Cardiovascular effects of congenital infections.
In the course of gestation, many bacteria, parasites, and viruses may infect the pregnant woman, but few cross the placenta to affect the fetus and fewer still affect the fetal heart. Although the incidence of fetal cardiac infection is low, the effect on the fetus is major. In terms of frequency, rubella virus, Toxoplasma gondii, and Coxsackie virus B are the principal infectious agents affecting the fetal heart, but any number of organisms may cross the placenta to affect the fetus. The pathogenesis of infection of the fetal heart relates to the agent and to the time of gestation when the infection occurs. The agent affects the heart along one or more of three separate pathways: inhibition of cell growth, cytolysis, and interference with the blood supply. Most agents cause cytolysis, stimulating inflammation and scarring. Although several agents carry the suspicion of teratogenicity, only rubella virus has been incriminated with certainty as capable of functioning along each of the three pathways with the potential to serve as teratogen.
Rosenberg
H S
HS
Department of Pediatrics, University of Texas Medical School, Houston 77225.
D018376:Cardiovascular Abnormalities; D002318:Cardiovascular Diseases / Q000235:genetics* / Q000473:pathology; D000013:Congenital Abnormalities / Q000473:pathology; D029822:Enterovirus B, Human / Q000472:pathogenicity; D005260:Female; D005318:Fetal Heart / Q000382:microbiology; D006801:Humans; D007231:Infant, Newborn; D007232:Infant, Newborn, Diseases / Q000209:etiology / Q000473:pathology; D009205:Myocarditis / Q000209:etiology; D010493:Pericarditis / Q000209:etiology; D011247:Pregnancy; D012410:Rubella Syndrome, Congenital / Q000209:etiology; D014125:Toxoplasmosis, Congenital / Q000209:etiology