Cefotaxime diffused consistently and in therapeutic levels into the cerebrospinal fluid (CSF) of 13 children successfully treated for bacterial meningitis. CSF cefotaxime levels early (6.0 ,ug/mI) and late (1.2 ,ug/ml) in treatment were severalfold the MBCs for the infecting organisms. After a single 40-mg/kg dose to each of five infants with ventriculostomies, mean CSF levels of cefotaxime were 6.4, 5.7, and 4.5 ,ug/mI at 2, 4, and 6 h, respectively.
We examined the minimal inhibitory concentrations and minimal bactericidal concentrations of chloramphenicol, ampicillin, ticarcillin, cefamandole, cefazolin, cefoxitin, cefotaxime, ceforanide, and moxalactam for 100 isolates ofHaemophilus influenzae, 25 of which produced fl-lactamase. Susceptibility was not influenced by the capsular characteristic of the organism. The mean minimal inhibitory concentrations of cefamandole, ticarcillin, and ampicillin for f-lactamase-producing strains were 3-, 120-, and 400-fold higher than their respective mean minimal inhibitory concentrations for ,8-lactamase-negative strains. No such difference was noted for the other antibiotics. We performed time-kill curve studies, using chloramphenicoL ampicillin, cefamandole, cefotaxime, and moxalactam with two concentrations of the antimicrobial agents (4 or 20 times the minimal inhibitory concentrations) and two inoculum sizes (10' or 106 colony-forming units per ml).The inoculum size had no appreciable effect on the rate of killing of fi-lactamasenegative strains. The rates at which ,B-lactamase-producing strains were killed by chloramphenicoL cefotaxime, and moxalactam were not influenced by the inoculum size. Whereas cefamandole in high concentrations was able to kill at 106 colony-forming units/ml of inoculum, it had only a temporary inhibiting effect at low drug concentrations. Methicillin and the ,-lactamase inhibitor CP-45,899 were able to neutralize the inactivation of cefamandole by a large inoculum of ,-lactamase-producing H. influenzae.
. .iwenty-pretekm and term female neonates were exchange-transfused with males donor f r e s h blood during t h e i r f i r s t days o f l i f e because o f hyperbilirubinaemia o r severe septicaemia. In ord e r t o .study t h e presence o f donor lymphocytes i n t h e neonat e s p e r i p h e r a l blood, chromosome s t u d i e s were performed inmediat e l y a f t e r , l 2 and 72 hours following t h e exchange t r a n s f u s i o n . We used t h e f l u o r e s c e n t -b i n d i n g technique i n o r d e r t o d i s t i nguish t h e d o n o r ' s c e l l s by t h e presence o f t h e Y-chromosone o r o t h e r f l u o r e s c e n t markers i n a t l e a s t 300 m i t o t i c f i g u r e s i n each speciment. We found t h a t i n jaundiced babies immediately following exchange t r a n s f u s i o n l e s s than 10% o f t h e lymphocytes came from t h e donor and 12 hours l a t e r only 1-2% were s t i l l present.However i n neonates exchange-transfusion f o r septicaemia t h e percentage o f d o n o r ' s lymphocytes immediately following t h e proceedure sometimes reached 50% and dropped t o l e s s than 10% by 12 hours.This shows t h e i n a b i l i t y o f t h e depressed by t h e i nf e c t i o n host defence mechanisms o f t h e newborn t o deal with t h e d o n o r ' s 1 ymphocytes. reactive oxygen metabolites by t h e PMN into the surrounding milieu results in autoinjury and is associated with diffuse capillary leak syndromes (septic shock, ARDS).NADPH oxidoreductase, t h e superoxide anion generating enzyme, is a PMN membrane bound flavoprotein normally dormant but inducible by a variety of agents. We studied the specific activity of this enzyme in critically ill children t o determine if detection of its activation might provide an early clue of impending in inflammatory amplification injury. Venous blood specimens from 12 healthy young adult controls reflec ed an induced enzyme b u t s i g n i f i c a n t a g e d i f f e r e n c e s w e r e o b s e r v e d . I n t h e i n t e n s i v e c a r e n u r s e r y t h e p r e v a l e n c e o f CMV v i r u r i a ( c o n g e n i t a l a n d a c q u i r e d i n f e c t i o n s ) w a s 3 . 3 % ( 1 8 o f 5 5 1 n e w b o r n s w i t h v i r u r i a ) . On t h e n u r s i n g u n i t s f o r c h i l d r e n a g e s 0 t o 2 y r s , t h e p r e v a l e n c e o f CMV v i r u r i a w ' a s 6 . 8 % ( 3 2 o f 5 4 4 p o s i t i v e , P < 0 . 0 1 , C h i s q u a r e z 7 . 3 , w h e n c o m p a r e d t o n e w b o r n s ) . T h e p r e v a l e n c e o f CMV v i r u r i a o n a n u r s i n g u n i t f o r c h i l d r e n a g e s 2 t o 5 y r s w a s 7 . 2 % ( 2 7 o f 3 8 2 ) , s i m i l a r t o t h a t f o r c h i l d r e n 0 t o 2 y r s ( P > 0 . 5 C h l s q u a r e = 0 . 0 0 4 ) . On a n u r s i n g u n i t f o r c h i l d r e n a g e s 5 t o 1 2 y r s t h e p r e v a l e n c e o f CMV v i r u r i a d e c r e a s e d t o 4 . 2 % ( 2 0 o f 4 7 6 , P -0 . 0 1 , C h i s q u a r e z 6 . 6 w h e n c o m p a r e d t o c h i l d r e n 2 t o 5 y r s ) . F o r 1 2 t o 1 8 y e a ...
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