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Certain population groups are at risk for inadequate prenatal care and transmission of perinatal infections. Philadelphia's birth cohort comprises largely at-risk groups and its infant mortality rate is among the nation's highest. This study identifies factors associated with infectious disease screening, treatment, and prevention in Philadelphia. Delivery charts for a probability sample of 550 patients were reviewed. Demographic factors associated with prenatal and delivery care were identified through Pearson chi-square, analysis of variance, and stepwise logistic regression analysis. Nonstandard and incomplete documentation complicated abstraction. Some prenatal care was noted in 95% of the records and screening varied by disease. Factors independently associated with care include maternal race, insurance status, and maternal age. Screening for infections with well-established recommendations (hepatitis B virus, rubella, syphilis) occurred more often than for group B streptococcus, HIV, hepatitis C virus, and varicella. Adoption of standard reporting forms and processes could improve practice and aid in quality improvement efforts and patient communication.

The cytoplasmically inherited [KIL-d] element epigenetically regulates killer virus gene expression in Saccharomyces cerevisiae. [KIL-d] results in variegated defects in expression of the M double-stranded RNA viral segment in haploid cells that are “healed” in diploids. We report that the [KIL-d] element is spontaneously lost with a frequency of 10−4–10−5 and reappears with variegated phenotypic expression with a frequency of ≥10−3. This high rate of loss and higher rate of reappearance is unlike any known nucleic acid replicon but resembles the behavior of yeast prions. However, [KIL-d] is distinct from the known yeast prions in its relative guanidinium hydrochloride incurability and independence of Hsp104 protein for its maintenance. Despite its transmissibility by successive cytoplasmic transfers, multiple cytoplasmic nucleic acids have been proven not to carry the [KIL-d] trait. [KIL-d] epigenetically regulates the expression of the M double-stranded RNA satellite virus genome, but fails to alter the expression of M cDNA. This specificity remained even after a cycle of mating and meiosis. Due to its unique genetic properties and viral RNA specificity, [KIL-d] represents a new type of genetic element that interacts with a viral RNA genome.

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