scholarly journals Extended-Spectrum Beta-Lactamase Bacteria From Urine Isolates in Children

2015 ◽  
Vol 20 (5) ◽  
pp. 373-377
Author(s):  
Lisa A. Degnan ◽  
Aaron M. Milstone ◽  
Marie Diener-West ◽  
Carlton K. K. Lee

OBJECTIVES: Multidrug-resistant Gram-negative bacteria, including extended-spectrum beta-lactamase (ESBL)–producing organisms, are a growing problem. The primary objective of this study was to describe the proportion of children with ESBL-producing urinary isolates at a tertiary medical center as well as these organisms' susceptibility patterns. The secondary objective was to identify the risk factors for acquiring ESBL urinary pathogens. METHODS: This retrospective study evaluated a cohort of children with ESBL urinary isolates, admitted to a tertiary children's hospital during a 6-year period. The proportion of patients with an ESBL-producing urinary isolate among all patients who grew a Gram-negative isolate is described together with the organism's susceptibility pattern. Patients with non-ESBL Gram-negative urinary organisms were used as a control group for identifying patient risk factors for ESBL. RESULTS: A total of 7.8% (29 of 370) of patients in our cohort grew Gram-negative urinary isolates with an ESBL strain. Most of the ESBL organisms isolated were sensitive to carbapenems (100% of ESBL organisms susceptible to ertapenem and 93.8% susceptible to meropenem) and amikacin (92.3% of ESBL organisms susceptible). Patients with longer hospitalization, recent antibiotic use, and recent intensive care unit admission were found to be at increased risk for ESBL organisms in the urine. CONCLUSIONS: When selecting empiric antibiotic therapy for suspected urinary tract infection in children, it may be prudent to consider the risk factors identified for acquiring an ESBL urinary pathogen.

2014 ◽  
Vol 27 (6) ◽  
pp. 562-566 ◽  
Author(s):  
Christopher J. Destache

The use of aminoglycoside (AG) antibiotics has declined over the past 15 years primarily due to comparable potency of other antimicrobials and the nephrotoxicity potential of AG drugs. However, resurgence in the use of AG antimicrobials is occurring due to multidrug-resistant gram-negative nosocomial infections. Multidrug-resistant Pseudomonas and Acinetobacter isolates as well as extended-spectrum beta-lactamase–producing Enterobacteriaceae continue to force clinicians to consider AG therapy for nosocomial infections in hospitalized patients and enterococcal endocarditis. Additionally, AGs are still indicated in the treatment of pulmonary exacerbations of cystic fibrosis. Along with the use of AG antibiotics is the associated renal insufficiency complication. This review discusses the mechanism for AG-induced nephrotoxicity. Patient- and drug-related risk factors are discussed to help identify patients at increased risk. The issue of serum-level monitoring is discussed relative to the development of nephrotoxicity.


2019 ◽  
Vol 4 ◽  
pp. 160
Author(s):  
Joseph M. Lewis ◽  
Rebecca Lester ◽  
Paul Garner ◽  
Nicholas A. Feasey

Background: Extended-spectrum beta-lactamase producing Enterobacteriaceae (ESBL-E) threaten human health; and, in areas of sub-Saharan Africa (sSA) where carbapenems are not available, may render ESBL-E infections untreatable. Gut mucosal colonisation probably occurs before infection, making prevention of colonisation an attractive target for intervention, but the epidemiology of ESBL-E in sSA is poorly described. Objectives: Describe ESBL-E colonisation prevalence in sSA and risk factors associated with colonisation. Methods: Studies included were prospective cross-sectional or cohort studies reporting gut mucosal ESBL-E colonisation in any population in sSA. We searched PubMed and Scopus on 18 December 2018. We summarise the range of prevalence across sites and tabulated risk factors for colonisation. The protocol was registered (Prospero ID CRD42019123559). Results: From 2975 abstracts we identified 32 studies including a total of 8619 participants from a range of countries and settings. Six studies were longitudinal; no longitudinal studies followed patients beyond hospital discharge.  Prevalence varied between 5 and 84% with a median of 31%, with a relationship to setting: pooled ESBL-E colonisation in community studies was 18% (95% CI 12 to 28, 12 studies); in studies recruiting people at admission to hospital colonisation was 32% (95% CI 24 to 41% 8 studies); and for inpatients, colonisation was 55% (95% CI 49 to 60%, 7 studies). Antimicrobial use was associated with increased risk of ESBL-E colonisation, and protected water sources or water treatment by boiling may reduce risk. Conclusions: ESBL-E colonisation is common in sSA, but how people become carriers and why is not well understood. To inform the design of interventions to interrupt transmission in this setting requires longitudinal, community studies.


2020 ◽  
Vol 4 ◽  
pp. 160
Author(s):  
Joseph M. Lewis ◽  
Rebecca Lester ◽  
Paul Garner ◽  
Nicholas A. Feasey

Background: Extended-spectrum beta-lactamase producing Enterobacteriaceae (ESBL-E) threaten human health; and, in areas of sub-Saharan Africa (sSA) where carbapenems are not available, may render ESBL-E infections untreatable. Gut mucosal colonisation probably occurs before infection, making prevention of colonisation an attractive target for intervention, but the epidemiology of ESBL-E in sSA is poorly described. Objectives: Describe ESBL-E colonisation prevalence in sSA and risk factors associated with colonisation. Methods: Studies included were prospective cross-sectional or cohort studies reporting gut mucosal ESBL-E colonisation in any population in sSA. We searched PubMed and Scopus on 18 December 2018. We summarise the range of prevalence across sites and tabulated risk factors for colonisation. The protocol was registered (Prospero ID CRD42019123559). Results: From 2975 abstracts we identified 32 studies including a total of 8619 participants from a range of countries and settings. Six studies were longitudinal; no longitudinal studies followed patients beyond hospital discharge.  Prevalence varied between 5 and 84% with a median of 31%, with a relationship to setting: pooled ESBL-E colonisation in community studies was 18% (95% CI 12 to 28, 12 studies); in studies recruiting people at admission to hospital colonisation was 32% (95% CI 24 to 41% 8 studies); and for inpatients, colonisation was 55% (95% CI 49 to 60%, 7 studies). Antimicrobial use was associated with increased risk of ESBL-E colonisation, and protected water sources or water treatment by boiling may reduce risk. Conclusions: ESBL-E colonisation is common in sSA, but how people become carriers and why is not well understood. To inform the design of interventions to interrupt transmission in this setting requires longitudinal, community studies.


Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 782-786
Author(s):  
Tsukasa Kuwana ◽  
Junko Yamaguchi ◽  
Kosaku Kinoshita ◽  
Satoshi Hori ◽  
Shingo Ihara ◽  
...  

AbstractCarbapenems are frequently used to treat infections caused by extended-spectrum beta-lactamase-producing Enterobacteriaceae (ESBL-E), but carbapenem-resistant Enterobacteriaceae bacteria are a clinical concern. Although cephamycins (cefmetazole; CMZ) have been shown to be effective against mild cases of ESBL-E infection, data on their use for severe ESBL-E infections with sepsis or septic shock remain scarce. Herein, we discuss a de-escalation therapy to CMZ that could be used after empiric antibiotic therapy in ICU patients with sepsis or septic shock caused by ESBL-E bacteremia. A sequence of 25 cases diagnosed with sepsis or septic shock caused by ESBL-E bacteria was evaluated. The attending infectious disease specialist physicians selected the antibiotics and decided the de-escalation timing. The median SOFA (Sequential Organ Failure Assessment) and APACHE II (Acute Physiology and Chronic Health Evaluation II) severity scores were 8 and 30; the rate of septic shock was 60%. Infections originated most frequently with urinary tract infection (UTI) (56%) and Escherichia coli (85%). Eleven patients were de-escalated to CMZ after vital signs were stable, and all survived. No patients died of UTI regardless of with or without de-escalation. The median timing of de-escalation antibiotic therapy after admission was 4 days (range, 3–6 days). At the time of de-escalation, the median SOFA score fell from 8 to 5, the median APACHE II score from 28 to 22, and the rate of septic shock from 55% to 0%. We conclude that for sepsis in UTI caused by ESBL-E bacteremia, de-escalation therapy from broad-spectrum antibiotics to CMZ is a potential treatment option when vital signs are stable.


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