Inhibition of spores to prevent the recurrence of Clostridioides difficile infection - A possibility or an improbability?

Chiu, Chun Wei; Tsai, Pei Jane; Lee, Ching Chi; Ko, Wen Chien; Hung, Yuan‐Pin

doi:10.1016/j.jmii.2021.06.002

Cited by 11 publications

(7 citation statements)

References 60 publications

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“…Spore germination is triggered by certain compounds such as the primary bile acid, cholic acid, and cholesterol derivatives, including taurocholate. On the other hand, chenodeoxycholate is able to inhibit the germination of C. difficile spores [ 9 , 10 , 11 ]. Once germination has begun, the vegetative cells are able to colonize the colon and start producing toxins [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Make It Less difficile: Understanding Genetic Evolution and Global Spread of Clostridioides difficile

Mengoli

Barone

Fabbrini

et al. 2022

Genes

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Clostridioides difficile is an obligate anaerobic pathogen among the most common causes of healthcare-associated infections. It poses a global threat due to the clinical outcomes of infection and resistance to antibiotics recommended by international guidelines for its eradication. In particular, C. difficile infection can lead to fulminant colitis associated with shock, hypotension, megacolon, and, in severe cases, death. It is therefore of the utmost urgency to fully characterize this pathogen and better understand its spread, in order to reduce infection rates and improve therapy success. This review aims to provide a state-of-the-art overview of the genetic variation of C. difficile, with particular regard to pathogenic genes and the correlation with clinical issues of its infection. We also summarize the current typing techniques and, based on them, the global distribution of the most common ribotypes. Finally, we discuss genomic surveillance actions and new genetic engineering strategies as future perspectives to make it less difficile.

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Section: Introductionmentioning

confidence: 99%

Make It Less difficile: Understanding Genetic Evolution and Global Spread of Clostridioides difficile

Mengoli

Barone

Fabbrini

et al. 2022

Genes

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“…Vancomycin is in a class of medications called glycopeptide antibiotics and its oral administration kills gram-positive bacteria in the intestine, such as Clostridioides difficile (C. difficile). Mechanistically vancomycin inhibits bacterial cell wall formation and has little effect on spore germination [11]. Antibioticinduced gut microbial disturbance can result in many negative effects including diarrhea and pathogen colonization, therefore use of probiotics as a means to protect against these effects has been investigated [12].…”

Section: Introductionmentioning

confidence: 99%

Targeting the Gut Microbiota and Host Immunity with a Bacilli-Species Probiotic during Antibiotic Exposure in Mice

et al. 2022

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Antibiotic therapy is necessary for the treatment of bacterial infections; however, it can also disrupt the balance and function of commensal gut microbes and negatively affect the host. Probiotics have been tested as a means to counteract the negative effects of antibiotic therapy, but many probiotics are also likely destroyed by antibiotics when taken together. Here we aimed to test the efficacy of a non-pathogenic spore-forming Bacillus-species containing a probiotic blend provided during antibiotic therapy on host immune defenses in mice. Mice were exposed to antibiotics and supplemented with or without the probiotic blend and compared to control mice. Fecal and cecal contents were analyzed for gut microbes, and intestinal tissue was tested for the expression of key enzymes involved in vitamin A metabolism, serum amyloid A, and inflammatory markers in the intestine. The probiotic blend protected against antibiotic-induced overgrowth of gram-negative bacteria and gammaproteobacteria in the cecum which correlated with host immune responses. Regional responses in mRNA expression of enzymes involved with vitamin A metabolism occurred between antibiotic groups, and intestinal inflammatory markers were mitigated with the probiotic blend. These data suggest prophylactic supplementation with a spore-forming Bacillus-containing probiotic may protect against antibiotic-induced dysregulation of host immune responses.

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“…Clostridioides difficile is well known to cause gastrointestinal infections, ranging from mild diarrhea to pseudomembranous colitis or toxic megacolon. [1][2][3] Because innate immunity plays a crucial role in the occurrence and development of C. difficile infections (CDIs), 1,4 impaired host immunity, such as the presence of hematological malignancy or polymorphisms of immune genes (such as IL-8 or toll-like receptors), is linked to the increased incidence and recurrence rates of CDIs. 1,4,5 The association between immunosuppressant drugs and the occurrence or development of CDIs is ambiguous and seems to be one body two sides.…”

Section: Introductionmentioning

confidence: 99%

Impacts of Corticosteroid Therapy at Acute Stage of Hospital-Onset Clostridioides difficile Infections

Lee¹,

Lee²,

Chiu³

et al. 2022

IDR

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Introduction The influence of corticosteroid therapy before or after the onset of Clostridioides difficile infections (CDIs) on the clinical outcomes of adults with hospital-onset CDIs was investigated. Materials and Methods A clinical study was conducted on the medical wards of a teaching hospital between January 2013 and April 2020. Adults (aged ≥ 20 years) with hospital-onset CDIs (ie, symptom onset at least 48 hours after hospitalization) were included. “Corticosteroid therapy during acute CDIs” was defined as the receipt of a corticosteroid at the prednisolone equivalent (PE) dose of ≥10 mg for at least 48 hours within one week after the CDI diagnosis. “Prior corticosteroid exposure” was defined as the receipt of a corticosteroid at the PE dose of ≥5 mg PE for at least 48 hours within one month before the CDI diagnosis. Results Of the 243 adults with hospital-onset CDIs, patients (44, 18.1%) who received corticosteroid therapy during acute CDIs were more likely to have prior corticosteroid exposure (86.4% vs 11.9%, P <0.001) and CDI episodes in intensive care units (31.8% vs 10.8%, P =0.001). Of note, a crucial association between corticosteroid therapy during acute CDIs and CDI recurrence was evidenced (13.6% vs 1.5%, P =0.002). Prior corticosteroid exposure was not associated with favorable CDI outcomes in terms of successful treatment (78.3% vs 74.9%, P =0.89), in-hospital crude mortality (17.4% vs 24.0%, P =0.61), or CDI recurrence (4.3% vs 5.3%, P = 1.00). However, for 177 patients without prior corticosteroid exposure, corticosteroid therapy during acute CDIs was linked to a higher proportion of CDI recurrence (33.3% vs 5.3%, P =0.046). Conclusion Corticosteroid therapy during acute CDIs might impact the recurrence of CDIs, particularly in those with a lack of prior corticosteroid exposure.

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Inhibition of spores to prevent the recurrence of Clostridioides difficile infection - A possibility or an improbability?

Cited by 11 publications

References 60 publications

Make It Less difficile: Understanding Genetic Evolution and Global Spread of Clostridioides difficile

Make It Less difficile: Understanding Genetic Evolution and Global Spread of Clostridioides difficile

Targeting the Gut Microbiota and Host Immunity with a Bacilli-Species Probiotic during Antibiotic Exposure in Mice

Impacts of Corticosteroid Therapy at Acute Stage of Hospital-Onset Clostridioides difficile Infections

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