A retrospective cohort study of antibiotic exposure and vancomycin-resistant Enterococcus recolonization

2019 ◽  
Vol 40 (4) ◽  
pp. 414-419
Author(s):  
Heather Y. Hughes ◽  
Robin T. Odom ◽  
Angela V. Michelin ◽  
Evan S. Snitkin ◽  
Ninet Sinaii ◽  
...  

AbstractObjective:In the National Institutes of Health (NIH) Clinical Center, patients colonized or infected with vancomycin-resistant Enterococcus (VRE) are placed in contact isolation until they are deemed “decolonized,” defined as having 3 consecutive perirectal swabs negative for VRE. Some decolonized patients later develop recurrent growth of VRE from surveillance or clinical cultures (ie, “recolonized”), although that finding may represent recrudescence or new acquisition of VRE. We describe the dynamics of VRE colonization and infection and their relationship to receipt of antibiotics.Methods:In this retrospective cohort study of patients at the National Institutes of Health Clinical Center, baseline characteristics were collected via chart review. Antibiotic exposure and hospital days were calculated as proportions of VRE decolonized days. Using survival analysis, we assessed the relationship between antibiotic exposure and time to VRE recolonization in a subcohort analysis of 72 decolonized patients.Results:In total, 350 patients were either colonized or infected with VRE. Among polymerase chain reaction (PCR)-positive, culture (Cx)-negative (PCR+/Cx−) patients, PCR had a 39% positive predictive value for colonization. Colonization with VRE was significantly associated with VRE infection. Among 72 patients who met decolonization criteria, 21 (29%) subsequently became recolonized. VRE recolonization was 4.3 (P = .001) and 2.0 (P = .22) times higher in patients with proportions of antibiotic days and antianaerobic antibiotic days above the median, respectively.Conclusion:Colonization is associated with clinical VRE infection and increased mortality. Despite negative perirectal cultures, re-exposure to antibiotics increases the risk of VRE recolonization.

2018 ◽  
Vol 5 (2) ◽  
Author(s):  
Maroun Sfeir ◽  
Marissa Walsh ◽  
Rossana Rosa ◽  
Laura Aragon ◽  
Sze Yan Liu ◽  
...  

Abstract Background Infections caused by Mycobacterium abscessus group strains are usually resistant to multiple antimicrobials and challenging to treat worldwide. We describe the risk factors, treatment, and clinical outcomes of patients in 2 large academic medical centers in the United States. Methods A retrospective cohort study of hospitalized adults with a positive culture for M. abscessus in Miami, Florida (January 1, 2011, to December 31, 2014). Demographics, comorbidities, the source of infection, antimicrobial susceptibilities, and clinical outcomes were analyzed. Early treatment failure was defined as death and/or infection relapse characterized either by persistent positive culture for M. abscessus within 12 weeks of treatment initiation and/or lack of radiographic improvement. Results One hundred eight patients were analyzed. The mean age was 50.81 ± 21.03 years, 57 (52.8%) were females, and 41 (38%) Hispanics. Eleven (10.2%) had end-stage renal disease, 34 (31.5%) were on immunosuppressive therapy, and 40% had chronic lung disease. Fifty-nine organisms (54.6%) were isolated in respiratory sources, 21 (19.4%) in blood, 10 (9.2%) skin and soft tissue, and 9 (8.3%) intra-abdominal. Antimicrobial susceptibility reports were available for 64 (59.3%) of the patients. Most of the isolates were susceptible to clarithromycin, amikacin, and tigecycline (93.8%, 93.8%, and 89.1%, respectively). None of the isolates were susceptible to trimethoprim/sulfamethoxazole, and only 1 (1.6%) was susceptible to ciprofloxacin. Thirty-six (33.3%) patients early failed treatment; of those, 17 (15.7%) died while hospitalized. On multivariate analysis, risk factors significantly associated with early treatment failure were disseminated infection (odds ratio [OR], 11.79; 95% confidence interval [CI], 1.53–81.69; P = .04), acute kidney injury (OR, 6.55; 95% CI, 2.4–31.25; P = .018), organ transplantation (OR, 2.37; 95% CI, 2.7–23.1; P = .005), immunosuppressive therapy (OR, 2.81; 95% CI, 1.6–21.4; P = .002), intravenous amikacin treatment (OR, 4.1; 95% CI, 0.9–21; P = .04), clarithromycin resistance (OR,79.5; 95% CI, 6.2–3717.1, P < .001), and presence of prosthetic device (OR, 5.43; 95% CI, 1.57–18.81; P = .008). Receiving macrolide treatment was found to be protective against early treatment failure (OR, 0.13; 95% CI, 0.002–1.8; P = .04). Conclusions Our cohort of 108 M. abscessus complex isolates in Miami, Florida, showed an in-hospital mortality of 15.7%. Most infections were respiratory. Clarithromycin and amikacin were the most likely agents to be susceptible in vitro. Resistance to fluoroquinolone and trimethoprim/sulfamethoxazole was highly common. Macrolide resistance, immunosuppression, and renal disease were significantly associated with early treatment failure.


2015 ◽  
Vol 2 (suppl_1) ◽  
Author(s):  
Heather Y. Hughes ◽  
Robin T. Odom ◽  
Angela V. Michelin ◽  
Evan S. Snitkin ◽  
Ninet Sinaii ◽  
...  

2019 ◽  
Vol 71 (3) ◽  
pp. 645-651 ◽  
Author(s):  
Vanessa W Stevens ◽  
Karim Khader ◽  
Kelly Echevarria ◽  
Richard E Nelson ◽  
Yue Zhang ◽  
...  

Abstract Background Vancomycin is now a preferred treatment for all cases of Clostridioides difficile infection (CDI), regardless of disease severity. Concerns remain that a large-scale shift to oral vancomycin may increase selection pressure for vancomycin-resistant Enterococci (VRE). We evaluated the risk of VRE following oral vancomycin or metronidazole treatment among patients with CDI. Methods We conducted a retrospective cohort study of patients with CDI in the US Department of Veterans Affairs health system between 1 January 2006 and 31 December 2016. Patients were included if they were treated with metronidazole or oral vancomycin and had no history of VRE in the previous year. Missing data were handled by multiple imputation of 50 datasets. Patients treated with oral vancomycin were compared to those treated with metronidazole after balancing on patient characteristics using propensity score matching in each imputed dataset. Patients were followed for VRE isolated from a clinical culture within 3 months. Results Patients treated with oral vancomycin were no more likely to develop VRE within 3 months than metronidazole-treated patients (adjusted relative risk, 0.96; 95% confidence interval [CI], .77 to 1.20), equating to an absolute risk difference of −0.11% (95% CI, −.68% to .47%). Similar results were observed at 6 months. Conclusions Our results suggest that oral vancomycin and metronidazole are equally likely to impact patients’ risk of VRE. In the setting of stable CDI incidence, replacement of metronidazole with oral vancomycin is unlikely to be a significant driver of increased risk of VRE at the patient level. In this multicenter, retrospective cohort study of patients with Clostridioides difficile infection, the use of oral vancomycin did not increase the risk of vancomycin-resistant Enterococci infection at 3 or 6 months compared to metronidazole.


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