Vancomycin Delays Clindamycin-Induced Fatality in the Hamster Model of Clostridioides [Clostridium] Difficile Infection

Authors

Amelia E. Fox-King, University of Nevada, Las VegasFollow
Chrisabelle Mefferd, University of Nevada, Las VegasFollow
Jacqueline R. Phan, University of Nevada, Las VegasFollow
Nancy O. Nou, University of Nevada, Las VegasFollow
Ernesto Abel-Santos, University of Nevada, Las VegasFollow
Brian P. Hedlund, University of Nevada, Las VegasFollow

Funder

Center for Academic Enrichment and Outreach

Document Type

Poster

Publication Date

10-9-2018

Publisher

University of Nevada, Las Vegas; Center for Academic Enrichment and Outreach

Publisher Location

Las Vegas (Nev.)

Abstract

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.

Keywords

Clostridioides [Clostridium] difficile; C. difficile; Vancomycin; Clindamycin; Hamster model

Disciplines

Bacteria | Digestive System Diseases | Disease Modeling | Medical Biochemistry | Medical Microbiology | Pathogenic Microbiology

File Format

pdf

File Size

4.120 KB

Language

English

Rights

IN COPYRIGHT. For more information about this rights statement, please visit http://rightsstatements.org/vocab/InC/1.0/

Repository Citation

Fox-King, A. E., Mefferd, C., Phan, J. R., Nou, N. O., Abel-Santos, E., Hedlund, B. P. (2018). Vancomycin Delays Clindamycin-Induced Fatality in the Hamster Model of Clostridioides [Clostridium] Difficile Infection.
Available at: https://digitalscholarship.unlv.edu/lsamp_posters/4