The Physician Who Smeared Himself with Smallpox

An Essay

Preface

This essay draws on Daniel Roytas’s Can You Catch a Cold? Untold History and Human Experiments, which documents historical challenges to germ theory and the extensive record of failed disease transmission experiments conducted between 1798 and the mid-twentieth century.

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On January 21, 1901, Dr. Matthew Joseph Rodermund, an American ophthalmologist, visited a young female patient suffering from smallpox. Upon entering her room, he asked the girl’s mother if she feared contracting the disease. When she replied she was not afraid, Rodermund burst open several pustules on the girl’s face and arms and collected the fetid pus. He then smeared it across his own face, hands, beard, and clothes.

Without washing, Rodermund returned home and ate dinner with his family. He consulted patients at his medical practice. He played cards at the local Businessmen’s Club, touching the faces and hands of at least ten people that evening. The next day, still covered in smallpox pus, he travelled by train to a nearby town, mingling with those he encountered. He consulted with twenty-seven more patients, again touching their faces and hands. For nearly forty-eight hours, Rodermund had been covered in the bodily fluids of a smallpox patient, which he had deliberately rubbed onto the faces and hands of at least thirty-seven unsuspecting individuals.

When news broke of his actions, Rodermund was held under police guard in a quarantine facility. He escaped that same evening, travelled to a nearby town to visit an acquaintance, and was arrested for the second time in twenty-four hours. After four days in quarantine, he was released. The police could find nothing to charge him with.

Not a single case of smallpox occurred — neither in Rodermund nor in any of the thirty-seven people he had directly exposed.

The result made headlines across the United States. Media outlets continue to report on Rodermund’s exploits to this day. The attention is understandable. Smallpox was considered one of the most contagious diseases known to medicine. Direct contact with infectious material from active pustules represented the most concentrated possible exposure. By every principle of contagion theory, Rodermund should have contracted smallpox. So should at least some of the dozens of people whose faces he touched with pus-covered hands. The expected outcome was an outbreak. The actual outcome was nothing.

Rodermund was not surprised. He had performed this experiment dozens of times over fifteen years. Each time, the result was negative.

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A Pattern, Not an Anomaly

Rodermund’s smallpox experiments were dramatic, but they were not unique. A century of documented self-inoculation experiments had produced similarly confounding results across multiple diseases considered highly contagious.

In 1798, Renée Desgenettes, physician-in-chief of Napoleon Bonaparte’s army in Egypt, faced an outbreak of bubonic plague among French troops after they liberated a fortress from the Ottoman Empire. The soldiers were terrified. To quell their fears about contagion, Desgenettes dipped a lancet into the suppurating wound of a plague victim — a “bubo,” the swollen lymph node characteristic of the disease — and pricked himself in the groin and armpit with the contaminated instrument. He remained completely well. The soldiers’ fears subsided.

Napoleon himself reinforced the demonstration. He grabbed the corpses of soldiers who had died from plague with his bare hands and lifted them about. He remained unaffected. Following the Battle of the Pyramids, Bonaparte, Desgenettes, and their staff occupied quarters at Murad Bay where sixty enemy soldiers had died of plague just days prior. Despite living within those pestilent walls for some time, not a single Frenchman contracted the disease.

In 1835, Antoine-Barthélémy Clot, known as Clot-Bey, a physician and sergeant major in Napoleon’s army, conducted a more systematic test. He took blood from a plague bubo and injected it into five Egyptian prisoners. Only one became unwell, and Clot-Bey attributed this not to the injection but to the man’s three prior days of residence in a plague-ridden hospital. Clot-Bey then injected himself six separate times with blood from another bubo. When he failed to fall ill, he injected himself with pus taken directly from the open wound of a man dying of the disease. Like Desgenettes before him, Clot-Bey remained completely unaffected.

Throughout the 1800s, at least fifty self-inoculation and human-to-human transmission experiments were performed across a range of diseases considered infectious. The methods were crude by modern standards — direct injection, skin-to-skin contact with infectious material, deliberate exposure to bodily fluids. The results were consistent: these experiments largely failed to reproduce the disease under investigation. The pattern held across plague, smallpox, and other conditions assumed to spread readily from person to person.

These early experiments did not prove that contagion was impossible. They did demonstrate that the relationship between exposure to infectious material and the development of disease was far less predictable than contagion theory suggested. A physician could inject himself with plague pus and remain healthy. A doctor could smear smallpox across his face for fifteen years without consequence. The expected chain of transmission — contact with pathogen leads to infection leads to disease — broke down repeatedly under direct experimental test.

The experiments also revealed something else: the willingness of trained physicians to stake their lives on the conviction that germ theory was wrong. Desgenettes, Clot-Bey, and Rodermund were not performing stunts. They were testing a hypothesis. Their survival was data.

The Medical Faction Rodermund Represented

Rodermund was not a lone eccentric. He belonged to a substantial faction within the medical profession that openly contested germ theory from its inception. These physicians were not marginal figures operating outside the mainstream. They included hospital presidents, university professors, pioneers of disease prevention, and some of the most influential medical minds of the nineteenth century.

The division between “contagionists” and “anti-contagionists” shaped medical discourse for decades. Contagionists subscribed to germ theory: one specific microorganism causes one specific disease. Pathogenic microbes invade the body, replicate, and produce illness. The interaction between germs and the immune system is a battle. Disease is the problem, and the solution lies in combating pathogens through antiseptics, vaccines, and antimicrobial drugs.

Anti-contagionists held a different view. They generally subscribed to one of two perspectives: terrain theory or zymotic theory. Terrain theory, conceived by Antoine Béchamp, Claude Bernard, and other sanitarian physicians, held that the body’s internal environment — its “terrain” or “soil” — determined whether disease occurred. The body exists in dynamic equilibrium, constantly working to maintain homeostasis. From this perspective, disease and symptoms are not the problem but an adaptive response to the problem — the body’s effort to restore balance after disruption by toxins, nutritional deficiencies, trauma, or environmental insults.

Zymotic theory proposed that specific diseases were caused by exposure to specific poisons or toxins rather than living microorganisms. The two theories shared a fundamental premise: germs were not the primary cause of disease. Environmental conditions were.

Dr. John W. Hodge, an outspoken advocate of sanitarian medicine, addressed the assumption that physicians universally accepted germ theory. In a 1905 journal article, he wrote: “There is a popular impression among the misinformed that the medical profession is unanimous in its acceptance of the germ theory of disease... This impression is grossly erroneous. Many of the most advanced thinkers in the medical profession, both in this country and abroad, are frank in the expression of their convictions that the germ theory has no scientific basis upon which to rest its claims.”

The roster of anti-contagionists included figures of considerable standing. Rudolph Virchow, considered one of the most brilliant and influential physicians of his era, opposed germ theory. Sir John Simon was a pioneer of disease prevention. Sir Edwin Chadwick shaped public health policy. Professor John Burdon-Sanderson acknowledged that “the influence of the environment upon organisms such as bacteria is so great that it appears as if it were almost paramount.” Dr. Stephen Mackenzie, senior physician at a leading London hospital, formally addressed the Medical Society in 1902 to warn that the profession was giving too much credence to the germ and too little to the body.

These physicians framed the debate in terms of “seed and soil.” W.H. Dickinson, senior physician to St. George’s Hospital in London, argued that treating disease should focus on the soil, not the seed, because the activity and growth of the seed is determined by the conditions of the soil in which it grows. Mackenzie believed physicians should treat infectious diseases by rendering the terrain unfavourable to the growth of pathogenic microbes rather than attempting to destroy the microbes themselves.

The anti-contagionists were labelled “sanitarian heretics” — an ironic term given that their views were, by and large, reasonable and supported by clinical observation. Modern scholars have looked upon them more favourably, describing them as scientists, reformers, and advocates for improved living conditions. They believed disease arose from raw sewage, garbage, rotting organic matter, poor sanitation, squalid housing, poisons, toxins, and nutritional deficiencies. They advocated treatment through dietary and lifestyle modifications, improved hygiene, fresh air, sunlight, and rest. These approaches had been accepted medical practice for over two thousand years in various forms.

Rodermund, then, was not conducting a rogue experiment. He was testing the hypothesis shared by a substantial portion of the medical establishment: that germs could not cause disease in healthy tissue, and that exposure to infectious material would not produce illness in a person whose internal terrain remained sound.

The Surgeons’ Evidence

The anti-contagionist position was not merely theoretical. It was supported by clinical observations from surgeons who worked directly with infected wounds, bacteria-laden tissue, and the practical realities of preventing post-operative complications.

Dr. Lawson Tait, surgeon and president of two large hospitals in Britain, addressed medical doctors at the annual Birmingham and Midland County Branch meeting in 1887. He argued that bacteria did not cause disease but were merely agents responsible for decomposing tissue devoid of “vitality.” There was an enormous difference, Tait observed, between living and dead matter, and in the way microorganisms interact with each. From his surgical observations, he concluded that bacteria could not attack living, healthy tissue. The phenomena of decomposition must not be mistaken for that of disease.

Tait’s position was informed by experiments he conducted over three years involving one hundred women who underwent ovariectomy. In fifty women, he performed surgery adhering to strict Listerian principles of antisepsis — sterilisation of wounds and instruments with carbolic acid. In the other fifty, he operated without such precautions, using only general cleanliness and cold water. The women operated on without Listerian infection control had a significantly lower mortality rate, better post-operative outcomes, shorter recovery times, and fewer complications.

These results were not anomalous. Professor Victor von Bruns, Dr. John Lowe, Dr. Thomas Keith, and Dr. Geo Bantock all reported that Listerian methods not only failed to improve surgical outcomes but were actively harmful. Tait achieved similar results operating on compound fractures. Suppuration — pus discharging from a wound — occurred when following Listerian principles. Using pure water to clean hands, instruments, and wounds resulted in uncomplicated healing.

Tait’s explanation centred on the food source of bacteria rather than the bacteria themselves. He regarded pus in an abscess as partially decomposed dead tissue that had become liquefied. Although the pus was full of bacteria, the healthy living tissue immediately adjacent remained free from germs. When pus was drained from an abscess, the bacteria were starved of their food source and evacuated the area, resolving the so-called infection. Despite not removing every last germ, the abscess would heal without complication. If bacteria were the cause of disease, Tait asked, why did they not re-infect the healthy surrounding tissue despite being left inside the clean surgical wound?

In 1890, Tait published further observations on the saprophytic action of bacteria — their consumption of dead and dying organic matter. If a piece of dead tissue was introduced into a man’s leg, it would result in rapid proliferation of germs. These organisms were not there to prey upon healthy tissue. They were there to break down the lifeless foreign matter. No bacteria would grow, Tait noted, when a shard of ivory or a lead bullet penetrated tissue. The foreign material was inorganic and therefore not prone to microbial decomposition. No infection occurred because bacteria could not use inorganic matter as a food source.

Dead and devitalised tissue may lie dormant until bacteria come in contact with it, at which point they go to work consuming the compromised tissue. The metabolic waste products of this process — some of which are toxic — produce symptoms associated with bacterial infection. But if bacteria were introduced into tissue that was vitalised and healthy, no decomposition or infection would take place.

Professor Hugh Cabot, in an address to a major medical association in 1921, described how surgical operations during the First World War cast considerable doubt on germs as the cause of disease. When men were admitted with battle wounds, the key to successful treatment was completely excising the damaged tissue. The presence of germs was neither here nor there — of no great importance. Bacteria were already present in wounds before surgery began. Wounds were almost never completely free from bacteria even after surgeons finished operating. It was not the removal of germs that prevented infection, Cabot concluded, but the removal of devitalised tissue. Germs grow on dead tissue and clotted blood, not on tissue in normal condition.

Dr. George Wilson, addressing the Section of State Medicine in 1899, stated that pathogenic germs are only found in necrosed — dead — tissue. Rather than causing the tissue death, germs perform a benign function, changing dead tissue into harmless by-products that can be removed by the body. Dr. Geo Granville Bantock reinforced this view: bacteria were not causative of disease but scavengers of tissue devoid of vitality. Dr. S.K. Das compared bacteria to the insect that consumes fallen fruit. The insect doesn’t attack fruit still hanging on the tree; it waits until the fruit has dropped and begun to decay. Bacteria function the same way. For healthy tissue, they remain absent or inactive. For diseased tissue, they actively seek it out and assist in breaking it down — a pattern mistaken for pathogenesis.

What Happened to These Ideas

The anti-contagionist perspective did not disappear because it was refuted. It was pushed aside.

As germ theory gained wider acceptance, discourse between the two factions became stifled. The contagionists were increasingly legitimised while the anti-contagionists were dismissed. Viewpoints seen to directly challenge germ theory were labelled heretical and discarded. The sanitarian perspective — which had shaped medical thinking for over two millennia in various forms — was overturned almost overnight.

The transition was not driven by decisive experimental evidence. Human transmission experiments continued to produce confounding results well into the twentieth century. During the 1918 Spanish influenza pandemic, the U.S. Navy conducted extensive experiments at military quarantine hospitals, partnering with over fifty high-ranking officers, the Surgeon General, and professors from leading universities. More than 160 sailors volunteered for experiments designed to transmit influenza through direct exposure to sick patients, injection of bodily fluids, and other aggressive methods. The infection rate was less than two per cent.

Other researchers attempting human-to-human transmission of influenza and the common cold produced similarly disappointing results. Anna Williams, Mary Nevin, and Caroline Gurley failed to infect any of forty-five healthy participants inoculated with bodily secretions from cold and flu patients. Robert Robertson and Robert Groves were unable to infect one hundred volunteers exposed to filtered mucus secretions. The pattern held across dozens of experiments: direct exposure to infectious material did not reliably produce disease.

When positive results did occur, they were plagued by methodological problems — no control groups, no blinding, no isolated pathogen as an independent variable. The most compelling evidence for contagious transmission came from the least reliable experimental methods. In one particularly telling result, researcher Paul Schmidt observed a substantially higher rate of flu symptoms from an inert substance — saline — than from infectious material. If a neutral solution produced more illness than sick secretions, the entire premise of transmission experiments was called into question.

Rodermund’s smallpox experiment remains unexplained by contagion theory. He exposed himself and thirty-seven others to concentrated infectious material under conditions that should have guaranteed transmission. Nothing happened. He had repeated this experiment for fifteen years with the same result. The pattern matched what Desgenettes observed with plague, what Clot-Bey demonstrated through self-injection, and what dozens of other physicians documented across the nineteenth century.

The anti-contagionists offered an explanation: germs cannot attack healthy, vitalised tissue. The terrain determines whether disease occurs, not the presence of microorganisms. Bacteria are scavengers that arrive to clean up damaged tissue, not invaders that cause the damage. This framework accounts for Rodermund’s result. His terrain was sound. The smallpox material had nothing to act upon.

Whether this explanation is correct remains an open question. What is not open to question is the historical record. Trained physicians repeatedly exposed themselves to the most feared diseases of their era and remained healthy. The expected chain of contagion broke down under direct test. These results were not hidden or suppressed — they made headlines. They were published in medical journals. They were discussed at professional meetings.

Then they were forgotten.

The ideas that Rodermund represented — terrain theory, the saprophytic role of bacteria, the primacy of the internal environment — disappeared into what one scholar called “the fog of time.” Germ theory became medical orthodoxy. The physicians who contested it became historical footnotes, remembered if at all as curiosities or cranks rather than as representatives of a substantial and reasoned alternative to the framework that now dominates medicine.

Rodermund smeared smallpox pus across his face and touched thirty-seven people. None of them got sick. The question is not whether this happened — it is documented, reported, and never disputed. The question is what it means. Contagion theory has no satisfying answer. The sanitarian physicians who were Rodermund’s intellectual allies believed they did. Their explanation may be wrong. But their question — why didn’t anyone get sick? — has never been adequately addressed.

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References

Roytas, Daniel. Can You Catch a Cold? Untold History and Human Experiments. 2024.

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