Serratia marcescens: The Red-Pigment Hospital Pathogen and How to Identify It

For centuries, people reported bread and communion wafers that appeared to be spotted with fresh blood, and treated it as a miracle or an omen. The cause turned out to be a bacterium that grows a bright red pigment: Serratia marcescens. For a long time it was thought harmless, and scientists even sprayed it over cities to track how germs spread, assuming it could not cause disease.

That assumption was wrong. Serratia marcescens is now a well-known cause of hospital-acquired infection, especially in intensive care units and in patients with catheters and breathing tubes. This page is about the organism behind the red color: how it causes infection, why it is so hard to treat, and how the laboratory identifies it.

Overview

Serratia is a genus of Gram-negative rods in the family Enterobacteriaceae. The genus has more than 15 species, but one matters most in medicine: Serratia marcescens, the species found most often in clinical specimens and the main cause of Serratia infections. A few other species (S. liquefaciens, S. odorifera) turn up in clinical material occasionally.

S. marcescens is best known for two things: some strains produce a striking red pigment, and it is an important cause of hospital-acquired (nosocomial) infection. It is an opportunistic pathogen, meaning it rarely troubles healthy people but readily infects patients who are already vulnerable, especially those with medical devices in place.

Figure: Dark red colonies of Serratia marcescens in MacConkey Agar

The red pigment: prodigiosin

Some strains of S. marcescens produce prodigiosin, a red pigment. This is the organism's signature and the reason for its long, strange history.

Two practical points about the pigment matter in the laboratory:

• It is temperature-dependent. Prodigiosin is produced best at around room temperature (25 to 28°C) and is often not produced at 37°C. So a Serratia growing from a patient at body temperature may look ordinary and pale, while the same strain left at room temperature turns red. A colorless clinical isolate does not rule out Serratia.
• Not all strains make it. Many clinical S. marcescens strains are non-pigmented. The red color, when present, is a strong clue, but its absence means nothing.

The pigment is not thought to be a major cause of disease. Its importance is as an identification clue and as the reason the organism was noticed for centuries.

Virulence factors and how Serratia causes disease

S. marcescens is not aggressive in the way Salmonella or Shigella are. It succeeds by living on surfaces, spreading in hospitals, and resisting antibiotics. Each factor below explains part of that.

Biofilm formation (the key factor). This is the heart of Serratia pathogenesis. The organism attaches to plastic and metal surfaces, catheters, breathing tubes, contact lenses, and the inside of medical equipment, and builds a biofilm, a community of bacteria wrapped in a protective slime layer. Inside a biofilm, the organism is shielded from both the immune system and antibiotics. This is why Serratia infections cluster around devices, and why they are hard to clear: the biofilm protects the bacteria and is also a reservoir that keeps re-seeding the infection.

Attachment (pili/fimbriae). Serratia uses surface pili to stick to host cells and to surfaces, the necessary first step before biofilm can form.

Endotoxin (LPS). As a Gram-negative organism, its lipopolysaccharide can trigger the inflammatory response of sepsis and endotoxic shock when the organism reaches the blood.

Secreted enzymes. Serratia releases several enzymes (including a protease, lipase, and chitinase) that break down host tissue and help it obtain nutrients. These contribute to tissue damage in wound and eye infections.

How it spreads and causes infection

S. marcescens lives in wet places: tap water, sinks, soap solutions, and moist medical equipment such as nebulizers, ventilator tubing, and bronchoscopes. It spreads from these reservoirs, and from patient to patient, mainly on the hands of hospital staff. Once it reaches a vulnerable site, usually via a catheter, a breathing tube, or a surgical wound, it attaches, forms biofilm, and establishes infection. This is why hand hygiene and equipment decontamination are central to preventing Serratia outbreaks.

Diseases it causes

S. marcescens causes urinary tract infection (often catheter-related), wound and surgical-site infection, pneumonia (often ventilator-associated), bloodstream infection and endotoxic shock, and endocarditis, which is classically seen in people who inject drugs. Eye infections linked to contact lenses also occur. Most of these appear in hospitalized or otherwise vulnerable patients.

Identifying Serratia in the laboratory

Gram stain. Serratia is a Gram-negative rod. It is motile.

On the plate.

• Blood agar and MacConkey: grows well on both. On MacConkey it is a late (slow) lactose fermenter, so it usually looks pale at 24 hours and may turn slightly pink on longer incubation. Do not expect the bright pink of E. coli.
• Nutrient agar or TSA at room temperature: pigmented strains produce the red prodigiosin color, best seen at 25 to 28°C, not at 37°C.

Figure: Serratia marcescens grew as bright, glossy red colonies on the TSA plate

What distinguishes Serratia from other coliforms. Three enzyme tests are the classic Serratia markers and separate it from most other Enterobacteriaceae: it is DNase-positive, lipase-positive, and gelatinase-positive. Among the Enterobacteriaceae, this trio is unusual and is the practical way to confirm Serratia when the pigment is absent.

The identification panel.

Antibiotic resistance

Serratia is often resistant to multiple antibiotics, which is a large part of why it is a problem in hospitals. Two things drive this. First, it carries an inducible chromosomal AmpC beta-lactamase, so it can appear susceptible to some cephalosporins at first and then become resistant during treatment. For this reason Serratia is one of the organisms for which many clinicians avoid relying on third-generation cephalosporins even when the isolate tests susceptible. It is also intrinsically resistant to polymyxins (colistin). Second, its biofilm shields it from antibiotics that would otherwise work.

The practical result: Serratia infections often need carbapenems or other agents guided by susceptibility testing, and device removal is frequently part of clearing a biofilm-associated infection.

How to remember

Red pigment, room temperature. Serratia makes red prodigiosin, but only in the cold (around 25°C), not at body temperature. Picture the "miracle" bleeding bread sitting out at room temperature turning red.

The device organism. Serratia lives on wet hospital surfaces and builds biofilm on catheters and tubes. If you picture Serratia, picture it as a slime layer on a plastic tube, not a free-swimming invader. That one image explains its infections (device-related), its spread (staff hands, wet equipment), and its resistance (biofilm shields it).

DNase-positive coliform. The bench trick: a slow-lactose Gram-negative rod that is DNase, gelatinase, and lipase positive is Serratia. Most Enterobacteriaceae are DNase-negative, so a DNase-positive coliform is a strong pointer.

AmpC, like the rest of the SPACE group. Serratia is one of the organisms that can turn on AmpC and defeat cephalosporins mid-treatment. It sits with Enterobacter, Citrobacter, Providencia, and Morganella in that group.

Key exam facts in one table

Where students get confused

The pigment is not reliable. Two traps: many clinical strains make no pigment at all, and even pigmented strains often do not show red at 37°C. So a plain-looking colony can still be Serratia. Use the biochemical tests, especially DNase, not the color, to identify it.

Lactose fermentation. Serratia is a late lactose fermenter, not a brisk one and not a true non-fermenter. It often reads pale at 24 hours.

It is an opportunist, not an aggressive pathogen. Serratia rarely infects healthy people. Its danger is in hospitals, in vulnerable patients with devices. Understanding it as a biofilm-and-device organism explains its whole clinical behavior.

AmpC and cephalosporins. Serratia can test susceptible to a cephalosporin and then become resistant during treatment, because it can switch on its AmpC enzyme. This is a classic trap and the reason cephalosporins are often avoided for serious Serratia infection.

Was it ever really harmless? Serratia was historically treated as non-pathogenic and used as a tracer organism sprayed into the environment. That was a mistake; it is a genuine opportunistic pathogen.

References

1. Tille, P. M. (2022). Bailey & Scott's Diagnostic Microbiology (15th ed.). Elsevier.
2. Procop, G. W., et al. (2017). Koneman's Color Atlas and Textbook of Diagnostic Microbiology (7th ed.). Wolters Kluwer.
3. Mahlen, S. D. (2011). Serratia infections: from military experiments to current practice. Clinical Microbiology Reviews, 24(4), 755–791. https://doi.org/10.1128/CMR.00017-11
4. Gupta, V., Sharma, S., Pal, K., Goyal, P., Agarwal, D., & Chander, J. (2021). Serratia, no longer an uncommon opportunistic pathogen. Infectious Disorders Drug Targets, 21(7), e300821191666. https://doi.org/10.2174/1871526521666210222125215