title: Clinical and microbiologic characteristics of tcdA-negative variant Clostridium difficile infections.
abstract: BACKGROUND
  The tcdA-negative variant (A-B+) of Clostridium difficile is prevalent in East Asian countries. However, the risk factors and clinical characteristics of A-B+C. difficile infections (CDI) are not clearly documented. The objective of this study was to investigate these characteristics.
  
  
  METHODS
  From September 2008 through January 2010, the clinical characteristics, medication history and treatment outcomes of CDI patients were recorded prospectively. Toxin characterization and antibiotic susceptibility tests were performed on stool isolates of C. difficile.
  
  
  RESULTS
  During the study period, we identified 22 cases of CDI caused by tcdA-negative tcdB-positive (A-B+) strains and 105 cases caused by tcdA-positive tcdB-positive (A+B+) strains. There was no significant difference in disease severity or clinical characteristics between the two groups. Previous use of clindamycin and young age were identified as significant risk factors for the acquisition of A-B+ CDI (OR = 4.738, 95% CI 1.48-15.157, p = 0.009 and OR = 0.966, 95% CI 0.935-0.998, p = 0.038, respectively) in logistic regression.Rates of resistance to clindamycin were 100% and 69.6% in the A-B+ and A+B+ isolates, respectively (p = 0.006), and the ermB gene was identified in 17 of 21 A-B+ isolates (81%). Resistance to moxifloxacin was also more frequent in the A-B+ than in the A+B+ isolates (95.2% vs. 63.7%, p = 0.004).
  
  
  CONCLUSIONS
  The clinical course of A-B+ CDI is not different from that of A+B+ CDI. Clindamycin use is a significant risk factor for the acquisition of tcdA-negative variant strains.
authors.affiliation: Department of Internal Medicine, Hanyang University College of Medicine, Seoul, Korea.
authors.forename: Jieun
authors.initials: J
authors.lastname: Kim
authors.forename: Hyunjoo
authors.initials: H
authors.lastname: Pai
authors.forename: Mi-Ran
authors.initials: MR
authors.lastname: Seo
authors.forename: Jung Oak
authors.initials: JO
authors.lastname: Kang
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D001372:Aza Compounds / Q000494:pharmacology / Q000627:therapeutic use; D001426:Bacterial Proteins / Q000378:metabolism*; D001427:Bacterial Toxins / Q000378:metabolism*; D002981:Clindamycin / Q000494:pharmacology / Q000627:therapeutic use; D016360:Clostridioides difficile / Q000187:drug effects / Q000302:isolation & purification*; D003015:Clostridium Infections / Q000188:drug therapy / Q000378:metabolism / Q000382:microbiology*; D003967:Diarrhea / Q000188:drug therapy / Q000382:microbiology; D004352:Drug Resistance, Microbial; D004768:Enterotoxins / Q000378:metabolism*; D005243:Feces / Q000382:microbiology; D005260:Female; D024841:Fluoroquinolones; D006801:Humans; D008297:Male; D008826:Microbial Sensitivity Tests; D008875:Middle Aged; D000077266:Moxifloxacin; D011446:Prospective Studies; D011804:Quinolines / Q000494:pharmacology / Q000627:therapeutic use; D012307:Risk Factors; D012720:Severity of Illness Index; D016896:Treatment Outcome
chemical_list: D000900:Anti-Bacterial Agents; D001372:Aza Compounds; D001426:Bacterial Proteins; D001427:Bacterial Toxins; D004768:Enterotoxins; D024841:Fluoroquinolones; D011804:Quinolines; C041348:tcdA protein, Clostridium difficile; D002981:Clindamycin; D000077266:Moxifloxacin