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At 1:15 p.m. on Monday, August 8th, 1904, a British physician named M. H. Gordon took some soil he had “richly impregnated with a living emulsion” of the virulent bacterium,¹ Serratia marcescens, and sprinkled it near a lamp post in front of the U.K. House of Commons. Gordon knew that was the exact spot Members of Parliament had to cross before their 2 p.m. session. His hope was for the politicians to step on the contaminated ground and spread the bacteria inside the Debating Chamber.

Gordon wasn’t executing a terrorist attack. Rather, he had been appointed by a committee to study how germs spread inside the House of Commons following an outbreak of influenza among its members. Gordon had chosen Serratia marcescens because the bacterium forms easily recognizable red colonies. For his experiment, he placed numerous open Petri dishes inside the Debating Chamber on which the colonies could grow. Gordon’s idea was simple: politicians’ boots would carry contaminated soil and spread Serratia marcescens into the building; he would go away with his Petri dishes and reveal colonies of the bacterium to point at faults in the House of Commons’ ventilation system.

But despite placing hundreds of Petri dishes around the chamber, Gordon wasn’t able to retrieve more than a handful of colonies. Suspecting the microbe might not spread easily by means of boots, he followed this up with a theatrical experiment: Inside the Debating Chamber, he gargled a suspension of Serratia marcescens and recited Shakespeare’s “King Henry V” and “Julius Caesar” for one hour to no one but an audience of open Petri dishes. This time, copious colonies of Serratia marcescens appeared, leading him to conclude that speech can transmit microbes as far as 70 feet (21 meters) away.²

Indeed, Serratia marcescens’ vivid blood-red color has prompted its use in a wide range of experiments that have increased our understanding of how germs disperse within human bodies, buildings, and populations. Sightings of the striking microbe outside the lab have awakened both fear and awe in the general population.

The awareness that certain strains of Serratia marcescens can cause severe harm to humans — counter-intuitively, the paler varieties are most dangerous — only became evident decades after Gordon’s investigations. Before then, hospitals deliberately sprayed Serratia marcescens inside their facilities to investigate microbial dispersion, and laboratory handbooks demonstrated transmission by handshake by having students coat their fingers in the microbe. While greater awareness of its dangers eventually led to its discontinuation in tracing experiments, Serratia marcescens remains an important subject of biomedical research.

Its scientific journey began over 200 years ago with a bloody polenta.

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Blood Masquerade

When growing on solid substances, like foodstuffs or Petri dishes filled with agar, Serratia marcescens forms red colonies reminiscent of blood, earning it the informal moniker “masquerader of blood.” Its appearance on the polenta of a wealthy Paduan farmer during a particularly hot and humid summer in 1819 — ideal conditions for its flourishing — prompted the flurry of investigation that gave it its scientific name.

After the farmer, Antonio Pittarello, discovered the red-spotted food in his house near Padua, the resultant hubbub of curiosity seekers and the spiritually appalled so disturbed the neighborhood that the local District Commissioner appointed Dr. Vicenze Sette (a physician, surgeon, and district health officer) to investigate the discovery. Also taking an interest in the mysterious “bloody polenta” was Bartolomeo Bizio (1791-1862), a young pharmacy student who joined the investigation on his own. In the meantime, red spots started to appear on food in hundreds of homes throughout Pittarello’s village as well as in villages close by.

Through a series of ingenious experiments, Sette and Bizio reproduced the red spots on fresh polenta independently in their own home laboratories. Both concluded (erroneously) that the cause was a microscopic fungus.³ Sette called it Zaogalactina imetrofa (from the Latin, “slime living on food”); Bizio called it Serratia⁴ to honor an Italian Benedictine monk and physicist, Serafino Serrati (whom he felt had not gotten adequate credit for his contributions to the invention of the steamboat) and marcescens (from the Latin, “to decay”) since, much to his disappointment, the microbe’s red color fades easily.

Racing to gain acclaim for identifying the source of the “bloody polenta” before Sette, Bizio made two deft moves. First, by citing Lazzaro Spallanzani, a pioneering biologist known for having worked to disprove the theory of spontaneous generation, he hoped to lend credibility to his findings; indeed, by demonstrating a biological origin for the “bloody polenta,” Bizio again refuted spontaneous generation decades before Louis Pasteur. And second, Bizio quickly published his discoveries in a Venetian newspaper.⁵ Sette was furious about being scooped by Bizio’s article, although Bizio’s results didn’t contradict his own.

As Bizio reported in a letter to a priest, Angelo Bellani, three years after the event:

For several days succeeding its publication, there was much discussion of my experiments in the columns of this newspaper [The Official Gazette]; and to make them still more well known, an enterprising publisher printed them in a small pamphlet which he sold in the streets, so that the general public as well as educated persons came to know about them.

By recreating red spots of Serratia marcescens on fresh polenta, Bizio grew pure colonies of microbes more than half a century before the “culture plate technique” developed by Robert Koch, Walther and Fanny Angelina Hesse, and Julius Petri.⁶ The significance of Bizio’s experiments has survived over the centuries, showing the falsehood of a dismissive remark made by renowned bacterial systematist S. T. Cowan, who said: “I believe we shall not lose anything by ignoring all work before the pioneer [sic] work of Pasteur.”

The bacteriological investigations of another predecessor of Pasteur, the naturalist Christian Gottfried Ehrenberg (1795-1876), have survived as well. In 1848, several decades after the bloody polenta first appeared in Padua, red spots began popping up on boiled potatoes in Germany. Unaware of Bizio’s work, Ehrenberg observed the phenomenon and called the organism responsible Monas prodigiosa, one of the many names that Serratia marcescens has held over the centuries. Ehrenberg studied historical records and concluded that the bacterium was most likely responsible for more than 100 documented cases of so-called “miraculous blood.”

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Specifically, Serratia marcescens holds a large but unintended place in two of the world’s religions due to this shocking resemblance to blood. The 1264 “Miracle of Bolsena” of a Host “bleeding” with Serratia marcescens was believed to have contributed to the establishment of the Holy Communion, a central sacrament of the Greek Orthodox and Roman Catholic church. Additionally, the infamous antisemitic “blood libels” might have been due to this microbe, with thousands of Jews executed as heretics following accusations of having stabbed holy wafers in what was most likely a naturally occurring outbreak of Serratia marcescens on the starchy substratum.

It is difficult to verify if Serratia marcescens was the precise biological cause of such “miracles” or “heresies,” however, since many microorganisms, such as mold or yeast, are often red or pink and grow readily on food. But it seems likely, for as researchers have pointed out: “We know of no organism [ … ] looking more like drops of fresh blood than Serratia marcescens.”

With its centuries-long history, it’s perhaps no surprise that Serratia marcescens has had so many different names and presents “one of the most confusing taxonomies in the bacterial world.” In 1924, bacteriologists rehabilitated Bizio’s Linnean appellation, retaining Ehrenberg’s “term of miracle (prodigium) bacterium for use as a trivial or common name.” By the end of the 19th century, however, due to its vivid hue, Serratia marcescens had become one of “the cornerstones of modern bacteriology.”

Fake Blood, Real Threat

Specifically, Serratia marcescens’ striking color made it the microbe of choice for several decades amongst bacteriologists studying how pathogens spread through buildings and cities.

In 1897, German bacteriologist Carl Flügge used the bacteria to perform experiments which served as a template for Gordon’s (but without the Shakespearean flair).⁷ Flügge was the first to demonstrate that mouth droplets carry bacteria. His findings spurred surgeon Johann Mikulicz to develop a precursor of today’s face mask, and were a major driver of the six feet (two meters) “social distancing” policy during the COVID-19 pandemic.

In 1919, military doctors proved that utensils can indirectly transmit microbes by applying Serratia marcescens on the mouth and lips of “donor soldiers” before their meals. In 1926, bacteriologists traced how handshakes transmit microbes by smearing the bacterium on the hands of test subjects. In 1937, dentists detected bacteremia (entry of bacteria into the blood system) following dental extraction by spreading the pathogen around the gum of teeth. In 1945, military staff correlated air quality with the progression of illness by exposing test subjects to huge quantities of aerosolized Serratia marcescens. In 1957, doctors demonstrated urinary tract infections through catheters by applying Serratia marcescens on genitalia of semi-comatose patients, one of whom died shortly after.⁸

More ominously, Nazi Germany studied the spread of the pathogen in the Paris Métro and the London Underground, as reported in a 1934 article by investigative journalist Henry Wickham Steed, Aerial Warfare: Secret German Plans. The French and U.K. governments took Steed’s article very seriously, as the underground systems in both Paris and London had functioned as shelters during WWI and would again in WWII.

The U.S. military also deployed Serratia marcescens in a spectacular way in September 1950. In a secret project called “Operation Sea Spray,” the Navy sprayed enormous quantities of the pathogen along the coast of San Francisco to study large-scale, open-air transmission of germs in biological warfare. Navy scientists also set up monitoring stations and traced the microbe up to 50 miles inland, but experts disputed any scientific and epidemiological merit of the experiments. Notably, “Operation Sea Spray” coincided with the first recorded nosocomial outbreak of Serratia marcescens, with eleven inpatients infected at Stanford Hospital between September 1950 and February 1951. Two of them got bacteremia; one died of heart failure.⁹

(In November 1976, the Long Island newspaper Newsday leaked information about “Operation Sea Spray.” Contrary to other biowarfare experiments that flew under the radar, this led to a public Hearing at the Senate in March and May of 1977.¹⁰ Surprisingly, however, in August 1977, an investigation by the U.S. Centers for Disease Control concluded that the strain used by the U.S. Military was not related to any infection within the population.)

That Serratia marcescens was so widely used in experiments involving human subjects should startle us; especially since the scientific community was accumulating evidence that the bacterium could be deadly. As early as 1903, infectologist E. Bertarelli showed that the bacterium was lethal to mice, rats, and guinea pigs “following inoculation of massive doses of Bacillus prodigiosus” (one of the microbe’s many names). The first report of human infection by Serratia marcescens followed in 1913, when a healthy young man sought medical help after becoming troubled by a foul-smelling red sputum, which he mistakenly took for blood.¹¹ Doctors found no sign of blood cells in the sputum but saw a large number of intestinal bacteria, which grew on agar into distinctive red colonies. The patient later recovered without complications.

Among those with weakened immune systems, Serratia marcescens has been involved “in every conceivable kind of infection.” It can affect an individual’s mouth and throat, lungs, gut, urinary tract, blood, heart, wounded skin, eyes, and central nervous system. When susceptible patients are infected by a virulent form of the pathogen, symptoms may include discoloration of extremities, shock, convulsions, deafness, delirium, and coma. Mortality of affected patients (especially in the case of sepsis, or the spread of bacteria in the bloodstream) runs as high as 30-40 percent. Indeed, by the late 1960s, the bacterium was unequivocally declared as a cause of serious infections, including death.

Infections with Serratia marcescens haven’t ceased to be a cause for concern,¹² and clinicians have wondered if there aren’t many more infections with Serratia marcescens going unrecognized. As recently as 2017, the World Health Organization listed Serratia among bacteria for which new antibiotics are urgently needed.

Modern Wonders

Serratia marcescens striking red color comes from a pigment aptly called “prodigiosin.” Clinicians have observed an inverse correlation between a strain’s high levels of prodigiosin and its ability to cause infections. This might explain why past studies designed to take advantage of Serratia marcescens’ vivid appearance have caused little harm. By using bright red colonies as markers for their experiments, like M. H. Gordon’s in the U.K. Parliament, researchers might have unwittingly selected a less virulent strain of Serratia marcescens.

Prodigiosin is an alkaloid with immunosuppressive, anticarcinogenic, and antimicrobial properties. Scientists do not yet fully understand why the bacterium produces prodigiosin, but have noticed that environmental conditions influence red pigmentation (for example, a rise in temperature reduces the bacterium’s vivid color). They speculate that the molecule might be important for cell dormancy, dispersal in the environment, or for gaining advantages over competing microbes.

Prodigiosin has many uses as a biomedicine, including the inhibition of microbes such as bacteria, fungi, algae, and viruses. Researchers are still investigating the mechanisms by which prodigiosin acts on a target cell, and have observed adverse effects on the cell membrane as well as in organelles within the cell. Prodigiosin has also contributed to research on microbial “secondary metabolites;” molecules, including antibiotics, which are not involved in primary physiological functions like growth or reproduction, but nonetheless help protect an organism. Researchers showed before the discovery of penicillin, the first antibiotic, that Serratia marcescens inhibits Vibrio bacteria. In 1983, prodigiosin was also used as a molecular marker to clone, for the first time, a gene involved in the biosynthesis of an antibiotic.

A formula named Coley’s Toxin containing Serratia marcescens has been used for over a century to stimulate the immune system to fight off cancers. (Its namesake, William Coley, is considered the “Father of Immunotherapy.”) Prodigiosin has shown activity against cancer cells, among others, by inducing DNA cleavage and apoptosis (cell death). Prodigiosin is also being investigated for therapies that require inhibition of the immune system.

In nature, Serratia marcescens is part of a complex web of ecological interactions. It can inhibit parasites (like the malaria agent Plasmodium falciparum), kill insects (like the cockroach Blattella germanica by acting synergistically with a fungus), or enhance growth of some plants while killing others. Researchers have also used Serratia marcescens as a model to study how environmental species evolve into pathogens. When confronted with a natural predator (like the protist Tetrahymena thermophila), the bacterium acquires traits that contribute to its virulence. In 2011, researchers also observed that Serratia marcescens had begun to infect corals, the first instance of a “reverse zoonosis” in marine habitats, a situation in which a pathogen moves from humans to animals.

As of early 2025, Serratia marcescens stands among the top 30 most studied microbes, topping species such as Agrobacterium tumefaciens (a widely used model microbe to genetically engineer plants), Legionella pneumophila (the cause of Legionnaire’s disease), Clostridioides difficile (a common diarrhea-causing bacterium affecting the intestinal tract), and Mycobacterium smegmatis (a model organism for the study of the pathogen causing tuberculosis, M. tuberculosis). Through surprising sightings and curious experiments, this microbe has left an enormous mark culturally, clinically, and scientifically. Its vivid blood-red color has elicited both wonder and alarm in the eyes of the beholder even as its actual dangers have often been ignored.

It is no wonder, then, that Alexander Fleming, that giant of microbial investigation, also paid notice. Fleming used it in a painting method he developed, called microbial art (or “agar art”). When working in this medium, artists take a Petri dish filled with agar and, using a lab tool called a loop, inoculate sections of the plate with various species of microbes that produce different hues. As the microbes grow, their living pigments form an image. For yellow, Fleming used Staphylococcus; for blue, Bacillus violaceus; and for brilliant red, of course, Serratia marcescens.

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This article is accompanied by an interview with the author. Listen on Spotify or Apple Music.

Corrado Nai is a science writer with a Ph.D. in microbiology. He has published articles in Smithsonian Magazine, New Scientist, Reactor (formerly Tor.com), Small Things Considered, and elsewhere. He is writing a graphic novel about the forgotten woman who introduced agar to microbiology, Fanny Angelina Hesse (1850-1934), based on unpublished historical material he helped resurface. Corrado lives in Jakarta with his wife and daughter.

Cite: Nai C. “A Brief History of the Miracle Bacterium.” Asimov Press (2025). DOI: 10.62211/48yk-73gf

Lead image by Ella Watkins-Dulaney, adapted from Benutzer:Brudersohn (CC BY3.0).

Footnotes

1. I use “virulent bacterium” and “pathogen” interchangeably to refer to a disease-causing microbe. Usually, “pathogen” refers to a species whereas strains (that is, lineages of bacteria) within a species can be more or less “virulent.”
2. Gordon’s 250+ page report is dramatic. In some experiments he made bacteriological analyses of the Ministerial versus the Opposition side of the Chamber; in others he placed open Petri dishes even on the top of the Clock Tower. In his speech experiment, he retrieved more colonies when he repeated the test with the ventilation system on than with the ventilation system off. Despite inconclusive bacteriology findings, he suggested 14 substantive modifications to the ventilation system.
3. Christian Gottfried Ehrenberg thought it was an animal, botanist Camille Montagne an algae.
4. Serratia marcescens is the first bacterium to be ever named after a person. The genus name Serratia is only predated by Vibrio (Otto Müller, 1773) and Polyangium (Heinrich Link, 1809).
5. The modern counterpart of Bizio’s newspaper article, published in the Gazzetta Privilegiata di Venezia on 24 August 1819, would be a preprint.
6. Koch was the first to streak bacteria into single colonies in the 1870s; the Hesse couple introduced agar to the laboratory in 1881; and Petri perfected his Petri dishes in 1887. The “culture plate technique” continues to be used unaltered to this day.
7. The original German article is available here: Carl Flügge (1897), Ueber Luftinfection. Zeitschrift für Hygiene 25:179-224.
8. It’s uncertain if Serratia marcescens was the cause of death, as doctors were not granted the rights for an autopsy.
9. The Stanford Hospital case marked the first case of endocarditis (inflammation of the heart) by Serratia marcescens.
10. The Hearing discussed classified Military biowarfare experiments that took place using Serratia marcescens until 1968, including in the New York City Subway. The Military admitted knowing about the Stanford Hospital outbreak.
11. This appearance of red sputum without the presence of blood was later named “pseudohaemoptysis.”
12. A dramatic outbreak happened in the mid-1970s and involved epidemics in four different hospitals in Nashville, Tennessee, caused by rotating staff likely transmitting the pathogen by hand. The virulent strain of Serratia marcescenswas resistant to all antibiotics and infected over 200 patients, killing eight. Then, in one of those hospitals, a much more severe epidemic with Klebsiella pneumoniae infected about 400 patients, killing 18. Clinicians attributed this outbreak to co-infection and in vivo transmission of antibiotic-resistant genes from Serratia to Klebsiella. More recently, outbreaks of Serratia marcescens have occurred within prisons due to contaminated disinfectants and amongst intravenous opioid users due to contaminated syringes. In 2004, biotech company Chiron Corporation lost an enormous quantity of flu vaccines due to contamination with Serratia marcescens.