Norman F. Jacobs
University of Illinois at Chicago
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The Journal of Pediatrics | 1981
Suma Pyati; Rosita S. Pildes; Rajam S. Ramamurthy; Norman F. Jacobs
GROUP B BETA HEMOLYTIC STREPTOCOCCUS is currently the leading cause of sepsis or meningitis or both during the first two months of life? 6 In our nursery, early-onset GBS infection accounts for 2 to 11% of the overall neonatal mortality. Reasons for the emergence of GBS as the predominant pathogen remain unexplained. In view of the prevalence of the organism in our population, we examined some of the epidemiologic factors associated with neonatal GBS infection. In this report, we analyzed only the data pertaining to early-onset disease, since complete information on all inborn infants who acquired late-onset disease in the first few months of life is not available. PATIENTS AND METHODS Early-onset GBS infected infants, identified prospectively, were all born at Cook County Hospital, Chicago, from 1972 through 1979 and had onset of symptoms in the first five days of life. GBS was isolated from peripheral venous blood and/or cerebrospinal fluid. Cultures were routinely obtained by the house staff from all infants at high risk for developing infection, infants suspected of sepsis, and symptomatic infants. In addition, blood and CSF cultures were routinely obtained immediately following death from all infants who died. The GBS were identified using streptococcal A (bacitracin) discs on sheep blood agar, bile esculin agar, and either the hippurate hydrolysis test or the cAMP test. The data for the entire eight years were examined first. Subsequently, data from 1972 through 1975 were pooled (period 1) and compared with data from 1976 through 1979 (period 2). The GBS infection rate is defined as the
Sexually Transmitted Diseases | 1978
Norman F. Jacobs; Eugene S. Arum; Stephen J. Kraus
An isolate of Chlamydia trachomatis obtained from a man with nongonococcal urethritis was used to produce experimental ure-thral and pharyngeal infections in chimpanzees. After urethral inoculation of only 8 χ 101 inclusion-forming units (IFU), infections were established in three of three animals; urethral discharges developed in two. The infections persisted for five to nine weeks. Larger inocula (7 χ 102 and 1 χ 105 IFU) produced pharyngeal infections in two animals. The third animals pharynx was not infected by 1 χ 105 IFU. Chlamydial complement-fixing antibodies increased significantly in sera of two of three animals. This study provides an animal model for study of mucosal infection by C. trachomatis. The relative resistance of the chimpanzee pharynx to infection parallels clinical observations in man.
Sexually Transmitted Diseases | 1978
Sumner E. Thompson; Gladys H. Reynolds; Helen B. Short; Clyde Thornsberry; James W. Biddle; Norman F. Jacobs; Michael F. Rein; Akbar A. Zaidi; Frank E. Young; Jonas A. Shulman
The arginine-hypoxanthine-uracil auxotype has been linked with the propensity of gonococci to cause disseminated infections. Gonococci recovered from 25 patients with disseminated gonococcal infections were compared with gonococci recovered from matched controls, patients with uncomplicated gonorrhea selected during the same month. Minimal inhibitory concentrations of penicillin, tetracycline, crythromycin, and ampicillin, and the nutritional requirements (auxotypes) for prolinc alone, arginine alone, arginine, hypoxanthine and uracil together, serine alone and cysteine-cystine (wild type) were analyzed by discriminant analysis. Significant susceptibility to penicillin characterized strains causing disseminated infections, and a proline requirement was the most common auxotype (48%) among strains isolated in Atlanta. Together the minimal inhibitory concentration of penicillin and the proline auxotype best separated the strains causing disseminated gonococcal infections from those causing gonorrhea. The arginine-hypoxanthine-uracil auxotype was found in only 24% of strains causing disseminated infections. A trait other than auxotype must determine the capacity of the organisms to disseminate.
Indian Journal of Pediatrics | 1994
Jagjit S. Teji; Gopal Srinivasan; Rosita S. Pildes; Robert J. Rydman; Norman F. Jacobs
Guidelines for management of asymptomatic term and preterm neonates born to mothers with prolonged rupture of membranes (PROM) have not been clearly established. A survey was conducted to identify current management practice of neonatologists in midwestern states and to find if there is consensus among physicians with regard to management of PROM without choriomnionitis, with chorioamnionitis but without treatment prior to delivery, and with intrapartum maternal antibiotic therapy prior to delivery. One hundred thirty seven responses to the questionnaire were received. Management of asymptomatic at risk neonates varied in different clinical scenarios. Preterm neonates were screened (94% vs 82%, p < 0.001) and treated (64% vs 41%, p<0.001) more often than term babies. In the absence of maternal symptoms of chorioamnionitis, term neonates were usually observed or treated based on screening test results. With maternal symptoms, 94% of physicians ordered screening test. Prematurity and perceived severity of maternal illness significantly influenced the decision to treat routinely irrespective of screening test results. Physicians favour routine treatment of infants born to mothers who had received intrapartum antibiotic therapy; opinion was divided about management of term asymptomatic infant born to mothers with chorioamnionitis without intrapartum antibiotic therapy. Lumbar punctures were not routinely done for term or preterm neonates prior to antibiotic therapy. Further studies are needed to answer questions regarding the benefits and risks of routine therapy of high risk neonates vs routine clinical observation and selective therapy of only infants who develop symptoms.
JAMA Pediatrics | 1998
Tessy Joseph; Suma Pyati; Norman F. Jacobs
JAMA Pediatrics | 1994
Medha Kamat; Suma Pyati; Rosita S. Pildes; Norman F. Jacobs; Marietta Luayon; Robert Muldoon; Paul S. Levy
JAMA | 1977
Norman F. Jacobs; Sumner E. Thompson
JAMA | 1976
Norman F. Jacobs
JAMA | 1980
Sumner E. Thompson; Norman F. Jacobs; Fernando Zacarias; Michael F. Rein; Jonas A. Shulman
JAMA | 1981
Sumner E. Thompson; Norman F. Jacobs; Fernando Zacarias; Michael F. Rein; Jonas A. Shulman