Infection due to extended-spectrum beta-lactamase-producing Salmonella enterica subsp. enterica serotype infantis in a neonatal unit

OBJECTIVE: To describe the investigation and control of an outbreak of extended-spectrum beta-lactamase producing Salmonella enterica subsp. enterica serotype Infantis in a neonatal unit in Brazil. METHODS: A case-control study for risk factors for Salmonella Infantis systemic infection, environmental cultures, and evaluation of staffing and overcrowding and an assessment of infection control practices were performed. RESULTS: During July 1998 to June 1999, 140 Salmonella Infantis culture-positive patients were identified in the neonatal unit. Presence of a peripheral intravascular catheter was identified as an independent risk factor (odds ratio = 4.98; 95% CI = 1.59-19.31; P =.01) and each 250-g increase in birth weight as a protective factor (odds ratio = 0.76; 95% CI = 0.57-0.95; P =.03). Hospital stay was significantly longer and costs higher in case patients than in control patients. Salmonella Infantis was isolated from multiple environmental sources. Neonatal unit personnel were observed to make several breaks in infection control practices. The unit was understaffed and overcrowded. Prompt case identification, cohorting of patients, enhanced staff hand hygiene, and environmental cleaning terminated the outbreak. CONCLUSIONS: Inadequate infection control practices, nursery overcrowding, and understaffing can have an adverse effect on patient morbidity, mortality rates, and hospital cost.     

Genomics of Neisseria meningitidis

An important feature of disease caused by Neisseria meningitidis is the propensity to invade the meninges. Much progress has been made in our understanding of how this pathogen circumvents the physical properties of this cellular barrier. This review will address the new possibilities offered by the recent availability of meningococcal genome sequences.     

Accuracy of sonography with a hydration test in differentiating between excretory renal obstruction and renal sinus cysts

PURPOSE: The aim of this prospective study was to determine whether sonography with a hydration test to induce diuresis can be used to reliably differentiate between excretory renal obstruction and renal sinus cysts. METHODS: We performed sonographic examination of all patients diagnosed with minimal or moderate obstruction of the intrarenal collecting system or renal sinus cysts on the basis of excretory urography, CT, or both between September 1, 1998, and October 31, 1999. The largest fluid-filled structures in the renal sinus were sonographically measured before and after each patient ingested 1.5 l of water. Cases in which the maximum diameters of the largest anechoic structures increased by at least 10% after hydration were diagnosed with excretory renal obstruction. The sonographic diagnoses were compared with the final diagnoses on excretory urography, CT, or both. RESULTS: Both kidneys were affected in 16 of the 36 patients examined, for a total of 52 kidneys. The sonographic diagnosis was consistent with the results of urography or CT in 48 (92%) of the 52 kidneys. The sonographic approach had a specificity of 92% and a sensitivity of 93% for the diagnosis of excretory renal obstruction, with only 1 false-negative and 3 false-positive results. CONCLUSIONS: When used with the stimulated diuresis test, sonography can reliably distinguish between excretory renal obstruction and renal sinus cysts and can be used as an alternative to other imaging techniques such as urography.     

Alanylation of teichoic acids protects Staphylococcus aureus against Toll-like receptor 2-dependent host defense in a mouse tissue cage infection model

Staphylococcus aureus is inherently resistant to cationic antimicrobial peptides because of alanylation of cell envelope teichoic acids. To test the effect of alanylated teichoic acids on virulence and host defense mediated by Toll-like receptor 2 (TLR2), wild-type (wt) S. aureus ATCC35556 (S.a.113) and its isogenic mutant expressing unalanylated teichoic acids (dlt(-)) were compared in a tissue cage infection model that used C57BL/6 wt and TLR2-deficient mice. The minimum infective doses (MID) to establish persistent infection with S.a.113 were 10(3) and 10(2) colony-forming units (cfu) in wt and TLR2(-/-) mice, respectively. The corresponding MID for dlt(-) were 5x105 and 10(3) cfu in wt and TLR2(-/-) mice, respectively. Both mouse strains showed bacterial-load-dependent inflammation with elevations in tumor necrosis factor, macrophage inflammatory protein 2, and leukocytes, with increasing proportions of dead cells. These findings indicate that alanylated teichoic acids contribute to virulence of S. aureus, and TLR2 mediates host defense, which partly targets alanylated teichoic acids.     

Management of myocardial infarction in Spain in the year 2000. The PRIAMHO II study

INTRODUCTION AND OBJECTIVES: Hospital registries are useful tools to measure the degree of implementation of new treatments and clinical practice guidelines. PATIENTS AND METHOD: The hospital registry described here was developed in the prospective PRIAMHO II study, which involved a random selection of Spanish hospitals with a coronary intensive care unit and external quality control. This study investigated patients admitted to the coronary care unit with acute myocardial infarction. Demographic and clinical characteristics were recorded, as well as the management, clinical course and survival after 28 days and one year. RESULTS: From May 15 to December 15 2000 we included in the registry 6,221 patients from the 58 hospitals that complied with the quality control requirements (71.6% of all participating hospitals). Acute mortality was 9.6%; 28-day and one-year mortality were 11.4% and 16.5%, respectively. Of the patients with ST elevation-myocardial infarction of less than 12 hours' duration, 71.6% were reperfused and 89.3% received fibrinolysis with a median door-to-needle time of 48 minutes. Ejection fraction was measured in 81% of the patients, and 43% were tested for inducible ischemia. About nine-tenths (91%) of the patients were discharged on least one antiplatelet drug, 56% on a beta blocker, 45% on an ACE inhibitor, and 45% on a lipid-lowering agent, with a coefficient of variation between hospitals greater than 25% for the last three drugs. CONCLUSIONS: The percentage of patients with ST elevation treated with reperfusion should increase, as it probably will thanks to the increasing use of primary angioplasty. The door-to-needle time was longer than the recommended interval. In-hospital risk stratification was good but nonsystematic for the evaluation of ejection fraction, and unsatisfactory for inducible ischemia testing. At discharge the percentages of patients receiving beta blockers, ACE inhibitors and statins were not optimal, and there were wide variations in prescribing practices between hospitals.     

Comparison of kinetics of induction of DNA adducts and gene mutations by a nitrofuran compound, 7-methoxy-2-nitronaphtho[2,1-b]furan (R7000), in the caecum and small intestine of Big Blue mice

In previous experiments, i.p. injection of the 5 nitronaphthofuran derivative 7-methoxy-2-nitronaphtho[2,1-b]furan (R7000) to lacI transgenic Big Blue mice led to an increase in the mutant frequency (MF), especially in the caecum and the small intestine. In the present work, the in vivo genotoxicity of R7000 in these two target organs was further investigated. Big Blue mice were treated with a single daily i.p. injection of R7000 of 0.05-0.5 mg/day for five consecutive days and killed 28 days later. These treatments led to significant increases in MF of 1.8-, 3- and 5.4-fold at 0.1, 0.2 and 0.5 mg/day R7000, respectively, in the small intestine. In the caecum, a mutagenic effect, of 4.5-fold, was only observed at the highest dose. DNA adduct formation and MFs resulting from R7000 were also analysed in parallel at various times after the last injection. R7000 led to 14 and seven different nucleotide modifications in the caecum and small intestine, respectively. Three hours after the final injection the level of induced DNA adducts was 10 times higher in the caecum than in the small intestine. From 3 h to 5 days after the final injection, 93 and 58% of DNA adducts disappeared in the caecum and small intestine, respectively. The resulting MF values were similar when comparing the two organs. Analysis of the R7000-induced mutation spectrum in the caecum showed that single G:C and large, > or =3 bp deletions and GC-->CG transversions were the first induced mutations at the end of the treatment. Fifteen days later, the R7000 mutation specificity characteristics already reported in Escherichia coli and in the small intestine of Big Blue mice were evident in the caecum, with the two major events being GC-->TA transversions and deletions of one G:C base pair. In both organs, a relationship between the decrease in R7000-DNA adducts and induction of MF was evident. However, the efficiency of this compound in damaging DNA was not correlated with the capacity of DNA lesions to lead to mutations. Some discrepancies in the R7000 genotoxic effects between the two organs were observed, which may be attributable to differences in the metabolic activation pathway of the compound, as well as to DNA repair proficiency in each tissue.     

Position paper of the ESICM Working Group on Nutrition and Metabolism. Metabolic basis of nutrition in intensive care unit patients: ten critical questions

The metabolic changes associated with critical illness involve several pathways acting at different steps of the utilization of nutritive substrates. The understanding of the role of these pathways and of their complex regulation has led to the development of new strategies for the metabolic and nutritional management of critically ill patients, including the development of new products for nutritional support. The rationale for changing the profile of nutritional support solutions by adding novel substrates is also discussed. This review focuses on the metabolic specificities of critically ill patients and also includes an analysis of the adequacy of tools to monitor the metabolic status and the adequacy of the nutritional support.