Prevention of healthcare-associated Clostridium difficile infection: What works?

Prevention of Clostridium difficile infection (CDI) has become extremely important because of increases in CDI incidence and severity. Unfortunately CDI prevention efforts are hampered by lack of data to support optimal prevention methods, especially for endemic CDI. Studies are needed to define optimal prevention practices and to investigate novel prevention methods

A randomized, placebo-controlled trial of fidaxomicin for prophylaxis of Clostridium difficile-associated diarrhea in adults undergoing hematopoietic stem cell transplantation

Background: Clostridium difficile-associated diarrhea (CDAD) is common during hematopoietic stem-cell transplantation (HSCT) and is associated with increased morbidity and mortality. We evaluated fidaxomicin for prevention of CDAD in HSCT patients. Methods: In this double-blind study, subjects undergoing HSCT with fluoroquinolone prophylaxis stratified by transplant type (autologous/allogeneic) were randomized to once-daily oral fidaxomicin (200 mg) or a matching placebo. Dosing began within 2 days of starting conditioning or fluoroquinolone prophylaxis and continued until 7 days after neutrophil engraftment or completion of fluoroquinolone prophylaxis/clinically-indicated antimicrobials for up to 40 days. The primary endpoint was CDAD incidence through 30 days after study medication. The primary endpoint analysis counted confirmed CDAD, receipt of CDAD-effective medications (for any indication), and missing CDAD assessment (for any reason, including death) as failures; this composite analysis is referred to as prophylaxis failure to distinguish from the pre-specified sensitivity analysis, which counted only confirmed CDAD (by toxin immunoassay or nucleic acid amplification test) as failure. Results: Of 611 subjects enrolled, 600 were treated and analyzed. Prophylaxis failure was similar in fidaxomicin and placebo recipients (28.6% vs 30.8%; difference 2.2% [-5.1, 9.5], P = .278). However, most failures were due to non-CDAD events. Confirmed CDAD was lower in fidaxomicin vs placebo recipients (4.3% vs 10.7%; difference 6.4% [2.2, 10.6], P = .0014). Drug-related adverse events occurred in 15.0% of fidaxomicin recipients and 20.0% of placebo recipients. Conclusions: While no difference was demonstrated between arms in the primary analysis, results of the sensitivity analysis demonstrated that fidaxomicin significantly reduced the incidence of CDAD in HSCT recipients. Clinical Trials Registration: NCT01691248

Pitfalls associated with the use of molecular diagnostic panels in the diagnosis of cryptococcal meningitis

Abstract We report the case of a kidney transplantation patient on chronic immunosuppressive therapy presenting with subacute meningitis. The final diagnosis of cryptococcal meningitis was delayed due to 2 false-negative cryptococcal results on a molecular diagnostic panel. Caution with such platforms in suspected cryptococcal meningitis is needed.</jats:p

Clostridium difficile infection in the United States: A national study assessing preventive practices used and perceptions of practice evidence

We surveyed 571 US hospitals about practices used to prevent Clostridium difficile infection (CDI). Most hospitals reported regularly using key CDI prevention practices, and perceived their strength of evidence as high. The largest discrepancy between regular use and perceived evidence strength occurred with antimicrobial stewardship programs.Infect. Control Hosp. Epidemiol. 2015;36(8):969–971</jats:p

Risk factors for recurrent Clostridium difficile infection (CDI) hospitalization among hospitalized patients with an initial CDI episode: A retrospective cohort study

BACKGROUND: Recurrent Clostridium difficile infection (rCDI) is observed in up to 25% of patients with an initial CDI episode (iCDI). We assessed risk factors for rCDI among patients hospitalized with iCDI. METHODS: We performed a retrospective cohort study at Barnes-Jewish Hospital from 1/1/03 to 12/31/09. iCDI was defined as a positive toxin assay for C. difficile with no CDI in previous 60 days, and rCDI as a repeat positive toxin ≤42 days of stopping iCDI treatment. Three demographic, 13 chronic and 12 acute disease characteristics, and 21 processes of care were assessed for association with rCDI. Cox modeling identified independent risk factors for rCDI. RESULTS: 425 (10.1%) of 4,200 patients enrolled developed rCDI. Of the eight risk factors for rCDI on multivariate analyses, the strongest three were 1) high-risk antimicrobials following completion of iCDI treatment (HR 2.95, 95% CI 2.25-3.86), 2) community-onset healthcare-associated iCDI (HR 1.80, 95% CI 1.41-2.29) and 3) fluoroquinolones after completion of iCDI treatment (HR 1.56, 95% CI 1.63-2.08). Other risk factors included gastric acid suppression, ≥2 hospitalizations within prior 60 days, age, and IV vancomycin after iCDI treatment ended. CONCLUSIONS: The rCDI rate was 10.1%. Recognizing such modifiable risk factors as certain antimicrobial treatments and gastric acid suppression may help optimize prevention efforts