Problem The authors review embryofetal pathologies in humans caused by antibodies to maternal autoantigens and paternal alloantigens. They consider the variable percentages of miscarriages, developmental delays, intrauterine growth retardation, perinatal deaths and birth defects of unknown etiology, because a part of these percentages may be caused by analog human isoantibodies to the studied ones in the chick embryos.
Method of study A total of 81 chick embryos whose dams had been immunized against soluble foreign transitory antigens and soluble paternal alloantigens from chick embryos have been macroscopically analyzed. The development was interrupted at random to know anomalies then existing; but 29/81 eggs (35.8%) were incubated until hatching. Each class of anomaly was analyzed by statistical methods; 66 control embryos were studied using the same methods.
Results Transmission of the induced isoantibodies to the embryos caused: monstrosity 8.6%; death by functional abnormality 3.7%; digested embryos 7.4%; malformation 1.2%; developmental delay 30.8%; developmental delay together with intraovo growth retardation 11.1; intraovo growth retardation 15.1%; normal 25.9%. Of the mentioned 29 eggs, 19 embryos died before being born, six died in under 1 week, but only four poults survived more than 1 week. Three chicks exhibited congenital abnormalities: transitory ataxia and dysphagia, and one of them also scoliosis, while a fourth remained healthy.
Conclusion If pathogenic activity by these isoantibodies can be shown to occur naturally in humans, as has been postulated, it could account for some miscarriage, developmental delay, fetal and perinatal death and birth defects of currently unknown etiology.