Thirty healthy gravid patients of six to 20 weeks' gestation each received a single dose of 7.5 mg of amikacin/kg within 24 hr prior to elective hysterectomy. The half-life (t1/2) of amikacin in maternal serum was 2.07 hr. The mean peak concentration of amikacin in the sera of these patients was slightly lower than that in nonpregnant adults. Two-thirds of the placental samples had amikacin concentrations of greater than or equal to 8 microng/g during the 20-hr interval between drug injection and delivery time. In fetal kidney the concentration of amikacin peaked at a level of 22.4 microng/g at 12 hr after administration. The peak concentration of amikacin in fetal urine was 24 microng/ml, and the t1/2 was 3.2 hr. High levels of the drug in fetal urine and low levels in fetal serum (less than 4 microng/ml) and amniotic fluid (less than 3 microng/ml) were unrelated to high levels found in fetal kidney. Levels of amikacin in fetal lung were 1.4-8.0 microng/g during intervals of 1-16 hr between administration of the drug and time of delivery. With the increasing number of drugs available for use, both potential benefits and risks for the fetus must be considered when prescribing an antibiotic to treat the infected gravid patient, and it should be kept in mind that low levels in body fluid may not be equated with safety.
Maternal-fetal transfer of cefazolin was investigated with use of a single 14-mg/kg intramuscular dose administered to 40 gravidas before elective hysterectomy. The half-life of cefazolin in maternal serum was 1.5 hr with mean concentrations at 2 and 4 hr of 39 and 16 microgram/ml, respectively. By microbiological assay, cefazolin was not detected in brain, cerebrospinal fluid, lung, liver, or kidney of the fetus but was present in concentrations of 1-11 microgram/ml in 12 of 27 individual samples of fetal serum from 0.75 to 10.66 hr. Cefazolin appeared in fetal urine from 2.17 to 19.5 hr at levels of less than 5 microgram/ml with a half-life of 5.4 hr. Cefazolin was present in the amniotic fluid of fetuses older than 14 weeks in concentrations of less than 1 microgram/ml from 9 to 21.75 hr. After administration of a single dose to the mother early in pregnancy, the fetal distribution of cefazolin is limited to the body fluids.
To investigate the maternal-fetal transfer o f Cefazolin, (CEZ), a new a n t i b i o t i c , and i t s d i s t r i b u t i o n i n the fetus, a s i n g l e 14 mg/kg I.M. dose was administered t o 41 gravidas (18-1st trimester, 23-2nd trimester) % t o 684 hours p r i o r t o therapeutic abortion and s t e r i l i z a t i o n by hysterectomy. CEZ concentration was assayed microbiologically i n maternal serum, myometrium, placenta, f e t a l tissues (brain, lung, l i v e r and kidney) and f e t a l f l u i d s (amniotic, CSF, urine and serum). Maternal serum h a l f -l i f e o f CEZ was 2.2 hours w i t h a peak serum concentration o f 63 ug/ml a t To. H a l f -l i f e and maximum CEZ concentrations were 3.2 hours and 0.16 ug/ml f o r placenta, 3.9 hours and 7.5 ug/ml f o r cord blood, and 9.4 hours and 0.8 u g h 1 f o r amniotic f l u i d . CEZ was not detected i n f e t a l CSF, brain, kidney, lung o r l i v e r . CEZ was mini m a l l y 6 lug/ml) detected i n f e t a l u r i n e from 2 t o 12 hours.Only three myometrial samples between % and 1 3/4 hours had minimal CEZ concentrations. There were no differences i n CEZ concentrations noted i n any tissues o r f l u i d s w i t h increasi n g weeks' gestation.No accumulation o f CEZ was demonstrated i n the fetus. Fetal serum concentrations were 5 t o 10% o f the maternal serum and i n the MIC range o f susceptible organisms. N-9, N-11, N-13, and N-27 were m s t ccmron to CF patients. Types N-7 and N-11 w e found rmst frequently in those with severe i q x h w n t or -tion Between June, 1972 and March, 1973, an epidemic of idiopathic gastroenteritis affected 59 infants in the nursery of this hospital. Microbiological evidence obtained by prevalence surveys established an enterotoxigenic E. coli 0142/ K86/H6 as the etiology of the outbreak. Clinical illness frequently was severe, resulting in 4 deaths and in intractable diarrhea in an additional 17 babies. Attack rates were found to be highest for low-birth-weight infants during the first two weeks of life. No predisposition was found to be associated with prior antibiotic therapy, gavage feeding, oxygen therapy, or birth by Caesarian section. Environmental microbiologic data incriminates the hands of personnel as potential transmission vehicles; hand carriage of the epidemic strain was not decreased by intensive handwashing with 3% hexachlorophene soap. Parenteral antibiotic treatment of affected babies was found to be associated with protracted illness, while oral colistin therapy successfully limited the course of diarrhea in all treated infants. Neonatal infection by an enteropathogenic bacterium not identified by traditional techniques and the resultant inappropriate use of parenteral antibiotic therapy are shown to be important causative factors in "idiopathic intractable diarrhea of infancy."PARAINFLUENZA VIRUS EPIDRMI0IX)GY. Carl D. Rrandt, Hyun W. Kim, Robert N. Chanock, Robert H. Parrott. George Washington University and Research Foundation of Children's Hospital, Washington, D.C. 20009Between October 195...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.