Mentor: John Alumasa, Ph.D.

Antibiotic-resistant bacteria remain a serious threat to global health that needs urgent resolution. It is estimated that infections caused by resistant microbes will result in over 50 million deaths annually by 2050, surpassing those from cancer-related complications (Naghavi). Bacteria use various survival strategies to evade the effects of antibiotics, including forming biofilms. Bacterial biofilms are assemblies of surface-associated cells enclosed in a mucus-like extracellular polysaccharide (EPS) matrix that offers several benefits to the microbes, including protection from antibiotic treatments. Biofilms are particularly dangerous in clinical settings because they facilitate bacterial attachment to lung, skin, or gut tissue, leading to medical complications. The EPS matrix has been attributed to blocking access to antibiotics, thereby reducing their clinical effectiveness. Moreover, bacterial cells encapsulated within biofilms experience enhanced horizontal gene transfer, enabling the exchange of antibiotic resistance genes. The rampant, unchecked spread of biofilms poses a serious threat, warranting mitigation strategies. Several methods are currently being investigated to curb biofilm growth or destroy mature biofilms, including the use of surfactants or genetic manipulation of resident bacterial populations to prevent cell adhesion. While some of these techniques are effective in laboratory settings, their applicability in real-world settings is limited, for example, due to potential reagent toxicity or procedural limitations when applied to patients. Recent approaches involving combinations of antibiofilm growth agents and antibiotics have become center stage. This work aimed to optimize conditions for growing biofilms in our laboratory to investigate similar combinatorial strategies for targeting bacterial cells sheltered within biofilms. A biofilm-forming, non-pathogenic Gram-positive species, Bacillus subtilis, was used as a model in this work to investigate and optimize various growth conditions. Preliminary work on the assessment of the growth surface revealed over 3-fold greater biofilm formation in a plate-well than in a pegged lid. Likewise, biofilm formation increased with temperature and incubation duration. The antibiotics investigated demonstrated a dose-dependent cell-growth-inhibition profile. However, while erythromycin inhibited biofilm growth, amoxicillin appeared to promote it, suggesting an undocumented phenomenon. Future studies will investigate antibiotic-sodium selenite combinations to target bacterial cells growing within mature biofilms. This study will provide vital information on the potential use of sodium selenite to inhibit biofilm growth, which will assist in the ongoing fight to tackle antibiotic resistance in pathogenic bacterial species.

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