The bacterium Serratia marcescens (S. marcescens) is a common environmental organism known for its distinctive appearance and increasing role in healthcare settings. Many people encounter this microbe as the pinkish-red film that forms in moist areas like shower stalls or sink drains. Its presence in diverse environments and notable hardiness lead to the question of whether it possesses the highly resistant survival structure known as an endospore.
What Serratia marcescens Is
Serratia marcescens is classified as a rod-shaped, Gram-negative bacterium belonging to the family Yersiniaceae. This microbe is ubiquitous, thriving in habitats including soil, water, and on the surfaces of plants and insects. Its ability to grow across a temperature range of 5°C to 40°C allows it to persist in many ecological niches.
The most recognizable characteristic of this species is its ability to produce prodigiosin, a bright red pigment. This pigment is synthesized at room temperature (typically 20°C to 30°C), giving colonies the reddish or pink color that led to its discovery in 1819. While it exists widely in the environment, S. marcescens is now recognized as an opportunistic human pathogen. It is frequently associated with nosocomial (hospital-acquired) infections, causing issues like urinary tract infections, bloodstream infections, and pneumonia in vulnerable patients.
The Endospore Formation Distinction
The definitive answer is that Serratia marcescens does not form endospores. Endospores are dormant, highly resistant structures produced by certain bacteria to survive extreme conditions like desiccation, heat, and harsh chemicals. They allow the bacterial cell to remain viable for potentially hundreds of years.
The capability to form endospores is a trait almost exclusively restricted to bacteria within the phylum Firmicutes, which includes the Gram-positive genera Bacillus and Clostridium. S. marcescens is classified as a Gram-negative bacterium in the phylum Proteobacteria, and therefore lacks the genetic machinery required for this complex process. Earlier studies suggested that S. marcescens might form spores, but analysis confirmed the observed structures were only aggregates of cellular debris, not true endospores.
How S. marcescens Persists in Environments
Despite lacking endospores, S. marcescens is remarkably persistent, especially in moist environments. Its primary survival strategy is the formation of biofilms, which are communities of bacteria encased in a self-produced matrix of sugars and proteins. This protective layer anchors the bacteria to surfaces, such as plumbing fixtures or medical devices, shielding them from environmental stresses and some disinfectants.
The organism also possesses inherent resistance mechanisms beyond the physical protection of the biofilm. It has high metabolic versatility, allowing it to adapt and survive even in nutrient-deficient places or disinfectant solutions. Furthermore, the bacteria can employ efflux pumps—specialized proteins that actively pump toxic compounds, including antibiotics and disinfectants, out of the cell. These combined non-spore mechanisms allow S. marcescens to maintain a formidable presence in clinical and domestic settings.
Disinfection Protocols and Non-Spore Forming Bacteria
The fact that Serratia marcescens is not a spore-former has significant practical implications for cleaning and sterilization procedures. Endospores from true spore-formers require specialized chemical agents (sporicides) or extreme physical methods, such as high-pressure steam sterilization. In contrast, the vegetative cells of S. marcescens are susceptible to standard, hospital-grade, non-sporicidal disinfectants.
Routine cleaning agents, such as alcohol-based cleaners, bleach solutions, and common quaternary ammonium compounds, are generally effective at killing S. marcescens on surfaces. This distinction is critical in healthcare settings, where surfaces must be routinely disinfected to prevent the spread of opportunistic pathogens. While the organism’s biofilm offers some protection, using appropriate friction combined with effective disinfectants is sufficient to control this bacterium.