Fetal damage caused by parvoviral infections.
The single-stranded DNA parvoviruses occur in humans and many species of animals. In general, they are species-specific and capable of producing disease at any stage of life. Parvoviruses have a requirement to replicate in cells in a permissive S-phase of DNA mitosis. The infections may be cytolytic to select cell groups resulting in specific developmental defects or may produce more generalized effects such as anemia, pancytopenia, or hemorrhage. The fetus is at particular risk for damage because of the vast number of cells in active mitosis. The teratogenic effects may be severe, often resulting in fetal death. Infections in childhood and adulthood are more frequently mild to subclinical. Some of the teratogenic effects recognized in animal species have been identified in humans. With increased knowledge of parvovirus effects in animals, more pathogenic effects may be related to human parvoviral disease. The need for vaccination, currently used annually in many domestic animal species, continues to be evaluated for humans.
Animal Health and Care Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.
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D000818:Animals; D000013:Congenital Abnormalities / Q000382:microbiology*; D005260:Female; D005315:Fetal Diseases / Q000382:microbiology*; D005865:Gestational Age; D006801:Humans; D010322:Parvoviridae Infections / Q000150:complications* / Q000151:congenital / Q000503:physiopathology*; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000503:physiopathology*; D011297:Prenatal Exposure Delayed Effects