Journal
MICROORGANISMS
Volume 11, Issue 9, Pages -Publisher
MDPI
DOI: 10.3390/microorganisms11092161
Keywords
Clostridioides difficile; colonization; toxin production; pathogenicity of toxins; antibiotics; fidaxomicin; sequestering or inactivating toxin production; quorum quenching; immunization; bacteriotherapy
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This article summarizes factors affecting the colonization of C. difficile and the pathogenicity of toxins TcdA and TcdB, and evaluates different approaches for the treatment of CDI.
Clostridioides difficile is considered a nosocomial pathogen that flares up in patients exposed to antibiotic treatment. However, four out of ten patients diagnosed with C. difficile infection (CDI) acquired the infection from non-hospitalized individuals, many of whom have not been treated with antibiotics. Treatment of recurrent CDI (rCDI) with antibiotics, especially vancomycin (VAN) and metronidazole (MNZ), increases the risk of experiencing a relapse by as much as 70%. Fidaxomicin, on the other hand, proved more effective than VAN and MNZ by preventing the initial transcription of RNA toxin genes. Alternative forms of treatment include quorum quenching (QQ) that blocks toxin synthesis, binding of small anion molecules such as tolevamer to toxins, monoclonal antibodies, such as bezlotoxumab and actoxumab, bacteriophage therapy, probiotics, and fecal microbial transplants (FMTs). This review summarizes factors that affect the colonization of C. difficile and the pathogenicity of toxins TcdA and TcdB. The different approaches experimented with in the destruction of C. difficile and treatment of CDI are evaluated.
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