Epidemics of Diarrhea Caused by a Clindamycin-Resistant Strain of<i>Clostridium difficile</i>in Four Hospitals

Johnson, Stuart; Samore, Matthew H.; Farrow, Kylie A; Killgore, George; Tenover, Fred C.; Lyras, Dena; Rood, Julian I.; DeGirolami, Paola C.; Baltch, Aldona L.; Rafferty, Mary Ellen; Pear, Suzanne M.; Gerding, Dale N.

doi:10.1056/nejm199911253412203

Cited by 354 publications

(235 citation statements)

References 24 publications

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“…Quality-control strains (Bacteroides fragilis NCTC 11295, Bacteroides thetaiotaomicron ATCC 29741, Escherichia coli ATCC 25922 and Staphylococcus aureus ATCC 25923) were always included. A 688 bp fragment of the ermB gene for erythromycin resistance was amplified using specific primer pairs 2980 (59-AATAAGTAAACAGGTAACGTT-39) and 2981 (59-GCTCCTTGGAAGCTGTCAGTAG-39) (Johnson et al, 1999 (Pituch et al, 2006) generated products of 630 and 399 bp for the tcdA and tcdB genes, respectively. PCR to detect deletion of repeat sequences in the tcdA gene with the NK9/ NKV011 (Pituch et al, 2006) primer pair for the 144 A 2 B + CDT 2 strains generated a 700 bp product similar to that obtained for the Japanese GAI 95 601 C. difficile strain and for the prevalent group of A 2 B + strains of PCR ribotype 017.…”

Section: Methodsmentioning

confidence: 99%

Characterization and antimicrobial susceptibility of Clostridium difficile strains isolated from adult patients with diarrhoea hospitalized in two university hospitals in Poland, 2004–2006

Pituch

Obuch-Woszczatyński

Wultańska

et al. 2011

Journal of Medical Microbiology

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Characterization and antimicrobial susceptibility of Clostridium difficile strains isolated from adult patients with diarrhoea hospitalized in two university hospitals in Poland, 2004Poland, -2006 This study analysed 330 Clostridium difficile strains isolated from patients with C. difficile infection who were hospitalized in two university hospitals (H1 and H2) in Warsaw, Poland, over the period [2004][2005][2006]. Strains were investigated for the presence of tcdA (A), tcdB (B) and binary toxin (CDT) genes, and antimicrobial susceptibility was determined against nine agents. Among the 330 C. difficile isolates, 150 (45.4 %) were classified as A + B + CDT " , 18 (5.5 %) as A + B + CDT + , 144 (43.6 %) as A " B + CDT " and 18 (5.5 %) as A " B " CDT " . The predominant PCR ribotype in hospitals H1 and H2 was type 017 and accounted for 48.3 and 40.0 %, respectively. Only one PCR ribotype 027 strain was found. The rates of resistance to erythromycin and clindamycin in hospitals H1 and H2 were 53.6 and 53.6 %, and 48.6 and 47.5 %, respectively, whereas resistance rates to the newer fluoroquinolones gatifloxacin and moxifloxacin were 38.5 and 38.5 % (H1) and 38.4 and 40.1 % (H2). Erythromycin resistance was frequently associated with resistance to clindamycin and newer fluoroquinolones in strains belonging to type 017. No metronidazole-and vancomycin-resistant isolates were found, although two C. difficile isolates had elevated MIC values of metronidazole (MIC range 1.0"1.5 mg l "1 ) and 15 strains revealed elevated MIC values for vancomycin (MIC range 1.5-2.0 mg l "1 ). In conclusion, an increase in non-027 CDT-producing C. difficile strains was observed in Poland, but C. difficile PCR ribotype 017 remains a major circulating type. INTRODUCTIONClostridium difficile is a major cause of antibioticassociated diarrhoea in hospitalized patients (Freeman et al., 2010). Toxigenic isolates usually produce two toxins: toxin A (A) and toxin B (B). A 2 B + strains do not produce detectable amounts of toxin A due to a deletion in the repeating sequence of the tcdA gene encoding the toxin (Kato et al., 1998). Some C. difficile strains produce a third additional toxin, called C. difficile binary toxin (CDT), which can enhance the attachment of C. difficile to intestinal epithelial cells (Schwan et al., 2009)

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Section: Methodsmentioning

confidence: 99%

Characterization and antimicrobial susceptibility of Clostridium difficile strains isolated from adult patients with diarrhoea hospitalized in two university hospitals in Poland, 2004–2006

Pituch

Obuch-Woszczatyński

Wultańska

et al. 2011

Journal of Medical Microbiology

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“…22 Some strains of C. difficile appear to have enhanced capability for spreading and causing outbreaks. These include the J strain described in 1999 23 …”

Section: Organism Descriptionmentioning

confidence: 99%

Laboratory Diagnosis of Clostridium difficile Infection

Tenover¹,

Baron²,

Peterson

et al. 2011

The Journal of Molecular Diagnostics

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The laboratory diagnosis of Clostridium difficile infection (CDI) continues to be challenging. Recent guidelines from professional societies in the United States note that enzyme immunoassays for toxins A and B do not have adequate sensitivity to be used alone for detecting CDI, yet the optimal method for diagnosing this infection remains unclear. Nucleic acid amplification tests (NAATs) that target chromosomal toxin genes (usually the toxin B gene, tcdB) show high sensitivity and specificity, provide rapid results, and are amenable to both batch and on-demand testing, but these tests were not universally recommended for routine use in the recent guidelines. Rather, two-step algorithms that use glutamate dehydrogenase (GDH) assays to screen for C. difficile in stool specimens, followed by either direct cytotoxin testing or culture to identify toxin-producing C. difficile isolates, were recommended in one guideline and either GDH algorithms or NAATs were recommended in another guideline. Unfortunately, neither culture nor direct cytotoxin testing is widely available. In addition, this two-step approach requires 48 to 92 hours to complete, which may delay the initiation of therapy and critical infection control measures. Recent studies also show the sensitivity of several GDH assays to be <90%. This review considers the role of NAATs for diagnosing CDI and explores their potential advantages over two-step algorithms, including shorter time to results, while providing comparable, if not superior, accuracy.

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“…Antibiotic resistance is a common characteristic of endemic C. difficile strains. Outbreaks in the 1990s are attributed to the emergence and international spread of virulent clindamycin-resistant strains, whilst globally disseminated strains of the 027/BI/NAP1 lineage exhibit resistance to the fluoroquinolones [1,3].…”

Section: Introductionmentioning

confidence: 99%

Identification of a novel mutation at the primary dimer interface of GyrA conferring fluoroquinolone resistance in Clostridium difficile

Aogáin

Kilkenny

Walsh

et al. 2015

Journal of Global Antimicrobial Resistance

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Epidemics of Diarrhea Caused by a Clindamycin-Resistant Strain ofClostridium difficilein Four Hospitals

Cited by 354 publications

References 24 publications

Characterization and antimicrobial susceptibility of Clostridium difficile strains isolated from adult patients with diarrhoea hospitalized in two university hospitals in Poland, 2004–2006

Characterization and antimicrobial susceptibility of Clostridium difficile strains isolated from adult patients with diarrhoea hospitalized in two university hospitals in Poland, 2004–2006

Laboratory Diagnosis of Clostridium difficile Infection

Identification of a novel mutation at the primary dimer interface of GyrA conferring fluoroquinolone resistance in Clostridium difficile

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