Objective: To assess the risk of maternal parvovirus B19 infection from exposure to various sources and the fetal morbidity of those infections.
Methods: We obtained demographic and occupational information about pregnant women exposed to sources of B19 and about the nature and duration of the exposures. We performed serologic testing 10-14 days after exposure using an indirect capture enzyme-linked immunosorbent assay. Women with immunoglobulin (Ig) M were examined with weekly ultrasound until 12 weeks after exposure, and the outcome of the pregnancy was ascertained from interviews with patients and their obstetricians. Logistic regression analysis was used to determine risk factors for maternal immunity and infection by B19.
Results: Of 618 pregnant women exposed, 307 (49.7%) were immune to B19, 259 remained susceptible after exposure, and 52 (16.7% of all susceptibles) contracted B19 infection. None of the 52 fetuses of infected women developed nonimmune hydrops, and there were no fetal deaths attributable to B19 in this group. The relative risk of maternal B19 infection was 2.8 if the source was a related child living in the household (95% confidence interval 1.7, 4.6; P < .001). No significant differences were found for maternal B19 infection in eight categories of maternal occupation. Maternal symptoms of polyarthralgia (46%), fever (19%), and nonspecific rash (38%) were significantly more common (P < .001) in IgM-positive patients than in noninfected women (4.1%, 2.8%, and 5.7%, respectively). Only 17 (33%) of the IgM-positive women were entirely asymptomatic.
Conclusion: The risk of maternal B19 infection in pregnancy could not be predicted by a gravida's occupation, but it was significantly higher when the source of exposure was her own child. The fetal risk of nonimmune hydrops after maternal B19 infection must be very low. As a consequence, exclusion of pregnant women from the workplace during endemic periods with seasonal clusters of cases is not justified. Weekly fetal ultrasound evaluation in these cases carries a low yield.
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http://dx.doi.org/10.1016/s0029-7844(97)00701-1 | DOI Listing |
Virol J
January 2025
Laboratório de Desenvolvimento Tecnológico em Virologia, Instituto Oswaldo cruz, Fundação Oswaldo Cruz, Rio de Janeiro, RJ, Brasil.
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National Blood Centre, Istituto Superiore di Sanità, Rome, Italy.
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Department of Physiopathology, Faculty of Medicine, Medical University of Gdansk, 80-210 Gdansk, Poland.
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January 2025
Universidade Federal de São Paulo, Departamento de Medicina, São Paulo, SP, Brazil.
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View Article and Find Full Text PDFPLoS One
January 2025
Department of Biophysics, School of Biological Sciences, Tarbiat Modares University, Tehran, Iran.
Multiple sclerosis (MS) is a devastating autoimmune disease that leads to the destruction of the myelin sheath in the human central nervous system (CNS). Infection by viruses and bacteria has been found to be strongly associated with the onset of MS or its severity. We postulated that the immune system's attack on the myelin sheath could be triggered by viruses and bacteria antigens that resemble myelin sheath components.
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