Biomedical subjects
Publications and source records attributed to E O Mason.
Two hundred and ten pneumococcal isolates underwent ceftizoxime disk (30 micrograms) screening to predict cephalosporin resistance. Forty-six isolates failed screening with 36 (78%) demonstrating intermediate/resistant MICs. Sensitivity and specificity were 100 and 95%, respectively. The ceftizoxime disk screen is an effective method of identifying potentially cephalosporin-resistant isolates.
OBJECTIVE: Data are scarce regarding the effects of nutrient fortification and storage on the immunoprotective properties of human milk. These effects are important considerations when feeding premature infants. We hypothesized that total bacterial colony counts (TBCC) and immunoglobulin A (IgA) concentration were not affected by the addition of fortifier even when tested under extreme storage conditions and that osmolality of fortified human milk does not increase with storage. METHODS: Ten frozen and five fresh milk samples from mothers of premature infants were divided into fortified and unfortified milk, and stored for 72 hours at either refrigerator or room temperature. Aliquots were obtained at 0 to 72 hours for TBCC, osmolality, and total IgA, and analyzed by repeated measures analysis of variance (ANOVA). RESULTS: Log10 TBCC in milk stored at refrigerator temperature for 0, 24, 48, and 72 hours were significantly greater in fortified vs unfortified milk; both increased similarly with storage. Osmolality was greater in fortified than unfortified milk; both increased by approximately 4% with storage. IgA concentration was not affected by fortification or storage. To simulate the usual nursery use of fortified human milk, a separate evaluation was performed. Fortified milk was stored at refrigerator temperature for 20 hours, warmed in a 40 degrees C laboratory incubator for 20 minutes, and placed in a 34 degrees C infant incubator for 4 hours. Samples for TBCC were obtained at 0, 20, and 24 hours and analyzed by repeated measures ANOVA. Log10 TBCC in fortified, refrigerated milk did not change over the 20-hour storage but increased during the simulated 4-hour usage. CONCLUSIONS: These findings may warrant consideration when using human milk in the neonatal nursery but support recommendations to use commercially fortified human milk within 24 hours.
Genetically engineered mice, which lack normal expression of intercellular adhesion molecule 1 (ICAM-1), were used to study the role of ICAM-1 in the host defense against disseminated candidiasis. The responses of ICAM-1-deficient mice and normal wild type mice were compared following an intravenous challenge with Candida albicans. ICAM-1-deficient mice lost more weight (P < .001) and had a significantly higher mortality (P < .001). Quantitative cultures revealed a greater tissue fungal burden in ICAM-1-deficient mice compared with normal mice, in both the kidney (P < .001) and the brain (P = .007). Extensive inflammation, composed primarily of histiocytes admixed with lymphocytes and occasional neutrophils, was present in the renal tissue of ICAM-1-deficient mice; this contrasted with a more localized and predominantly neutrophilic infiltrate in normal mice. This work suggests that the loss of ICAM-1 significantly impairs host defense against C. albicans, by impairing either neutrophil migration or phagocyte activation or both.
Two oxazolidinones and ceftriaxone, imipenem, rifampin, and vancomycin were tested against 162 penicillin-intermediate and 68 penicillin-resistant strains of pneumococci. U-100592 is two- to fourfold more active than U-100766 against penicillin-resistant pneumococci. The MICs of U-100592 at which 90% of the isolates were inhibited were 0.25 and 0.5 microgram/ml for penicillin-intermediate and -resistant strains, respectively, and 0.5 microgram/ml for ceftriaxone-susceptible, -intermediate, and -resistant strains. U-100592 MICs for 7 of 230 strains (2 from blood, 3 from middle-ear fluid, and 2 from the upper respiratory tract) were 1 microgram/ml.
Vancomycin susceptibility testing of Streptococcus pneumoniae by the E-test consistently resulted in MICs that were at the upper limit of the 1-microgram/ml susceptible category defined by current National Committee for Clinical Laboratory Standards guidelines and were always higher than MICs obtained by microbroth dilution. Three of five E-test results for S. pneumoniae ATCC 49619 were higher than the acceptable limits.
Mice genetically deficient in the gene encoding for intercellular adhesion molecule-1 (ICAM-1) production were compared with wild-type mice after injection with Haemophilus influenzae type b (Hib) or Streptococcus pneumoniae. The incidence of Hib bacteremia was greater in the ICAM-1-deficient mice than wild-type mice (P = .007), but mortality was greater for wild-type mice at 24 h (P = .03). In contrast, the incidence of S. pneumoniae bacteremia was equivalent but mortality was greater in ICAM-1-deficient mice at 24 h (P = .0003). More ICAM-1-deficient mice had cerebrospinal fluid cultures (CSF) positive for Hib (P = .04), whereas all animals at sacrifice had CSF cultures positive for S. pneumoniae. CSF white blood cell counts and histology of the meninges and cochlea were no different between groups for either organism. ICAM-1 deficiency may be protective early in Hib infection but has a detrimental effect in S. pneumoniae infection.
The contribution of intercellular adhesion molecule 1 (ICAM-1) during systemic and local bacterial infections was studied in transgenic ICAM-1-deficient and control mice that were injected intraperitoneally (ip) or intradermally (id) with Escherichia coli, Pseudomonas aeruginosa, or Staphylococcus aureus. Mortality rates, blood cultures, white blood cell (WBC) counts and absolute neutrophil counts (ANCs) were obtained daily until cultures were sterile. Six and 24 h after injections, autopsies were done on randomly selected ip-inoculated mice and biopsies were done on randomly selected id-inoculated mice. Survival rates were similar. In ICAM-1-deficient mice, ip P. aeruginosa resulted in higher incidences of bacteremia at 24 h (P = .003) and 48 h (P = .002); id S. aureus resulted in larger skin lesions (P = .026). Leukocytosis persisted in ICAM-1-deficient mice 6 h after ip injection of E. coli; however, WBC counts and ANCs in peritoneal fluid did not differ. Although the inflammatory responses were similar histologically in ICAM-1-deficient and normal mice, differences in site- and stimulus-specific susceptibilities were noted.
Surveillance by 33 laboratories in 19 states during a 4 1/2 month period between December 1993 and April 1994 found that 263 of 1627 (16.2%) isolates of Streptococcus pneumoniae were resistant to penicillin. One hundred and seventy (10.4%) isolates were determined to be intermediately resistant to penicillin (MICs 0.1-1.0 mg/L and 93 (5.7%) were found to be highly resistant to penicillin (MICs > 2.0 mg/L). MIC90s for intermediately penicillin resistant strains were: amoxycillin/clavulanate 2.0 mg/L, cefaclor 64 mg/L, cefixime 32 mg/L, cefprozil 8 mg/L and loracarbef 128 mg/L. MIC90s for highly penicillin resistant strains were: amoxycillin/clavulanate 4.0 mg/L, cefaclor > or = 128 mg/L cefixime 64 mg/L, cefprozil 32 mg/L and loracarbef > or = 128 mg/L.
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The MICs of penicillin and cefotaxime for a range of penicillin-susceptible and penicillin-resistant isolates of Streptococcus pneumoniae were unchanged by the addition of gentamicin. In time-kill studies the rate of killing was greater for 18 of 20 isolates in the presence of gentamicin. However, mean differences in killing after 6 h of incubation were modest, not exceeding 1 log10 unit.
OBJECTIVE: To determine whether treatment with dexamethasone and ceftriaxone for children with bacterial meningitis reduces the frequency of either sensorineural hearing loss or other neurologic sequelae. DESIGN: This was a prospective, multicentered, placebo-controlled clinical trial. Subjects were followed for 1 year. SETTING: The study was conducted in six children's hospitals located in Pittsburgh, Houston, Los Angeles, Chicago, Washington, D.C., and Columbus, Ohio. PATIENTS: Enrolled were 173 children, 8 weeks to 12 years of age, with suspected bacterial meningitis; 143 children were evaluable. Eighty-seven percent of patients were followed for at least 6 weeks to 3 months, and 67% were followed for 1 year. INTERVENTIONS: Subjects were randomized to receive ceftriaxone with or without dexamethasone (0.15 mg/kg every 6 hours for 4 days). Auditory brainstem responses (ABR) were measured within 24 hours of admission. MAIN OUTCOME MEASURES: Hearing, development, and neurologic sequelae were assessed at the time of discharge and 6 weeks and 1 year later. MAIN RESULTS: One hundred forty-three patients (69 received dexamethasone and 74 received placebo) with bacterial meningitis were evaluable: Haemophilus influenzae type b (83), Streptococcus pneumoniae (33), Neisseria meningitidis (24), and three others. Overall, there was no significant difference in auditory outcome between dexamethasone and placebo recipients. Twenty-two children had bilateral moderate or more severe hearing loss at the time of the first ABR. At follow-up, the resolution of hearing impairment was nearly identical for each group. Nine of ten children who remained persistently deaf were deaf at the time of the first ABR. There were no differences in neurologic or developmental outcome between groups. CONCLUSION: All but one child with persistent bilateral moderate or more severe hearing loss had demonstrable deafness at the time of the first ABR. Dexamethasone did not significantly improve audiologic, neurologic, or developmental outcome in children with bacterial meningitis.
OBJECTIVE: The clinical diagnosis of sepsis remains difficult, particularly in the young child, and would be improved by a rapid and reliable method for identification of bacteria in blood and other body fluids. Polymerase chain reaction (PCR) amplification of highly conserved DNA sequences found in all bacteria would permit fast and sensitive determination of the presence of bacteria in clinical specimens. METHODOLOGY: A primer pair for highly conserved regions of bacterial DNA encoding 16S ribosomal RNA (rDNA) was utilized for PCR amplification. PCR products were analyzed by gel electrophoresis, and, after modification of the primers, by an automated 96-well plate reader. RESULTS: rDNA was amplified from 12 different species of bacteria, including Gram-negative and -positive organisms. No signal was observed when total human DNA was used as template. Colorimetric analysis of amplified sequences using a 96-well format was also successful. CONCLUSIONS: We conclude that a single primer pair designed to anneal to a highly conserved region of bacterial DNA can amplify DNA specimens from a variety of different bacteria, while not amplifying human DNA. Such a molecular genetics approach can be fully automated with existing robotic technology. Because of speed, sensitivity, and cost, molecular triage of patients with signs and symptoms of possible bacterial infection will decrease morbidity and mortality among those with unrecognized bacteremia who are managed as outpatients, and will dramatically reduce hospital expenses from individuals who are admitted and are not bacteremic.
Multilocus enzyme electrophoresis was used to genetically characterize sequential isolates of coagulase-negative staphylococci (CONS) from 3 neonates with persistent bacteremia and organisms cultured from several sites in 23 children with presumed catheter-related sepsis (CRS). For 2 of 3 neonates and 21 (91%) of 23 of the patients with presumed CRS, the same CONS clone was isolated from multiple consecutive blood cultures (mean, 7.3 isolates; range, 3-19). For the 23 children with presumed CRS, 7 (30%) had catheter hub (CH) and 7 (30%) had catheter exist site (CES) cultures positive for CONS; cultures from 3 of these patients (from both CH and CES) grew CONS. Genetic analysis of isolates recovered from the CH and peripheral and central venous catheter blood cultures of all 7 patients revealed clonal identity of the strain grown from all sites. In contrast, only 4 (57%) of 7 of the CONS isolates from the CES were the same clone as that isolated from the blood. These data suggest that repetitive isolation of CONS during the course of CRS is due to ongoing bacteremia, not culture contamination with distinct CONS isolates. The results also are consistent with the hypothesis that the CH is a more likely site of initial colonization by CONS than the exist site in patients with CRS.
The increasing prevalence of intermediately and highly penicillin-resistant strains of Streptococcus pneumoniae is a problem worldwide. However, optimal management of patients with middle ear and sinus infections caused by resistant pneumococci has not been established. We performed agar dilution susceptibility studies on 71 strains of penicillin-resistant pneumococci (minimum inhibitory concentration (MIC), > or = 0.1 microgram/ml) recovered from middle ear and sinus cultures of Houston children against 13 oral antibiotics with the use of both established and newly proposed National Committee for Clinical Laboratory Standards susceptibility criteria. Of the 62 middle ear isolates 35 (56%) were intermediately resistant and 27 (44%) were highly resistant to penicillin. Of the 9 sinus isolates tested, 5 (56%) were intermediately resistant (MIC between 0.1 and 1 micrograms/ml) and 4 (44%) were highly resistant (MIC > or = 2 micrograms/ml) to penicillin. The MIC90 increased with increasing penicillin resistance for the antibiotics tested except for rifampin, ciprofloxacin, loracarbef, clindamycin and trimethoprim-sulfamethoxazole. None of the highly penicillin-resistant isolates was susceptible to loracarbef or trimethoprim-sulfamethoxazole. The MIC90 values for clindamycin and rifampin were similar for the intermediately and highly penicillin-resistant groups, and the number of susceptible isolates in each group remained greater than 90% for both antibiotics. Thirty-five isolates were resistant to erythromycin but susceptible to clindamycin, a susceptibility pattern distinctly different from that seen in South Africa and Europe, where clindamycin resistance parallels erythromycin resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
Children with meningitis due to Streptococcus pneumoniae isolates that are relatively or fully resistant to penicillin and have decreased susceptibility to broad-spectrum cephalosporins (MIC, > or = 2.0 micrograms/ml) who have failed treatment with broad-spectrum cephalosporins have been reported. The National Committee for Clinical Laboratory Standards has newly revised guidelines indicating that S. pneumoniae isolates associated with meningitis for which the MICs are > or = 0.5 micrograms/ml should be considered resistant to broad-spectrum cephalosporins. This recommendation is not clearly based on data related to clinical outcome and may be too conservative. We present data on five children who had S. pneumoniae meningitis due to isolates that were relatively or fully resistant to penicillin (MIC range, 0.125 to 4.0 micrograms/ml) and had cefotaxime or ceftriaxone MICs of 0.50 to 2.0 micrograms/ml. Their clinical courses and outcomes were comparable to those of five children with S. pneumoniae meningitis due to strains that were relatively or fully resistant to penicillin and were inhibited by cefotaxime at concentrations of < or = 0.25 micrograms/ml, as well as to those of 25 patients with S. pneumoniae meningitis due to penicillin-susceptible isolates identified during the same period. Children with meningitis due to S. pneumoniae with cefotaxime or ceftriaxone MICs of < or = 1.0 micrograms/ml may be adequately treated with these antibiotics. Further clinical data are required before solid recommendations can be made regarding cephalosporin breakpoints for S. pneumoniae.
We compared the E test (AB Biodisk North America, Inc., Culver City, Calif.) with the National Committee for Clinical Laboratory Standards broth microdilution method for the determination of MICs of penicillin and cefotaxime for 108 isolates of Streptococcus pneumoniae. The E test was performed following manufacturer's recommendations with Mueller-Hinton blood agar, and the broth microdilution procedure was performed with lysed horse blood-supplemented Mueller-Hinton broth. The microdilution method classified 26 isolates as highly penicillin resistant (MIC, > or = 2 micrograms/ml), 33 as intermediately resistant to penicillin (MIC, > or = 0.1 < 2.0 micrograms/ml), and 49 as susceptible to penicillin (MIC, < 0.1 micrograms/ml). Discordant results obtained with the E test for penicillin susceptibility testing compared with broth microdilution occurred for 19 of the 108 isolates tested. Cefotaxime MICs for 90% of isolates found highly resistant, intermediately resistant, and susceptible to penicillin by broth microdilution were 2.0, 0.5, and 0.06 micrograms/ml, respectively. There were 16 susceptibility category changes when the E test was used to determine cefotaxime MICs. All of the discrepancies in the penicillin and cefotaxime MICs determined by the E test occurred at the susceptibility category breakpoints, and all represented differences of only one twofold dilution factor. Properly performed and controlled, the E test should be a reliable quantitative procedure for more accurately predicting the susceptibility of S. pneumoniae to several antibiotics.
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A sample of 48 penicillin-resistant Streptococcus pneumoniae (PRSP) strains recovered between January 1989 and May 1991, primarily from infected children in Houston, was characterized by multilocus enzyme electrophoresis and repetitive extragenic palindromic-polymerase chain reaction genomic profiling. A heterogeneous array of 22 clonal genotypes was identified, but 64% of the PRSP strains in the sample were assigned to five clones that are closely similar in overall chromosomal character and express serotype 6 capsule. A close genetic association between these five clones and penicillin-resistant 6B clones recovered in Alaska, Iceland, and Spain was identified by multilocus enzyme electrophoresis. Taken together, the results suggest either that the common resistant 6B clones in Alaska, Iceland, Spain, and Houston have a recent ancestor or that isolates of a certain pneumococcal phylogenetic lineage are more likely to develop penicillin resistance.