23 Infectious Diseases in Pregnancy

This chapter covers the major types of infections that occur during pregnancy and are likely to cause complications for the fetus—excluding human papilloma virus, which is covered in Chapter 6, and puerperal endometritus (Chapter 22). Also covered are the most recent, evidence-based approaches for diagnosing and managing major infectious diseases in pregnancy.

Definitions

Viral Infections

Viral infections are hard to treat because viruses live inside the body’s cells, and they are often “protected” from treatments by their host cells. Antibiotics do not generally work against viral infections. Although a few antiviral medicines are available. However, vaccines are the best way to prevent a woman from getting many viral diseases. In addition to human papilloma virus (see Chapter 6), other major viral infections for which pregnant women need to be monitored include cytomegalovirus, herpes simplex virus, and human immunodeficiency virus (HIV).

Cytomegalovirus

Cytomegalovirus (CMV) is a double-stranded DNA virus and a member of the herpes virus family. It is endemic throughout the world, afecting individuals in all social and demographic areas. It represents the most common cause of congenital viral infection.

Clinical Manifestations

Among healthy individuals, viral transmission typically requires repeated and prolonged contact. Infection is mainly asymptomatic, with incubation periods varying from 20 days to 2 months. The infection may result in complications throughout the body (Fig. 23.1). Symptoms usually involve fever, malaise, headache, and myalgia. Lymphadenopathy may be present. Laboratory findings may include elevated liver enzymes, atypical lymphocytes, and thrombocytopenia. Individuals with chronic CMV infection may develop pneumonia, gastroenteritis, retinitis, or encephalitis.

Fig. 23.1 Cytomegalovirus infection can impact many organs and systems in the body, including the brain, eyes, lungs, stomach, intestines, and liver.

During the initial infection, viremia occurs. Peak titers of immunoglobulin M (IgM) antibodies can usually be detected 1–3 months after the onset of infection. Viral titers decline to undetectable levels by 12 months, but they can persist up to 18 months.

After the resolution of the primary infection, the virus establishes latency within host tissues and can be isolated in blood and secretions. Most infections resolve spontaneously within 2–6 weeks. Secondary complications of primary CMV infection include hepatitis and pneumonia.

Diagnosis of Maternal and Fetal Infection

Approximately 50% of pregnant patients are seropositive for CMV antibodies. The incidence of primary infection during pregnancy ranges from 1% to 4%, with 5% to 68% of patients presenting clinical symptoms.

Initially, diagnosis of maternal infection is established by determining the IgG, IgM, and IgG avidity indexes in the blood (Fig. 23.2). When these results indicate high probability of a recent infection, the mother should be counseled and offered more invasive diagnostic testing for fetal infection.

A first-time (primary) CMV infection during pregnancy results in a 30–40% risk of vertical transmission to the fetus. In contrast, the risk of transmission with recurrent maternal infection is between 0.2% and 1.8%.

The most likely pathway for congenital CMV is via blood transmission to the fetus. Placental infection occurs first, followed by replication of the virus and transfer to the fetus. Once the fetal infection occurs, the virus replicates in the renal tubular endothelium and is excreted into the amniotic fluid. The cycle then can repeat itself. Finally, neonates can acquire the infection through breastfeeding.

Only 10–15% of infected neonates are symptomatic at birth. Among infected infants, asymptomatic at birth, 5–15% will develop sequelae later in life (Table 23.1; Evidence Box 23.1).

The symptoms of congenital, fetal CMV infection appear to be related to the timing of maternal infection. Infection during the first half of pregnancy, for example, is associated with symptomatic disease, whereas infection in the latter half is more commonly associated with initially asymptomatic disease.

Prevention

Because there are no effective therapies for congenital CMV infection, prevention in the mother is ideal. Several vaccines have been developed that prevent maternal CMV infection. However, many physicians are reluctant to use these vaccines to immunize women of childbearing age, because their safety has not been properly established. Also, reports of new infections in previously immune patients have raised questions about the efficacy of CMV vaccination in general.

Fig. 23.2a, b Diagnostic options flow chart, if maternal cytomegalo-virus (CMV) infection is suspected.

Table 23.1 Abnormalities associated with congenital cytomegalovirus infection

Antenatal ultrasonographic findings	Early postnatal findings	Late findings
Microcephaly	Microcephaly	Developmental delay
Periventricular calcifications	Periventricular calcifications	Mental retardation
Intracranial hemorrhage	Ventriculomegaly	Seizures
Ventriculomegaly	Chorioretinitis	Visual impairment
Echogenic bowel	Hyperbilirubinemia	Sensorineural hearing loss
Hepatosplenomegaly	Hepatosplenomegaly
Fetal Growth Restriction	Hepatitis
	Growth delay

 

Herpes simplex virus (HSV) is a double-stranded DNA virus (Fig 23.3) transmitted by direct and intimate contact. Following primary infection, the virus remains latent in neuronal ganglia to reactivate at later times. There are two identified strains of HSV: type 1, which causes oropharyngeal lesions; and type 2, which is responsible for genital tract infections. Twenty-two percent of pregnant women are seropositive for HSV-2 and more than 2% of women acquire the infection during pregnancy.

Clinical Manifestations

Only 30% of pregnant women are symptomatic to primary infection, with manifestations ranging from mild discomfort to widespread genital lesions associated with pain, dysuria, tender regional lymph node enlargement, fever, and malaise.

Fig. 23.3 The herpes simplex virus, pictured here, causes long-term persistent infection in most affected individuals.

HSV infections are classifed as primary, nonprimary first episode, and recurrent (Table 23.2). Lesions are usually preceded by paresthesias, followed by the eruption of vesicles, which rupture forming a shallow-based ulcer that develops into a crust. Eventually all lesions heal without scarring.

Diagnosis

Isolation of HSV in cell culture is performed in patients who present with genital lesions. The sensitivity of viral culture is low, and decreases with reactivations and as lesions begin to heal.

Commercially-available polymerase chain reaction (PCR) assays for HSV are more sensitive and can be used instead of cell cultures. The lack of HSV detection both by PCR and in culture does not exclude HSV infection, because viral shedding is intermittent.

In women who lack lesions, use type-specific serology for HSV, or diagnostic culture and/or PCR assay. If infection is suspected and all tests are negative, repeat serology in 6 weeks.

Perinatal Transmission

Transmission to the fetus can occur during the antepartum or intrapartum period by different mechanisms. Antepartum infections are associated with a potential risk for hematogenous spread to the fetus. On the other hand, when intrapartum transmission occurs, it is usually secondary to direct exposure to maternal viral shedding in vaginal secretions. Finally, neonatal transmission may occur secondary to close contact with infected individuals.

Perinatal transmission rates vary according to the type of infection:

• primary: 50%
  
• nonprimary first episode: 33%
  
• recurrent: 0–4%

All pregnant women must be asked during prenatal care about any history of genital herpes and counseled to avoid intercourse with infected individuals. If they do become infected, either one of the antiviral drugs acyclovir or valacyclovir may be administered, depending on the scenario (Table 23.3).

At the onset of labor, women should be questioned about symptoms of genital herpes and carefully evaluated for presence of vaginal or cervical lesions. Women without evidence of genital herpes can deliver vaginally, while those with either primary or recurrent lesions should undergo cesarean section to decrease the risk of perinatal transmission (Fig. 23.4).

Pregnancy in the HIV Era

Women account for a disportionately increasing number of new cases of HIV infection throughout the world. The prevalence of infected women of childbearing age has also increased as a result of the decreasing mortality associated with the advent of combined antiretroviral therapy and higher rates of heterosexual transmission.

In 2005, UNAIDS (the Joint United Nations Program on HIV/AIDS) estimated that 38.6 million people had HIV, of whom 17.3 million were women (with most being in their reproductive years). At least 3.28 million pregnant women infected with HIV are estimated to give birth each year, with more than 75% of these in sub-Saharan Africa. Most of the annual 700 000 new infections of HIV in children in sub-Saharan Africa occur via vertical transmission.

Fig. 23.4 Intrapartum approach for women with herpes simplex virus.

The management of HIV infection during pregnancy involves two major goals: the prevention of disease progression in the mother, and vertical transmission to the new born.

Human Immunodeficiency Virus

The HIV virus particle is 100–120 nm in diameter, with a spherical morphology. Its cone-shaped core is surrounded by a lipid matrix containing key surface antigens and glycoproteins. The viral core contains two copies of genomic RNA, reverse transcriptase, integrase, and proteases (Fig. 23.5). Gp120, a glycoprotein present in the viral surface, binds to cells bearing CD4 receptors, causing a change in their shape. This allows the virus to bind to other receptors on the cell and to fuse its membrane with the cell’s membrane. Once this occurs, HIV empties it contents into the cytoplasm of the cell.

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