Chronically persistent bacterial infections are an enormous health problem and are prevalent in many medical settings. Often, the bacteria that cause these infections exhibit a small colony variant phenotype, grow slowly, produce biofilms and are resistant to antibiotics. In this study, I used Providencia rettgeri, an opportunistic human pathogen and a natural pathogen of Drosophila melanogaster. From previous research in the Lazzaro Lab, it was found that Providencia rettgeri also has a small colony variant (S strain) phenotype. Therefore, I hypothesized that our isolated S strain is a canonical small colony variant with an ability to persist in the host, Drosophila melanogaster. After conducting various experiments to determine the growth dynamics, biofilm capabilities and antibiotic resistance of the Providencia rettgeri S strain, I concluded that the S strain (small colony phenotype) of Providencia rettgeri is most likely not a suitable model strain for studying small colony variants and their implication in persistent infections. This is because although the S strain did exhibit slower growth and diminished host lethality compared to the wildtype strain (L strain), its ability to produce biofilms and its antibiotic resistance were either equal to or worse than the L strain. Although this strain may not be a canonical small colony variant, it’s slow growth and ability to persist in the host represents an interesting physiology worthy of continued study. A rescue experiment is currently in the works to determine if an identified mutation in the penicillin binding protein gene in the S strain is responsible for the small colony/low host lethality phenotype. The wildtype version of this gene, which is involved in cell wall synthesis and interactions with antibiotics, is hypothesized to restore the large colony size and advanced growth demonstrated by the wildtype strain when expressed in the mutant (S) background.