K. Bombicino

Impact of heteroresistance to colistin in meningitis caused by Acinetobacter baumannii

We read with interest the paper by Li and colleagues concerning colistin hetero-resistance in Acinetobacter baumannii clinical isolates. The incidence of colistin-heteroresistance is still not well known due to its difficult detection. Moreover, its clinical impact has only been discussed in our previous report and in a communication of David. In a recent review of patients with meningitis due to A. baumannii treated with colistin, heteroresistant isolates have not been described. The aim of the present work is to report our experience regarding the clinical impact of colistin-heteroresistance in post neurosurgical meningitis caused by A. baumannii. Seven isolates were recovered from two cases (patients 1 and 2) of A. baumannii colistin heteroresistant in post neurosurgical meningitis were detected in the intensive care unit of Hospital de Clinicas Jose de San Martin of Buenos Aires city during the period 2004e2009. The selection intra-treatment with colistin of A. baumannii colistinresistant was analyzed. Strains were identified by phenotypic tests and genomospecies was determined by ARDRA (Amplified ribosomal DNA restriction analysis). Minimal inhibitory concentrations (MICs) to colistin (against the resistant subpopulations and the original strains) and the other antimicrobials (ampicillinesulbactam, ceftriaxone, ceftazidima, imipenem, meropenem, amikacin, gentamicin and levofloxacin) were performed by dilution method in cation-adjusted MuellerHinton agar and interpreted according to the Clinical and Laboratory Standards Institute. Pulsed-field electrophoresis (PFGE) was performed with ApaI as described previously. Population analysis profiles (PAPs) were determined according to a previous report. Timeekill studies were performed twice and thus, results were analyzed by using mean colony count values from the duplicate plates for each isolate, with the following concentrations: colistin sulfate: 4,8,12 and 80 MIC and rifampicin 4 mg/ ml. This study was performed with the colistin susceptible heteroresistant isolates from each patient (Ab86 and

Effects of endothelin-3 on water and sodium excretion during extracellular volume expansion

The aim of the present study was to elucidate the role of an IV dose of endothelin-3 (ET-3) (5 ng Kg-1 min-1) on mean arterial pressure (MAP), on diuresis and natriuresis in control and in volume expanded anesthetized rats. A systemic infusion of ET-3 in normal rats (Group I) increased MAP and produced a trend of increasing diuresis, without changes in natriuresis. A 10% body weight expansion (Group II) increased diuresis and natriuresis without changes in MAP. The simultaneous infusion of ET-3 and expansion with saline (Group III) resulted in an increase in MAP, an enhanced diuretic response, and a natriuresis of similar magnitude to that observed in Group II. These results suggest that the diuresis produced by a low dose of exogenous ET-3 in control rats, is independent of sodium excretion. Furthermore, the enhanced diuresis caused by ET-3 during expansion is greater than the addition of ET-3 and expansion effects, suggesting that new mechanisms are triggered in order to maintain volume and salt homeostasis in this state.