Serratia marcescens: Morphology, Pigment, Biofilm, and Motility

Serratia marcescens is a Gram-negative bacterium best known for the vivid red pigment it can produce on shower curtains, bathroom tiles, and laboratory plates. But behind that eye-catching color is an organism with a remarkably flexible toolkit: it switches between different cell shapes depending on its environment, builds resilient biofilms on medical devices and household surfaces, and deploys multiple modes of movement to colonize new territory.¹ Understanding these four traits together explains why this single species causes problems in hospitals while also attracting interest from bioengineers and drug developers.

Cell Shape and Surface Architecture

S. marcescens is a rod-shaped bacterium, roughly two micrometers long and about 0.8 micrometers wide under standard laboratory conditions. High-resolution imaging of intact cells has measured those dimensions precisely: around 2,000 nanometers in length and 800 nanometers in width, with relatively little variation from cell to cell.¹² That puts it in roughly the same size range as E. coli, its more famous relative in the family Enterobacteriaceae.

The outer membrane, however, is anything but featureless. Atomic force microscopy has revealed funnel-like pores dotting the membrane surface, each made up of protein subunits arranged in a doughnut-shaped ring. Some of these pores are composed of six to eight subunits with lateral diameters around 56 to 66 nanometers, while others are built from four subunits and sit slightly differently on the membrane plane.³ These pores are channels for transporting molecules across the outer membrane, and their variety hints at the bacterium’s ability to interact with a wide range of chemical environments. The cell surface also features protrusions described as looking like miniature mountain ranges under high magnification, giving the membrane a surprisingly rugged topology.

One biochemical trait useful for identifying S. marcescens in clinical labs is its production of DNase, an enzyme that chews up DNA. This feature helps distinguish it from closely related bacteria in the same family.⁴ Along with its pigment production and characteristic colony appearance, DNase activity remains a standard screening marker in diagnostic microbiology.

Prodigiosin and Why the Bacterium Turns Red

The red pigment that makes S. marcescens famous is prodigiosin, a molecule the bacterium assembles from two smaller building blocks through separate internal pathways. One pathway produces a single-ring compound called MAP, and the other produces a two-ring compound called MBC. A final enzyme, PigC, joins the two pieces together to create the finished red molecule.⁵ More than a dozen pig genes encode the proteins involved, and the whole set is organized in an operon, meaning the genes are read and activated as a coordinated unit.

Prodigiosin is not just decoration. It has antibacterial activity against other species, can reduce the ability of competing bacteria to form biofilms, and inhibits the production of protease enzymes that rival microbes use as weapons.⁶ Laboratory tests have shown antibacterial effects against both Gram-positive and Gram-negative organisms. In one study, prodigiosin suppressed biofilm formation in Pseudomonas aeruginosa by up to about 58 percent at higher concentrations and showed no toxic effect on normal human skin cells at 100 micrograms per milliliter.⁷ These properties have made prodigiosin a candidate for pharmaceutical development, particularly as an anticancer and antimicrobial agent, though clinical use remains distant.

Temperature Controls the Color

If you culture S. marcescens at human body temperature (37 °C), you will almost certainly see no red pigment at all. Grow the same strain at around 27–30 °C and colonies turn brilliantly red. This is one of the most distinctive features of the organism and a reliable way to miss it in clinical samples if only standard incubation temperatures are used.

Early work established that pigment production happens over a narrow temperature band even though the bacterium itself grows comfortably across a much wider range. At 27 °C in rich medium, cells reach peak numbers within a day or two, but prodigiosin does not peak until about four days later, during the period when the culture has stopped actively dividing.⁸ The pigment is a classic secondary metabolite, meaning the bacterium invests in it only after the main growth phase is over. No prodigiosin forms at 38 °C, but if cultures grown at that temperature are shifted down to 27 °C within about 36 to 48 hours, pigment production resumes normally.⁹

The mechanism behind this temperature switch turns out to be transcriptional. The pig genes are simply not read at 37 °C. Researchers showed this by hooking the operon to an externally inducible promoter: when forced to transcribe the pigment genes at the normally non-permissive temperature, the cells produced prodigiosin just fine. A regulatory protein called HexS is part of the control system that keeps the operon silent at higher temperatures.¹⁰ In other words, the cellular machinery needed to assemble prodigiosin works fine at body temperature; it is the gene-reading step that gets blocked. Why exactly S. marcescens would want to suppress its pigment at mammalian body temperature remains an open question, but it may reflect a shift toward a more stealth-oriented infection strategy inside a warm-blooded host.

How Biofilms Form and Why They Matter

S. marcescens readily forms biofilms on a wide variety of surfaces, from catheter tubing and contact lens cases to shower drains and water pipes. These biofilms are communities of cells embedded in a self-produced matrix of sugars, proteins, and other polymers collectively called extracellular polymeric substances (EPS). The EPS of S. marcescens contains both polysaccharides and proteins, and the sugar portion has been characterized as a complex mixture including glucose, rhamnose, galactose, and unusual heptose sugars arranged into two distinct polysaccharide structures: a rhamnoglucan and a heptoglucan.¹¹ Both contain lipid material, giving the matrix a hydrophobic quality that helps it stick to surfaces and resist removal by flowing water or cleaning agents.

Exposure to certain anti-fouling compounds can reduce EPS production. Lipophilic bismuth thiols, for example, lowered total polysaccharide and protein content in EPS from both S. marcescens and E. coli at concentrations below the level needed to kill the cells outright.¹² Strategies like these, targeting the biofilm matrix rather than the bacteria directly, are of growing interest because biofilm-dwelling cells are notoriously harder to kill with standard antibiotics than free-floating ones.

Quorum Sensing Ties It All Together

Biofilm development in S. marcescens does not happen at random. The cells coordinate through a chemical communication system called quorum sensing (QS). Individual bacteria release small signaling molecules, and when the local concentration of those molecules rises high enough, the population collectively shifts its behavior. In S. marcescens, the primary signals are N-acyl homoserine lactones, including N-hexanoyl homoserine lactone.¹³

Quorum sensing in this species does not just control biofilm maturation and eventual sloughing (the release of chunks of biofilm to colonize new sites).¹⁴ It also regulates prodigiosin production, protease and lipase secretion, and swarming motility.¹⁵ In practical terms, this means a single communication circuit links many of the traits covered in this article. Disrupting quorum sensing has been explored as a strategy to disarm the bacterium: compounds that jam QS signals can simultaneously reduce biofilm formation, pigment output, and surface movement.

Swimming, Swarming, and Cellular Shape-Shifting

When floating in liquid, S. marcescens behaves like many other flagellated bacteria: it swims using one or a small number of flagella.¹⁶ This swimming mode allows individual cells to navigate toward nutrients or away from threats using chemotaxis, the ability to steer by sensing chemical gradients.

On a solid surface, however, something dramatic happens. The cells stop dividing normally, elongate considerably, and sprout anywhere from ten to a hundred flagella covering their sides.¹⁷ These elongated, heavily flagellated “swarmer” cells move in coordinated rafts across the agar surface, a behavior visually distinct from swimming. The transition requires a surface of the right consistency, typically agar concentrations around 0.7 to 0.85 percent.¹⁸

Like pigment production, swarming is temperature sensitive. Colonies swarm well at 30 °C but not at 37 °C on standard nutrient agar. A two-component signaling system called RssAB helps enforce this restriction. When the sensor kinase gene rssA is disrupted, mutant cells swarm vigorously even at 37 °C, start swarming at lower cell densities, and tolerate higher agar concentrations.¹⁹ This suggests the bacterium actively suppresses swarming under conditions resembling a mammalian host, paralleling the suppression of prodigiosin at the same temperature.

Surfactants Grease the Way

Flagella alone are not enough for efficient surface movement. S. marcescens also secretes biosurfactants called serrawettins, cyclic lipopeptides that reduce the surface tension at the interface between the cell and whatever it is crawling on. Serrawettin W2, one of the best-characterized examples, is a ring-shaped molecule made of a fatty acid linked to five amino acids.²⁰

What makes serrawettins interesting is that they enable two different kinds of surface spreading. On soft agar where flagella are active, adding serrawettin speeds up swarming. On harder agar where flagella alone cannot drive movement, serrawettin still promotes spreading, suggesting a flagellum-independent mode of surface translocation. Importantly, serrawettins do not help cells move beneath the agar surface, only on top of it, consistent with a surfactant mechanism that specifically wets the cell-surface interface.²⁰ Recent work has even shown that alternating electric fields at frequencies near the natural resonant frequency of the cells can enhance this surfactant-assisted swarming, a finding with potential applications in micro-scale bioengineering.²¹

Clinical Significance and Antibiotic Resistance

For decades, S. marcescens was considered harmless. Its bright pigment made it a convenient tracer organism, and the U.S. military sprayed it over populated areas during the 1950s and 1960s to study how biological agents might spread through cities. The experiments exposed both civilians and military personnel, a fact that became public in the 1970s and led to congressional hearings.²² It is now recognized as a genuine opportunistic pathogen that causes hospital-acquired infections, particularly urinary tract infections in catheterized or elderly patients.²³

The resistance picture is sobering. S. marcescens carries a chromosomal AmpC beta-lactamase that can be induced or constitutively overproduced through mutation, conferring high-level resistance to many cephalosporins. A single amino acid change in the AmpC enzyme increased its efficiency against ceftazidime more than a thousand-fold in laboratory-selected mutants.²⁴ Beyond this intrinsic mechanism, strains isolated from water and clinical settings increasingly carry plasmid-borne resistance genes against carbapenems, considered last-resort antibiotics.²⁵ A retrospective study of 242 clinical cases found that patients with multidrug-resistant S. marcescens bloodstream infections had a 28-day mortality rate of 50 percent, compared with 12 percent for those with non-resistant strains.²⁶

Insect Models and the Immune Evasion Playbook

S. marcescens has become a useful tool for studying how bacteria evade host immune defenses, particularly in the fruit fly Drosophila melanogaster. When injected directly into the fly’s body cavity, S. marcescens resists the insect’s main humoral immune pathway and kills the host within a day. This resistance depends on the bacterium’s lipopolysaccharide O-antigen, a sugar structure on the outer membrane that shields the cell from antimicrobial peptides.²⁷ Because Drosophila immune pathways share evolutionary roots with parts of the mammalian immune system, these experiments provide insight into how S. marcescens survives inside a host more broadly.

Phage Therapy and Combination Approaches

With antibiotic options narrowing, researchers are turning to bacteriophages, viruses that specifically infect and kill bacteria. In one reported case involving a patient with a refractory lung infection caused by multidrug-resistant S. marcescens, investigators isolated a phage called Spe5P4. Genome analysis confirmed the phage carried no virulence or antibiotic-resistance genes, making it a reasonable candidate for therapeutic use.²⁸ While single-case reports are far from definitive, they represent early steps toward phage-based treatment for Serratia infections where antibiotics have failed.

Biofilm-dwelling cells pose a particular challenge. A recent laboratory study tested a triple combination of phages, sub-lethal doses of antibiotics, and antimicrobial peptides against multidrug-resistant S. marcescens biofilms. Phages plus antibiotics reduced biofilm mass but could not fully clear it. Adding antimicrobial peptides to the mix eliminated over 99.99 percent of both free-floating and biofilm-associated cells.²⁹ The result underscores a recurring theme: no single weapon is likely to work against biofilm infections, but layered strategies that attack from different angles can be remarkably effective.

Research Uses Beyond Medicine

The vigorous collective motion of swarming S. marcescens has attracted physicists and engineers. In one set of experiments, dense carpets of S. marcescens cells deposited inside microfluidic channels self-organized to pump fluid at speeds as high as 25 micrometers per second, functioning as tiny living pumps without any external power source.³⁰ Researchers studying how active and passive particles interact have used S. marcescens swarms to probe fundamental questions about collective motion in living systems. When part of a swarm is immobilized by UV light, the still-active bacteria at the boundary collide with and gradually dislodge the passive cells, recovering the swarm’s original collective motion in a process that resembles a phase boundary moving through a material.³¹

The swimming dynamics of individual S. marcescens cells have also proven more complex than simple random walks. Mathematical analysis has shown that the trajectories of swimming cells are multi-fractal, meaning different aspects of their movement scale in different ways depending on bacterial density and the concentration of chemical attractants in the environment.³² These findings feed into broader efforts to model how living systems move, with potential applications in designing micro-robots or understanding how pathogens navigate tissue.

Outside the physics lab, S. marcescens strains isolated from soil have shown promise as biocontrol agents. Some produce a cocktail of enzymes including chitinase, protease, and cellulase, alongside plant-growth-promoting compounds. In tea plantations, for example, a rhizosphere strain demonstrated efficacy against root rot disease, combining direct antifungal activity with stimulation of plant defenses.³³ The same enzymatic versatility that makes S. marcescens a problem in hospitals makes certain environmental strains useful allies in agriculture.