To assess the effectiveness of selective digestive decontamination (SDD) for eradicating carbapenem-resistant Klebsiella pneumoniae (CRKP) oropharyngeal and gastrointestinal carriage.

A randomized, double-blind, placebo-controlled trial with 7 weeks of follow-up per patient.

A 1,000-bed tertiary-care university hospital.

Adults with CRKP-positive rectal swab cultures.

Patients were blindly randomized (1:1) over a 20-month period. The SDD arm received oral gentamicin and polymyxin E gel (0.5 g 4 times per day) and oral solutions of gentamicin (80 mg 4 times per day) and polymyxin E (1 × 106 units 4 times per day for 7 days). The placebo arm received oral placebo gel 4 times per day and 2 placebo oral solutions 4 times per day for 7 days. Strict contact precautions were applied. Samples obtained from the throat, groin, and urine were also cultured.

Forty patients (mean age ± standard deviation, 71 ± 16 years; 65% male) were included. At screening, greater than or equal to 30% of oropharyngeal, greater than or equal to 60% of skin, and greater than or equal to 35% of urine cultures yielded CRKP isolates. All throat cultures became negative in the SDD arm after 3 days (P< .0001). The percentages of rectal cultures that were positive for CRKP were significandy reduced at 2 weeks. At that time, 16.1% of rectal cultures in the placebo arm and 61.1% in the SDD arm were negative (odds ratio, 0.13; 95% confidence interval, 0.02–0.74; P<.0016). A difference between the percentages in the 2 arms was still maintained at 6 weeks (33.3% vs 58.5%). Groin colonization prevalence did not change in either arm, and the prevalence of urine colonization increased in the placebo arm.

This SDD regimen could be a suitable decolonization therapy for selected patients colonized with CRKP, such as transplant recipients or immunocompromised patients pending chemotherapy and patients who require major intestinal or oropharyngeal surgery. Moreover, in outbreaks caused by CRKP infections that are uncontrolled by routine infection control measures, SDD could provide additional infection containment.

Infect Control Hosp Epidemiol 2012;33(1):14-19

To devise a local strategy for eradication of a hospital-wide outbreak caused by carbapenem-resistant Klebsiella pneumoniae (CRKP).

Quasi-experimental, before-and-after, interrupted time-series study.

A 1,000-bed tertiary-care university teaching hospital.

Retrospectively, all relevant data were collected from the medical records of patients with CRKP infections from May 2006 through April 2007, the preintervention period. From May 1, 2007, through May 1, 2010, the postintervention period, the intervention was applied and prospectively followed. The 5 key elements of this strategy were an emergency department flagging system, the building of a cohort ward, the eradication of clusters, environmental and personnel hand cultures, and a carbapenem-restriction policy. The demographic and clinical parameters of patients colonized by and/or infected with CRKP were collected from medical records.

A total of 10,680 rectal cultures were performed for 8,376 patients; 433 (5.16%) and 370 (4.4%) were CRKP-colonized and CRKP-infected patients, respectively, and 789 (98%) of 803 patients were admitted to the CRKP cohort ward. The CRKP infection density was reduced from 5.26 to 0.18 per 10,000 patient-days (P<.001), and no nosocomial CRKP infections were diagnosed. Twenty-three percent of environmental cultures were found to be positive. Meropenem use was reduced from 283 ± 70.92 to 118 ± 74.32 defined daily doses per 1,000 patient-days (P<.001).

This intervention produced an enormous impact on patient location, surveillance cultures, and antibiotic policies and a massive investment in infection control resources.

To determine the attributable (direct) mortality and morbidity caused by carbapenem-resistant Klebsiella pneumoniae bacteremia.

A matched retrospective, historical cohort design, using a stepwise procedure to stringendy match the best control subjects to the best case subjects.

A 1,000-bed tertiary-care university teaching hospital.

Case subjects were defined as adult patients with carbapenem-resistant K. pneumoniae bacteremia during the period from October 2005 through October 2008. Control subjects were defined as patients who were very similar to case subjects except that they did not have bacteremia.

Matching potential control subjects to case subjects was performed at a 1:1 ratio using a computerized record system. The criteria used included same hospitalization period, similar Charlson comorbidity index, same underlying disease, same age within 10 years, and same sex. Demographic and clinical characteristics were collected from medical records.

During the study period, 319 patients developed an infection due to carbapenem-resistant K. pneumoniae. Of these 319 patients, 39 (12.2%) developed a bloodstream infection, for an overall rate of 0.59 episodes of carbapenem-resistant K. pneumoniae bacteremia per 10,000 patient-days. We excluded 7 patients from our study, leaving a total of 32 case subjects in our cohort. Case subjects were significandy more likely than control subjects (n = 32) to require care in an intensive care unit (12 case subjects [37.5%] vs 3 control subjects [9.4%]), ventilator support (17 case subjects [53.1%] vs 8 control subjects [25%]), and use of a central venous catheter (19 case subjects [59.4%] vs 9 control subjects [28.1%]). For case subjects, the crude mortality rate was 71.9% (ie, 23 of the 32 case subjects died); for control subjects, the crude mortality rate was 21.9% (ie, 7 of the 32 control subjects died) (P < .001. For case subjects, the attributable mortality was 50% (95% confidence interval [CI], 15.3%-98.6%). A mortality risk ratio of 3.3 (95% CI, 2.9-28.5) was found for case subjects with carbapenem-resistant K. pneumoniae bacteremia.

Patients with carbapenem-resistant K. pneumoniae require more intensive and invasive care. We have shown that the crude and attributable mortality rates associated with carbapenem-resistant K. pneumoniae bacteremia were striking.

To implement a comprehensive infection control (IC) program for prevention of cardiac device-associated infections (CDIs).

Prospective before-after trial with 2 years of follow-up.

A tertiary-care, university-affiliated medical center.

A consecutive sample of all adults undergoing cardiac device implantation between 1997 and 2002.

An IC program was implemented during late 2001 and included staff education, preoperative modification of patient risk factors, intraoperative control of strict aseptic technique, surgical scrubbing and attire, control of environmental risk factors, optimization of antibiotic prophylaxis, postoperative wound care, and active surveillance. The clinical endpoint was CDI rates.

Between 1997 and 2000, there were 7 CDIs among 725 procedures (mean annual CDI incidence, 1%). During the first 9 months of 2001, there were 7 CDIs among 167 procedures (4.2%; P = .007): CDIs increased from 7 among 576 to 3 among 124 following pacemaker implantation (P = .39) and from 0 among 149 to 4 among 43 following cardioverter-defibrillator implantation (P = .002). Of the 14 CDIs, 5 involved superficial wounds, 7 involved deep wounds, and 2 involved endocarditis. Following intervention, there were no cases of CDI among 316 procedures during 24 months of follow-up (4.2% reduction; P = .0005).

We observed a high CDI rate associated with substantial morbidity. IC measures had an impact on CDI. Although the relative weight of each measure in the prevention of CDI remains unknown, our results suggest that implementation of a comprehensive IC program is feasible and efficacious in this setting.