No single diagnostic test for cytomegalovirus (CMV) infection is currently available for pregnant women at all stages of gestation. Improved accuracy in estimating the timing of primary infections can be used to identify women at higher risk of giving birth to congenitally infected infants. A diagnostic algorithm utilizing immunoglobulin G (IgG), IgM, and IgG avidity was used to prospectively screen serum from 600 pregnant women enrolled from two groups: <20 weeks gestation (n ‫؍‬ 396) or >20 weeks gestation (n ‫؍‬ 204). PCR testing of urine and/or blood was performed on all seropositive women (n ‫؍‬ 341). The majority (56.8%) of women were CMV IgG seropositive, with 5.5% being also CMV IgM positive. In the IgM-positive women, 1.2% had a low-avidity IgG, indicating a primary CMV infection and a high risk of intrauterine transmission. Two infants with asymptomatic CMV infection were born of mothers who had seroconverted in the second trimester of pregnancy. Baseline, age-stratified CMV serostatus was established from 1,018 blood donors. Baseline seropositivity from a blood donor population increased with age from 34.9% seroprevalence at less than 20 years of age to 72% seroprevalence at 50 years of age. Women at high risk of intrauterine transmission of CMV were identified at all stages of gestation. Women infected with CMV during late gestation may be more likely to transmit the virus, so failure to detect seroconversions in late gestation may result in failure to detect infected neonates.Human cytomegalovirus (CMV) is the most common cause of congenital malformation resulting from viral intrauterine infection in developed countries (12,21,48). Primary CMV infection occurs in 0.15 to 2.0% of all pregnancies and may be transmitted to the fetus in up to 40% of cases (48). Up to 15% of intrauterine CMV infections result in symptomatic congenital disease at birth, and 10 to 15% of those born with asymptomatic congenital CMV will develop significant clinical sequelae in infancy (7,10,18). In utero transmission of CMV can occur during primary maternal infection, reactivation, or reinfection of seropositive mothers. Most concern centers on primary maternal infection, due to the potential for significant fetal damage when the infection is acquired and transmitted during the first trimester (30, 48). Perinatal infections can result through virus transmission from many parts of the birth canal (39); however, the majority of these infections are asymptomatic (43).The usefulness of prenatal testing for CMV has been questioned due to the absence of clearly effective intervention (1, 27) and to evidence for severe congenital malformation resulting from viral reactivation (6,8,20). Continuing advancements in technology, however, mean reliable and inexpensive serologic tests are available, prenatal diagnostic procedures with acceptable negative predictive values (NPV) can be performed, and trials of neonatal antiviral treatments are ongoing (25,34,37,50,52). Proposed diagnostic algorithms have focused on first-trimester screeni...

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Objectives To examine the seroprevalence of hepatitis C virus (HCV) in the Australian injecting drug‐using community in the 1970s, and to compare the profile of HCV genotypes with that seen in the 1990s. Design Investigation of stored sera that were collected from injecting drug users in the 1970s and comparison with sera collected in the 1990s. Setting Inner Sydney, 1974‐1975 and 1994‐1996. Patients The 1970s group comprised 141 consecutive injecting drug users who attended the Brisbane Street Methadone Clinic. The 1990s group comprised 88 consecutive, injecting drug users of European origin who were HCV antibody‐ positive and attended a primary healthcare facility (the Kirketon Road Centre). Main outcome measures HCV antibody prevalence (1970s); profile of HCV serotypes (1970s and 1990s); and serological evidence of hepatitis A and B. Results 84% of the 1970s group were HCV antibody‐positive, of whom 92% were infected with HCV serotype 1 and 1% with serotype 3. In contrast, in the 1990s group, 69% were infected with HCV serotype 1 and 25% with serotype 3. The HCV‐positive subjects from the early group were more likely than those from the recent group to have serological evidence of previous HBV infection. Conclusions The high prevalence of HCV among injecting drug users in the 1970s in Australia confirms an epidemic that has been present for at least 25 years. Over this period, the proportion of HCV genotype 1 infections has decreased and genotype 3 infections have emerged.

We report three cases with misleading cytomegalovirus (CMV) or Epstein-Barr virus (EBV) immunoglobulin M (IgM) results during primary human immunodeficiency virus (HIV) infection. We determined the rate of positive anti-CMV IgM assays or anti-EBV capsid antigen IgM assays in sera from a group of well-characterized subjects with primary HIV infection as 2.9% (1/35; 95%CI: 0.15-16.6%) for each infection. The rate of positive anti-EBV capsid antigen IgM assays in subjects with positive hepatitis A virus IgM assays was 30% (6/20; 95%CI: 14.6-51.9%). Clinicians need to consider the limitations of IgM assays for diagnosis of herpesvirus infections, and consider testing for other infections with overlapping clinical manifestations.