Serratia marcescens (S. marcescens)

Serratia marcescens is a Gram-negative, rod-shaped bacterium in the Enterobacteriaceae family that functions as a significant opportunistic human pathogen [6][14]. It is primarily recognized as a cause of nosocomial (hospital-acquired) infections, including urinary tract infections, pneumonia, surgical wound infections, and bloodstream infections, particularly among immunocompromised individuals and neonates in intensive care units [6][11]. Historically notable for its production of the red pigment prodigiosin, S. marcescens is clinically challenging due to its extensive intrinsic and acquired antibiotic resistance profiles [3][11]. Most strains possess chromosomally encoded AmpC beta-lactamases, which confer resistance to penicillins and early-generation cephalosporins, and the species is intrinsically resistant to colistin and macrolides [11][13]. Therapeutic management typically requires susceptibility-guided treatment, often involving carbapenems, aminoglycosides, or fourth-generation cephalosporins like cefepime [8][13]. Because Serratia marcescens is a whole organism (pathogen) rather than a single molecular target like a receptor or enzyme, it does not fit the classical definition of a single therapeutic target molecule [1][11].

Other names

Bacillus prodigiosusMonas prodigiosaS. marcescens

Antibacterial agents targeting this organism act through diverse mechanisms: beta-lactams (e.g., carbapenems, cephalosporins) inhibit cell wall peptidoglycan synthesis; aminoglycosides (e.g., amikacin) inhibit protein synthesis by binding to the 30S ribosomal subunit; and fluoroquinolones inhibit DNA gyrase and topoisomerase IV [8][11][13].