Melissa Chan, aged 36 years, presents for her second antenatal visit. Her blood tests indicate that she is Hep Be Ag positive and Hep Bc Ag negative and Hep Bs Ab negative. She is concerned that her baby may catch hepatitis B.
Melissa is infected with Hepatitis B virus. Since she is HBeAg positive and HBsAb negative she would either be in the early phase of an acute infection or a highly infective carrier. Her baby would be at very high risk of being infected; usually during delivery (around 90% of babies are infected from HBeAg positive mothers).
In addition to the routine obstetric history, it would be important to ascertain how Melissa became infected with Hepatitis B virus – exchange of body fluids through sexual transmission, injecting drugs, needle stick injuries, blood transfusions, tattoos, acupuncture needles.
In addition, a medical history to ascertain symptoms and signs referrable to hepatitis B (flu-like illness, lethargy, loss of appetite, pruritus, nausea, right upper quadrant pain, joint pain, dark urine and yellow sclera) to determine when she was infected, although many infections can be subclinical.
In addition to the routine obstetric and medical examination, particular examination for signs of injecting drug use, tattoos, jaundice, enlarged tender liver or very firm liver if she has chronic hepatitis.
If Melissa has not had HIV and Hepatitis C serology, those should be performed.
With respect to her hepatitis B, the following tests should be done:
Mother:
Melissa should be informed that she is highly infective and counselled on modes of transmission and prevention of transmission (saliva, blood and sexual transmission - if injecting drug user, referral to a methadone program; otherwise not sharing needles, use needle exchange service, use of condoms). Her sexual partner should be assessed for hepatitis B status and if negative, should be immunised.
Baby:
With respect to the baby, vertical transmission which occurs mainly during delivery, can be prevented in >95% of babies at risk through hepatitis B immune globulin (HBIG), and hepatitis B vaccine (HBV).
In utero and in the early newborn period, the foetus and baby has an underdeveloped immune system. Defence against infections is mostly provided by the intrauterine environment and passive transfer of maternal antibodies.
Maternal antibodies present wane after 4-6 months. The following are present in colostrum and breast milk:
The teratogenic effects of rubella were first noted in 1941 by an Australian ophthalmologist, who recognized several cases of congenital cataract following a large outbreak of rubella. Maternal rubella is now rare in many industrialized countries that have rubella vaccination programmes. However, in many developing countries, congenital rubella syndrome remains a major cause of developmental anomalies, particularly blindness and deafness.
The risk of foetal infection and damage is greatest during the first 8 weeks of pregnancy and damage is rare after 16 weeks. Congenital rubella syndrome may include a number of clinical features, some of which may not present until adolescence or adulthood:
Congenital rubella is preventable by immunization in childhood. Routine antenatal screening and postpartum immunisation of susceptible women provides additional protection.
Syphilis is a sexually transmitted infection caused by Treponema pallidum. Congenital syphilis is now a rare disease in most countries but it remains a severe, adverse pregnancy outcome in many less developed countries. Untreated syphilis in pregnancy can cause stillbirth, preterm labour and intrauterine growth restriction. Later in life, a range of neurological disorders can occur, including paretic neurosyphilis; all these manifestations respond poorly to treatment.
At least 50% of infants with congenital syphilis are asymptomatic, so diagnosis may rely on serology. Clinical features typical of congenital syphilis include:
The diagnosis is confirmed by serological tests on the mother and infant:
| Primary CMV | Reactivation CMV | |
|---|---|---|
| Infection Status of Mother in Pregnancy |
|
|
| Infection of Foetus in Pregnancy |
|
|
| Incidence of Congenital Infection | Overall incidence of congenital infection due to primary maternal infection is 1 in 1000 | Overall incidence of congenital infection is 1-2% - the majority are unaffected |
Toxoplasma gondii is a protozoan parasite that infects up to a third of the world's population. Infection is mainly acquired by ingestion of food or water that is contaminated with oocysts shed by cats or by eating undercooked or raw meat containing tissue cysts. Primary infection is usually subclinical but may cause lymphadenopathy or ocular disease. Infection acquired during pregnancy may cause severe damage to the foetus. The risk of foetal infection increases but that of foetal damage decreases with advancing gestation. There is geographical variation in the incidence of congenital infection; in Australia it is estimated to be less than 1 in 1000 births.
Signs of severe symptomatic congenital toxoplasmosis include:
Toxoplasmosis during pregnancy is ideally diagnosed by showing seroconversion. More commonly it is suspected because specific IgM is detected in serum by antenatal screening. IgM can remain detectable for many months and, in the absence of symptoms, further testing is needed. Tests for the avidity of IgG antibodies can discriminate between recently acquired and previous infection. If recent infection is confirmed or cannot be excluded, treatment of the mother with spiramycin can reduce the risk of vertical transmission.
Appropriate management depends on diagnosis of intrauterine infection by amniotic fluid PCR at about 18 weeks gestation. If foetal infection occurs during the first trimester, termination of pregnancy is often recommended. If infection occurs during the second or third trimester, treatment of the mother with a combination of pyrimethamine and a sulphonamide is likely to reduce sequelae of the disease in the newborn.
Specific IgM in the infant's serum or persistence of IgG beyond the first few months of life are evidence of congenital toxoplasmosis. T. gondii may be detected in tissue by histological examination or PCR, or in CSF by PCR. Treatment of a congenitally infected infant with spiramycin, pyrimethamine and a sulphonamide can reduce progressive damage after birth.
The risk of foetal varicella syndrome in children exposed to varicella-zoster virus (VZV) in utero is:
VZV infection of the newborn results from transmission from a mother with chickenpox to her infant around the time of delivery, in circumstances where the infant lacks the protection of maternal antibodies. The likelihood of such infection depends on the timing of delivery in relation to when the mother develops the chickenpox rash.
Zoster immune globulin (ZIG) can prevent or modify varicella if given within 4 days (preferably 48 hours) of exposure to:
Immunisation of susceptible women of child-bearing age with varicella vaccine will protect the foetus from the risk of congenital varicella.
Group B streptococcus can cause neonatal sepsis, pneumonia, meningitis and, less frequently, focal infections such as osteomyelitis, septic arthritis or cellulitis.
Investigations for suspected Group B strep sepsis may include:
Supportive Care:
Monitoring and management of temperature control, fluids and electrolytes, acid base balance, oxygen and nutrition.
Antibiotic Treatment:
High-dose intravenous penicillin plus synergistic gentamicin or cefotaxime should be used until the organism and sensitivities are confirmed, at which time penicillin alone (if organism sensitive) can be used for the duration of treatment.