Is Ivermectin a BioWeapon from Unit 731. Hundreds of Millions of People. 38 Years in Africa. Over 5 billion Treatments. Merck USA’s Largest Drug Donation Program.
“Are we allowing the entire world to become a kill box—where governments can identify, track, and strike people anywhere with little public oversight?”
Long before ivermectin became a household name during the COVID-19 pandemic, it had already become one of the most important medicines ever used in global public health. This episode traces the complete history of ivermectin, from its discovery by Satoshi Ōmura and development by William C. Campbell at Merck to the early human clinical trials led by Dr. Mohammed A. Aziz that demonstrated the drug’s effectiveness against river blindness (onchocerciasis).
The episode follows the launch of Merck’s Mectizan Donation Program in 1987, now recognized as the world’s largest long-term drug donation program, with more than five billion treatments distributed. It examines how Merck, the World Health Organization (WHO), the World Bank, the Carter Center, ministries of health, scientists, nonprofit organizations, and hundreds of thousands of community-directed health workers built one of the largest disease-control campaigns in modern history across Africa, Yemen, and Latin America.
The discussion explains how river blindness is transmitted by blackflies (Simulium), why Onchocerca volvulus proved so difficult to eliminate, how ivermectin kills the parasite’s microfilariae but not the long-lived adult worms, and why repeated treatment programs have continued for decades. The episode also explores Loa loa, Wolbachia bacteria, doxycycline therapy, tropical medicine research, and the scientific challenges surrounding neglected tropical diseases.
The program also examines the broader history of tropical medicine through researchers including Dr. R. W. Ashford and others whose work connected Papua New Guinea, Africa, the Amazon Basin, Yemen, Brazil, and Venezuela. Their research crossed multiple diseases, including river blindness, cyclospora, and other neglected tropical infections, illustrating how global health networks evolved over several decades.
Finally, the episode explores the remarkable humanitarian legacy of the ivermectin campaign while asking larger historical questions about medicine, international development, Africa, scientific research, and the institutions that shaped one of the largest public health efforts in modern history. It also serves as the foundation for the next episode examining Walter Rodney and his analysis of Africa, development, global power, and the historical forces that continue to influence the continent today.
Clips:
How Does Ivermectin Work? – YouTube
Why is ivermectin toxic to dogs?
Tom Petty And The Heartbreakers – Runnin’ Down A Dream (Official Music Video) – YouTube
Tim Truth | Substack
Cancer and Aspirin: We Were Wrong About Aspirin (New Evidence)
River Blindness Treatment: Medications and Surgery | Inciteful Med Resources
Program: Mass Drug Administration to Control Onchocerciasis (aka River Blindness) | GiveWell
First Step as a Researcher – Wiping Blackboards | S&T articles archive| Sakura Science Club
How they use hormones to flip sex: Hormones
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River blindness is caused by a parasitic worm called Onchocerca volvulus.
It is spread by infected blackflies.
The adult worms live under the skin for 10–15 years and produce millions of tiny baby worms called microfilariae.
Those baby worms cause:
- severe itching
- skin disease
- eye damage
- blindness
Ivermectin is the medicine used to control river blindness.
Its main job is to kill the baby worms (microfilariae).
By removing the baby worms, it:
- relieves itching
- helps prevent blindness
- reduces the chance blackflies spread the disease to other people
Loa loa is a completely different parasite.
It causes Loiasis (African eye worm disease) and is spread by deer flies, not blackflies.
In parts of Central Africa, some people are infected with both river blindness and Loa loa.
Most people tolerate ivermectin well. However, people carrying extremely large numbers of Loa loa larvae in their blood can, in rare cases, develop serious neurological complications after treatment because so many parasites die at once and the body reacts intensely to their sudden destruction.
Wolbachia bacteriaThere is one more important piece.
Many adult river blindness worms contain Wolbachia, a type of bacteria that lives inside the worms.
The worms depend on these bacteria to survive and reproduce.
Scientists discovered that if they kill the Wolbachia bacteria with the antibiotic doxycycline, the adult worms gradually become sterile and eventually die.
So today there are two different treatment approaches:
- Ivermectin rapidly kills the baby worms, reducing symptoms and transmission.
- Doxycycline attacks the Wolbachia bacteria living inside the adult worms, weakening and eventually killing the adult worms themselves.
Think of it this way:
- Onchocerca volvulus = the parasite that causes river blindness.
- Microfilariae = the baby worms that cause most of the symptoms.
- Ivermectin = kills the baby worms.
- Wolbachia = bacteria living inside the adult worms that help them survive.
- Doxycycline = kills the Wolbachia bacteria, causing the adult worms to become sterile and eventually die.
- Loa loa = a separate parasite that can create rare but serious complications if a person has an extremely heavy infection when treated with ivermectin.
These are the four key pieces that explain why river blindness treatment has evolved over the past four decades.
Here is a single research table focusing on the most influential English-language public promoters of ivermectin during the COVID-19 era and whether discussions of side effects were a significant part of their public messaging.
Across this group, the dominant public themes were:
- Ivermectin’s long history of use against parasites.
- Its Nobel Prize association.
- Claims regarding COVID-19 effectiveness.
- Government and media censorship.
- Regulatory decisions.
Topics that generally received much less attention included:
- Rare neurological complications in people with high Loa loa microfilarial burdens in Central Africa.
- Mazzotti reactions after parasite death.
- Overdose toxicity.
- Drug interactions.
- Differences between approved antiparasitic use and proposed COVID-19 use.
This table reflects the general emphasis of their publicly available content rather than asserting that they never mentioned side effects. Several did discuss safety, but the uncommon adverse reactions associated with specific circumstances (such as Loa loa coinfection) were not a prominent or recurring theme in their public advocacy.
The timeline is surprisingly short once the program reached the relevant regions.
- 1987 – Merck announces the Mectizan Donation Program for river blindness.
- 1988 – Large-scale ivermectin distribution begins in endemic countries.
- 1989–1991 – Physicians in parts of Cameroon begin reporting rare cases of coma and severe neurological illness after ivermectin treatment. At first, the cause is unknown.
- 1992–1994 – Additional cases are documented as treatment expands into more Loa loa-endemic areas of Central Africa. Investigators begin to suspect the events are geographically linked.
- 1995–1997 – Detailed investigations identify very high Loa loa microfilarial loads as the major risk factor. A landmark 1997 Lancet paper establishes the association.
- Late 1990s – WHO, national programs, and researchers revise treatment strategies in affected regions, eventually leading to geographic risk mapping, enhanced surveillance, and later screening approaches.
So the progression was roughly:
- 1989–early 1990s: “People are developing severe neurological illness after ivermectin. Why?”
- Mid-1990s: “These cases all seem to occur where Loa loa is common.”
- 1995–1997: “Patients with the most severe reactions have extraordinarily high Loa loa microfilarial burdens.”
That finding did not mean ivermectin played no role—the neurological syndrome occurred after ivermectin treatment. Rather, the evidence indicated that the risk was concentrated in a very specific group of patients with heavy Loa loa infections, which allowed treatment programs to be modified instead of concluding that ivermectin posed the same risk to everyone.
- Penicillin (most forms)
- Heparin
- Insulin
- Most large antibody drugs
- Many antibiotics unless the meninges are inflamed
These drugs work elsewhere in the body and either are too large or too water-soluble to enter the brain easily.
Where ivermectin fitsIvermectin is actually interesting because under normal conditions it penetrates the human brain very poorly. Several protective mechanisms keep it out.
The most important is P-glycoprotein (P-gp), a transporter in the blood–brain barrier that actively pumps ivermectin back into the bloodstream if small amounts enter the barrier.
Problems can occur when:
- someone receives an overdose,
- the blood–brain barrier is impaired,
- P-glycoprotein is absent or inhibited,
- or there are unusual biological circumstances.
This is also why certain dog breeds (such as Collies with MDR1/ABCB1 gene mutations) can develop severe ivermectin toxicity at doses tolerated by most dogs—their protective transporter does not function normally.
The broader perspectiveOne reason the blood–brain barrier became such a focus during COVID discussions is that people asked whether ivermectin itself was causing neurological symptoms. Years of research, including investigations during river blindness programs, found that the rare severe neurological events in people with extremely high Loa loa infections were much more strongly associated with the massive parasite burden and its rapid clearance than with ivermectin routinely crossing into the brain at therapeutic doses.
So the key point is:
- Many common medicines intentionally cross the blood–brain barrier.
- Ivermectin is generally designed not to, and the body has active mechanisms to keep it out of the brain.
- When neurological toxicity occurs, researchers look not only at the drug itself but also at dose, genetics, the integrity of the blood–brain barrier, drug interactions, and the underlying disease.
So if you compare them:
- Morphine, Valium, Prozac, alcohol, nicotine: specifically need to reach the brain.
- Ivermectin: normally kept out of the brain by protective mechanisms.
- Statins: mainly act in the liver; some cross the blood–brain barrier more than others, but they are not intended to produce their primary effect in the brain.
In most humans and most dogs, ivermectin does not readily cross the blood-brain barrier in clinically significant amounts at approved doses.
The reason is that both species have a protective transport protein called P-glycoprotein, produced by the ABCB1 (formerly MDR1) gene. This protein acts like a pump that moves ivermectin back out of the brain and into the bloodstream.
However, there are exceptions.
In dogsSome dogs inherit an ABCB1 (MDR1) gene mutation. In those dogs:
- The P-glycoprotein pump doesn’t work properly.
- More ivermectin can enter and remain in the brain.
- High doses can produce neurological toxicity, including tremors, seizures, coma, and sometimes death.
This is why certain herding breeds are much more susceptible.
In humansMost people also have functioning P-glycoprotein at the blood-brain barrier, so approved doses of ivermectin generally result in very low concentrations in the brain.
Researchers have studied this extensively because the question naturally arose: if ivermectin affects nerve cells in parasites, what prevents it from affecting ours?
Under certain circumstances—such as:
- very large overdoses,
- severe impairment of the blood-brain barrier,
- or possibly rare genetic differences affecting drug transport—
more ivermectin may enter the human brain, and neurological toxicity has been reported. These cases are uncommon and are not the expected outcome at approved therapeutic doses.
The key pointThe blood-brain barrier is not an absolute wall. It is a highly selective barrier with active transport systems.
So a more accurate way to think about it is:
- Most dogs and most humans: P-glycoprotein keeps brain exposure very low at recommended doses.
- Some dogs with the ABCB1 mutation: Significantly more ivermectin can enter the brain, especially at higher doses.
- Humans: Brain exposure is usually low at approved doses, but higher exposure can occur under unusual circumstances such as overdose or impaired barrier function.
So it would not be accurate to say ivermectin “crosses the blood-brain barrier in dogs like humans” in a simple yes/no sense. It is capable of crossing to some extent in both species, but under normal conditions protective transport mechanisms keep brain concentrations low, and those protections can fail or be overwhelmed in certain situations.
1975–1978
- Satoshi Ōmura (Japan) and Merck scientists discover and develop avermectins.
- Early studies focus on safety, including why ivermectin generally does not affect the mammalian brain.
1981
- Ivermectin is introduced in veterinary medicine.
1987
- Merck launches the Mectizan Donation Program for river blindness.
- At this point, there is no recognized link between ivermectin and severe neurological reactions in people with high Loa loa infections.
1988–1991
- Mass treatment expands across Africa.
- Most programs proceed without reports of unusual neurological complications.
1989–1993
- As treatment reaches parts of Cameroon and neighboring Central African countries, physicians begin reporting rare cases of coma and encephalopathy after ivermectin treatment.
1994–1995
- More cases are documented.
- Researchers begin to suspect there is a common factor because the cases cluster geographically.
1995–1997
- Investigations identify the cause:
- Patients with severe reactions have extremely high Loa loa microfilarial loads.
- The neurological illness is linked to the rapid death of massive numbers of Loa loa microfilariae after ivermectin treatment.
1997
- A landmark study in The Lancet establishes the association between very high Loa loa infection and post-ivermectin encephalopathy.
Late 1990s
- WHO, national programs, and researchers revise treatment strategies in high-risk areas.
- Enhanced surveillance and mapping of Loa loa-endemic regions begin.
2000s
- Programs adopt risk-reduction measures, including better geographic screening and, later, targeted “test-and-not-treat” approaches in some regions.
2010s–Present
- The Loa loa complication remains a recognized but uncommon risk in specific areas of Central Africa.
- It is now incorporated into tropical medicine guidelines, and the large wave of unexpected cases seen in the early years of mass treatment has not recurred at the same scale after these program changes.
This timeline shows that it took about 8–10 years from the start of the Mectizan Donation Program in 1987 until researchers clearly identified very high Loa loa infection as the major risk factor for these rare neurological complications.
In ivermectin’s case, the key insight of the 1990s was that the neurological complications were not primarily due to ivermectin acting directly on the brain at normal doses. Instead, they were strongly associated with people who had extraordinarily high Loa loa infections, where rapid killing of massive numbers of microfilariae triggered the severe reaction.
It’s also true that if researchers had not identified a specific risk factor, the repeated occurrence of unexplained severe neurological events could have undermined confidence in ivermectin much more broadly. Public health programs generally depend on being able to explain adverse events and reduce their occurrence. Identifying the association with Loa loa gave investigators a biologically plausible explanation and a basis for changing practice.
Before that discovery, clinicians were seeing rare but alarming neurological events after ivermectin treatment in certain areas, without a clear explanation. Once researchers recognized that the cases clustered in people with very high Loa loa microfilarial loads.Early development (1970s–early 1980s) focused on questions such as:
- Is ivermectin toxic to mammals?
- Does it enter the brain?
- What dose is safe?
- How is it metabolized?
- What are the effects in laboratory animals and early human studies?
Those studies generally involved healthy animals, veterinary species, and controlled human trials. They were not designed to detect a rare interaction that would occur only in people with extremely high Loa loa microfilarial burdens living in certain regions of Central Africa.
The Loa loa problem became apparent only when several conditions came together:
- Millions of people were treated in mass campaigns.
- Treatment expanded into areas where Loa loa was common.
- A very small subset of people had exceptionally high parasite loads.
- Clinicians observed a pattern of severe neurological illness after treatment and investigated it.
So it wasn’t that researchers ignored brain safety for 8–10 years. Rather, they had identified one safety issue (how ivermectin itself behaves in mammals), while a different, population-specific safety issue emerged only after large-scale use revealed it.
That sequence is not unique to ivermectin. Some rare adverse reactions are discovered only after a medicine is used in very large and diverse populations because clinical trials are usually far too small to detect events that occur, for example, once in tens of thousands or hundreds of thousands of people.
In ivermectin’s case, the key insight of the 1990s was that the neurological complications were not primarily due to ivermectin acting directly on the brain at normal doses. Instead, they were strongly associated with people who had extraordinarily high Loa loa infections, where rapid killing of massive numbers of microfilariae triggered the severe reaction.
If you’re comparing countries, the other major powers that also did not have endemic river blindness include:
- Russia
- China
- Japan
- Most of Europe
- Canada
- United States
- Australia
The large, decades-long ivermectin donation campaigns instead focused on endemic regions in Africa, Yemen, and limited parts of Latin America.
From April 1, 1965, Satoshi Omura became a researcher at the Kitasato Institute.
The Kitasato Institute is a research institute founded by Shibasaburo Kitasato, an outstanding medical scientist of modern Japan. He was born in 1852, graduated from the University of Tokyo School of Medicine, and studied in Germany at Robert Koch’s laboratory.
Shibasaburo did a lot of work to pioneer cutting edge medical research at the time, such as pursuing pure culture of tetanus bacteria. His efforts were so dedicated that he sacrificed sleep for his experiments.
In the experiment to plant bacteria in the medium, he did not take any meals and continued his work for 10 hours straight, which astonished Koch. After he completed his overseas studies of six years and six months, Shibasaburo returned home, and founded the Kitasato Institute.
Omura had joined this distinguished institute, but he was hired as an assistant to Director Toju Hata, and his first job was to note down what was taught in his class and to wipe the blackboard.
Omura realized that he was not yet accepted as a full-fledged researcher at Kitasato. So every morning, he came to the lab at six o’clock, to clean the room and to write-up the final copy of each academic paper.
Back then, there were not any word processors or computers. Writing up the final draft was a very important task. Omura worked hard, trying to find any typos or inadvertent mistakes made by the author. In the end, fixing such mistakes really is an indispensable task, Omura thought to himself.
It was around that time that an unfamiliar foreign visitor came to the laboratory. It was Professor Yoshida Zen’ichi of Kyoto University who guided in the visitor from abroad. Professor Yoshida was a famous scholar who served as Chairman of Japan’s Chemical Society at that time.
The foreigner who visited the lab was Paul von Rague Schleyer, a professor at Princeton University and a famous scholar in the field of organic chemistry. He had read Omura’s paper written in English. Omura had written this paper during his graduate school days at Tokyo University of Science. Professor von Schleyer and Omura exchanged views on determining chemical substance structures using NMR. Omura was deeply impressed because it was his first time to meet such a distinguished foreign researcher. Because Omura had written his paper in English, researchers outside Japan could also read and evaluated it.
“It was from this instance, I think, that I clearly made up my mind to become a researcher,” Omura recalls.
Highly Evaluated for His ThesesOmura’s salary at that time was not high, so life was not easy. However, his wife Fumiko supported the household by opening a private tutoring class or by individually tutoring students. Fumiko who was bright-natured cooperated without any complaints. When Omura got his Nobel Prize, one reporter asked how he felt. “The first person I broke this great news to was my deceased wife, who supported me during my hardest times. I talked to her in my heart,”responded Omura.
Omura started his research on chemical structure determination. The Kitasato laboratory already had equipment for nuclear magnetic resonance (NMR) and infrared spectroscopy (IR). However, the only person who could read and decipher the data was Omura. That was because he was able to use the NMR at Tokyo Industrial Testing Laboratory. It was the only NMR in Japan at that time. Omura felt that his efforts had come to fruition after all his sleepless nights conducting experiments during his master’s program at Tokyo Science University.
Omura’s research to investigate the structure of leucomycin had proceeded smoothly, and he was finally able to determine its structure. Subsequently, Director Hata had instructed Omura to perform separation, crystallization and structure determination of cerulenin. Hata was beginning to evaluate Omura’s work highly and Omura was given new challenges one after the other.
Cerulenin is an antibiotic produced by a certain microorganism. Omura performed this task well and published it as a paper. Both of these tasks were pioneering attempts using NMR to determine the structure of natural substances.
Suffering from Neurosis – Fumiko Saves OmuraThe research progresses steadily and Omura wrote papers one after another and presented them. However, Omura gradually lost the purpose in his research. Was his research really useful or not?
Even when he went to the laboratory, he was thinking to himself in silence. His wife Fumiko quickly noticed this negative change and took him to the hospital. The doctor told Omura that he is working too much and that he needs a hobby. Lending his ear to the doctor, Omura takes up golf.
Still, dark feelings crept up in his mind while thinking about his future. Omura sought advice from other researchers outside the institute whom he met during academic meetings.
He also went to an international conference held in Europe with Fumiko to distract himself from depressing moods. After he returns from Europe, Omura went to seek advice from a famous chemistry researcher on how to direct his future research. He gives an unexpected advice to Omura.
“Go study in the United Sates! It’s good to experience the American research environment and think about your next step.”
Omura was taken aback. The idea of studying abroad had never occurred to him until then. These words changed Omura’s life.
Source: First Step as a Researcher – Wiping Blackboards | S&T articles archive| Sakura Science Club
From Imperial Army Microbiology to Ivermectin The Kitasato Scientific LineageWhen most people hear the story of ivermectin, they usually begin with Japanese scientist Dr. Satoshi Ōmura, who collected soil samples during the 1970s and discovered a microorganism that eventually led to the development of avermectin. Merck scientists in the United States later recognized the extraordinary antiparasitic properties of that microorganism and developed ivermectin.
That is the familiar story.
What is discussed far less often is how Ōmura became the scientist who made that discovery.
Scientists do not appear out of nowhere. They are trained by other scientists, who themselves were trained by earlier generations. This report follows that scientific lineage through one institution—the Kitasato Institute in Japan—and asks how knowledge, research traditions and scientific leadership passed from one generation to the next.
The timeline begins long before ivermectin existed.
From Imperial Army Microbiology to Ivermectin
The Kitasato Scientific Lineage
When most people hear the story of ivermectin, they usually begin with Japanese scientist Dr. Satoshi Ōmura.
During the 1970s, Ōmura and his research group collected soil samples from different parts of Japan, searching for microorganisms that might produce useful medicines. One of those samples contained a previously unknown strain of bacteria that produced a family of compounds later named avermectins.
That discovery was only the Japanese half of the story.
Shibasaburo Kitasato: The FounderThe story begins with Dr. Shibasaburo Kitasato, born in 1853.
Kitasato was one of the founders of modern Japanese bacteriology. During the late nineteenth and early twentieth centuries, he became internationally respected for research involving tetanus, plague, cholera and other infectious diseases.
This was a period when scientists were beginning to prove that particular microorganisms caused particular diseases. Governments were also developing formal systems for sanitation, quarantine and epidemic control.
Kitasato became one of Japan’s leading authorities in this new field. His work extended beyond the laboratory into public health, quarantine and military sanitation.
He eventually established what became the Kitasato Institute, one of Japan’s most important centers for bacteriology, microbiology and infectious-disease research.
The institute trained scientists, maintained laboratories and created a professional network that survived Kitasato’s death in 1931.
Kitasato therefore established more than a research facility. He established a scientific tradition.
Sahachiro Hata: From Bacteriology to Drug DevelopmentOne of Shibasaburo Kitasato’s most important associates was Dr. Sahachiro Hata.
The similar names can be confusing, so the relationship should be clear from the beginning:
Shibasaburo Kitasato founded the institute. Sahachiro Hata was one of his leading students and associates.
Sahachiro Hata became a prominent Japanese bacteriologist. He conducted research on plague under Kitasato and later traveled to Germany to work with scientist Paul Ehrlich.
At that time, syphilis was a widespread and often devastating disease. Ehrlich was searching for a chemical that could kill the organism responsible for syphilis without killing the patient.
Ehrlich and Hata tested hundreds of chemical compounds. Their work produced arsphenamine, commonly known as Salvarsan, in 1909.
Salvarsan became one of the first widely successful drugs specifically directed against an infectious organism. It was an important early step toward modern antimicrobial medicine.
Sahachiro Hata’s career also included military medical service and work in South Manchuria before the Second World War. He later became deputy director of the Kitasato Institute.
His career brought several fields together inside the same scientific tradition:
bacteriology, infectious disease, drug development, military medicine, quarantine and work connected with Manchuria.
Sahachiro Hata is also important because of his relationship to the next central figure.
Toju Hata was his adopted son and heir.
Toju had been born into the Fujimatsu family. After his adoption, he took the Hata family name and entered the same scientific and institutional world associated with Sahachiro Hata and the Kitasato Institute.
Toju Hata: The Bridge Between War and Postwar MedicineDr. Toju Hata joined the Kitasato Institute in 1936 as a young microbiologist.
He was entering both the institute founded by Shibasaburo Kitasato and the scientific world in which his adoptive father, Sahachiro Hata, had become a major figure.
One year later, in 1937, Japan’s war in China expanded dramatically. Toju Hata was drafted into the Imperial Japanese Army and sent to Manchuria.
Manchuria was a major center of Japanese military operations. It was also a major center of military medicine, epidemic prevention, bacteriology and biological-warfare activity.
The publicly available accounts of Toju Hata’s career provide very little information about this assignment.
They state that he served in Manchuria, but they do not identify his Army unit, commanding officer, military hospital, laboratory, location or precise duties.
In 1938, Hata was transferred from Manchuria to the Ninoshima Army Quarantine Station near Hiroshima.
Ninoshima was a major military quarantine and disinfection facility. Japanese soldiers returning from overseas passed through the station before reentering the country.
They could be medically examined, isolated, bathed and disinfected. Their uniforms, equipment and possessions could also be disinfected.
The purpose was to stop diseases carried by military personnel from spreading inside Japan.
Hata was therefore not serving in an unrelated Army position. He was a trained microbiologist assigned to the Army’s system of quarantine, infectious-disease control and large-scale disinfection.
The Wider Military Medical System and Unit 731To understand why Hata’s wartime career matters, it is necessary to understand the structure of Japanese military medicine.
The Imperial Japanese Army operated military hospitals, quarantine stations, sanitation departments, bacteriology laboratories, epidemic-prevention organizations and water-purification units.
Some of these organizations performed ordinary military health work. Disease could disable armies as effectively as enemy fire. Cholera, typhoid, dysentery and other infections had to be detected, contained and prevented.
But the same military medical system also contained Japan’s secret biological-warfare program.
The organization later known as Unit 731 officially operated under the name Kwantung Army Epidemic Prevention and Water Purification Department.
That title made it sound like a conventional public-health organization responsible for safe water, military sanitation and epidemic control.
Behind that public identity, Unit 731 conducted biological-warfare research, produced disease agents and carried out lethal experiments on prisoners.
Unit 731 did not operate in complete isolation from the rest of Japanese military medicine. It existed inside a wider professional system involving Army physicians, bacteriologists, laboratories, hospitals, epidemic-prevention units and water-purification organizations.
Toju Hata’s documented wartime career placed him inside that same broad professional environment.
He was a microbiologist.
He served in Manchuria while Unit 731 was operating and expanding there.
He was then transferred to an Army quarantine station devoted to disease control and disinfection.
His exact Manchurian unit and duties remain unidentified in the public accounts of his life.
Toju Hata Returns to KitasatoAfter Japan’s surrender in 1945, Toju Hata returned to the Kitasato Institute and resumed scientific research.
Medical research was entering a new era.
Penicillin had shown that one microorganism could produce a substance capable of killing another microorganism. Scientists around the world began collecting soil, growing bacteria and fungi, and testing the chemicals those organisms produced.
Soil became one of the principal places scientists searched for new medicines.
Toju Hata became an important figure in Japan’s postwar search for antibiotics and other biologically active compounds.
His research was associated with leucomycin, an antibiotic used against bacterial infections, and mitomycin, a microbial compound later used in cancer treatment.
The Kitasato laboratories continued searching for microorganisms that produced useful chemicals.
This was not a complete break from the institute’s earlier history. Kitasato had always concentrated on microorganisms, infectious disease and medical treatment.
The postwar difference was the growing effort to screen large numbers of microorganisms systematically and turn the chemicals they produced into drugs.
Toju Hata eventually became director of the Kitasato Institute and the first president of Kitasato University. Under his leadership, the institution became one of Japan’s leading centers for antibiotic and microbial-drug research.
Satoshi Ōmura Enters Toju Hata’s Research WorldSatoshi Ōmura was born in 1935 and was ten years old when the Second World War ended.
He later trained in chemistry, pharmacy, fermentation science and microbiology.
Ōmura joined the Kitasato Institute in 1965.
At that time, Toju Hata was director.
This is the important connection.
Ōmura did not arrive at an institution with no history behind it. He entered a laboratory culture that Toju Hata had helped shape through years of postwar antibiotic research.
Hata was also more than a distant administrator.
He and Ōmura conducted research together and published scientific papers together.
Their work included the study of kinamycin, an antibiotic produced by a microorganism obtained from Japanese soil.
The research method was straightforward but labor-intensive.
Scientists collected soil from different locations.
They separated microorganisms from those samples.
They grew the organisms under controlled conditions.
They examined the chemicals produced during fermentation.
They tested those chemicals to determine whether they affected bacteria, parasites, tumors or other biological targets.
Ōmura became highly skilled at finding unusual microorganisms and identifying the compounds they produced.
The Japanese portion of the ivermectin story therefore grew directly out of the Kitasato Institute’s established program of searching soil microorganisms for medicines.
How Merck Became InvolvedThe Kitasato Institute could discover microorganisms and identify promising natural compounds, but developing a commercial medicine required far greater resources.
A pharmaceutical company had the laboratories, chemists, animal-testing programs, manufacturing facilities and regulatory experience needed to turn a promising natural substance into a usable drug.
That is why Merck became part of the story.
Merck was a major American pharmaceutical company with large research laboratories in New Jersey.
Ōmura developed a working relationship with Dr. Max Tishler, a respected pharmaceutical chemist who had held senior positions at Merck.
Through that relationship, Kitasato sent promising microorganisms and fermentation products to Merck so they could be tested against a much wider range of diseases and biological targets.
The partnership divided the work according to expertise.
Kitasato specialized in locating unusual microorganisms and studying the chemicals they produced.
Merck had the resources to test those chemicals extensively, alter them chemically and develop them into medicines.
That collaboration connected Japanese soil research with an American pharmaceutical-development program.
William C. Campbell and the AvermectinsDr. William C. Campbell was a parasitologist working at Merck.
A parasitologist studies organisms that survive by living in or on other organisms. Campbell’s particular work included parasitic worms that infected livestock.
Those infections caused disease in cattle, sheep, horses and other animals. They also created major economic losses for agriculture.
Merck was therefore actively searching for better veterinary treatments.
When the microorganism selected by Ōmura’s group reached Merck, scientists grew it and studied the substances it produced.
Campbell and his colleagues tested those substances against parasitic worms.
The activity was unusually powerful.
The natural compounds produced by the microorganism became known as avermectins.
These natural compounds were not yet ivermectin.
Merck chemists modified one of them to improve its usefulness, safety and effectiveness.
That chemically modified compound became ivermectin.
Merck introduced ivermectin first as a veterinary medicine in the early 1980s. It became highly successful in treating parasitic infections in livestock and other animals.
From Veterinary Medicine to River BlindnessAfter ivermectin proved successful in animals, William Campbell proposed testing it against the parasite responsible for river blindness, also known as onchocerciasis.
River blindness is caused by a parasitic worm spread through the bites of infected blackflies.
Adult worms live inside the human body for years and release large numbers of microscopic larvae called microfilariae.
Those larvae move through the skin and eyes, causing intense itching, skin disease, impaired vision and sometimes blindness.
Human studies showed that ivermectin could dramatically reduce the number of microfilariae.
The treatment did not normally kill all the long-lived adult worms, so doses had to be repeated over many years.
In 1987, Merck introduced the human form of ivermectin under the name Mectizan and announced that it would donate the medicine for river-blindness programs.
The project grew into an enormous international campaign involving Merck, the World Health Organization, governments, nonprofit organizations, health workers and communities across Africa and other affected regions.
ConclusionThe story of ivermectin is often reduced to three statements.
Satoshi Ōmura found a microorganism in Japanese soil.
William Campbell and Merck discovered that its compounds killed parasites.
Merck developed ivermectin.
That summary leaves out the scientific tradition that produced the discovery.
Shibasaburo Kitasato established Japan’s modern bacteriology and infectious-disease research system.
His associate Sahachiro Hata carried that work into antimicrobial drug development, military medicine and South Manchuria.
Sahachiro’s adopted son, Toju Hata, entered the Kitasato Institute as a microbiologist, served in the Imperial Japanese Army in Manchuria, transferred to the Ninoshima Army Quarantine Station and returned after the war to become a leader
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