Biomedical subjects
Publications and source records attributed to M S Amstey.
Postpartum ultrasonographic examination of a patient with a retained placenta showed findings consistent with placenta accreta. The diagnosis was confirmed after surgery with histopathologic examination of the uterus. This case illustrates the possible clinical application of ultrasonography in the postpartum diagnosis of placenta accreta.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A case of midtrimester septic abortion due to Hemophilus influenza is discussed on the basis that the pathogeneses of the septic abortion was due to the hematogenous spread of the organism orginating from upper respiratory infection. The absence of ruptured membranes and the elevated antibody titer at the onset of the pelvic infection were in keeping with this hypothesis. Additional data on the bacteriology of this organism and the probability of the occurrence of a type b organism with original ampicillin resistance are presented.
A cluster of 5 patients with puerperal infection due to group A beta hemolytic streptococcus (GABHS) is described. The most striking clinical signs included the early onset of uterine tenderness followed by an abrupt temperature elevation to greater than or equal to 102 F. At the time of uterine tenderness (Day 2, postpartum), 4 of 5 patients had gram-stained lochial smears showing a predominance of gram-positive cocci. The cluster of cases occurred with no source of the infection identified after 365 culture attempts. Therapy was rapidly successful with intravenous penicillin.
Clinical impressions and observations of genital herpesvirus infections indicate that lesions are more persistent and more severe during pregnancy. Several explanations are possible: an altered immune state, increased vascularity and blood flow, and/or increased viral infectivity due to increase in one or more hormones during pregnancy. Studies presented here were directed toward investigating the latter possibility. Herpesvirus, type 2, isolated from a genital lesion was titrated in WI-38 cells in the absence and presence of estriol, progesterone, human chorionic gonadotropin (hCG) and human placental lactogen. Two other deoxyribonucleic acid (DNA) viruses, adenovirus type 7 and vaccinia virus, were included for control purposes. Although estriol significantly inhibited and hCG significantly enhanced the single-cycle production of herpesvirus, there was little or no effect on these hormones on adenovirus. Progesterone, after 48 hours but not after two hours of preincubation, inhibited production of herpesvirus and vaccinia virus but had no effect on aderiovirus. When end-point titers were measured after multiple cycles of viral growth, there were no differences in viral titers with any of the hormones, except for a slight reduction with estriol. Except for the uniform effect of progesterone on DNA viruses, hormonal effects on viral production cannot be generalized from experiments with one virus.
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Non-Group A or D beta hemolytic streptococci were identified in the vaginas of 5-11% of prenatal patients. More than 97% of organisms so identified have been found to be specifically Group B beta hemolytic streptococci (GB-BHS). The differences may have been related to seasonal changes. These organisms were found in 5% of preabortion patients--none of whom developed any infectious morbidity even though no therapy was used prior to the abortion. Of 100 gynecologic patients undergoing major gynecologic surgery, 17% had preoperative cultures positive for GB-BHS. However, the morbidity (18%) was the same for the culture-positive and culture-negative patients.
Pregnant mice at 10 days of gestation were more susceptible to vaginal inoculation with herpesvirus, type 2, than were nonpregnant mice. This mouse model system also was used to compare delivery through a birth canal contaminated with herpesvirus, type 2, to delivery after maternal paranteral inoculation by the same virus. Approximately 26 per cent of newborn mice either died or had evidence of disseminated herpesvirus infections after delivering through a vagina inoculated with herpesvirus, whereas only 4 per cent of newborn mice died after subcutaneous inoculation of pregnant animals. Only 1 per cent of neonates delivered of subcutaneously inoculated pregnant mice had any evidence of herpesvirus infection. Pregnant mice immunized to herpesvirus, type 1, had significantly less newborn infection after delivery through a herpesvirus-inoculated birth canal when compared to nonimmunized mice.
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A 4 year survey of a low socioeconomic prenatal population in a large outpatient clinic revealed an incidence of 4.4% gonorrhea by cervical culture. These patients who were culture-positive had a 7.6% perinatal mortality rate compared to a 3.0% perinatal mortality rate among culture-negative patients from the same clinic. The immaturity and prematurity rate was significantly higher in the culture-positive group as was the incidence of premature rupture of the membranes and prolonged premature rupture of membranes.