User:EKL49/Serratia marcescens

Antibiotic Resistance
Traditionally, infections by S. marcescens have been treated with cefepime, carbapenems (Siedner et al., 2014; Tamma et al., 2022 as cited in Tavares-Carreon et al., 2023), aminoglycoside amikacin, gentamicin and tobramycin (Bertrand & Dowzicky, 2012; Sader et al., 2014 as cited in Tavares-Carreon et al., 2023). However, recent clinical data has shown declining efficacy for gentamicin and tobramycin, part of a trend towards increasing resistance and a narrowing of treatment options. The development of these resistances to common antibiotics is partially due to adaptive resistance through overexposure and selection of resistant strains, but S. marcescens also has intrinsic resistance from sources such as lipopolysaccharide modifications, which can reduce antibiotic penetration, and adaptive resistance through biofilm production (Tavares-Carreon et al., 2023). Biofilm production increases antibiotic resistance because bacteria at the bottom of the biofilm are less exposed to antibiotics, the bacteria in the biofilm do not grow as quickly, and there are faster rates of horizontal gene transfer which allows resistance genes to spread easily within the population. . In 2017, the World Health Organization (WHO) listed Serratia as among the most critical group of bacteria for which new antibiotics are urgently needed due to its resistance to multiple drugs and threat to hospitals, nursing homes, and patients who use ventilators and blood catheters.

Preventing Biofilm Formation (Phloretin)
Biofilm formation is a main cause of how S. marcescens gain drug resistance. Therefore prevention against S. marcescens can be made easier through disrupting its process, specifically through disturbing quorum sensing. A particular phenolic compound called phloretin which “is abundant in the peel/skin and root bark of juicy fruits, such as apples and pears” is an effective method for such as well as reducing the virulence of S. marcescens.

Phloretin not only disrupts the structure of biofilms but increases the level of ethanolamine, a critical ingredient of the cell membrane responsible for sustaining membrane permeability. The increase of ethanolamine increases the permeability of the membrane. Therefore the changed biofilm structure and increased membrane permeability allows for antibiotics to enter the biofilm cells easier, inhibiting spread.

Phloretin impacts the virulence factors of S. marcescens through inhibiting protease activity (responsible for the spoilage of dairy products), prodigiosin production (a virulence factor that plays a vital role in host infection), EPS production (crucial for quorum sensing), as well as repressing swimming and swarming motility (essential for attachment and development of S. marcescens biofilms). All of these effects reduce biofilm formation and pathogenicity.

Studies have shown that phloretin could also inhibit the biofilm formation and virulence of other bacterias such as Streptococcus mutans and Escherichia coli.

Removing Biofilms (Chloramphenicol)
Recent studies examining the effectiveness of existing treatments for S. marcescens have both reiterated the ability for Red Mold to gain adaptive immunity to various antibiotics, but also demonstrated potentials for new treatments that are more effective than existing treatments. The current standard for treatment of S. marcescens, according to the Infectious Disease Society of America, is a process known as antibiotic lock therapy (ALT) which involves holding various antibiotic chemicals in and around affected regions, primarily in catheters and other enclosed tubing (O’Grady et al., 2011). Such a treatment method is the standard for dealing with various types of biofilms or other mold-growths, but there has not yet been any proven effectiveness in dealing with the growth of S marcescens colonies, neither in vivo nor in vitro (Ray et al. Ann Clin Microbiol Antimicrob 2017). To that end, the study performed by Ray et al. demonstrates the potential for S. marcescens to develop resistance to antibiotics. Colonies were treated with various industry-grade antimicrobial chemicals, like ceftriaxone, kanamycin, and gentamicin, at several levels of magnitude greater than the planktonic minimum inhibitory concentration, but the colonies continued to grow despite high concentrations of the chemicals. However, when treated with chloramphenicol, described as “a last resort antibiotic used to treat infections such as tetracycline-resistant cholera“ by Ray et al., the biofilms demonstrated significant reductions in growth at multiple levels of treatment concentration.