Vancomycin Delays Clindamycin-Induced Fatality in the Hamster Model of Clostridioides [Clostridium] Difficile Infection
Center for Academic Enrichment and Outreach
University of Nevada, Las Vegas; Center for Academic Enrichment and Outreach
Las Vegas (Nev.)
Antibiotics can leave the host gut microbiome susceptible to Clostridioides [Clostridium] difficile colonization and lethal toxin production. For instance, clindamycin-induced susceptibility to C. difficile infection (CDI) results in rapid fatality in hamster models, yet vancomycin has been shown to offer increased survival in hamsters challenged with C. difficile. We aim to develop an antibiotic treatment that will facilitate CDI susceptibility without prompt fatality in hamster models. An antibiotic regimen starting with a continuous vancomycin treatment along with a single clindamycin dosage is thought to reduce the major disruption in the indigenous gut microbiome and prevent clindamycin-induced death. Quantitative polymerase chain reaction (qPCR) of the rpsJ gene was used to determine the abundance of C. difficile in the hamster gut flora over the course of an antibiotic treatment, while toxin A and B production was quantified using a toxin immunoassay (ELISA). The vancomycin-centered antibiotic regimen significantly increased survival rates during administration, whereas clindamycin-induced fatalities occurred after a single dosage. qPCR determined that C. difficile proliferation was rapid. C. difficile was detected in feces two days post-C. difficile challenge in vancomycin and clindamycin-treated animals, with C. difficile remaining in high abundance (>108 gene copies/g feces), until death the following day. Vancomycin administered continuously for five days with one clindamycin treatment postponed C. difficile toxin production, while still leaving hosts susceptible to infection. These results suggest that incorporating vancomycin into an antibiotic regimen will delay clindamycin-induced death whilst permitting C. difficile susceptibility, but it cannot delay the rapid pathogenesis of CDI and subsequent fatalities in the hamster model.
Clostridioides [Clostridium] difficile; C. difficile; Vancomycin; Clindamycin; Hamster model
Bacteria | Digestive System Diseases | Disease Modeling | Medical Biochemistry | Medical Microbiology | Pathogenic Microbiology
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Fox-King, A. E.,
Phan, J. R.,
Nou, N. O.,
Hedlund, B. P.
Vancomycin Delays Clindamycin-Induced Fatality in the Hamster Model of Clostridioides [Clostridium] Difficile Infection.
Available at: https://digitalscholarship.unlv.edu/lsamp_posters/4
Bacteria Commons, Digestive System Diseases Commons, Disease Modeling Commons, Medical Biochemistry Commons, Medical Microbiology Commons, Pathogenic Microbiology Commons