Honors Program

Honors in Health Sciences: Microbiology

Date of Award

5-2018

Thesis Professor(s)

Dr. Sean James Fox

Thesis Professor Department

Health Sciences

Thesis Reader(s)

Dr. Patrick Brown, Dr. Mark Giroux

Abstract

Members of the Staphylococcus genus are known to cause serious human infections in the clinical environment. Many species of this genus are typically found among the normal flora of the skin, nasal cavities, and the linings of the throat; however, the bacterium becomes an opportunistic infection when there is a break in the physical barriers or when a contaminated medical device is implanted in the human body. As more resistant strains are beginning to appear it is becoming drastically harder to treat patients infected with this bacterium. One such strain is Methicillin Resistant Staphylococcus aureus (MRSA). MRSA is a major problem occurring nosocomially as it is highly resistant against Beta-lactam antibiotics, including vancomycin, and as a result this bacterium may be the cause of toxic-shock syndrome in the body, leading to death. Recently, there have been published studies detailing bacterial-bacterial interactions that inhibit the growth of harmful pathogens. In this study, we expand upon an inhibitory interaction previously identified by our lab between Alcaligenes and Staphylococcus. Prior work has shown that Alcaligenes faecalis may have bacteriostatic or bactericidal effects on Staphylococcus aureus. Therefore, we wanted to examine if this inhibitory effect is: 1) produced by other members of the Alcaligenes genus (A. faecalis and A. viscolactis) ; 2) applied to other members of the Staphylococcus genus (S. aureus, S. epidermidis, S. capitis, and S.saprophyticus). A. faecalis inhibits all Staphylococcus species tested, albeit at varying levels, with S. aureus being inhibited the most and S. epidermidis the least. Additionally, inhibitory action was shared among Alcaligenes species as both A. faecalis and A. viscolactis inhibited S. aureus strains. This inhibition appears to require live Alcaligenes cells as heat-killed and the cell free supernatant of A. faecalis and A. viscolactis did not cause inhibition of S. aureus. Although it is possible that the solution may not have been concentrated enough to show proper inhibition. The mechanism is density dependent as increasing the concentration of A. faecalis cells greatly increases the amount of inhibition of S. aureus. Lastly, this interaction ultimately appears to be bactericidal as, LIVE/DEAD viability staining shows S. aureus cells as being compromised. Taken together, these results show a unique previously unreported interaction between Alcaligenes and Staphylococcus. The mechanism by which this interaction occurs is unknown, but could potentially provide new therapeutic targets to combat antimicrobial resistant strains of Staphylococcus.

Publisher

East Tennessee State University

Document Type

Honors Thesis - Withheld

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.

Copyright

Copyright by the authors.

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