Infections in pregnancy

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Chapter 30 Infections in pregnancy

Michael Flynn

Urinary tract infection

Syphilis

Incidence. Incidence in Australia is 2 in 1000.

Screening

• This should be performed with a specific Treponena pallidum assay (e.g. T. pallidum haemagglutination assay (TPHA) or T. pallidum particle assay or syphilis enzyme immunoassay (EIA)).

• Syphilis may be transmitted to the fetus in the second trimester, with the following consequences:

• premature delivery in 20%

• intrauterine fetal death (IUFD) in 20%

• subclinical infection in 20%

• congenital infection in 40%

Clinical syndromes

Management of syphilis

• Early syphilis (primary, secondary or latent of <12 months): treat with benzathine penicillin 2.4 million units intramuscularly weekly for 2 weeks, or erythromycin 500 mg four times a day for 15 days.

• Late syphilis (incubation >12 months): treat with intramuscular benzathine penicillin 2.4 million units weekly for 3 weeks, or erythromycin 500 mg four times a day for 30 days.

• Check for other sexually transmitted diseases, and treat the partner.

Toxoplasmosis

• Toxoplasma gondii is an obligate intracellular organism. The birth prevalence is 0.23 in 1000 births to non-immune mothers. The rate of maternal infection is 1.6 in 1000.

• The risk of transmission rises with increasing gestational age. However, the fetus is more severely affected if infected before 20 weeks gestation, and is usually asymptomatic if infected in the third trimester.

• Congenital toxoplasmosis can result in microcephalus, hydrocephalus, seizures, reduced intellect, chorioretinitis, cataract, hepatitis and pneumonitis.

• Primary infection is rare in pregnancy in Australia.

• Selective testing is recommended only for those women at increased risk and, preferentially, this testing is prior to pregnancy. Symptoms of acute toxoplasmosis include malaise, fever and cervical lymphadenopathy.

• Immunoglobulin M (IgM) is not a reliable marker of recent infection.

• If IgG-positive and IgM-positive and symptoms suggestive of infection, then repeat and check IgG titres and IgG avidity (suggestive of infection within 3 months).

• If the above is suggestive of recent acute maternal toxoplasmosis, then treatment depends on gestational age.

• Consider treatment with sulfadoxine and pyrimethamine and folic acid or spiramycin.

• Ultrasound and amniocentesis help with diagnosis.

Rubella

• The incubation period is 14–21 days; then a rash develops which lasts 2–7 days.

• Fewer than 5% of women are not immune to rubella at antenatal clinic screening.

Possible outcomes of maternal rubella infection

• no effect on the fetus

• placental infection only

• placental/fetal infection causing asymptomatic infection but affecting organs

• death of fetus (abortion, IUFD)

• congenital rubella syndrome (bilateral cataracts, IUGR, congenital heart disease, especially patent ductus arteriosus, sensorineural deafness and microphthalmia)

Risk to fetus of maternal infection

• At <8 weeks gestation, up to 85% of the fetuses are infected and all infected fetuses will develop complications such as cardiac, eye, ear and neurological defects.

• At <12 weeks gestation, 50%–80% of fetuses are infected, and of these 65%–85% have clinical defects.

• Between 13 and 16 weeks gestation, 30% of fetuses are infected and one-third suffer sensorineural deafness.

• At >16 weeks gestation, 10% of fetuses are infected, with rare clinical manifestations.

Diagnosis of maternal rubella

• four-fold rise in IgG titres

• rubella-specific IgM antibody (false-positives occur with rheumatic factor)

• reinfection: low IgM and rapid rise in IgG

• reinfection occurring more often with vaccination (80%) than with natural immunity (3.4%)

Diagnosis of intrauterine/congenital rubella

• rubella polymerase chain reaction (PCR), culture and fetal IgM can be performed following chorionic villus sampling, amniocentesis of fetal blood sampling

• virus isolated from infant’s pharynx, urine and cerebrospinal fluid in the first 3 months of life

• IgM rubella-specific antibody present in cord blood

• persistence of rubella antibodies after 6 months

Vaccination

It is advisable not to vaccinate during or within 3 months of pregnancy. However, if vaccination occurs in pregnancy or 3 months before pregnancy, the risk to the fetus is negligible. Rubella vaccination affords protection in 95% of cases. The vaccine consists of attenuated virus given subcutaneously.

Hepatitis B

The incubation period ranges from 50 to 180 days.

Hepatitis B virus (HBV)

• The infective particle consists of two shells, the outer surface antigen (HBsAg) and the inner core (HBcAg).

• The organism cannot be cultured, and diagnosis is dependent on the presence of serological markers of antigen and antibody to the viral particle.

• The surface antigen (HBsAg) is the first to appear and is present throughout the acute infective stage until the presence of surface antibody (anti-HBs), which signals recovery and immunity.

• The hepatitis Be antigen (HBeAg) is a soluble protein derived from the core. It is detected in the acute phase of the infection and continues to be present as long as viral replication persists. This represents high infectivity.

• Chronic carriers of hepatitis B have HBsAg in their blood for more than 6 months.

Factors in perinatal transmission

The major risk to the neonate is vertical transmission, mostly at the time of delivery:

• About 85%–90% of infants will develop hepatitis B if their mothers are HBeAg-positive.

• Fewer than 5% of infants will be infected if the mother is anti-HBe-positive.

• Intrauterine transmission occurs in only 3%–8% of infants of HBeAg-positive mothers.

Prevention of hepatitis B

• Hepatitis B immunoglobulin and vaccine has 94% efficacy in preventing perinatal transmission.

• Hepatitis B immunoglobulin alone has an efficacy of 71%, while hepatitis B vaccine alone has 75% efficacy.

• Therefore, to prevent transmission to the newborn, it is necessary to give the baby 0.5 mL hepatitis B immunoglobulin (intramuscularly) at delivery and hepatitis B vaccine within 1 week of delivery and to repeat at 1 and 6 months.

• There is no evidence that caesarean section reduces the perinatal transmission of hepatitis B.

• With vaccine and immunoglobulin given, breastfeeding poses no additional risk of vertical transmission.

Hepatitis C

• Screen at first antenatal visit, especially if from high-risk group (intravenous drug use, high-risk ethnic groups, tattoos).

• Vertical transmission is 6% if the hepatitis C virus is ribonucleic acid (RNA)-positive. Risk is proportional to RNA load.

• There is no clear evidence of mode of delivery and reduction of perinatal transmission.

• Decreased use of internal monitoring devices may reduce risk of vertical transmission.

• Hepatitis C virus has been found in breast milk, although studies have not shown a higher risk of vertical transmission during breastfeeding.

Human immunodeficiency virus (HIV) and pregnancy

Transmission to the neonate

• Transplacental: data from termination of pregnancies at 16–24 weeks gestation show that up to 66% of fetuses are infected.

• Labour and delivery: transmission occurs when the neonate is exposed to infected blood.

• Postpartum transmission: occurs through breastfeeding. In industrialised countries, HIV-infected mothers are advised not to breastfeed.

Managing HIV in pregnancy

• Adopt an appropriate multidisciplinary approach with adequate counselling.

• At the first visit, perform the routine screening tests plus those for Toxoplasma, cytomegalovirus, tuberculosis, Cryptococcus and Candida.

• Cervical cytology and colposcopy are essential.

• Review immune status with CD4 lymphocyte count and viral RNA copy number.

• Avoid invasive testing (amniocentesis, chorionic villus sampling, cordocentesis).

• Studies in 1994 confirmed that antiretroviral therapy in pregnant women from the second trimester and continued in infants for 6 weeks after birth reduces transmission from 25% to 8%. Antenatal administration of zidovudine plus intravenous loading dose just predelivery and neonatal oral administration for 6 weeks is preferred protocol.

• In 1999, studies confirmed that elective caesarean section reduces transmission by 50%–80%.

• The risk of transmission through breastfeeding is thought to be 16%.

• The risk of transmission is minimised when there are undetectable viral copy numbers and rupture of membranes <4 hours.

• These strategies will minimise mother-to-infant transmission.

• Ultrasound assessment of growth and wellbeing is appropriate in the third trimester.

• Elective caesarean section is at 38 weeks.

Cytomegalovirus

Cytomegalovirus (CMV) is a herpes virus and the commonest cause of intrauterine infection. Primary infection occurs in 1 in 300 pregnancies, with fetal infection occurring in 40% of these, and 10% of infected fetuses having congenital problems.

Most primary infections are asymptomatic, but suspect in viral illness with atypical lymphocytes which is monospot-negative.

Fetal complications

These include IUFD, IUGR, hepa-tosplenomegaly, central nervous system complications and neonatal jaundice. The major long-term effect is neurosensory deafness.

Diagnosis

• If IgM-positive, then repeat 2–4 weeks later and check IgG avidity.

• IgM can remain positive for up to 2 years after infection.

• Direct viral detection can be via CMV fluorescence antibody, CMV isolation or PCR of maternal fluids.

• Once primary infection is confirmed, fetal diagnosis can be via amniocentesis or fetal blood sampling. However, positive results do not predict any degree of fetal damage.

Pathogenesis of fetal complications

• This includes placental infection.

• Fetal infection causes cytolysis with areas of focal necrosis and healing by fibrosis and calcification. The risk of fetal infection from primary maternal infection is 40%–50%, but the severity of fetal damage is variable and unpredictable.

• Of infants exposed to CMV in utero, 95% may be asymptomatic at birth. Of these, 5% may develop long-term sequelae (sensorineural deafness, epilepsy or learning disability).

• The 5% of exposed neonates who are symptomatic at birth are usually affected by a primary infection. The prognosis is almost invariably associated with long-term defects.

Antenatal advice

• A woman with primary infection during pregnancy has about a 4% risk of delivering a baby with a CMV-related disorder. Half of these cases are restricted to hearing loss.

• All pregnant women should be advised about simple infection control mechanisms to reduce transmission risk (e.g. hand-washing after nappy changes and contact with respiratory secretions in children under age 2).

• There is no therapy that alters the disease course; therefore, counselling and support are required.

• The risk of transmission is equal throughout the pregnancy; however, an adverse neurological outcome is more frequent in the first half of pregnancy.

Listeriosis

Listeria is a small, non-sporing, gram-positive rod-shaped bacterium. Those infected may present with malaise, headache, fever, diarrhoea and abdominal pain.

Bacteriological investigations include blood and urine cultures, and cervical swab culture. Amniocentesis with Gram stain and culture is definitive diagnosis.

Complications of listeriosis in pregnancy

• fetal: IUFD and premature labour; mortality rate if untreated is 40% in the second and third trimesters

• neonatal: microabscesses in liver, lungs, adrenals and central nervous system; treatment of maternal listeriosis is with amoxycillin, gentamicin and delivery dependent on gestation

Varicella zoster

It is known as chickenpox in the primary infection and as shingles with reactivation of the infection. Up to 4% of pregnant women are not immune. The incubation period lasts 14–18 days. The contagious period lasts 7 days after the rash disappears.

Infection in early pregnancy

Abnormalities in the fetus occur in 1%–2% of cases, especially if infection has occurred between 8 and 21 weeks gestation. Effects on the fetus include microcephaly, convulsions, mental retardation and limb abnormalities.

Infection in late pregnancy

In late pregnancy, the severity of perinatal infection is dependent on timing before delivery. Up to 5 days before delivery, maternal IgG is protective and neonatal infection is usually mild. If infection occurs 5 days before or after delivery, there is a risk of severe neonatal varicella infection, with a 30% mortality rate.

Group B streptococcus

This is the leading cause of early-onset neonatal sepsis. Colonisation of the vagina occurs in up to 20% of women at some stage during pregnancy. The reservoir of group B streptococcus (GBS) also occurs in the gastrointestinal tract. This recolonises the genital tract after treatment, so there is no need to treat the asymptomatic woman unless in labour.

Neonatal sepsis occurs with an incidence of 3 in 1000, although 1%–2% of infants will be colonised at birth.

Management

• Antepartum treatment is relatively ineffective because the gastrointestinal tract is the primary reservoir.

• Intrapartum antibiotics are used in the prevention of neonatal sepsis; also to reduce maternal morbidity. This has led to a 7% decline in the incidence of GBS disease. Guidelines for prevention suggest either a risk-based or screening approach to identify those patients requiring intrapartum antibiotics. It is probable that screening has a more protective approach than the risk-based approach.

• Screening is via low vaginal or anorectal swab between 35 and 37 weeks.

• Clinical risk factors include <37 weeks gestation, rupture of membranes >18 hours, maternal fever >38°C.

• All women with a previously affected GBS child or GBS bacteruria in pregnancy should be treated intrapartum.

• Intrapartum treatment with a penicillin antibiotic is used in those with a positive antenatal culture and in high-risk groups. If penicillin allergy, then use erythromycin or clindamycin.

Herpes simplex

• Incidence of newborn infection is rare (1 in 10,000 to 1 in 40,000).

• Up to 60% of neonates with herpes infection do not have associated maternal history or signs of herpes at the time of delivery. Primary genital herpes is more likely to cause severe infection and neonatal symptoms than recurrent infection.

• Congenital or transplacental spread is rare and is associated with primary infection.

• Vertical transmission at time of vaginal delivery may occur in up to 40%–50% of deliveries from women with primary infection, and in up to 3%–8% with recurrent infection.

Risk factors for intrapartum infection

• maternal primary infection

• multiple lesions

• premature delivery

• premature rupture of membranes

Management

• If lesions are present and membranes have been ruptured for <4 hours, a caesarean section reduces the risk of transmission, particularly in primary infections in women who are herpes simplex antibody negative.

• Acyclovir shortens the duration of viral shedding, especially during the primary attack.

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