Review of Current Literature on the Economic Burden of<i>Clostridium difficile</i>Infection

Dubberke, Erik R.; Wertheimer, Albert I.

doi:10.1086/592981

Cited by 171 publications

(140 citation statements)

References 45 publications

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“…Today, CDI is a huge social and economic burden 1 causing an estimated $3.2 billion of health care cost to US hospitals alone. 2,3 Advanced age ( 65 years), antibiotic use, immunosuppression, exposure to health care system and long-time hospitalization are major risk factors for CDI. 4 C. difficile toxins A (TcdA) and B (TcdB) are the major virulence factors.…”

Section: Introductionmentioning

confidence: 99%

A chimeric protein comprising the glucosyltransferase and cysteine proteinase domains of toxin B and the receptor binding domain of toxin A induces protective immunity againstClostridium difficileinfection in mice and hamsters

Wang

Yan

Kim

et al. 2015

Human Vaccines & Immunotherapeutics

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Section: Introductionmentioning

confidence: 99%

A chimeric protein comprising the glucosyltransferase and cysteine proteinase domains of toxin B and the receptor binding domain of toxin A induces protective immunity againstClostridium difficileinfection in mice and hamsters

Wang

Yan

Kim

et al. 2015

Human Vaccines & Immunotherapeutics

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“…Following several major outbreaks of C. difficile infection by hypervirulent strains in North America and Europe, the disease continues to be a major cause of diarrhoea in hospitalized patients and among the elderly in long-term care facilities. The mortality and morbidity associated with C. difficile infections is high, resulting in significant economic burden (Dubberke & Wertheimer, 2009). Regardless of the impact, there has been little improvement in C. difficile treatment in the last 30 years.…”

Section: Introductionmentioning

confidence: 99%

Killing kinetics of fidaxomicin and its major metabolite, OP-1118, against Clostridium difficile

Babakhani

Gomez

Robert

et al. 2011

Journal of Medical Microbiology

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The kinetics of bacterial killing for fidaxomicin and its major metabolite, OP-1118, were investigated against Clostridium difficile strains, including two clinical strains belonging to the restriction endonuclease analysis group BI (ORG 1687 and 1698), the ATCC 43255 strain and two laboratory-derived mutant strains with decreased susceptibility to fidaxomicin (ORG 919 and 1620). Both fidaxomicin and OP-1118 demonstrated time-dependent killing of C. difficile strains. Fidaxomicin (at 4¾ MIC) reduced bacterial counts of the ATCC 43255 strain, clinical strain ORG 1687 and the two laboratory-generated mutant strains by ¢3 logs within 48 h of exposure. The other BI strain, ORG 1698, was tested at 2¾ MIC fidaxomicin with bacterial counts decreasing 1 log in 48 h. Exposure to OP-1118 (at 4¾ MIC) also resulted in a ¢3 log drop in c.f.u. counts for the ATCC 43255 strain, the clinical BI strain ORG 1687 and the mutant strain ORG 919. Higher concentrations of OP-1118 (32¾ MIC) were required for a 3 log reduction in c.f.u. counts for the other BI strain, ORG 1698. In summary, the results indicate that both fidaxomicin and its major metabolite, OP-1118, are bactericidal against C. difficile strains, including the hypervirulent restriction endonuclease analysis group BI strains, at concentrations that are many fold below the detected faecal concentrations of these compounds after oral administration of fidaxomicin.

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“…The presentation of the disease can vary from mild diarrhea to severe colitis (3) and toxic dilatation that requires colectomy or may result in death. The use of proton pump inhibitors, residence in long-term-care facilities, and use of antibiotics are recognized risk factors (4,5). However, the increasing incidence of communityacquired CDI suggests that other contributory factors may be responsible for the spread of the disease (6,7).…”

mentioning

confidence: 99%

A Novel Quantitative Sampling Technique for Detection and Monitoring of Clostridium difficile Contamination in the Clinical Environment

2015

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The horizontal transmission of Clostridium difficile in the hospital environment is difficult to establish. Current methods to detect C. difficile spores on surfaces are not quantitative, lack sensitivity, and are protracted. We propose a novel rapid method to detect and quantify C. difficile contamination on surfaces. Sponge swabbing was compared to contact plate sampling to assess the in vitro recovery of C. difficile ribotype 027 contamination (ϳ10 0 , 10 1 , or 10 2 CFU of spores) from test surfaces (a bed rail, a stainless steel sheet, or a polypropylene work surface). Sponge swab contents were concentrated by vacuum filtration, and the filter membrane was plated onto selective agar. The efficacy of each technique for the recovery of C. difficile from sites in the clinical environment that are touched at a high frequency was evaluated. Contact plates recovered 19 to 32% of the total contamination on test surfaces, whereas sponge swabs recovered 76 to 94% of the total contamination, and contact plates failed to detect C. difficile contamination below a detection C lostridium difficile infection (CDI) remains one of the most clinically important health care-associated infections and continues to burden health care services and finances (1, 2). The presentation of the disease can vary from mild diarrhea to severe colitis (3) and toxic dilatation that requires colectomy or may result in death. The use of proton pump inhibitors, residence in long-term-care facilities, and use of antibiotics are recognized risk factors (4, 5). However, the increasing incidence of communityacquired CDI suggests that other contributory factors may be responsible for the spread of the disease (6, 7). The horizontal transmission of CDI is implicated in patients with or without diarrhea, who may shed spores of C. difficile to contaminate their surrounding surfaces (8). Spores of C. difficile can persist on hospital surfaces for months (9), posing a risk of spreading to surfaces beyond the near patient environment, such as via the hands of patients, visitors, and health care workers (10).To reduce the risk of transmission, patients considered to be sources of CDI should be isolated upon presentation of symptoms of diarrhea, and an enhanced cleaning protocol should be implemented (11). Decontamination of surfaces in the clinical environment using a sporicide is recommended for C. difficile-positive cases only (11). However, patients may remain asymptomatic, even though they are excreting C. difficile (3), and will not prompt the implementation of infection control measures in the absence of diarrhea. Consequently, patients with asymptomatic cases of C. difficile disease may continue to contaminate the clinical environment unhindered unless a carrier status is diagnosed.Assessment of surfaces in the patient environment to monitor contamination levels and the persistence of C. difficile spores is not routinely performed. Current methods to sample surfaces for C. difficile contamination are not quantitative, have a low sensitivity, and req...

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Review of Current Literature on the Economic Burden ofClostridium difficileInfection

Cited by 171 publications

References 45 publications

A chimeric protein comprising the glucosyltransferase and cysteine proteinase domains of toxin B and the receptor binding domain of toxin A induces protective immunity againstClostridium difficileinfection in mice and hamsters

A chimeric protein comprising the glucosyltransferase and cysteine proteinase domains of toxin B and the receptor binding domain of toxin A induces protective immunity againstClostridium difficileinfection in mice and hamsters

Killing kinetics of fidaxomicin and its major metabolite, OP-1118, against Clostridium difficile

A Novel Quantitative Sampling Technique for Detection and Monitoring of Clostridium difficile Contamination in the Clinical Environment

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