» Articles » PMID: 18808358

Emergence of Clostridium Difficile Infection Due to a New Hypervirulent Strain, Polymerase Chain Reaction Ribotype 078

Overview
Journal Clin Infect Dis
Date 2008 Sep 24
PMID 18808358
Citations 248
Authors
Affiliations
Soon will be listed here.
Abstract

Background: Since 2005, an increase in the prevalence of Clostridium difficile infection (CDI) due to polymerase chain reaction ribotype 078 has been noticed in The Netherlands. This strain has also been identified as the predominant strain in pigs and calves.

Methods: CDI caused by type 078 was studied in relation to CDI caused by the hypervirulent type 027 and by types other than 027 and 078. Human and porcine isolates were further investigated and characterized by multilocus variable number tandem repeat analysis.

Results: From February 2005 through February 2008, the incidence of type 078 among isolates obtained from 1687 patients increased from 3% to 13%. Compared with patients infected with type 027, patients infected with type 078 were younger (67.4 vs. 73.5 years; P < .01) and more frequently had community-associated disease (17.5% vs. 6.7%; odds ratio, 2.98; 95% confidence interval, 2.11-8.02); rates of severe diarrhea (38.9% vs. 40.0%) and attributable mortality (3.8% vs. 4.0%) were similar in both groups. Compared with patients infected with other types, patients infected with type 078 more frequently received fluoroquinolone therapy (29.4% vs. 19.8%; odds ratio, 2.17; 95% confidence interval, 1.06-4.44). Type 078 isolates contained genes for toxin A, toxin B, binary toxin, and a 39-base pair deletion in toxin regulator gene (tcdC), as well as a point mutation at position 184, resulting in a stop codon. Multilocus variable number tandem repeat analysis of 54 human and 11 porcine isolates revealed 4 clonal complexes containing both porcine and human isolates.

Conclusions: CDI due to type 078 and CDI due to type 027 present with similar severity, but CDI due to type 078 affects a younger population and is more frequently community associated. C. difficile type 078 isolates from humans and pigs are highly genetically related.

Citing Articles

Abundant geographical divergence of Clostridioides difficile infection in China: a prospective multicenter cross-sectional study.

Bai L, Xu T, Zhang W, Jiang Y, Gu W, Zhao W BMC Infect Dis. 2025; 25(1):185.

PMID: 39920584 PMC: 11806848. DOI: 10.1186/s12879-025-10552-y.


PPAR-γ agonist mitigates intestinal barrier dysfunction and inflammation induced by Clostridioides difficile SlpA in vitro.

Noori M, Azimirad M, Ghorbaninejad M, Meyfour A, Zali M, Yadegar A Sci Rep. 2024; 14(1):32087.

PMID: 39738433 PMC: 11686163. DOI: 10.1038/s41598-024-83815-4.


and Gut Microbiota: From Colonization to Infection and Treatment.

Spigaglia P Pathogens. 2024; 13(8).

PMID: 39204246 PMC: 11357127. DOI: 10.3390/pathogens13080646.


Fecal microbiota live - jslm (Rebyota™/RBL) for management of recurrent infection.

Boyle B, Khanna S Future Microbiol. 2024; 19(14):1243-1251.

PMID: 38989699 PMC: 11633411. DOI: 10.1080/17460913.2024.2364583.


Association of toxin-producing Clostridioides difficile with piglet diarrhea and potential transmission to humans.

Takeichi K, Fukuda A, Shono C, Ota N, Nakajima C, Suzuki Y J Vet Med Sci. 2024; 86(7):769-776.

PMID: 38797681 PMC: 11251813. DOI: 10.1292/jvms.24-0051.