risk of preterm delivery.

At term, clinical or histological chorioamnionitis are associated with a large increase in the risk of neonatal death, neonatal encephalopathy, and cerebral palsy. The relative contributions of infection and an inflammatory response associated with other risk factors (e.g. pre-eclampsia) are not known, although the limited but potentially devastating role played by bacteria such as GBS is clearly understood. Currently, with the exception of GBS, it remains unknown whether the use of antibiotics or antipyretics reduces the associated risks.

The most important infective organisms in pregnancy are described in this chapter: detailed discussion of their pathology and features in adults are described in Section 7.

Viral infections

Infections in pregnancyHIV

HIV/AIDS is caused by the HIV1 and HIV2 retroviruses. In 2005, there were 17.3 million women living with HIV worldwide, of whom three quarters were living in sub-Saharan Africa; in certain areas of sub-Saharan Africa up to 40% of the women attending antenatal services are HIV positive. HIV/AIDS is now globally the leading cause of death and disease in women of a childbearing age. In 2010, an estimated 91 500 people were living with HIV in the United Kingdom, 22 000 of who remain unaware of their diagnosis. The prevalence of HIV infection among women giving birth in the United Kingdom is monitored through an unlinked anonymous survey; in 2009 the estimated HIV prevalence was 2.2 per 1000 women giving birth. The predominant mode of infection is heterosexual sexual contact, and the risk of infection is 0.03 to 1% per episode of sexual intercourse. Universal antenatal HIV screening was implemented in the United Kingdom in 2000, and by 2010 the uptake was estimated to be 96%. In 2010, over 98% of all diagnosed pregnant women in the UK had received some form of antiretroviral treatment (ART) before delivery. The increase in diagnosis and treatment as well as the implementation of successful obstetric and neonatal interventions has led to a sharp decline in the incidence of mother-to-child transmission (MTCT), from 25.6% in 1993 to 1.2% in 2006. However, the incidence of MTCT remains as high as 20 to 30% in developing countries.

Pregnancy does not have an effect on the progression of HIV, but the effect of HIV on pregnancy remains unclear. There is some evidence suggesting an increase in the rates of preeclampsia, gestational diabetes and preterm delivery. This effect is higher in women on highly active antiretroviral therapy (HAART), although further studies are required to confirm these associations.

MTCT occurs largely, but not exclusively, during delivery or breastfeeding. Its prevalence is highest in developing countries, as a result of low rates of diagnosis and treatment, poor availability of obstetric care, and the high prevalence of breastfeeding. The issues surrounding breastfeeding in the developing world are complex, as its avoidance is associated with a high incidence of infant death due to the scarcity of safe drinking-water in these areas. Other factors influencing MTCT include concomitant sexually transmitted diseases (especially hepatitis C), preterm delivery, and high viral loads.

Practical prevention of MTCT needs to vary according to resources and availability of health care. A multidisciplinary approach is required to optimize obstetric and neonatal management. Under ideal circumstances, combination therapy using HAART is advised; zidovudine alone is less effective and allows the emergence of resistant strains. Women who are already taking ART for their own health should continue to do so during pregnancy and the postpartum period. ART exclusively taken to prevent MTCT should be commenced from 20 to 28 weeks and discontinued after delivery. Women should be screened and treated for other sexually transmitted infections early in gestation and again at 28 weeks. Antenatal blood tests include renal and liver function tests to look for drug toxicity. CD4 counts and viral loads should also be checked in each trimester and at 36 weeks. The treatment regimen should be modified if viraemia is not suppressed.

The mode of delivery should be individualized and is largely determined by the viral load at 36 weeks. Two large European cohort studies have shown MTCT rates of less than 0.5% in women with viral loads less than 50 copies/mL irrespective of the mode of delivery. This has led to an increase in planned vaginal deliveries in this group in the United Kingdom. Intrapartum strategies include the avoidance of early amniotomy, fetal blood sampling, and the use of fetal scalp electrodes; low-cavity forceps should be used in preference to ventouse if necessary. Planned caesarean section after 38 weeks remains the preferred modality of delivery in women with viral loads in excess of 50 copies/mL, those on zidovudine monotherapy, and in the presence of hepatitis C coinfection. ART should be given to the neonate for 4 weeks and breastfeeding should be avoided. Overall, these interventions can reduce the MTCT rate to less than 1%.

A different strategy is required in developing countries where resources are scarce: caesarean section is less readily available and associated with higher operative and future obstetric risks, and the avoidance of breastfeeding has more serious implications. In the absence of triple therapy, the World Health Organization recommends zidovudine monotherapy antenatally after 14 weeks, with the addition of single-dose nevirapine and lamuvudine in labour. In the most deprived areas the only ART is a single dose of nevirapine administered in labour (the only single-drug regime that reduces MTCT), which is unfortunately associated with high rates of drug resistance. Amniotomy is avoided as the rate of MTCT is directly related to the duration of ruptured membranes in women with high viral loads. Breastfeeding is exclusive, limited to 6 months, and combined with ART.


Up to 20% of women in North America and more in developing countries are nonimmune, hence small outbreaks of rubella still occur. Most women in the United Kingdom are immune as a result of widespread immunization programmes, and fewer than 10 affected neonates are born each year.

The incubation period is 14 to 21 days, with infectivity 7 days before and 7 days after the appearance of the characteristic rash, which is preceded by a short prodrome of low-grade fever, headache, malaise, and lymphadenopathy. Arthritis and arthralgia occur in up to 70% of adult women, and rare maternal complications are thrombocytopenia, acute postinfectious encephalitis, myocarditis, Guillain–Barré syndrome, relapsing encephalitis, optic neuritis, bone marrow aplasia, and progressive panencephalitis.

The fetus is at greatest risk during the first trimester, when 90% will be affected. Embryo resorption may occur in very early gestation, or abortion, or the congenital rubella syndrome. This consists of congenital heart disease—especially pulmonary arterial hypoplasia, patent ductus arteriosus, and coarctation of the aorta—learning difficulties, ocular defects such as cataracts, glaucoma, and microphthalmia, and sensorineural deafness. Between 12 and 16 weeks the sequelae are less severe, with sensorineural deafness predominating. At 25 weeks vertical transmission is approximately 25%, rising to 100% at term, but the fetus is almost invariably unaffected.

Congenital rubella can only be prevented by immunization; termination of pregnancy may be offered where infection has occurred in the first trimester. Immunization programmes vary worldwide, but in the United Kingdom rubella forms part of the MMR vaccination in early childhood. Immunity is routinely checked in early pregnancy, and postnatal vaccination is offered if a mother is nonimmune or has low immunity. The vaccine is live attenuated and therefore contraindicated in pregnancy, although inadvertent administration has not led to recorded problems.


The parvovirus B19 is the only pathogenic parvovirus in humans. Infectivity is high and via respiratory secretions, often from children. More than 50% of adults in Western countries are immune; 0.25% of women are infected in pregnancy, but infection can be epidemic. Viraemia appears about 7 days after infection and has disappeared within a few days, before symptoms occur. The classic ‘slapped cheek’ rash is not invariable and most have an arthralgia; 20% of adults have no symptoms. Pregnancy does not alter these symptoms.

Infection in pregnancy leads to a 9% excess risk of fetal loss, with an approximately 30% rate of fetal infection, largely with exposure before 20 weeks gestation. A characteristic effect is due to the parvovirus binding to the P antigen present on erythrocytes, erythroblasts, and myocardium. This can cause a predominantly aplastic anaemia that is of minimal significance in healthy children or adults. By contrast, the fetus is vulnerable, largely because of the short half-life of fetal red blood cells and the need for erythropoiesis, and it may develop a severe aplastic anaemia with a variable but occasionally severe thrombocytopenia. This is a cause of nonimmune hydrops (Fig. 14.15.1), exacerbated in some cases by cardiac dysfunction, which is self-limiting in more than 50% of cases but fatal in the rest. Fetal death typically occurs 3–6 weeks after infection and is very unusual more than after 18 weeks afterwards.

Fig. 14.15.1 Antenatal ultrasound scans: (a) fetal head showing ventriculomegaly secondary to congenital toxoplasmosis; (b) fetal abdomen showing intrahepatic calcification seen in congenital varicella infection; (c) fetal abdomen showing ascites in parvovirus infection.

Fig. 14.15.1
Antenatal ultrasound scans: (a) fetal head showing ventriculomegaly secondary to congenital toxoplasmosis; (b) fetal abdomen showing intrahepatic calcification seen in congenital varicella infection; (c) fetal abdomen showing ascites in parvovirus infection.

Parvovirus in pregnancy is encountered either during investigation of fetal hydrops, or where there has been maternal infection or contact with an infected individual. For the former, the diagnosis is made when the hydropic fetus is established to be anaemic, usually by the finding of a raised peak systolic velocity in the fetal middle cerebral artery, and by exclusion of other causes of hydrops. Maternal blood will usually show IgM; if IgG is present, a stored early-pregnancy booking sample can be checked for comparison. Viral identification by PCR of a fetal blood sample is more reliable. An in utero transfusion is given if the degree of anaemia appears to be increasing and the fetal state worsens. This involves injection of high haematocrit blood into the umbilical vein at the cord insertion. When the disease appears to be severe, an in utero platelet transfusion is recommended by some because of the potential for thrombocytopenia and reports of severe and fatal fetal bleeding during in utero transfusion.

Management of the woman infected by parvovirus involves close follow-up of the fetus, usually with ultrasound scans assessing the middle cerebral artery, at least every 2 weeks and up until 4 months after infection, when the mother can be reassured that her risk of fetal loss is low.

Long-term follow-up of babies affected in utero by parvovirus are reassuring, but there are reports both of fetal loss at transfusion and of severe cerebral damage following very severe fetal anaemia.

Cytomegalovirus (CMV)

CMV is the commonest congenital infection in developed countries. Immunity is present in up to 75% of women; less in higher socioeconomic classes or in developing countries. Infection in pregnancy occurs in about 1%. Maternal infection is usually asymptomatic but can cause an infectious mononucleosis-like illness.

Vertical transmission occurs during pregnancy following 40% of primary infections and less than 1% of secondary recurrences. After primary infection, 5 to 15% of neonates are symptomatic, and of these more than 80% develop severe neurological sequelae including mental impairment and sensorineural hearing loss. Even asymptomatic infants have a 5 to 15% risk of hearing impairment. Overall, the chance of normal childhood development without evidence of fetal damage is approximately 75%. The outcomes of CMV infection in pregnancy are shown in Fig. 14.15.2. Ultrasound abnormalities, particularly intracranial or hepatic calcifications, cerebral ventriculomegaly, oligohydramnios, and IUGR are detected in only 20%.

Fig. 14.15.2 The outcome of CMV infection in pregnancy.

Fig. 14.15.2
The outcome of CMV infection in pregnancy.

CMV is encountered in pregnancy usually because IgM is found incidentally, although it may be detected as part of the investigation of a fetus with abnormalities. CMV IgM is long lasting and its identification in pregnancy may predate the pregnancy, hence a negative retrospectively tested booking sample, or low IgG avidity, or rising IgG or IgM titres are required to confirm maternal infection. Vertical transmission is detected using amniocentesis and PCR, which needs to be performed no earlier than 20 weeks gestation and 6 weeks after maternal infection, or in the presence of ultrasound abnormalities (which have multiple causes), to exclude fetal infection. Ultrasound abnormalities, high viral load, and thrombocytopenia are associated with more severe sequelae, and fetal blood sampling later in the pregnancy may help determine the prognosis where ultrasound abnormalities are not detected. There is no effective therapy and termination of pregnancy may be offered: currently in the United Kingdom this can be performed late in the pregnancy. Intravenous ganciclovir given to the infant reduces hearing loss in the most severely affected. CMV screening is currently not recommended.

Herpes simplex (HSV)

HSV-2 is the predominant cause of genital herpes, but in up to 30% of cases it is HSV-1 that is responsible. In the United States of America the seroprevalence of HSV-1 and HSV-2 is 63% and 23% respectively, with about 90% of those seropositive to HSV-2 giving no history of infection. Primary infection in pregnancy occurs in 2% of susceptible women. This is usually asymptomatic, but primary herpes may be characterized by genital pain and ulceration, discharge, dysuria, lymphoedema, and systemic symptoms. The development of vesicles may occur for the first time in a woman previously infected: it does not necessarily imply recent transmission. A rare but severe manifestation of HSV infection in pregnancy is disseminated disease, with necrotizing hepatitis, thrombocytopenia, leucopenia, disseminated intravascular coagulopathy, and more than 50% mortality.

Herpes simplex is transmitted vertically at delivery, but very rarely during pregnancy. Transmission is almost 50% in active primary infection, with the greatest risk in late pregnancy, but nearer 1% with active recurrent herpes because of passive fetal immunity. Nevertheless, most neonatal herpes occurs in women without a history. It is rare (1.65/100 000 live births in the United Kingdom), although less so in the United States, but causes severe illness including encephalitis and death, particularly in preterm neonates.

Caesarean delivery is recommended when genital lesions from primary infection are evident at the time of delivery, and usually also where primary infection has occurred in the 6 weeks prior to delivery. This should be performed before, or as soon as possible after the membranes have ruptured. If vaginal delivery is unavoidable or the membranes have been ruptured for more than 4 h, then the neonate should be treated with aciclovir. Caesarean delivery is not advised if primary infection has occurred earlier in the pregnancy or where there is asymptomatic recurrent herpes. Where recurrent herpes is symptomatic at delivery the neonatal risk is extremely small and probably not an indication for caesarean section. Oral aciclovir may be safely used in pregnancy for all women with a primary episode and may prevent recurrences at term. Screening and searching for asymptomatic viral shedding is not advised.

Herpes zoster

In Western countries, more than 90% of adults are immune to varicella zoster virus (VZV), with infection only occurring in 3 per 1000 pregnancies. In developing countries, many more are nonimmune. Transmission is by respiratory droplets and personal contact with the vesicles. Primary infection causes chickenpox; reactivation of the virus that has lain dormant in sensory nerve root ganglia causes shingles. The incubation period is 10 to 21 days, infectivity being from 48 h before the rash appears to when all the vesicles are covered. Primary infection in pregnancy may be severe, with pneumonia in 10% and occasional maternal death. Maternal shingles is not associated with neonatal risk.

The principal risk to the fetus is with primary infection in late pregnancy, when varicella infection of the newborn occurs in 50% and is associated with a neonatal mortality approaching 30%. Infection between 20 and 36 weeks gestation, in the absence of preterm delivery, does not have sequelae. Before 20 weeks, however, 1 to 2% of fetuses develop the congenital varicella syndrome, characterized by neurological, optical, and limb anomalies. Ultrasound findings 5 weeks after infection include polyhydramnios and echogenic foci in the fetal liver (Fig. 14.15.1).

Maternal infection is confirmed by the presence of IgM; maternal IgG indicates immunity. A nonimmune mother with significant exposure should be given varicella zoster immune globulin (VZIG) within 10 days, and if chickenpox develops oral aciclovir is recommended within 24 h of the rash if the gestation exceeds 20 weeks. Careful fetal ultrasound evaluation is required when the mother is infected before 20 weeks. In late pregnancy, VZIG is given to the neonate if delivery occurs 5 days after or 2 days before maternal infection. Vigilance for neonatal infection is required: this has a mortality of up to 30% and is treated with aciclovir.

Hepatitis B

Less than 1% of pregnant women in Western countries are HepBsAg positive, although the incidence is rising; in parts of Africa and Asia the rate is 25%. Vertical transmission can occur throughout pregnancy and is particularly important because 90% of infected neonates become chronic carriers (in contrast to adults, 10% of whom become chronic carriers) that are both infectious and at risk of liver disease. The risk of transmission relates to maternal viral antigen status: in HepBsAg positive/HepBeAg negative mothers the risk is 5 to 20%; in HepBsAg positive/HepBeAg positive it is 70 to 90%.

Vertical transmission can be reduced by more than 90% by active neonatal immunization, using 0.5 ml hepatitis B vaccine. This is recommended to all infants born to HepBsAg positive mothers; additional passive immunization (200 IU of hepatitis B immunoglobulin within 12 h of birth) for infants born to HepBeAg positive or HepBsAb negative mothers is also advised. Targeted screening only identifies about half of chronic carriers, so universal screening has been advocated in developed countries, with the World Health Organization recommending universal vaccination in countries with high prevalence.

Hepatitis C

Worldwide, 3% of pregnant women have been infected with hepatitis C virus (HCV), but the figure is 30% in HIV-positive women. The principal risk factor in the United Kingdom, where about 0.5% of women have been infected, is intravenous drug abuse, and sexual transmission is unusual. Hepatitis C leads to chronic hepatitis in about 80%; progression is insidious and most pregnant women are asymptomatic. Liver transaminases may be normal, but tend to reduce during pregnancy if elevated. Antibody levels are usually detectable within 3 months after infection; the persistence of HCV antibody implies persistent infection and infectivity.

Interferon-α‎ with ribavirin reduces disease activity, but ribavirin may be teratogenic, hence interferon is used (rarely) for treatment of severe cases in pregnancy and (more commonly) postpartum. Vertical transmission of HCV occurs in approximately 6% if HCV is detectable by polymerase chain reaction (PCR) in the mother; otherwise the risk is very low. Coexisting HIV infection increases the rate of vertical transmission to 23%. Transmission is not thought to be significantly affected by mode of delivery. Transmission by breast feeding is unlikely. Elective caesarean section, formula feeding, and administration of immune globulin do not reduce vertical transmission to the neonate.

Maternal antibodies may persistent for months, hence PCR is used to confirm infection in infants. Infected infants usually remain viraemic and prone to chronic hepatitis.

Bacterial diseases

Bacterial vaginosis

This occurs when there is an overgrowth of anaerobic organisms such as Gardnerella vaginalis and Mycoplasma hominis, and characterized by excessive Gram-negative bacilli and cocco-bacillary organisms compared to lactobacilli on Gram staining. The prevalence varies from 5 to 20%, depending much on the diligence with which the diagnosis is sought. Bacterial vaginosis is not sexually transmitted, but is associated with sexually transmitted diseases and is rare before the onset of sexual activity. Three of four Amsel’s criteria are required for diagnosis: a thin white homogeneous discharge, clue cells, raised vaginal pH (>4.5), and a positive ‘whiff test’ (fishy odour when 10% KOH is added to the discharge). At least 50% of women with bacterial vaginosis have no symptoms, but an offensive, thin white discharge is often found.

Bacterial vaginosis is associated with late miscarriage and preterm birth. Prematurity is a major cause of neonatal mortality and morbidity in developed countries.

Symptomatic bacterial vaginosis is treated with oral clindamycin. In women with risk factors for preterm birth, particularly a prior history of this or late miscarriage, treatment of asymptomatic infection is indicated as it reduces the risk of recurrence. It is not known whether screening and treatment in low-risk women has the same effect. Vaginal clindamycin is not effective and metronidazole has paradoxically been associated with an increased risk of preterm delivery.

Infections in pregnancyStreptococci

Group A streptococci (Streptococcus pyogenes) are an important cause of puerperal sepsis worldwide. This bacterium is also the principal one responsible for the recent increase in maternal deaths from sepsis in the United Kingdom. In the 3-year period from 2006 to 2008 there were 13 maternal deaths associated with this organism. Typically the women developed sepsis during pregnancy, often before 24 weeks and despite intact membranes, and presented with a history of malaise or upper respiratory tract infection before they rapidly became severely unwell. Group A streptococcus is carried by 5 to 30% of the population, and spread by contact or droplets. Preventive strategies including strict hygiene; appropriate treatment requires identification and aggressive antibiotic treatment.

Group B streptococci (GBS, Streptococcus agalactiae) are an important cause of neonatal disease but cause less severe maternal disease. Up to 25% of pregnant women are colonized by GBS, usually without symptoms, although maternal urinary tract infection is not uncommon. GBS is associated with preterm delivery but it is ascending infection at the time of delivery that is best understood. Although 70% of neonates born to carriers are colonized, only 1 to 2% will develop disease of chorioamnionitis and fetal infection leading to early-onset neonatal streptococcal sepsis. The incidence of this is 0.5 to 3.7 per 1000 live births with a mortality of 6%. Intrauterine infection may also cause antepartum stillbirth. Infection usually occurs following rupture of the membranes: risk factors are prematurity, prolonged rupture of the membranes, intrapartum maternal fever, heavy colonization, low maternal antibody levels, and a previously affected infant.

Intrapartum high-dose intravenous penicillin greatly reduces early-onset neonatal disease. Preventive strategies are based on risk factors, either alone or in conjunction with screening. With the former approach, women are treated if they have a previous history, intrapartum fever, are in preterm labour, or where the membranes have been ruptured for more than 18 h. This leads to at least 70% of neonatal sepsis being prevented by treating approximately 18% of women. In the latter approach, a combined screening and risk-based strategy, third-trimester vaginal and anal swabs are taken, with women identified as carriers also being treated intrapartum. This leads to approximately 25% of all pregnant women being treated, with 86% of cases of sepsis prevented. The former is the currently preferred approach in the United Kingdom because of implications of cost and allergy to penicillin. Vaccines for GBS remain under development.


Infection is from salads contaminated with animal faeces, undercooked meats, unpasteurized milk, soft cheeses, some fruit, hummus, and patés. In the United Kingdom the incidence is up to 5 per 100 000 live births. Worldwide the incidence has fallen as a result of public health campaigns about the likely source of infection. Maternal disease manifests as bacteraemia, with fever, sore throat, headache, and chills: diarrhoea, pyelitis, and backache may also occur. It is treated with ampicillin with an aminoglycoside for synergy.

Infection of the fetus occurs transplacentally. Before 24 weeks gestation this usually results in miscarriage; after 24 weeks neonatal mortality is approximately 20%.


Chlamydia trachomatis is the most common sexually transmitted infection, with up to 7% of pregnant women being infected, depending on age, marital status, and socioeconomic class. Infection is mostly asymptomatic. Pelvic infection is very rare during pregnancy, but after delivery endometritis and salpingitis may lead to tubal damage and infertility, and 12% of induced abortions are followed by pelvic infection.

Maternal infection, particularly if recently acquired, is associated with preterm delivery and a significant cause of neonatal handicap. Treatment reduces but does not eradicate these risks. Neonatal conjunctivitis occurs in up to 50% of neonates exposed to chlamydia, with a smaller proportion developing pneumonia.

The identification of maternal infection warrants referral to a genitourinary medicine clinic, with contact tracing for treatment of sexual partners. Erythromycin is effective, and a single dose of azithromycin (1 g) ensures compliance and is also known to be safe. Tetracyclines are contraindicated in pregnancy as they cause tooth discoloration in the child. Reinfection rates are high and repeat testing is advised after at least 3 weeks to ensure a cure has been achieved. Screening or even prophylaxis of all mothers following abortion is cost-effective, but routine screening in pregnancy should currently be limited to those at risk of infection who are also at increased risk of preterm delivery.


Neisseria gonorrhoea is endemic in many developing countries, and having fallen to low rates in many areas of the developed world in the late 1980s and early 1990s is now gradually increasing again. Pharyngeal and disseminated systemic infection with fever, rash, and septic arthritis are more common in pregnancy, but salpingitis is rare. Cervical culture detects most infections; PCR testing is expensive and does not enable antibiotic sensitivity testing. As with nonpregnant women, 80% are asymptomatic.

Gonococcal cervicitis is associated with a fourfold increase in prematurity and chorioamnionitis. Further, 40% of neonates exposed to gonorrhoea at delivery will develop ophthalmia neonatorum. Gonococci have also been implicated in postpartum and postabortion endometritis and salpingitis.

Treatment is best with a single intramuscular dose of ceftriaxone (250 mg). Disseminated infection warrants intravenous therapy. Penicillinase-producing strains are common. The patient should be screened for other sexually transmitted infections and antichlamydia therapy is often given at the same time. A test of cure should be taken at least 3 days after antibiotics. Because of the frequency of infection and the serious risks, screening is warranted in high-risk groups such as those undergoing first-trimester termination.


The incidence of infection in pregnancy is 0.02% in the United Kingdom, but in Africa, South-East Asia, and Russia it is endemic. Pregnancy does not alter the clinical manifestations. Screening with nontreponemal tests (e.g. VDRL) is routine in many countries, including the United Kingdom. Sensitivity is highest in secondary syphilis and lowest early in the infection, and false-positive results occur with concomitant infections or autoimmune disease.

Vertical transmission is predominantly transplacental, occurring in up to 90% of untreated women, particularly those with early disease. Most affected pregnancies result in congenital syphilis, miscarriage, preterm delivery or perinatal death. Ultrasound examination of the infected fetus may be normal or show hepatomegaly and other abnormalities. At birth, babies exhibit rhinitis, osteitis, and skin bullae. Hutchinson’s triad of abnormal teeth, interstitial keratitis, and sensorineural deafness arise later in the untreated child.

Syphilis is usually diagnosed in pregnancy after the development of suggestive symptoms or a positive screen. A positive VDRL should be confirmed with a specific treponemal test (e.g. FTA-ABS). Treatment is with two intramuscular doses of benzyl penicillin (2.4 MU, 1 week apart). In true penicillin allergy, a 5- to 10-day regimen of high-dose oral ceftriaxone is recommended. VDRL titres should fall until undetectable or less than 1 in 4, otherwise retreatment is necessary. Treatment will prevent congenital infection in 98% of cases. The rare Jarisch–Herxheimer reaction to treatment may precipitate preterm labour. Screening in pregnancy is cost-effective, even where the disease is rare: 121 women were identified by antenatal screening in the United Kingdom from 1994 to 1997, with 18 600 tests needing to be performed to detect 1 case.


Mycobacterium tuberculosis infection (TB) is extremely common in the developing world. The proportion of younger people infected—including women of reproductive age—is rising, in part due to HIV infection. Pregnancy has little effect on the course of either symptomatic or latent TB, but the diagnosis may be delayed in pregnancy because of the nonspecific symptoms.

Congenital tuberculosis is acquired transplacentally and is potentially fatal but extremely rare; treatment is advised principally for maternal health. Coinfection with HIV should be considered. Isoniazid, ethambutol, pyrazinamide, and probably rifampicin are safe in pregnancy; streptomycin can cause ototoxicity. Vitamin B6 and vitamin K supplementation are indicated. Breastfeeding is not contraindicated. Infectivity is greatly reduced after 2 weeks of therapy, hence separation of mother and child is inappropriate.

Protozoal infections


In the United Kingdom and North America 15 to 20% of adults have antibodies to Toxoplasma gondii; infection in pregnancy occurs in 0.2%. It is more common in mainland Europe and in developing countries. Infection is acquired from contact with soil, uncooked meat, or contaminated salad, and is more common in women with HIV. The condition is frequently asymptomatic, but 10 to 20% of mothers have lymphadenopathy or a flu-like episode.

Vertical transmission occurs during pregnancy in about 30%. Transmission is lower (<10%) in early gestation, but has greater impact: over 75% will have clinically apparent disease. This includes the classic neonatal triad of chorioretinitis, cerebral calcification, and microcephaly. Ultrasound findings include intracranial calcification, cerebral ventriculomegaly (Fig. 14.15.3), ascites, and hepatomegaly. With increasing gestation, vertical transmission increases to about 75% by term, but the risks of severe sequelae are less. The highest risk for congenital toxoplasmosis with a poor outcome is therefore when maternal infection occurs around 20 to 24 weeks’ gestation. At this stage the risk of severe handicap is approximately 10%.

Fig. 14.15.3 MRI head of a 20-day-old baby with congenital toxoplasmosis, showing severe ventriculomegaly from hydrocephalus.

Fig. 14.15.3
MRI head of a 20-day-old baby with congenital toxoplasmosis, showing severe ventriculomegaly from hydrocephalus.

Toxoplasmosis is encountered in pregnancy either as part of investigations for abnormal fetal ultrasound appearances, or as a result of screening. Toxoplasmosis screening is imprecise: IgM may not be detected with proven disease, and it may also persist for months after infection. Infection is nevertheless unlikely in the previous 3 months if IgM is negative, or there is high-avidity IgG. Maternal infection is confirmed by a change from negative to positive IgG, or low to high levels of IgM. Mothers infected in pregnancy are treated with spiramycin with the aim of reducing vertical transmission, this being diagnosed or excluded using PCR on amniotic fluid taken after 18 weeks. Combination therapy of pyrimethamine and sulfadiazine with folinic acid is used if fetal infection is detected. Although reversal of ultrasound abnormalities has been recorded after therapy, there is no consistent evidence that treatment is effective when vertical transmission has occurred. In the neonate, diagnosis requires IgA or IgM testing because maternal IgG will persist for up to 1 year. Neonatal infection is treated for 1 year. Because of the perceived effectiveness of therapy in preventing vertical transmission, screening is widely practised in Europe.


In sub-Saharan Africa up to 8% of infant mortality is attributable to malaria in pregnancy. Pregnant women are more susceptible to malaria and complications such as cerebral malaria, pulmonary oedema, and renal failure occur more commonly.

Severe malarial anaemia of pregnancy causes spontaneous abortion, premature birth, IUGR, and stillbirth. Congenital malaria from transplacental spread occurs in approximately 1% of infected pregnancies. The newborns have fever, respiratory distress, pallor, anaemia, hepatomegaly, jaundice, and diarrhoea.

Prevention of malaria infection advocated by the World Health Organization involves insecticide-treated mosquito nets, intermittent preventive treatment with antimalarial drugs, and febrile malaria case management. Antimalarial drugs reduce parasitaemia, placental malaria, low birth weight, and—depending on their timing—perinatal death. Drugs used depend on the sensitivity of the relevant plasmodium locally and include proguanil, chloroquine, mefloquine, and artemisinin compounds. Most falciparum malaria is now resistant to mefloquine and chloroquine. Sulfadoxine–pyrimethamine is most commonly used as intermittent preventive treatment, this chemoprophylaxis involving two doses at least 1 month apart to all pregnant women in stable transmission areas. A third dose is recommended where HIV infection is common. Artemisinin combination therapy is increasingly used for febrile malaria because of resistance to other drugs and lower frequency of few side effects, although there are less safety data, particularly for the first trimester.


Infection in pregnancy can cause miscarriage, IUGR, and preterm delivery. Congenital infection occurs in about 10% and may be initially asymptomatic, but jaundice, anaemia, hepatosplenomegaly, encephalitis and pneumonitis can then develop. Diagnosis is through placental histology, blood smear examination for parasitaemia, and ELISA. There is no safe and reliable treatment in pregnancy.

Other conditions

Notes on other infections in pregnancy are given in Table 14.15.1.

Table 14.15.1 Notes on other infections in pregnancy




Transplacental transfer occurs, probably without any effect on the fetus


Vertical transmission has been reported rarely; if vaginal warts are massive they may obstruct delivery


50% have a mild respiratory or gastrointestinal illness; some have severe cramping abdominal pains simulating placental abruption that can lead to unnecessary emergency caesarean section; newborns with vertically acquired echoviral infections may have fulminant hepatic necrosis, severe coagulopathy from disseminated intravascular coagulopathy, and meningitis or myocarditis

Japanese B encephalitis virus

Particularly high mortality rates with fetal death have been reported in pregnancy

Lassa fever

Increased mortality for women in pregnancy, survival is improved by abortion and ribavirin (see Table 14.15.1)

Trichomonas vaginalis

Infections are common in pregnancy, can be transmitted to the newborn around birth, but there are no adverse effects on the fetus

Mycoplasma hominis

A commensal of the lower female genital tract; controversial disease role in newborns

Ureaplasma urealyticum

As for M. hominis

Lyme disease

Borrelia burgdorferi in gestation has a good prognosis if recognized early and treated aggressively; fetal death or disease, including meningoencephalitis, occurs without maternal treatment


Placental infection occurs in up to 25% in bilharzia infested areas, but there is no effect on gestational age or birth weight


The incidence of vaginal thrush increases with each trimester; rarely, vaginal thrush in pregnancy predisposes to congenital candidiasis

Antimicrobial agents in pregnancy

A guide to the safety of antimicrobial agents in pregnancy is given in Table 14.15.2.

Table 14.15.2 A guide to the safety of antimicrobial agents in pregnancy


Probably safe but limited human studies

Potential or proven risk in pregnancy, but benefits may outweigh risk

Fetal abnormalities, risk greater than benefit











Antiparasitic agents, except quinine




Antimycobacterial agents: INH, pyrazinamide, rifampicin, dapsone, ethambutol


Antimycobacterial agents: ethionamide, thalidomide, clofazimine/cycloserine


Aciclovir, valaciclovir, famciclovir




Adapted from: Gilbert DN, Moellering RC, Sande MA (2000). The Sandford guide to antimicrobial therapy, 13th edition. Antimicrobial Therapy, Inc, Sandford, USA.

Further reading

De Santis M, et al. (2006). Rubella infection in pregnancy. Reprod Toxicol, 21, 390–8.Find this resource:

Doroshenko A, Sherrard J, Pollard AJ (2006). Syphilis in pregnancy and the neonatal period. Int J STD AIDS, 17, 221–7.Find this resource:

Gibbs RS, Schrag S, Schuchat A (2004). Perinatal infections due to group B streptococci. Obstet Gynecol, 104, 1062–76.Find this resource:

Grether JK, Nelson KB (1997). Maternal infection and cerebral palsy in infants of normal birth weight. JAMA, 278, 207–11.Find this resource:

Levy R, et al. (1997). Infection by parvovirus B19 during pregnancy: a review. Obstet Gynecol Surv, 55, 254–9.Find this resource:

RCOG (2004). Management of HIV in pregnancy. Green Top Guideline 39. Royal College of Obstetricians and Gynaecologists, London.Find this resource:

    Ormerod P (2001). Tuberculosis in pregnancy and the puerperium. Thorax, 56, 494–9.Find this resource:

    Ornoy A, Diav-Citrin O (2006). Fetal effects of primary and secondary cytomegalovirus infection in pregnancy. Reprod Toxicol, 21, 399–409.Find this resource:

    Rorman E, et al. (2006). Congenital toxoplasmosis—prenatal aspects of Toxoplasma gondii infection. Reprod Toxicol, 21, 458–72.Find this resource:

    Steer P (2005). The epidemiology of preterm labor—a global perspective. J Perinat Med, 33, 273–6.Find this resource:

    Useful websites

    Centers for Disease Control. Malaria during pregnancy.

    NAM. Reproductive health.

    Royal College of Obstetricians and Gynaecologists. Infection and pregnancy—study group statement.