Seven Papers, Zero Pesticides

An essay on the myxomatosis programme and the questions it never asked

Preface

In 1859, a single act of homesickness triggered one of history’s most devastating ecological invasions. Thomas Austin, an English settler in Victoria, released twenty-four European rabbits onto his Australian estate so he could hunt them as he had back home. Within decades, their descendants numbered in the hundreds of millions.

The rabbits ate Australia. They stripped vegetation to bare earth, out-competed native species, accelerated erosion, and collapsed grazing land. Farmers tried everything: poisons, traps, shotguns, dynamite, ferrets, the world’s longest fence. Nothing worked. By the mid-twentieth century, Australia’s rabbit population had become a national emergency—a plague with no apparent solution.

Then, in 1950, government scientists announced they had found one. A disease called myxomatosis, reportedly fatal to European rabbits but harmless to other species, would be deliberately released into the wild. The result, according to official histories, was one of the most successful biological control programmes ever attempted: tens of millions of rabbits dead within months, entire populations collapsed, an ecological weapon that had finally matched the scale of the problem.

This is the story taught in textbooks, cited in scientific literature, and held up as proof that viruses can be weaponised against pest species. It is one of virology’s canonical success stories.

This essay examines what that story leaves out.

Acknowledgments

The analysis presented here builds on research first compiled by Dawn Lester and David Parker in What Really Makes You Ill? Why Everything You Thought You Knew About Disease Is Wrong (2019). Their work identified the myxomatosis programme as a case study in paradigm-bound investigation and documented many of the primary sources examined in this essay. The present work extends their analysis with additional documentation of the pesticide timeline, the virus isolation failures, and the evidentiary gaps in the CSIRO field studies.

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Between 1951 and 1965, Australian virologist Frank Fenner and his colleagues at the Commonwealth Scientific and Industrial Research Organisation (CSIRO) published seven papers documenting their field studies of myxomatosis in wild rabbit populations. These papers represent the most comprehensive scientific record of what is widely regarded as the first successful use of biological control against a vertebrate pest. They detail inoculation methods, mosquito vectors, mortality rates, geographic spread, and the gradual attenuation of virulence over time.

The seven papers contain no references to insecticides, pesticides, or agricultural chemicals of any kind.

This absence is remarkable. Australian farmers had been poisoning rabbits for nearly a century before the myxomatosis programme began. Strychnine, arsenic, cyanide, and phosphorus baits were standard tools of rabbit control throughout the late 19th and early 20th centuries. By the 1940s, a new generation of synthetic pesticides—organochlorines including DDT, chlordane, dieldrin, and heptachlor—had entered Australian agriculture. These were being applied across the same landscapes, near the same water sources, in the same years that CSIRO researchers were conducting their field trials.

The researchers never investigated whether these chemicals might be relevant to what they were observing.

This essay examines that gap—and a deeper one. The question is not whether pesticides definitively caused the rabbit die-offs attributed to myxomatosis; that case cannot be made from available evidence. The question is why a comprehensive research programme, spanning more than a decade and producing seven detailed papers, never considered the possibility. And beneath that question lies another: whether the “virus” blamed for myxomatosis was ever properly isolated in the first place.

If engineers investigating bridge collapses refused to record wind speed or structural load, and then declared metal fatigue the sole cause, we would not call that a complete investigation. The myxomatosis programme made an equivalent omission. It measured viral variables exhaustively and environmental variables not at all.

The myxomatosis story is typically presented as a triumph of virology. It may be more accurately understood as a case study in what happens when a theoretical framework—germ theory—determines in advance which questions get asked, which variables get measured, and which standards of evidence get applied.

The Conventional Narrative

The standard history runs as follows. European rabbits were introduced to Australia in 1859 and rapidly became an ecological catastrophe. Their numbers exploded into the hundreds of millions. They devastated grazing land, competed with native species, and contributed to erosion. Farmers tried everything: fencing, trapping, shooting, poisoning. Nothing worked at scale.

In 1896, Italian microbiologist Giuseppe Sanarelli observed a fatal disease in European rabbits he had imported to Uruguay. The disease was named myxomatosis. Researchers noted that while the presumed causative agent (later called myxoma virus) was devastating to European rabbits, it caused only mild illness in South American rabbit species—interpreted as evidence that these were the natural hosts. This species-specific lethality made myxomatosis an obvious candidate for biological control. The reasoning was never tested with purified material; it was inferred from the observation that crude preparations from sick animals killed European rabbits more reliably than South American ones.

Australia began experimenting with myxomatosis introduction in 1926. The early attempts failed. Further trials in the 1930s also failed. After World War II, CSIRO resumed the programme. Field trials in 1950 initially showed the same disappointing pattern as earlier efforts—the disease would kill inoculated rabbits but failed to spread.

Then, in the summer of 1950-51, something changed. An outbreak at one of four trial sites in the Murray Valley “escaped” and spread across the entire Murray-Darling basin, reportedly killing tens of millions of rabbits. Professor Fenner, who joined the CSIRO team in early 1951, would later describe this as the moment that inspired his career in myxomatosis research. The programme was declared a success. Subsequent years saw continued outbreaks, though with gradually decreasing mortality as both virus and host populations evolved.

This narrative presents myxomatosis as proof of concept for viral biological control. The variable early results are explained by the need for specific environmental conditions—particularly mosquito vectors and suitable weather. The 1950-51 success is attributed to unusually heavy rains that created ideal mosquito breeding conditions along the Murray River flats. The later attenuation is explained by co-evolution: less virulent viral strains were selected because they allowed infected rabbits to survive longer and spread the virus further, while more resistant rabbit populations emerged through natural selection.

The narrative is coherent. It is also incomplete.

What the Programme Actually Found

The consistency implied by the success story dissolves under examination. CSIRO’s own historical accounts acknowledge that early Australian and European trials were “disappointing” and often failed to spread. But the variability extended well beyond the pre-1950 period.

The Skokholm Island case is particularly instructive. In 1955, the journal Nature published a brief report titled “Failure of myxomatosis on Skokholm Island.” The paper documented three separate attempts to introduce myxomatosis to the rabbit population on this small Welsh island. In each attempt, rabbits inoculated with the virus developed disease and died within the expected timeframe of about fourteen days. But there was little or no spread to uninoculated rabbits.

The conventional explanation holds that the virus requires a vector—typically a biting insect—to transmit between animals. Skokholm presumably lacked sufficient vectors. But this explanation raises its own questions. If myxomatosis requires specific insect vectors to spread, what made the Murray-Darling conditions in 1950-51 so different from every previous Australian attempt? CSIRO researchers had been trying for decades in various locations. The answer offered is weather: unusually heavy rains produced unusually large mosquito populations.

Weather may well have been a factor. But “unusual weather” as an explanation does significant work in the myxomatosis literature. It explains why earlier attempts failed. It explains why the 1950-51 outbreak succeeded spectacularly. It explains geographic variation in mortality. At a certain point, a variable that explains everything explains nothing—it becomes a placeholder for conditions that were never systematically characterised, including the chemical environment that weather events would have mobilised and redistributed.

The attenuation pattern presents another puzzle. Initial mortality rates in 1950-51 reportedly exceeded 99%. By the mid-1950s, mortality had dropped substantially. By the 1980s, some rabbit populations showed mortality rates below 50%. The standard explanation—co-evolution of virus and host—is plausible. But it is also unfalsifiable in practice. Had mortality increased over time, this would have been attributed to viral evolution toward greater virulence. Had it stabilised at high levels, this would have been attributed to host-pathogen equilibrium. The framework accommodates any trajectory, which is precisely what makes it untestable against alternatives.

Fenner’s own papers document something else: researchers observed rabbits with scar tissue indicating recovery from the disease. Myxomatosis, in other words, was not inherently fatal even in susceptible European rabbits. Some animals survived. The case fatality rate was variable, not fixed—responsive to conditions that the research programme did not systematically investigate.

The Pesticide Timeline

While CSIRO researchers were focused on viral transmission, something else was happening across Australian agricultural landscapes—and specifically in the Murray-Darling basin where the 1950-51 “outbreak” occurred.

The Australian Department of the Environment records that organochlorine pesticides were introduced to Australia in the mid-1940s. These included DDT, chlordane, dieldrin, heptachlor, and aldrin. Government assessments describe them as “the first highly effective synthetic insecticides.” They saw widespread use in agriculture and pest control throughout the 1950s—the same decade as the myxomatosis programme’s most intensive field work.

These were not minor applications. DDT and its relatives were sprayed from aircraft, applied to crops, used to treat livestock, and deployed against mosquitoes. The chemicals were persistent, accumulating in soil and water. They were also toxic—sufficiently so that most were eventually banned, though not until the 1970s and 1980s. New South Wales government assessments from this period document organochlorine contamination of waterways and agricultural land throughout the Murray-Darling basin.

But organochlorines were only the latest addition to Australia’s chemical arsenal against pests. Rabbit poisoning had been practiced intensively since the 1860s. Historical records document the use of strychnine, arsenic, cyanide, and phosphorus baits across vast areas of agricultural land. A 1921 letter cited in ecological histories describes a “compulsory poison law” that required “every landowner in the Commonwealth to continually poison his land, from year’s end to year’s end.” The writer describes the landscape as “always covered more or less with the carcasses of poisoned rabbits.”

Some of these older poisons were persistent environmental contaminants. Arsenic, in particular, does not break down. Lead arsenate, used as a pesticide though not specifically for rabbits, similarly remains in soil indefinitely. Any rabbit population in Australian agricultural land during the mid-20th century was living in an environment contaminated by decades of accumulated toxins.

Sodium fluoroacetate, known as 1080, was introduced to Australian rabbit control programmes in the early 1950s—contemporaneous with the myxomatosis trials. Australian government records show that 1080 was being actively tested and deployed for rabbit control in New South Wales and Victoria during this period. This compound is an organofluorine, highly toxic to mammals, and it would become the dominant rabbit poison in subsequent decades. While 1080’s acute toxicity profile differs from the organochlorines—it disrupts cellular metabolism rather than causing the chronic tissue effects associated with chlorinated compounds—its introduction meant that multiple poisoning programmes were operating simultaneously with the myxomatosis trials.

The myxomatosis field studies were conducted primarily in riverside habitats. The second paper in Fenner’s series explicitly notes “a close connection was demonstrated, on the flats bordering the Murray River, between the distribution of these insects and myxomatosis activity.” Rabbits and mosquitoes both concentrate near water sources. So do pesticide residues—runoff from agricultural applications, accumulated deposits in sediments, and concentrated contamination in flood-prone areas. The 1950-51 “escape” occurred following heavy rains that would have mobilised these residues throughout the flood plains.

Seven papers. Detailed documentation of geography, weather, mosquito populations, viral strains, and mortality rates. No investigation of the chemical environment in which all of this was occurring.

The Encephalitis Coincidence

Fenner’s memoir, Nature, Nurture and Chance, contains a striking passage about the 1950-51 outbreak:

“The climatic conditions at the time of the outbreak of myxomatosis in the Murray-Darling Basin had been such that there was also an outbreak of encephalitis in that region...”

Human encephalitis and rabbit myxomatosis occurring simultaneously, in the same geographic area, under the same climatic conditions. The coincidence generated concern at the time. Researchers worried that the myxoma virus might somehow be responsible for human illness. Fenner reports that he and two colleagues were inoculated with the virus to demonstrate its safety for humans—they remained unaffected.

The human encephalitis cases were attributed to arboviruses transmitted by the same mosquito populations that had exploded following heavy rains. Culex annulirostris, the mosquito species associated with myxomatosis transmission in Australia, is also recognised as a major vector for Murray Valley encephalitis virus. Later laboratory work identified a flavivirus associated with Murray Valley encephalitis.

But there is another dimension to this coincidence that was never investigated. Organochlorine pesticides, which were being deployed intensively for mosquito control and agricultural pest management during this period, have documented neurotoxic effects. DDT and its metabolites can cause neurological symptoms including tremors, seizures, and altered mental status. These effects could produce neurological presentations clinically indistinguishable from what was being diagnosed as viral encephalitis. The simultaneous appearance of neurological disease in both humans and rabbits, in the same region, following the same weather events that would have mobilised pesticide residues, is compatible with shared chemical exposure as the cause.

This is not proof. It is a hypothesis that the available evidence does not rule out. The relevant point is that no one investigated it. The researchers were operating within a framework that attributed disease to infectious agents. Having identified presumptive viruses in both rabbit and human populations, they had no reason to look for chemical confounders. No contemporaneous toxicological work was conducted to measure pesticide exposures or to determine whether chemical and infectious factors might be operating together.

The geography reinforces the question. River flats and flood plains concentrate mosquitoes. They also concentrate pesticide runoff. Animals drinking from contaminated water sources, living in contaminated soil, exposed to residues mobilised by flooding—these are the conditions that characterised the Murray-Darling basin in 1950-51. The field studies documented where disease occurred without documenting what else was present in those locations.

What “Virus” Meant in Practice

The word “virus” carries specific connotations in contemporary usage: an ultramicroscopic infectious particle, a strand of genetic material in a protein coat, an entity that can be isolated, purified, and characterised at the molecular level.

This is not what “virus” meant in the myxomatosis research programme. The foundational material used in all major studies—the Standard Laboratory Strain (SLS)—was never properly isolated. A 2015 comprehensive review by Kerr and colleagues contains a remarkable admission: the SLS “was not a cloned virus in the sense of having been pock-purified on the chorioallantoic membrane of fertile eggs or cloned by limit dilution in rabbits.”

The authors justify this by citing Fenner and Marshall’s 1957 assertion that there was “no evidence that it was a mixture of virus populations based on repeatability of disease produced by inoculation of very low doses of virus.” The reasoning is circular: they knew they had a single agent because they got consistent results, and they got consistent results because they had a single agent. No independent verification was offered.

The SLS was derived from Martin’s strain B around 1910 and maintained by periodic passage in laboratory rabbits for over forty years. It was the source material for all subsequent field studies. Yet it was never purified or characterised as a specific infectious agent according to any rigorous standard.

Later laboratory work, conducted decades after the original field trials, has visualised particles under electron microscopy and sequenced genetic material from cell cultures, now labelled “myxoma virus.” But electron microscopy of unpurified samples cannot distinguish between pathogenic agents and the cellular debris, exosomes, and breakdown products present in any tissue preparation. Sequencing genetic material from a cell culture does not establish that the sequence originated from a disease-causing entity rather than from the host cells or contaminants. These methods demonstrate that particles and genetic material exist in laboratory preparations—which was never in dispute. They do not establish that a specific particle causes a specific disease, and they do not retroactively fix the design flaws of the original field programme. What actually killed rabbits in the Murray-Darling basin in 1950-51 cannot be determined from modern laboratory work, because the original studies never isolated a putative agent from the chemical environment, never controlled for pesticide exposures, and never designed experiments capable of distinguishing infectious effects from toxicological ones.

The actual isolation procedures used in the field programme are documented in the papers themselves. A 1963 British study by Chapple and Bowen describes the methods used to collect field strains. Researchers obtained “small pieces of eyelid and lung” from diseased rabbits, “received in 50% (v/v) glycerol saline.” The tissue was then processed:

The samples were “well washed with cold saline,” then “ground in a cold pestle and mortar with sterile sand,” suspended in a “special diluent,” and “lightly centrifuged to remove debris and sand.” The resulting supernatant was considered “isolated virus” and stored at -70°C.

The “special diluent” contained McIlvaine’s citric acid/di-sodium phosphate buffer, skim milk, penicillin, and streptomycin. What researchers called “virus” was everything soluble from diseased tissue that remained after grinding and light centrifugation—a complex mixture containing cellular debris, proteins, genetic material, buffer components, antibiotics, milk proteins, and whatever environmental contaminants the source animals had accumulated.

Australian studies followed identical procedures. Fenner, Marshall, and Woodroofe describe using “1% (w/v) suspensions” of spleen tissue from infected animals in phosphate buffers. Infectivity was demonstrated solely by “inoculating rabbits and recording the characteristic pyrexia which followed successful infection.” No purification, characterisation, or isolation of specific agents was performed.

When tissue culture methods were introduced, the pattern continued. Researchers harvested “culture fluids” from infected cell suspensions, “clarified by light centrifugation,” and stored them. The maintenance medium contained unheated ox serum and other additives. The resulting “virus suspensions” contained everything present in infected cell cultures except large cellular debris.

Throughout the reviewed literature—spanning decades and multiple countries—no researcher provided electron microscopy evidence of purified viral particles from field samples, biochemical characterisation of isolated material, demonstration that putative virus could be separated from all other biological components while retaining infectivity, or controls to exclude bacterial, chemical, or other causes of disease.

The quantification methods are equally problematic. “Virus” was measured by counting pocks on chorioallantoic membranes or recording disease symptoms in test animals. These methods measure biological effects of crude tissue preparations, not the presence of isolated viral entities. Pocks could represent localised tissue reactions to any component of the complex biological mixtures being tested.

Even claims about “clones” collapse under scrutiny. The 2015 review mentions that “tests of 127 clones prepared from single pocks did not produce any prolonged survival times,” but provides no evidence that individual pocks contained single, pure viral entities. The pocks themselves could represent tissue reactions to multiple agents within the crude inoculum.

This is not a minor technical point. The entire viral theory of myxomatosis rests on the assumption that disease was caused by a specific infectious agent. But no such agent was ever isolated from the complex biological preparations used in every study. The independent variable (the presumed virus) was never separated from the confounding variables (tissue components, chemical residues, buffer additives). What researchers termed “virus isolation” consisted of tissue grinding, filtering, and dilution—procedures that retained all soluble components of diseased tissue, including any toxic substances present.

Symptoms and Their Interpretation

Myxomatosis in rabbits presents with a recognisable syndrome: conjunctivitis (red, runny, swollen eyes), swelling of mucous membranes around the eyes, nose, mouth, and genitals, fever, lethargy, and respiratory distress. In severe cases, blindness and pneumonia precede death. The defining feature that gives the disease its name is the myxoma—gelatinous, mucinous swellings particularly around the head.

These specific pathological features are cited as evidence that myxomatosis is a distinct viral disease. The reasoning holds that if the same syndrome appears wherever the “virus” is introduced, this indicates a specific causative agent.

But this reasoning has limits. The clinical syndrome could result from the introduction of specific biological material—the crude tissue preparations themselves—rather than from any replicating agent. Rabbits on Skokholm Island developed the syndrome when injected but did not transmit it to cage-mates. This is consistent with reaction to an injected substance rather than contagion.

More broadly, the toxicological effects of the compounds present in mid-century Australian agricultural environments were never systematically studied in rabbit populations. Phosphorus compounds can cause tissue necrosis and mucous membrane damage. Arsenic produces a range of systemic effects including oedema. Organochlorines accumulate in tissues and can cause chronic pathological changes. Whether any of these could produce or contribute to the specific swellings characteristic of myxomatosis was never investigated—not because studies ruled it out, but because the question was never asked.

The symptom-matching argument cuts both ways. If researchers begin with the assumption that a disease is infectious, they will interpret any distinctive clinical picture as evidence of a specific pathogen. The same symptoms, in a different interpretive framework, might prompt investigation of specific toxic exposures. The presence of toxicants capable of producing tissue injury means that toxicological screening should have been part of the investigative design. Its absence is a methodological failure, not evidence that toxicants were irrelevant.

What the Gap Means

The absence of pesticide investigation in the myxomatosis papers is not evidence of a cover-up. It is evidence of a paradigm.

Germ theory, by the mid-20th century, had become the dominant framework for understanding disease. Infectious agents—bacteria, viruses, parasites—were the causes that researchers looked for. Environmental toxicology existed as a field, but it was not integrated into mainstream disease investigation. When animals or humans became sick, the reflex was to search for a pathogen.

This framework determined what data were collected. The CSIRO researchers meticulously documented viral transmission, mosquito populations, geographic spread, and mortality rates. They did not document pesticide applications, chemical contamination of water sources, or toxic residues in affected animals. The paradigm shaped the evidence base, and the evidence base now appears to confirm the paradigm.

The same framework determined what counted as “isolation.” Grinding tissue, suspending it in buffer, and centrifuging out debris was considered adequate because the goal was to obtain infectious material, not to characterise a specific agent. The procedures made sense within germ theory’s assumptions. They did not constitute proof that a specific virus existed or caused the observed disease.

The Skokholm Island failures illustrate the interpretive consequences. Inoculated rabbits died; uninoculated rabbits did not become sick. The standard explanation invokes insufficient vectors. But the data are more parsimoniously explained by a simpler hypothesis: there was no contagious agent—only a toxic inoculum that killed injected animals but did not propagate. The viral interpretation requires an additional explanatory layer (missing vectors) to account for the failure to spread. The toxic interpretation requires no such addition. The point is not merely that the trial design could not distinguish between these possibilities; it is that the simpler explanation was never considered because germ theory provided no category for it.

This critique is not directed at germ theory’s existence as a framework. It is directed at its monopoly over inquiry in environments saturated with industrial chemicals. When one theoretical lens determines all research questions, alternative explanations become invisible—not because they have been tested and rejected, but because they were never considered.

The Pattern Beyond Myxomatosis

The myxomatosis gap is not unique. A similar investigative pattern appears in other twentieth-century disease attributions where infectious explanations dominated inquiry while environmental chemical exposures went unexamined.

The polio epidemics of the mid-twentieth century peaked during the years of heaviest DDT and lead arsenate use and declined as these pesticides were restricted—a correlation that mainstream epidemiology attributes to vaccination but that matches the pesticide timeline with equal precision. BSE in cattle emerged in populations treated with organophosphate insecticides applied directly to animals’ spines, a connection investigated by farmer and researcher Mark Purdey through direct tissue sampling but largely ignored by establishment science.

Each of these cases requires its own in-depth treatment; the purpose here is not to settle those debates but to illustrate that the structural bias—infectious-first, toxicology-ignored—is recurring rather than unique to myxomatosis. This is not conspiracy. It is the normal operation of paradigm-bound science. Researchers ask the questions their training prepares them to ask. Funding flows to investigations that fit established frameworks. Careers are built on extending existing knowledge, not on challenging foundational assumptions. The result is a literature that appears comprehensive but that systematically excludes certain categories of explanation.

The Remaining Questions

The myxomatosis programme is typically cited as a success story—one of the few cases where viral biological control worked as intended. The millions of dead rabbits in 1950-51 are offered as proof that viruses can be weaponised against pest populations.

But the evidence, examined carefully, supports a more limited conclusion. Something killed large numbers of rabbits in the Murray-Darling basin in 1950-51. That event coincided with the introduction of material from sick rabbits into wild populations. It also coincided with unprecedented pesticide deployment, unusual weather that would have mobilised chemical residues, and a human encephalitis outbreak.

What the evidence does not establish is that a properly isolated virus, as distinct from toxic components of crude tissue preparations or environmental chemical exposure, was the cause. The investigation was not designed to make that distinction. The data to resolve the question were not collected. The “virus” itself was never purified from the material injected into test animals.

The later history complicates the narrative further. Mortality declined. Outbreaks continued but with diminishing impact. Rabbits remain abundant in Australia despite decades of myxomatosis circulation. The “success” of 1950-51 was never replicated at that scale. If a virus was responsible, it appears to have been a one-time weapon—effective under conditions that were never fully specified and never reproduced. This is a strange profile for a contagious pathogen.

An alternative reading of the same history: Australia’s most intensive period of rabbit mortality coincided with its most intensive period of agricultural chemical deployment. As pesticide use patterns changed—as some compounds were banned, as application methods evolved, as environmental concentrations shifted—rabbit mortality patterns also changed. The correlation is not proof. But it is a correlation that was never investigated.

What Would Resolution Require

To distinguish between viral and toxicological explanations for myxomatosis—or to determine their relative contributions—would require studies that have never been conducted.

Such studies would need to properly isolate and characterise the putative viral agent from field samples according to rigorous standards: electron microscopy of purified particles, biochemical characterisation, demonstration that purified material retains infectivity independent of other tissue components. They would need to document pesticide application patterns in areas where myxomatosis outbreaks occurred, measure chemical residues in affected and unaffected rabbits, and compare mortality rates in contaminated versus uncontaminated environments.

They would need to examine whether the clinical syndrome attributed to myxomatosis can be produced by specific pesticide exposures, whether crude tissue preparations used in historical inoculations contained chemical contaminants at biologically relevant concentrations, and whether disease transmission requires injection of foreign material or can occur through documented natural routes.

These studies are unlikely to be funded. They would challenge an established narrative. They would raise uncomfortable questions about the safety of pesticide programmes and the validity of biological control methods. They would require collaboration between virologists and toxicologists—disciplines that rarely intersect. The institutional barriers are substantial.

When an entire class of questions is never funded, absence of studies is not evidence of absence. It is evidence of institutional priorities.

The absence of such studies does not prove the toxicological hypothesis. It demonstrates that the hypothesis has not been tested. In an epistemically complete science, negative evidence—studies conducted that failed to find a connection—would carry weight. In the actual history of myxomatosis research, the relevant studies were never done.

Conclusion

Seven detailed papers documented the CSIRO myxomatosis programme over more than a decade. They established the viral theory of myxomatosis as canonical. They did not examine pesticide exposure as a confounder, despite intensive chemical deployment across the same landscapes during the same years. And they relied on a “virus” that was never isolated according to any rigorous standard—acknowledged in the literature itself as uncloned, unpurified, and characterised only by the disease it supposedly caused.

This gap does not prove that pesticides caused the rabbit die-offs. What it demonstrates is that the viral explanation was never established in the first place. The researchers asked certain questions and not others. The questions they asked were shaped by germ theory. The questions they did not ask—about environmental chemicals, about toxic confounders, about proper virus isolation—remain unanswered. A theory that rests on unpurified material, untested confounders, and circular reasoning is not a theory that has been validated; it is a theory that has been assumed.

The 1950-51 rabbit deaths in the Murray-Darling basin are a historical fact. The simultaneous human encephalitis outbreak is a historical fact. The introduction of organochlorine pesticides to Australian agriculture in the mid-1940s is a historical fact. The presence of accumulated toxins from decades of mandated poisoning is a historical fact. The Skokholm Island failures are a historical fact. The absence of proper virus isolation is documented in the researchers’ own papers.

The conclusion that a virus, and a virus alone, explains these facts is an interpretation built on unpurified material and untested assumptions. It has never been demonstrated. Until it is, the myxomatosis success story remains a case study in how theoretical commitments can shape investigation—and how what researchers fail to examine can become invisible in the historical record.

The rabbits died. The question of what killed them is less settled than the textbooks suggest.

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References

1. CSIRO. “Myxomatosis to control rabbits.” CSIROpedia. https://csiropedia.csiro.au/myxomatosis-to-control-rabbits/

2. NSW Environment. “Myxomatosis – Blue Plaques.” https://www.environment.nsw.gov.au/topics/heritage/blue-plaques/myxomatosis

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New Biology Clinic

For those of you looking for practitioners who actually understand terrain medicine and the principles we explore here, I want to share something valuable. Dr. Tom Cowan—whose books and podcasts have shaped much of my own thinking about health—has created the New Biology Clinic, a virtual practice staffed by wellness specialists who operate from the same foundational understanding. This isn’t about symptom suppression or the conventional model. It’s about personalized guidance rooted in how living systems actually work. The clinic offers individual and family memberships that include not just private consults, but group sessions covering movement, nutrition, breathwork, biofield tuning, and more. Everything is virtual, making it accessible wherever you are. If you’ve been searching for practitioners who won’t look at you blankly when you mention structured water or the importance of the extracellular matrix, this is worth exploring. Use discount code “Unbekoming” to get $100 off the member activation fee. You can learn more and sign up at newbiologyclinic.com