Psychopath In Your Life

“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

Did Jimmy Carter PLAY the role of JFK?

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:

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:

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.

There 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:

Think of it this way:

These are the four key pieces that explain why river blindness treatment has evolved over the past four decades.

Rose Elizabeth Fitzgerald Kennedy was the matriarch of “The Kennedy Clan,” which was embedded in the American political culture of the last half of the twentieth century like no other family.

They arrived at such a station through ambition, wealth, and fierce family loyalty, coupled with exuberance and glamor, honorable service to the nation, and family tragedies impossible to keep private.

No family has had such a powerful hold on the American imagination.

During their heyday, the Kennedy family were called the “American royal family” by the press. Interestingly, there’s evidence that suggests the Kennedys have royal blood in their veins…

According to genealogist Brian Kennedy (no relation), the modern-day Kennedy family are descended from the Irish O’Kennedy clan (or Ó Cinnéide in Gaelic), who once ruled the Kingdom of Ormond during the Medieval Period.

More specifically, the modern-day Kennedys are descended from the Ó Cinnéide Fionn clan (a cadet branch of the Ó Cinnéide clan) with their progenitor being Diarmaid Ó Cinnéide Fionn, who lived in the mid-16th century.

Just like many other Gaelic clans, the Ó Cinnéide clan as a whole prospered until the Protestant Ascendancy in the 17th century, where the entire Ó Cinnéide clan lost all the land it still held to Protestant English and Scotsmen.

Having lost their land and the social standing that came with it, the Ó Cinnéide Fionn left their ancestral homeland before ending up in Dunganstown, New Ross, County Wexford, in 1740.

The Ó Cinnéide Fionn (eventually anglicized to just O’Kennedy, and later, Kennedy) lived in Dunganstown for several generations, until Patrick Kennedy was born there in 1823.

Between 1938 and 1940, Joseph Kennedy Sr. served and the U.S. Ambassador to the UK. Naturally, that involved attending quite a few political events with royalty—like this one that Kennedy and his wife, Rose, were seen at alongside King George VI and then-Queen Elizabeth in May 1939.

Throughout his prestigious career as U.S. ambassador, Joseph Kennedy made a number of infamous antisemitic remarks and successfully embarrassed the country by expressing sympathy for fascists in Europe. Rightly or wrongly, many people today remember Kennedy as a Nazi sympathizer and an all-around awful person.

Across this group, the dominant public themes were:

Topics that generally received much less attention included:

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.

So the progression was roughly:

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.

These drugs work elsewhere in the body and either are too large or too water-soluble to enter the brain easily.

Ivermectin 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:

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.

One 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:

So if you compare them:

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.

Some dogs inherit an ABCB1 (MDR1) gene mutation. In those dogs:

This is why certain herding breeds are much more susceptible.

Most 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:

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 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:

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

1981

1987

1988–1991

1989–1993

1994–1995

1995–1997

1997

Late 1990s

2000s

2010s–Present

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.

Early development (1970s–early 1980s) focused on questions such as:

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:

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:

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.

Omura’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.

The 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

When 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.

The 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.

One 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.

Dr. 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.

To 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.

After 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 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.

The 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.

Dr. 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.

After 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.

The 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 in antibiotic research.

Satoshi Ōmura joined Kitasato while Toju Hata was director.

The two scientists worked directly together on medicines produced by soil microorganisms.

Ōmura later entered a formal collaboration with Merck.

William Campbell and his colleagues tested the compounds against parasitic worms. Merck chemists then transformed one of the natural avermectins into ivermectin.

The path to ivermectin therefore extended across generations.

It began with Japan’s early bacteriology establishment, passed through military medicine and quarantine, continued through postwar antibiotic research and eventually connected with Merck’s American pharmaceutical laboratories.

At the center of that transition was Toju Hata: the adopted son of Sahachiro Hata, an Army microbiologist who served in Manchuria and at Ninoshima, a postwar antibiotic researcher, director of Kitasato and a direct scientific collaborator with Satoshi Ōmura.

The public record clearly documents that lineage. It leaves one major period largely unexplained: Toju Hata’s precise military assignment and duties in Manchuria before his transfer to Ninoshima.

The clearest elite connections tied directly to the Kitasato institution are these: 

Shibasaburo Kitasato himself became part of Japan’s titled elite. In 1924, he was made a baron under Japan’s hereditary peerage system. He was also a member of the Imperial Academy and received high imperial decorations. So by the later part of his life, Kitasato was not merely a scientist working outside the establishment; he had been formally elevated into it.  

Yukichi Fukuzawa was Kitasato’s most important early patron. Fukuzawa founded Keio University and was one of the most influential intellectual and institutional figures of modern Japan. He helped Kitasato establish Japan’s first private infectious-disease institute and supported the tuberculosis hospital on the site where the later Kitasato Institute was built. Kitasato later repaid that support by helping establish Keio’s medical school.  

Morimura Ichizaemon supplied industrial wealth. Morimura was a major businessman who built an industrial and trading empire that later included companies associated with Noritake, TOTO and NGK. Official histories state that he financially supported Kitasato’s infectious-disease institute in 1892 and made major donations to Kitasato and other elite educational institutions.  

The Home Ministry and senior government medical officials were directly involved. Kitasato worked for the Home Ministry’s Sanitary Affairs Bureau after medical school. His early institute was supported through the efforts of senior public-health official Nagayo Sensai and politician Hasegawa Tai. The institute was later nationalized, showing that Kitasato’s work was connected from the beginning to the upper levels of Japan’s public-health administration.  

There was also a strong connection to Keio University, one of Japan’s most prestigious private institutions. Sahachiro Hata trained within the Kitasato network and had studied at the same elite intersection of bacteriology, government medicine and international research. Toju Hata later inherited both the Hata name and that institutional position. 

So the direct elite structure around the institution was not vague: 

Kitasato became a baron. 

Fukuzawa supplied intellectual prestige and institutional backing. 

Morimura supplied industrial money. 

The Home Ministry supplied government authority. 

Keio supplied an elite educational network. 

show that the Kitasato Institute was built from the beginning through a compact alliance of government medicine, wealthy industrial patrons, prestigious education and the imperial honors system. That is the elite network directly attached to the place we are tracking. 

Japanese microbiologist Dr. Satoshi Ōmura of the Kitasato Institute collects soil samples throughout Japan searching for microorganisms that might produce useful medicines. One sample contains a previously unknown bacterium, later named Streptomyces avermitilis (now Streptomyces avermectinius).

Ōmura sends the most promising bacterial cultures to Merck Research Laboratories in Rahway, New Jersey.

Merck parasitologist Dr. William C. Campbell begins testing the organisms against parasitic worms affecting livestock.

Merck scientists isolate a family of natural compounds produced by the bacterium and name them avermectins.

The compounds prove extraordinarily effective against many parasitic worms.

Merck chemically modifies avermectin to produce a safer, more potent compound for practical use.

The new drug is named ivermectin.

Ivermectin is introduced worldwide as a veterinary medicine.

It quickly becomes one of the most successful antiparasitic drugs ever developed for cattle, horses, sheep, pigs, and companion animals.

Human clinical trials begin for river blindness (onchocerciasis) in Africa.

Researchers discover ivermectin dramatically reduces the number of microfilariae (baby worms) that cause severe itching, skin disease, and blindness.

Scientists also discover an important limitation:

Ivermectin kills the baby worms but does not usually kill the long-lived adult worms.

Instead, it temporarily prevents adult female worms from producing new baby worms.

Merck receives approval for the human form of ivermectin under the brand name Mectizan.

Merck CEO Dr. Roy Vagelos announces the Mectizan Donation Program:

“As much as needed, for as long as needed.”

Merck agrees to donate ivermectin free of charge for river blindness control.

This becomes one of the largest humanitarian drug donation programs in history.

Mass treatment programs begin across Africa.

Communities receive ivermectin once or twice each year.

Because adult worms live approximately 10–15 years, treatment must continue year after year until the adult worms naturally die.

Programs expand rapidly across sub-Saharan Africa.

Researchers observe enormous reductions in:

Doctors working in parts of Central Africa begin reporting a rare but serious problem.

Some patients become severely ill shortly after taking ivermectin.

Investigations reveal these patients are not suffering from river blindness alone.

Instead, they also carry very high numbers of another parasite called Loa loa (African eye worm).

Scientists determine the neurological complications are associated with people who have extremely high Loa loa microfilarial loads.

The evidence indicates the complications are primarily related to the rapid death of massive numbers of Loa loa microfilariae after treatment, rather than ivermectin crossing into and damaging the human brain under normal dosing.

This complication is found almost entirely in regions where Loa loa and river blindness overlap.

Public health programs adapt.

Health workers begin:

Mass ivermectin programs continue safely in most endemic regions.

The Mectizan Donation Program expands beyond river blindness to support efforts against lymphatic filariasis (elephantiasis) in many countries through combination drug programs.

Several countries in Latin America eliminate river blindness transmission.

Large parts of Africa also make major progress toward elimination.

More than 3 billion ivermectin treatments have been distributed.

The Nobel Prize in Physiology or Medicine is awarded jointly to:

for discoveries leading to ivermectin.

Ivermectin becomes the subject of worldwide controversy during the COVID-19 pandemic, generating intense scientific, medical, and political debate far beyond its original role as an antiparasitic medicine.

The Mectizan Donation Program continues.

More than 5 billion treatments have now been donated worldwide.

River blindness has been eliminated or interrupted in several countries, while many African nations continue annual treatment campaigns.

Researchers continue studying new approaches—including doxycycline, which targets the Wolbachia bacteria living inside adult river blindness worms—in hopes of shortening treatment times and eventually eliminating the disease.

The program brought together:

One reason many public health historians point to the ivermectin program as a milestone is that it showed what could be accomplished when a pharmaceutical company, international organizations, governments, scientists, and local communities all committed to the same long-term goal. It became a model that later influenced medicine donation programs for trachoma, lymphatic filariasis, intestinal worms, schistosomiasis, and other neglected tropical diseases.

That’s why the legacy of ivermectin isn’t just more than 5 billion treatments. It’s also the public health infrastructure that grew around it—networks of researchers, health workers, ministries, NGOs, and international agencies that continued working together on other neglected tropical diseases long after the first ivermectin tablets were distributed.

1967 – Brazilian physicians examine a 3-year-old Yanomami child with two scalp nodules. When the nodules are surgically removed and examined, they identify Onchocerca volvulus, the parasitic worm that causes river blindness. This is the first recognized case in Brazil.

Late 1960s–Early 1970s – The discovery prompts Brazilian researchers to investigate neighboring Yanomami villages along the Brazil–Venezuela border. Rather than finding an isolated case, they discover that river blindness is already established throughout a remote region of the Amazon. Entomologists identify local Simulium blackflies capable of transmitting the parasite, confirming that an active transmission cycle exists.

1970s–1980s – Researchers continue mapping the endemic area, documenting infection in numerous Yanomami communities. The region is found to be one of the most isolated river blindness foci in the world, accessible mainly by aircraft, river travel, and long treks through dense rainforest.

1987 – Merck announces the Mectizan Donation Program, pledging to provide ivermectin free of charge for as long as needed to fight river blindness worldwide.

1990 – Brazil begins regular ivermectin distribution among the Yanomami as part of the Pan American Health Organization’s regional elimination program.

1992 – Brazil officially recognizes the Yanomami Indigenous Territory, protecting approximately 96,650 square kilometers (37,317 square miles) of rainforest. The protected area improves access for organized public health campaigns, although the remoteness of many villages continues to make treatment one of the most challenging river blindness programs anywhere in the world.

2000s–Present – Most endemic areas in the Americas eliminate river blindness through repeated ivermectin treatment. The Yanomami region on the Brazil–Venezuela border remains the last endemic focus in the Americas, requiring continued treatment because of its vast size, scattered villages, and difficult terrain.

The 1987 Merck ivermectin program changed global public health. Before then, no pharmaceutical company had committed to donating a medicine for as long as necessary to eliminate a disease. That pledge became the model for many later neglected tropical disease donation programs.

Since then, similar programs have followed:

From a historical standpoint, the ivermectin program is generally considered the first and the largest of these global medicine donation efforts, and it became the template for many of the others that followed.

Yes, there is considerable overlap, although not everyone works on both.

They are generally part of the same broad scientific community:

Within that community, people often specialize.

For example:

Even so, they attend many of the same conferences, publish in many of the same journals, belong to the same tropical medicine societies, and may collaborate on projects involving neglected tropical diseases.

One interesting connection in your research is R. W. Ashford.

Ashford is best known to you because he first described what became known as Cyclospora in Papua New Guinea in 1979.

But Ashford was not just a Cyclospora researcher. He was a broad tropical parasitologist. During his career he published on:

That was quite common, especially in the 1960s–1990s. Tropical medicine researchers often worked on multiple parasites, particularly if they were based in endemic countries or institutions like the Liverpool School of Tropical Medicine or the London School of Hygiene & Tropical Medicine.

So while the scientists studying Cyclospora and river blindness are not necessarily the same individuals, they are often members of the same broader research community. Many are trained in tropical medicine or parasitology and may work across several parasitic diseases during their careers. That is one reason you keep encountering some of the same institutions, journals, and organizations as you move from one tropical disease to another.

Unlike most countries affected by river blindness, Yemen is the only country outside Africa where onchocerciasis remains endemic. The disease in Yemen is known locally as sowda, a severe inflammatory skin form of the infection. Unlike much of Africa, blindness has been uncommon in Yemen; the disease has primarily caused intense itching, skin damage, and disability.

The first medical descriptions of onchocerciasis in Yemen are published. Physicians identify a distinctive form of skin disease that would later become known locally as sowda.

Merck launches the Mectizan Donation Program, promising to donate ivermectin for as long as needed to fight river blindness worldwide. Yemen eventually becomes one of the countries receiving donated medicine.

Yemen begins its first national ivermectin treatment program.

Unlike Africa, where ivermectin was generally distributed once or twice a year through mass campaigns, Yemeni doctors initially treated individual patients suffering from sowda. Because symptoms often returned within a few months, patients were commonly treated every three months.

The control program expands into additional endemic valleys along Yemen’s western mountains and Red Sea watershed. Treatment becomes integrated with the country’s National Leprosy Control Programme.

Researchers publish one of the first scientific reports describing the successful use of ivermectin for river blindness in Yemen.

The Ministry of Public Health establishes the National Onchocerciasis Control Program (NOCP) based in Taiz.

By this time, thousands of patients have already received ivermectin, and distribution continues to expand with assistance from local organizations and the Mectizan Donation Program.

Yemen combines ivermectin distribution with a campaign against lymphatic filariasis in areas where both diseases overlap, improving efficiency by treating multiple neglected tropical diseases together.

Health officials and international experts reassess Yemen’s program, shifting the goal from simply treating sick patients toward eliminating transmission through broader mass drug administration.

Despite civil war, humanitarian crises, and difficult terrain, Yemen continues ivermectin campaigns with support from the Ministry of Health, WHO, ESPEN, the Mectizan Donation Program, and international partners.

Nearly 500,000 Yemenis receive ivermectin during a nationwide campaign involving almost 1,000 treatment teams working across 33 endemic districts despite ongoing conflict.

Yemen carries out one of its largest-ever ivermectin campaigns, reaching remote mountain communities that had previously been difficult to access because of conflict and geography.

The elimination campaign continues. WHO describes Yemen as one of the world’s most challenging river blindness programs because of war, mountainous terrain, and isolated communities. Even so, mass ivermectin distribution remains the cornerstone of the country’s strategy to eliminate the disease.

Yemen occupies a unique place in the history of river blindness.

Yes. Yemen is still receiving ivermectin treatments today. Despite the civil war, WHO, the Yemen Ministry of Health, the Mectizan Donation Program, and their partners have continued annual mass drug administration campaigns.

The numbers are much smaller than in many African countries because Yemen has a much smaller endemic population.

1992

2000s

2019

2022

2025

Unlike the Africa-wide program, there is no published cumulative total of all ivermectin treatments given in Yemen since 1992. Based on the documented annual campaigns over more than 30 years, the cumulative number is in the millions of treatments, but it is not in the hundreds of millions like countries such as Nigeria or the Democratic Republic of the Congo. The available reports document individual campaign totals rather than a single lifetime cumulative figure.

For perspective:

It’s understandable to find that surprising. Yemen is often thought of in terms of conflict or geopolitics, not tropical medicine.

The explanation is mostly geographic and biological rather than political. Western Yemen has river valleys, fast-flowing streams, and the blackfly (Simulium) that transmits river blindness. Because the disease is present there, it naturally attracted the same tropical disease specialists who were already studying onchocerciasis in Africa.

Tropical medicine is also a relatively small scientific field. Researchers often specialize in neglected tropical diseases, not in one particular country. The same scientists and institutions may work in:

Institutions such as the Liverpool School of Tropical Medicine, the London School of Hygiene & Tropical Medicine, WHO, and other international research centers have historically sent researchers wherever these diseases occur. So it’s common to see the same names—such as R. W. Ashford and colleagues—appear in publications from several continents.

In other words, the researchers followed the diseases, not the countries. Because Yemen is the only country outside Africa where river blindness remains endemic, it became part of the same international tropical medicine network.

Here’s the distinction:

Blackflies need clean, fast-flowing water to reproduce. Their larvae attach themselves to rocks, logs, and vegetation in rivers and streams. That’s why river blindness became known as “river blindness.”

Countries with blackflies include:

If you’ve ever been fishing or hiking near a fast-moving stream and been attacked by tiny biting flies, there’s a good chance they were blackflies.

The reason Africa became the center of river blindness is not because Africa has blackflies and other places don’t. It’s because the particular blackfly species capable of transmitting Onchocerca volvulus became established there, along with the parasite itself. Yemen is the only country outside Africa where that transmission cycle persists today.

One fascinating thing about this field is exactly what you noticed: it is relatively small and specialized. There are experts in tropical medicine, but only a subset spend much of their careers on diseases like river blindness. As a result, you often see the same researchers, universities, and organizations appearing over decades as they move from one endemic region to another, following where these diseases occur.

“Can it be modified in the lab?” The answer is yes. Modern genetic engineering techniques such as CRISPR can, in principle, be applied to blackflies, although they are much more difficult to work with than mosquitoes because of their life cycle and breeding requirements.

So the short answer is:

Yes. It is biologically possible to modify a blackfly in a laboratory.

Yes. Yemen is not unique in having major problems from blackflies. In fact, Africa has experienced by far the greatest burden.

Some of the hardest-hit countries include:

Outside Africa:

One interesting historical point is that the blackflies themselves are widespread around the world, but the combination of the right blackfly species, the Onchocerca volvulus parasite, and the local environment made Africa—and to a much smaller extent Yemen and parts of Latin America—the places where river blindness became established.

One of the things that fascinated tropical medicine researchers was exactly this pattern. For well over a century, the disease was overwhelmingly concentrated in sub-Saharan Africa, with Yemen standing out as the only endemic country outside Africa in the Eastern Hemisphere, and then a handful of isolated foci in Latin America, including Venezuela and Brazil. Today, after decades of control efforts, active transmission remains primarily in Africa and Yemen, with only the Yanomami focus shared by Brazil and Venezuela still considered endemic in the Americas.

It occurs in the Amazon rainforest along the border of northern Brazil and southern Venezuela.

More specifically:

The disease occurs almost entirely among the Yanomami, an Indigenous people living in small, remote villages scattered through dense rainforest.

This is one of the biggest questions researchers have asked.

The leading scientific explanation is that river blindness did not originate in South America. Most evidence suggests it was introduced from West Africa during the trans-Atlantic slave trade, beginning in the 1500s. Infected people carried the parasite to the Americas, where compatible Simulium blackflies already existed in certain river systems. Once established, the parasite continued cycling between humans and blackflies in a handful of isolated regions.

Over time, six endemic areas developed in the Americas:

Through decades of ivermectin treatment, Mexico, Guatemala, Colombia, and Ecuador eliminated transmission, and most of Venezuela has as well. Today, the only remaining endemic transmission in the Americas is the shared Yanomami region on the Brazil–Venezuela border, largely because it is one of the most remote and difficult places in the world to reach consistently.

So geographically, it’s remarkable:

The Yanomami occupy one of the largest protected Indigenous territories on Earth.

Here are the key facts:

The territory contains:

It is also rich in natural resources, including:

The gold has been the biggest source of conflict. Illegal mining has brought:

It is one of the most remote inhabited regions in the world. Brazilian government sources estimate that about 98% of access is by aircraft, with very little road access.

One reason this area remained the last endemic focus of river blindness in the Americas is that it is immense, heavily forested, crossed by fast-flowing rivers where blackflies breed, and extremely difficult for health teams to reach consistently.

Illegal mining is the biggest criticism today.
Many Indigenous leaders and human rights organizations argue that illegal gold mining has brought malaria, mercury pollution, violence, food shortages, and disease into Yanomami territory. They say these problems—not river blindness—are now the greatest threat to the Yanomami.

2. Health care has been too inconsistent.
Critics say the government has often failed to provide continuous medical care because the territory is so remote. They argue that treatment teams have sometimes been unable to reach villages regularly, especially during periods of increased illegal mining or the COVID-19 pandemic.

3. Protection of Indigenous land.
Organizations such as the Hutukara Yanomami Association argue that protecting health requires protecting the territory itself. Their position is that as long as illegal miners continue to enter, health improvements will remain fragile because miners bring disease, contaminate rivers with mercury, and disrupt traditional food sources.

4. River blindness program.
There has been relatively little criticism of the ivermectin campaign itself. The main challenge discussed by researchers is logistical rather than ideological: reaching hundreds of small, scattered communities across roughly 230,000 km² of rainforest often requires aircraft, boats, and long treks on foot.

5. Some researchers question long-term dependence on repeated treatment.
A smaller scientific discussion concerns whether repeated ivermectin distribution alone is enough to eliminate transmission or whether additional strategies are needed. This is generally a debate about elimination strategy rather than opposition to treatment.

So if you’re looking at the Yanomami specifically, the criticism is not primarily “they’re getting too much ivermectin.” The dominant criticism is that illegal mining, weak protection of Indigenous territory, and interrupted health services have undermined both the Yanomami’s health and conservation efforts.

The two timelines overlap, but river blindness came first.

So the sequence is:

One important point: the illegal mining did not cause river blindness. The disease was already established in the Yanomami region decades before the gold rush. However, mining has made overall health conditions much worse by increasing malaria, polluting rivers with mercury, disrupting access to health care, and making disease control more difficult.

The biggest reason is that the medicine wasn’t free until 1987.

Here’s the timeline:

Even after the drug became free, there were several practical reasons it wasn’t immediate:

So the roughly three-year gap between 1987 and 1990 was not considered unusual. It reflected the time needed to organize a program in an extremely remote region after the donation program was launched.

The longer gap—from 1967 to 1987—is explained largely by the fact that ivermectin did not yet exist as a treatment. Before ivermectin, there was no practical, safe medicine that could be distributed repeatedly on a mass scale to entire communities. That changed with Merck’s donation program in 1987.

Yes. The Merck/Mectizan donation program absolutely extends to the Yanomami region.

In fact, the Yanomami Focus Area on the Brazil–Venezuela border is the last remaining endemic focus of river blindness in the Americas, so it has become one of the program’s highest priorities.

Here are some remarkable facts:

This is one of the most difficult public health operations in the world. The teams have to contend with:

So when people hear that Merck has donated more than 5 billion treatments, it includes not only large-scale campaigns in countries like Nigeria and the Democratic Republic of the Congo, but also extraordinary efforts to reach small, isolated populations like the Yanomami in the Amazon. Even though the Yanomami population is relatively small, their remote location has made them one of the most challenging groups to serve.

Yes. There are documented cases of river blindness among the Yanomami, and that is precisely why the region remains the last endemic focus in the Americas.

Some key facts:

The reason this region remains endemic is not because the disease is unusually severe there, but because it is extraordinarily difficult to eliminate. The Yanomami are highly mobile, living in small communities spread across dense rainforest, often reachable only by aircraft, boat, or long treks on foot. Missing even a portion of the population can allow transmission to continue.

One encouraging point is that mass blindness on the scale once seen in parts of West Africa has largely been prevented in the Yanomami region because of decades of repeated ivermectin treatment. The challenge now is eliminating the parasite completely so the treatments are no longer needed.

Yes. There are documented cases of river blindness among the Yanomami, and that is precisely why the region remains the last endemic focus in the Americas.

Some key facts:

The reason this region remains endemic is not because the disease is unusually severe there, but because it is extraordinarily difficult to eliminate. The Yanomami are highly mobile, living in small communities spread across dense rainforest, often reachable only by aircraft, boat, or long treks on foot. Missing even a portion of the population can allow transmission to continue.

One encouraging point is that mass blindness on the scale once seen in parts of West Africa has largely been prevented in the Yanomami region because of decades of repeated ivermectin treatment. The challenge now is eliminating the parasite completely so the treatments are no longer needed.

There are many people and organizations trying to help the Yanomami remain on their ancestral land. The situation is mixed: there has been measurable progress since Brazil declared a health emergency in 2023, but serious problems remain.

The main groups working to protect the Yanomami include:

There has been real progress:

However, the crisis is not over.

The biggest continuing problems are:

So the overall picture is that the Yanomami are not being abandoned. There is an ongoing effort by the Brazilian government, Indigenous organizations, and international groups to help them stay on their land and improve their health. At the same time, they continue to face persistent threats from illegal mining, malaria, environmental contamination, and the logistical challenge of delivering health care across one of the most remote rainforest regions in the world.

The one that made blackflies famous is river blindness.

For humans, this is by far the most important disease transmitted by blackflies. It has infected tens of millions of people over the last century and led to the world’s largest ivermectin donation program.

Even without transmitting disease, blackflies can be a serious problem.

Large swarms can cause:

In livestock, massive blackfly attacks have occasionally killed cattle or horses through blood loss and toxic reactions from thousands of bites.

One interesting fact is how specialized they are.

That specialization is one reason river blindness became such a distinct field within tropical medicine. Many researchers spend decades studying the biology of a single parasite (Onchocerca volvulus) and its relationship with a relatively small number of blackfly species.

No single person “discovered” blackflies because people had been bitten by them for thousands of years.

The scientific story began in the 1700s.

For centuries, blackflies were simply considered painful biting insects.

The breakthrough came in Africa.

Unlike mosquitoes, blackflies are:

It took decades of fieldwork, microscopy, and parasite studies to determine which species could actually transmit river blindness.

Scientists recognize:

One interesting historical point is that the insect was known long before the disease was understood. People had been bitten by blackflies for thousands of years, but it wasn’t until the late 19th and early 20th centuries that scientists connected certain blackflies to one of the world’s most important tropical diseases.

Here’s why only certain blackflies can transmit Onchocerca volvulus:

So it’s not just “a blackfly.” It’s a very specific combination:

This is actually common in parasitology. Many parasites have very specific vectors. For example:

River blindness is similar. Out of more than 2,000 blackfly species, only a relatively small number are capable of maintaining the complete life cycle of Onchocerca volvulus.

One of the remarkable aspects of this disease is that scientists still don’t know every molecular detail of why one blackfly species is a competent vector while a closely related species is not. They understand the overall life cycle well, but the exact genetic and biochemical interactions that make some flies susceptible and others resistant remain an active area of research. That is one reason river blindness has remained such a specialized field of tropical medicine.

Cyclospora and river blindness belong to the same broad world of tropical parasitology, but they present almost opposite scientific problems.

Cyclospora is microscopic and comparatively short-lived in a patient, yet scientists still cannot routinely grow it in a laboratory or reproduce its complete infection in an animal.

River blindness is caused by a large parasitic worm that scientists can examine at different life stages, but the worm lives for more than a decade and requires both a mammal and a blackfly to complete its life cycle.

The result is that both diseases have treatments and decades of research behind them, yet neither behaves like a familiar bacterial infection that can be grown overnight, exposed to hundreds of drugs, and quickly traced to its source.

1. Cyclospora: difficult to obtain and difficult to reproduce

What Cyclospora is

Cyclospora cayetanensis is a single-celled intestinal parasite. Humans are currently considered its only known host. The parasite reproduces inside cells lining the human intestine, and infected people pass immature oocysts in their feces. Those oocysts must remain outside the body—usually for at least one or two weeks under suitable environmental conditions—before becoming infectious.

That environmental stage explains why immediate person-to-person spread is considered unlikely. Someone does not normally become infected directly from a freshly contaminated bathroom surface; the organism first has to mature in the environment.

Why Cyclospora is so difficult to study

The single greatest obstacle is that researchers still lack a dependable laboratory supply of the organism.

There is no established animal model and no routine in-vitro or in-vivo culture system that continuously produces Cyclospora oocysts. Researchers usually must obtain organisms from stool donated by naturally infected people. Those samples may contain limited numbers of oocysts and require difficult purification before experiments can begin.

That creates a chain of problems:

Scientists cannot easily grow more organisms. With bacteria, one patient sample can sometimes generate millions or billions of organisms in culture. With Cyclospora, the supply may end when the human stool sample is exhausted.

Drug screening is restricted. Researchers cannot conveniently expose identical cultures to hundreds or thousands of possible treatments.

Its full life cycle remains partly hidden. Much of what is known about its development inside humans comes from a small number of intestinal biopsy specimens.

Human infectivity is difficult to measure. In a 2004 pilot study, seven volunteers swallowed preparations containing Cyclospora oocysts, but none developed detectable infection. That did not prove the parasite was harmless; it demonstrated how difficult it was to know whether the available organisms were mature, viable and infectious.

Why Cyclospora infections can persist

In an untreated person, the parasite can continue reproducing inside intestinal cells. Symptoms may improve and then return, producing the characteristic relapsing illness.

Persistence is also helped by practical problems:

This is very different from the persistence of river blindness. Cyclospora does not normally live in one patient for 10 or 15 years. Its difficulty lies more in diagnosis, environmental detection, research access and interruption of food or water contamination.

Why Cyclospora is difficult to find on food

The parasite may be unevenly scattered across a large shipment of produce. Contamination levels can be extremely low, yet still sufficient to cause illness. The organism cannot be enriched by growing it in culture after it is recovered from food.

A molecular test can detect Cyclospora DNA, but DNA detection does not automatically prove that the organism was alive or infectious. A negative food sample also does not prove that the shipment was never contaminated because investigators may simply have sampled an uncontaminated portion.

This explains why outbreak investigations often depend heavily on interviews, purchase records and traceback rather than on finding the parasite in a particular food sample.

2. Cyclospora progress over nearly 50 years

1977–1979: first observations

The earliest recognized human cases occurred in Papua New Guinea during the late 1970s. In 1979, R. W. Ashford published a description of an unidentified coccidian-like organism in human patients.

At that point, researchers could see the organism, but they did not know exactly what it was.

1980s–1994: identity gradually established

Similar organisms were reported in people with prolonged diarrhea in several countries. It was initially confused with cyanobacteria and other parasites. By the early 1990s, researchers established that it was a coccidian parasite, and the name Cyclospora cayetanensis became accepted.

Mid-1990s: major foodborne outbreaks

Large outbreaks associated with imported fresh produce demonstrated that Cyclospora was not merely an obscure tropical infection. The outbreaks forced public-health agencies to develop better surveillance and food-investigation methods.

By 1999, CDC scientists were still describing Cyclospora as an “enigma,” noting major gaps in knowledge about environmental survival and detection.

2000s: improved clinical diagnosis

Microscopy improved, and molecular methods such as polymerase chain reaction allowed laboratories to detect Cyclospora DNA more specifically. Multiplex gastrointestinal test panels later made clinical diagnosis easier in laboratories that used them.

However, improved diagnosis did not solve the central research problem: scientists still could not continuously cultivate the organism.

2010s: food testing improves

FDA developed and validated molecular methods for finding Cyclospora in selected high-risk produce. A validated FDA method was evaluated and published in 2018.

This was substantial progress because investigators could search directly for Cyclospora DNA on produce rather than relying exclusively on patient interviews.

But it did not become an easy universal test. Different foods contain substances that interfere with DNA extraction, and mixed foods such as salsa present additional problems.

2019–2026: coordinated research and genotyping

FDA established a dedicated Cyclospora task force in 2019 and developed a multiyear prevention, response and research plan.

Researchers have also worked on genotyping methods intended to compare Cyclospora found in patients, food, water or soil. FDA stated that these methods were being developed to characterize organisms from produce, mixed foods and environmental samples.

Environmental experiments have begun clarifying how moisture, temperature, soil and plant surfaces affect persistence. FDA-associated research has found that detection can continue for extended periods under moist conditions, although these experiments still do not amount to a complete culture system.

Bottom line after almost five decades

Since the first published description in 1979, scientists have made major progress in:

But after approximately 47 years, researchers still lack the central tool that would transform the field: a dependable continuous culture system or animal model.

That is why Cyclospora remains unusually difficult.

3. River blindness: a long-lived worm with two hosts

What causes it

River blindness is caused by Onchocerca volvulus, a filarial roundworm.

An infected blackfly bites a person and deposits immature larvae. Those larvae develop into adult worms inside nodules beneath the skin. Adult females produce enormous numbers of microscopic larvae called microfilariae. These migrate through the skin and eyes. When another blackfly takes a blood meal, it ingests microfilariae, which develop further inside the fly and can then infect another person.

The serious itching, skin injury and eye damage are caused largely by inflammatory reactions to dying microfilariae.

Why the worm is difficult to study

The full life cycle requires:

That cannot be reproduced quickly in an ordinary laboratory flask.

Adult worms mature very slowly. Work with the closely related cattle parasite Onchocerca ochengi indicates that development into fully mature, fertile adults can take roughly 279–532 days after infection.

Human infection models present obvious ethical obstacles. Chimpanzees were previously used in research, but infections could persist for six to nine years, making experiments extraordinarily slow and costly.

Researchers have therefore depended on:

These tools are useful, but none perfectly duplicates the complete natural human-blackfly cycle.

Why river blindness persists in an individual

Adult worms may survive in nodules for approximately 10–15 years or longer, and fertile females can release microfilariae through much of that period.

Ivermectin is highly effective at removing microfilariae and temporarily suppressing their production. This reduces itching, eye injury and transmission.

But ivermectin generally does not rapidly kill all adult worms. Once its suppressive effect diminishes, surviving females can resume releasing microfilariae.

That is why WHO recommends repeated treatment at least annually for approximately 10–15 years in many settings—long enough to outlast the reproductive life of the adult worms and interrupt transmission.

Why river blindness persists in a region

Even excellent medicine cannot eliminate transmission unless enough people receive it repeatedly.

Persistence is encouraged by:

WHO notes that Loa loa co-endemicity can require modified treatment strategies because ivermectin can cause severe adverse events in heavily infected individuals.

Thus, the difficulty is not merely inventing a medicine. It is maintaining a functioning delivery and surveillance system for decades.

4. River-blindness progress over more than 50 years

Before the 1970s

Scientists had already identified the worm, the blackfly vector and the relationship between infection, skin disease and blindness. However, control was limited and enormous West African river basins remained heavily affected.

1974–2002: attacking the blackfly

The Onchocerciasis Control Programme began in West Africa in 1974.

Its initial strategy was predominantly aerial spraying of insecticides into rivers to kill blackfly larvae. The programme operated until 2002 and brought the disease under control across much of the original 11-country area.

This was an immense technical achievement, but it required aircraft, repeated surveillance, insecticides, international financing and cross-border coordination.

1987–1989: ivermectin changes the strategy

Merck announced the ivermectin donation in 1987, and large-scale distribution was incorporated into African control efforts by approximately 1989.

Ivermectin allowed programs to treat people directly rather than relying only on blackfly control.

Its limitation remained clear: it was mainly a microfilaricide, not a reliably rapid killer of adult worms.

1990s–2015: community-directed treatment expands

The African Programme for Onchocerciasis Control operated from 1995 to 2015 and extended treatment into countries not covered by the original West African programme. Community-directed distribution allowed residents to organize local ivermectin delivery rather than relying solely on visiting medical teams.

Late 1990s–2000s: Wolbachia becomes a treatment target

Researchers discovered that adult filarial worms depend heavily on intracellular Wolbachia bacteria.

Courses of doxycycline that remove Wolbachia can sterilize female worms and gradually kill or permanently disable many adult worms. Early WHO research summaries reported that a six-week doxycycline regimen produced adult-worm sterility.

This was a major biological advance because it offered a way to attack the adult stage.

Its limitation is operational: a four- to six-week antibiotic course is far harder to deliver to entire populations than a single dose of ivermectin. Doxycycline is also unsuitable for some groups, including young children and pregnant women.

2018 onward: moxidectin and improved suppression

Moxidectin was developed as another treatment capable of suppressing microfilariae for longer than ivermectin in many patients. WHO-associated researchers had been investigating it since the late 1990s.

It offers another tool but does not entirely solve the problem of rapidly eliminating every adult worm.

2013–2025: national elimination becomes real

WHO verified elimination in:

Niger became the first African country verified as having eliminated transmission.

As of the end of 2024, WHO reported that approximately 25.5 million people lived in African areas where transmission had fallen sufficiently for ivermectin treatment to stop.

That is enormous progress, but it also demonstrates the timescale: Niger’s achievement followed more than 40 years of sustained control work.

5. The most important difference

Cyclospora is persistent mainly as a scientific and food-safety mystery.

Researchers can treat most diagnosed patients, but they cannot easily:

River blindness is persistent mainly as a biological and delivery problem.

Researchers understand much of its life cycle and have effective medicines, but:

6. Side-by-side conclusion

Neither disease is scientifically hopeless.

Cyclospora research has advanced from an unidentified object under a microscope to molecular detection, food testing and genetic analysis. But scientists still cannot grow it reliably, which keeps basic questions unanswered after nearly half a century.

River-blindness research has produced one of the largest and most successful parasite-control campaigns in history. Entire countries have eliminated transmission. But the biology of a 10- to 15-year adult worm means success has required decades of uninterrupted drug delivery, vector control and outside support.

That is what makes these two parasites stand out: the scientific community has made genuine progress, but neither organism has yielded to the ordinary laboratory and treatment methods used against many bacteria and viruses.

There are several parasites that have historically been difficult to study because of complex life cycles or limited laboratory models. Examples include:

What makes Cyclospora stand out is that for many years there was no simple, continuous laboratory culture system, which slowed work on diagnostics, drug screening, and understanding its biology.

What makes Onchocerca stand out is that it is a long-lived worm with a complicated life cycle involving both humans and blackflies, making laboratory research inherently difficult.

One thing you’ve probably noticed is that researchers working on tropical parasites often say things like:

You don’t hear those statements nearly as often in fields like E. coli, Staphylococcus, or influenza research, where laboratory systems are much more established.

So your observation is a reasonable one: within tropical parasitology, Cyclospora and river blindness are among the organisms that have posed particularly persistent technical challenges. The reasons differ, but both have required decades of work because their biology is much more complex than many familiar bacterial pathogens.

Discovered in the late-1970s, the pioneering drug ivermectin, a dihydro derivative of avermectin—originating solely from a single microorganism isolated at the Kitasato Intitute, Tokyo, Japan from Japanese soil—has had an immeasurably beneficial impact in improving the lives and welfare of billions of people throughout the world. Originally introduced as a veterinary drug, it kills a wide range of internal and external parasites in commercial livestock and companion animals. It was quickly discovered to be ideal in combating two of the world’s most devastating and disfiguring diseases which have plagued the world’s poor throughout the tropics for centuries. It is now being used free-of-charge as the sole tool in campaigns to eliminate both diseases globally. It has also been used to successfully overcome several other human diseases and new uses for it are continually being found. This paper looks in depth at the events surrounding ivermectin’s passage from being a huge success in Animal Health into its widespread use in humans, a development which has led many to describe it as a “wonder” drug.

Here’s the timeline:

The nickname “McNamara’s Morons” referred to Project 100,000, begun in 1966.

McNamara believed the military could both increase manpower and provide disadvantaged young men with education and job skills. The standards for enlistment were lowered so thousands of men who previously would have been rejected could enter the armed forces.

The program ultimately enlisted about 354,000 men.

Critics argued that:

The phrase “McNamara’s Morons” was coined by critics of the policy and is now widely regarded as derogatory.

After leaving the Pentagon in 1968, McNamara became President of the World Bank.

This is where his reputation becomes much more complicated.

During the 1970s he argued that economic development could not succeed if major tropical diseases kept millions of people trapped in poverty.

One disease he repeatedly highlighted was onchocerciasis (river blindness).

At the time:

McNamara viewed river blindness as both:

That perspective fit the World Bank’s mission because healthier populations were seen as essential for long-term growth.

In 1974, four major international organizations launched the OCP:

The initial program covered approximately:

Early control relied almost entirely on aerial larviciding—spraying rivers to kill blackfly larvae before ivermectin became available.

When Merck announced the donation of ivermectin in 1987, the program expanded dramatically because treatment of people could be combined with vector control.

McNamara’s legacy illustrates how the same individual can be remembered in very different ways depending on the context.

Both are well-documented parts of his historical record.

So when you see his name in the history of onchocerciasis, it reflects a later phase of his career—after the Vietnam War—when he used the World Bank’s financial influence to support large-scale international development and disease-control programs.

Yes. McNamara’s legacy is one of the most debated of any major American public official because it includes both the Vietnam War and later global development work.

Broadly speaking, historians and commentators tend to fall into a few perspectives:

The Onchocerciasis Control Programme is often cited as one of the World Bank’s major public health successes. McNamara’s advocacy helped secure political and financial support at a time when river blindness received relatively little international attention. However, that achievement has not erased the controversy surrounding his earlier career.

McNamara himself reflected publicly on Vietnam later in life. In his 1995 memoir, In Retrospect: The Tragedy and Lessons of Vietnam, he wrote that the United States had been “wrong, terribly wrong” in key aspects of its approach to the war. Some people viewed this as a meaningful acknowledgment of mistakes; others felt it came far too late and did not amount to full accountability.

In short, it is fair to say that many people view his support for global health initiatives—including the fight against river blindness—as a significant positive contribution. At the same time, many also believe that those accomplishments do not outweigh or erase the consequences of his decisions during the Vietnam War. Those two assessments often coexist in discussions of his historical legacy.

Before McNamara:

During McNamara’s presidency (1968–1981):

In that sense, many historians describe McNamara as having redirected the World Bank toward developing countries, particularly Africa.

At the same time, the World Bank was only one source of international finance. During roughly the same period, countries also received funding from:

One of the interesting historical questions—which economists and historians continue to debate—is whether the rapid expansion of development lending produced long-term self-sustaining growth or whether it also contributed to long-term debt dependence in some countries.

So a fair historical summary would be:

Robert McNamara was a pivotal figure in expanding World Bank lending to Africa and making poverty reduction, agriculture, education, and health central priorities. His tenure marked a major increase in international development financing for the region, although the long-term outcomes remain debated, with some countries experiencing significant gains and others later facing persistent debt challenges.

The World Bank was created in 1944 at the Bretton Woods Conference and officially began operations in 1946.

Here’s the timeline:

For over a decade, OCP operations were exclusively based on the spraying of insecticides by helicopters and aircraft over the breeding sites of vector blackflies in order to kill their larvae. Following the registration of ivermectin (produced under the brand name Mectizan®) for human use in 1987, in a hitherto unprecedented move and with unheralded commitment, Mectizan® was donated by the manufacturing company, Merck & Co. Inc., to treat onchocerciasis in all endemic countries for as long as it was needed. The resultant drug donation programme was the first, largest, longest running and most successful of all—and proved a model for all others that have followed. Ivermectin began to be distributed in 1988, with operations being organized through the independent Mectizan Donation Program (MDP) established and funded by Merck. Thereafter, OCP control operations changed from exclusive vector control to larviciding combined with ivermectin treatment or, in some areas, to ivermectin treatment alone. Ivermectin swiftly became the drug of choice for the treatment of Onchocerciasis due to its unique and potent microfilaricidal effects, the absence of severe side effects and its excellent safety. It is now the sole tool being used in disease elimination campaigns in the 16 other African countries where the disease exists, orchestrated by the African Programme for Onchocerciasis Control (APOC), which commenced operations in 1996. A single annual dose of 150 µg/kg of ivermectin, given orally, can reduce the level of skin microfilariae to zero and, by interfering with worm embryogenesis, can delay the build-up of new microfilariae for a period of up to two years. OCP was closed in December 2002 after virtually stopping disease transmission in all target nations except Sierra Leone where operations were hampered by civil war.

The process, from the discovery of ivermectin’s activity against onchocercal microfilariae to the successful distribution programme from 1988 onward, was neither an easy or direct path. Success was achieved through groundbreaking and innovative partnerships. The journey was a complex undertaking, incorporating scientific uncertainty, conflicting views, ambiguity, frustration, individual innovation and unexpected twists and turns. The actual discovery of ivermectin was an international team effort involving a unique, pioneering Public Sector/Private Sector partnership and the commitment and vision of several key individuals. Ivermectin’s development into a drug for human use also involved a number of organizational, individual and pharmacological variables—together with a large slice of luck, educated insight and personal commitment.

The origins of ivermectin as a human drug are inextricably linked with Onchocerciasis (or River Blindness), a chronic human filarial disease caused by infection with Onchocerca volvulus worms. The parasites are transmitted via the bite of infected blackflies of the genus Simulium, which breed in highly-oxygenated, fast-flowing rivers and watercourses. In the human body, immature larval forms of the parasite create nodules in subcutaneous tissue, where they mature into adult worms. After mating, female worms can release up to 1000 microfilariae a day for some 10–14 years. These move through the body, and when they die they cause a variety of conditions, including skin rashes, lesions, intense itching, oedema and skin depigmentation (Fig. 2 ). Microfilariae also invade the eye, causing visual impairment and loss of vision, onchocerciasis being the second leading cause of blindness caused by an infectious disease.17) The disease causes visual damage for some 1–2 million people, around half of who will become blind.18)

1940s–1950s
Scientists discover that soil microorganisms produce powerful natural chemicals. The discovery of antibiotics such as streptomycin convinces researchers that soil is a rich source of new medicines.

1950s–1960s
Research laboratories around the world begin collecting thousands of soil samples. The goal is not to find a cure for river blindness, but to discover any microorganism capable of producing useful compounds, including antibiotics and antiparasitic drugs.

1965
Dr. Satoshi Ōmura joins the Kitasato Institute in Tokyo, Japan. He specializes in isolating new species of Streptomyces bacteria from soil.

Late 1960s–Early 1970s
Ōmura and his team collect soil samples from across Japan, including parks, fields, mountains, and golf courses. Thousands of microorganisms are isolated and grown in the laboratory. Most prove to be unremarkable, but a small number appear promising.

Early 1970s
One soil sample collected near a golf course in Kawana, Shizuoka Prefecture, contains a previously unknown Streptomyces species. Ōmura identifies it as one of the most interesting organisms in his collection.

1973
Ōmura sends selected bacterial cultures to researchers at Merck & Co. in the United States, where parasitologist William C. Campbell is searching for new drugs to combat parasites in livestock.

At this point, the objective is entirely veterinary medicine. Farmers lose billions of dollars worldwide because parasitic worms reduce the health and productivity of cattle, sheep, horses, pigs, dogs, and other animals.

1974–1975
Campbell’s laboratory discovers that one of Ōmura’s bacterial cultures produces an extraordinarily powerful compound against parasitic worms. The compound is named avermectin.

1978
Merck scientists chemically modify avermectin to improve its safety and effectiveness. The new compound is named ivermectin.

1981
Ivermectin is introduced as a veterinary medicine. It rapidly becomes one of the most successful antiparasitic drugs ever developed for cattle, horses, sheep, pigs, and companion animals because it controls a wide variety of internal and external parasites.

Early 1980s
Researchers begin asking whether ivermectin might also work against human parasitic diseases. Studies focus on river blindness (Onchocerca volvulus), a disease affecting millions in Africa and parts of Latin America.

1987
Merck announces that it will donate ivermectin, marketed as Mectizan, free of charge for as long as necessary to treat river blindness. The Mectizan Donation Program begins and eventually becomes one of the largest pharmaceutical donation programs in history.

1998
The donation program expands to include efforts to eliminate lymphatic filariasis in countries where ivermectin is an appropriate treatment.

2015
Satoshi Ōmura and William C. Campbell receive the Nobel Prize in Physiology or Medicine for the discovery and development of avermectin and ivermectin, recognizing work that has transformed the treatment of parasitic diseases in both animals and humans.

The original research had nothing to do with river blindness.

Ōmura was searching Japanese soil for microorganisms that produced biologically active compounds. Campbell was searching for new medicines to protect livestock from parasitic worms. Only after ivermectin proved extraordinarily effective in animals did researchers investigate whether it could also treat human diseases. That unexpected progression eventually led to its worldwide use against river blindness and several other parasitic infections.

For many years, the standard approach was:

Then researchers made an important discovery.

Scientists discovered that Onchocerca volvulus, the worm that causes river blindness, contains bacteria called Wolbachia.

These bacteria are not simply infecting the worm—they live inside its cells and are essential for the worm’s biology.

Without Wolbachia, the adult worms become infertile and gradually die.

Doxycycline does not kill the worm directly.

Instead, it kills the Wolbachia bacteria inside the worm.

Without those bacteria:

So instead of attacking the worm itself, doxycycline attacks something the worm depends on.

Imagine a factory.

Ivermectin clears away the products already on the shelves (the baby worms), but the factory remains standing and eventually starts producing again.

Doxycycline shuts down the power plant. The factory can no longer make new products and eventually closes.

There are several practical reasons:

It can come closer to what parasitologists call macrofilaricidal therapy—treatment that targets the adult worms.

However, it is slower than ivermectin.

A common strategy in individual patient care is:

The discovery of Wolbachia transformed research on river blindness because it showed that the parasite has an Achilles’ heel. Instead of trying to poison the worm directly, scientists found they could target its essential bacterial partner.

Researchers continue to investigate other drugs that can kill adult Onchocerca worms more quickly than doxycycline, since a shorter, simpler treatment would be much easier to use in endemic regions.

This is actually a fascinating story because Wolbachia was discovered long before anyone knew it was the “Achilles’ heel” of river blindness.

1924
American scientists Marshall Hertig and S. Burt Wolbach were studying mosquitoes at Harvard Medical School.

While examining the reproductive tissues of the mosquito Culex pipiens under a microscope, they noticed tiny bacteria living inside the insect’s cells.

Because the organism was first described by Hertig and named in honor of Wolbach, it became known as Wolbachia pipientis.

At the time, they had no idea how widespread or important it would prove to be.

1930s–1970s
Scientists occasionally found Wolbachia in insects, but it was considered an odd curiosity.

No one knew it infected millions of insect species.

No one suspected it played a role in parasitic worms.

1978–1987
Ivermectin is developed and becomes the standard treatment for river blindness.

Researchers know ivermectin removes the baby worms, but they cannot explain why the adult worms survive for 10–15 years.

Early 1990s
Advances in molecular biology allow scientists to identify bacterial DNA inside parasitic worms.

Researchers discover that Onchocerca volvulus and several related filarial worms contain Wolbachia bacteria.

This is completely unexpected.

1995
A landmark study by Mark J. Taylor and colleagues demonstrates that the bacteria are not accidental passengers.

The worms depend on Wolbachia for normal survival and reproduction.

This changes the entire understanding of filarial biology.

Late 1990s
Researchers begin asking a simple question:

“If the worms cannot live without Wolbachia, what happens if we kill the bacteria?”

They test doxycycline, an inexpensive antibiotic already widely used for bacterial infections.

1999–2003
Clinical trials show that several weeks of doxycycline:

This is the first practical treatment shown to attack the long-lived adult worms indirectly.

2000s
The Liverpool School of Tropical Medicine and several international collaborators lead much of the research on doxycycline therapy for river blindness and lymphatic filariasis.

The work helps establish doxycycline as an important option for treating individual patients, although it is less practical than ivermectin for mass drug administration.

It happened through improvements in laboratory techniques.

Scientists used:

When they examined adult Onchocerca worms, they repeatedly found bacteria packed inside reproductive tissues and other cells.

The same bacterial DNA appeared over and over.

Eventually researchers realized:

These bacteria were not infecting the worms like a disease.

They were living with the worms in an essential partnership.

Without Wolbachia:

That discovery completely changed river blindness research. Before the 1990s, scientists were focused on killing the worms directly. After the discovery of Wolbachia, they realized they could instead target the bacteria that the worms required to survive.

There are really three main approaches to treating river blindness. Keeping it simple helps avoid the confusion.

The most common regimen is:

That works out to approximately:

4-week course

6-week course

So compared with ivermectin:

Mainly because it is much harder to use in mass campaigns.

Someone in a remote village has to:

By comparison, ivermectin can be distributed by a community health worker in a single visit once a year.

For most people, that’s essentially the whole story:

Those six points cover the key biology behind current treatment without getting into more specialized research on newer drugs and combination therapies.

However, based on the available evidence, there is no credible evidence that the ivermectin donation program was a covert program to kill people in Africa.

What is well documented is:

At the same time, there are legitimate issues that researchers and critics have discussed:

Africa has also experienced documented unethical medical research and exploitation in some historical contexts, so it’s understandable why people examine large-scale interventions carefully. But it is important to distinguish those documented cases from claims about a specific program. In the case of the ivermectin donation program, the published evidence supports the conclusion that it substantially reduced illness from river blindness rather than serving as a covert harm program.

European colonial powers established medical services throughout Africa. Some work genuinely reduced diseases such as smallpox and sleeping sickness, but medicine was also used to support colonial administration, labor systems, and military control.

Researchers often viewed African populations as convenient subjects for large-scale experiments or interventions that would not have been acceptable in Europe.

Large epidemics of sleeping sickness (African trypanosomiasis) affected Central and East Africa.

Colonial governments introduced mass screening and treatment campaigns. Some drugs available at the time, such as atoxyl (an arsenic-containing compound), caused serious side effects, including blindness, because they were used before modern clinical trial standards existed.

The intent was to control disease, but treatment programs often involved compulsory examinations and treatment with medicines that were incompletely understood.

In several colonies, health authorities imposed compulsory vaccinations, quarantines, relocations, and medical examinations.

These programs sometimes reduced disease transmission but were frequently carried out without informed consent or meaningful community choice.

European governments established tropical medicine institutes across Africa.

Many produced valuable scientific discoveries, but ethical oversight varied greatly by modern standards.

Questions about informed consent, risk disclosure, and participant autonomy were often secondary to research objectives.

One of the best-documented examples is Project Coast, South Africa’s secret chemical and biological warfare program.

Directed by Wouter Basson, it operated during the apartheid era.

Investigations after apartheid found that the program researched chemical and biological agents for military purposes and has been linked to unethical human experimentation and covert operations. The extent of every allegation remains debated, but the existence of the program itself is well documented.

During the Cold War, African countries became arenas for proxy conflicts involving the United States, Soviet Union, Cuba, China, France, and others.

Medical programs sometimes overlapped with intelligence, military logistics, or geopolitical competition, although that does not mean humanitarian health programs were fronts for intelligence operations.

Africa became the epicenter of the global HIV epidemic.

This period saw enormous investments in research, vaccine trials, treatment studies, and prevention programs.

Most of these studies were conducted under increasingly strict ethical rules compared with earlier decades, but debates continued over:

These debates influenced international research ethics and helped strengthen protections for participants.

Today, most international research involving human participants is expected to follow principles established in documents such as the Declaration of Helsinki and the CIOMS International Ethical Guidelines, along with review by institutional ethics committees and local regulatory authorities.

These safeguards were developed in part because of historical abuses—not only in Africa, but also in Europe, North America, Asia, and elsewhere.

The historical record shows that:

At the same time, it’s important to evaluate each modern program—whether related to malaria, river blindness, HIV, or vaccination—on its own evidence rather than assuming it resembles past abuses. Historical precedent can justify careful scrutiny, but it does not by itself demonstrate that a current program is unethical or harmful.

The campaigns relied much more on community organization and repeated local engagement than on mass advertising. There wasn’t one global strategy; approaches evolved over time and varied by country. Researchers have also documented both successes and challenges.

Common elements included:

Programs generally did not claim the medicine had no risks. Instead, they developed procedures to manage concerns:

No.

Some communities were hesitant or refused treatment for reasons including:

This is one of the biggest points of confusion.

Ivermectin does not reliably kill the adult Onchocerca worms, which can live for roughly 10–15 years in the body. Instead, it suppresses or kills the microfilariae—the immature worms responsible for disease—and temporarily reduces the adult worms’ production of new microfilariae.

As a result, annual or semiannual treatment was intended to keep microfilarial levels low until the adult worms died naturally. At the same time, repeated community-wide treatment reduced the number of microfilariae available for blackflies to transmit, helping interrupt the parasite’s life cycle over many years.

So the rationale for annual dosing was based on the parasite’s biology rather than a one-time cure. Researchers have continued to look for drugs that are more effective at killing the adult worms, because that could shorten treatment programs substantially.

For the river blindness (onchocerciasis) mass treatment programs, the number is actually surprisingly small.

The tablets are usually 3 mg each, and the dose is based on body weight (or sometimes height).

Typical once-yearly dose:

So for most adults, the annual treatment is typically:

Many programs give one dose per year, although in some areas with higher transmission they give it twice per year (every six months).

That means, over the long term:

This also helps explain how the donation program reached such enormous totals. When people hear “billions of ivermectin treatments,” a treatment usually means one annual dose, which for most adults consists of only 3 or 4 tablets, not bottles of medication. The cumulative total became so large because tens or hundreds of millions of people received those few tablets year after year.

Richard W. Ashford and the Liverpool doxycycline researchers were in the same broad scientific field: tropical parasitology. In fact, Ashford spent much of his career at the Liverpool School of Tropical Medicine and later became Professor of Parasite and Vector Biology there.

However, “tropical parasitology” is a very broad discipline. Within it, researchers often specialize in different parasite groups:

So they were very much in the same academic community. They:

One particularly interesting overlap is David Molyneux. He was one of Liverpool’s leading experts on filarial diseases while Ashford was a professor there. Their careers overlapped at Liverpool, and they would almost certainly have known each other professionally, even though they focused on different parasites.

So if you’re tracing the scientific network, it is reasonable to view them as belonging to the same Liverpool School of Tropical Medicine ecosystem. Ashford was not one of the scientists who developed anti-Wolbachia therapy, but he was part of the same institutional and professional community from which that work emerged.

Onchocerca volvulus

Discovered

The adult worm was first scientifically described in 1874 by Irish physician John O’Neill, who found it in skin nodules from patients in West Africa.

How it spreadsies breed in fast-flowing rivers and streams.

That is why the disease became known as river blindness.

What happens

The adult worms live in nodules beneath the skin.

They produce millions of baby worms called microfilariae.

Those baby worms travel through:

The adult worms may live 10–15 years.

Loa loa (African Eye Worm)

The parasite

Loa loa

First described

The worm was first described scientifically in the late 1700s after European physicians observed a worm moving beneath the eye of people returning from West Africa.

The species was formally named during the 1800s.

Where it occurs

Mainly the rainforests of

How it spreads

Not by blackflies.

It is spread by deer flies (Chrysops), also called mango flies.

The major difference

River blindness

Adult worms stay under the skin.

Baby worms travel through

Loa loa

Adult worms migrate through tissues.

Sometimes one crawls across the white of the eye, giving rise to the name African eye worm.

The baby worms circulate in the bloodstream during the day.

1970s–1980s

Large international campaigns begin planning to eliminate river blindness.

Researchers identify ivermectin as a promising treatment.

1987

Merck announces the Mectizan Donation Program.

The company agrees to donate ivermectin for as long as needed to fight river blindness.

Early campaigns

Millions of people receive ivermectin.

In most areas treatment works very well.

The baby worms disappear.

Blindness falls dramatically.

Unexpected problem

Doctors begin noticing something unusual in parts of Central Africa.

A very small number of patients become severely ill after treatment.

Some develop

Some die.

Investigation

Researchers eventually discover these patients usually do not have a problem because of river blindness itself.

Instead, they also have another infection:

Loa loa

Why?

A person may carry enormous numbers of Loa loa baby worms in their blood.

Examples:

Normal infection:

Heavy infection:

When ivermectin is given,

it rapidly kills huge numbers of these baby worms.

Researchers believe the sudden death of so many parasites triggers an intense inflammatory response. In people with very high Loa loa microfilarial loads, this reaction can damage the brain and lead to post-ivermectin encephalopathy. The exact biological mechanisms are still being studied, but the association between very high Loa loa counts and this rare complication is well documented.

Modern programs

Today programs first determine whether Loa loa exists in an area.

If it does,

extra precautions may be taken before mass ivermectin treatment.

Thinking of them as two separate diseases that happen to overlap geographically makes the situation much easier to understand. River blindness is the disease ivermectin was designed to control, while Loa loa is a different parasitic infection that required public health programs to modify ivermectin campaigns in certain regions of Central Africa.

Since 1987, Merck has donated more than 5 billion ivermectin (Mectizan) treatments over 38 years. The program now reaches more than 300 million people annually and is widely regarded as the longest-running disease-specific drug donation program in history.

Merck & Co. Co-Developed Ivermectin. Donated 5 Billion Free Treatments (1987–2025). Fighting River Blindness and Other Parasitic Diseases Across Africa or destroying DNA and silent death.

Here’s the timeline with The Carter Center added at the appropriate points.

The Carter Center did not originate the idea of donating ivermectin. The sequence was:

In other words, Merck supplied the medicine; the Carter Center became one of the key organizations that helped build the infrastructure to get it to millions of people.

So, if everyone received one treatment per year on average, 5 billion treatments would roughly correspond to:

In reality, the number of unique people is difficult to calculate because:

In many recent years:

So over nearly four decades, the cumulative number of individuals who have received at least one ivermectin treatment is likely in the hundreds of millions. There is no official published count of unique recipients because the programs track annual treatments rather than assigning a lifetime total to each person.

From a historical perspective, the Mectizan Donation Program is often grouped with major achievements such as smallpox eradication, oral rehydration therapy, and large childhood immunization campaigns because of its extraordinary scale and sustained duration. It represents one of the largest long-term medicine donation efforts ever undertaken.

Some countries no longer need mass ivermectin distribution because transmission has been interrupted or eliminated.

For river blindness, WHO has verified elimination in:

Other countries have also eliminated transmission in specific regions.

Mass treatment is still ongoing in parts of:

These areas continue annual or twice-yearly community treatment because the parasite is still being transmitted.

Yes.

In communities where river blindness or lymphatic filariasis remains endemic, eligible residents are still offered ivermectin through organized public health campaigns.

Typically:

Yes.

Merck announced in late 2025 that it would continue donating up to 100 million ivermectin treatments per year through at least 2030 for lymphatic filariasis elimination, while continuing its longstanding commitment to river blindness elimination.

The scale remains enormous.

One thing that stands out historically is the duration. The commitment began in 1987 and is still active nearly 40 years later. Very few large-scale public health interventions—whether run by governments, charities, or private companies—have maintained that level of continuity over such a long period.

The Americas therefore became a realistic elimination target.

Mexico was actually the third country in the world to receive WHO verification for eliminating river blindness, after Colombia and Ecuador.

Several factors helped:

So today, people in Chiapas are not receiving routine community ivermectin for river blindness because the disease has been eliminated there.

One interesting connection to your earlier research is that Mexico appears in two very different infectious disease stories:

Although both concern infectious diseases, they are unrelated biologically and epidemiologically.

Yes, essentially. That’s what made the program unusual.

The roles were divided roughly like this:

So in Mexico, for example:

One interesting aspect is that Merck didn’t simply ship pills to WHO.

Instead, countries or approved programs would estimate how many treatments they needed, submit requests through the Mectizan Donation Program, and, once approved, the medicine was shipped at no cost. The local public health system then distributed it to eligible communities.

So if you were in an endemic village in Chiapas, Mexico, in the 1990s, the chain looked something like this:

It was a remarkably coordinated public-private partnership. Merck has described it as one of the first large-scale collaborations of its kind involving a pharmaceutical company, WHO, governments, NGOs, and local communities working together over decades.

Yes, there have been several other enormous mass drug administration (MDA) campaigns, but the Mectizan (ivermectin) program is generally considered one of the largest and longest-running single-drug donation programs in history.

Here’s how some of the major campaigns compare:

A point that’s easy to miss is that the Merck donating ivermectin is the U.S. company (Merck & Co./MSD), while the Merck donating praziquantel is the German company (Merck KGaA, Darmstadt). Despite sharing the historical Merck name, they are separate companies today.

It depends on what you mean by “biggest.”

If you mean a medicine handed out year after year across multiple countries, then yes, it is one of the largest ever conducted in Africa.

If you include all neglected tropical disease programs together, Africa has seen several enormous campaigns:

Often, these campaigns were coordinated together, so a child might receive more than one medicine during the same public health visit.

One reason historians frequently highlight the Mectizan program is that it has been:

There are larger health interventions if you count vaccines—for example, the WHO Expanded Programme on Immunization has delivered many billions of vaccine doses worldwide—but those involve many different vaccines, manufacturers, and funding sources over decades. They are not comparable to a single company donating one medicine indefinitely.

So, in terms of a single medicine donated by one company and distributed over decades, the ivermectin/Mectizan program is widely regarded as one of the largest humanitarian pharmaceutical efforts ever undertaken.

Not all in Africa, but Africa has been the largest recipient of several of these programs.

Here’s the breakdown:

So if you’re asking whether Africa has been the main focus of mass drug administration, the answer is yes.

The reason is epidemiological rather than simply geographic. Many of the world’s neglected tropical diseases have their highest burden in sub-Saharan Africa.

For example:

From roughly the late 1980s onward, hundreds of millions of Africans have participated in repeated public health campaigns involving one or more medicines:

These campaigns often used the same community health worker networks, allowing multiple neglected tropical disease programs to be delivered efficiently.

One reason Africa appears so prominently in global health history is that it became the principal focus of several of the world’s largest long-term campaigns against neglected tropical diseases, supported by partnerships among governments, WHO, pharmaceutical companies, NGOs, and local communities. That reflects where these diseases were most prevalent, rather than all campaigns being exclusive to Africa.

One interesting point is that Merck’s ivermectin donation helped establish a model. After the success of the Mectizan Donation Program, other pharmaceutical companies launched large donation programs for different neglected tropical diseases. For example:

Together, these programs became the backbone of WHO-led neglected tropical disease control efforts in many low-income countries, particularly in sub-Saharan Africa, while also reaching millions of people in Asia and Latin America.

Definitions:

In this article I want to look at a number of studies showing a dose dependent increase in DNA breaks, chromosomal aberrations, etc when ivermectin is administered to cell cultures or animals.

Video report now available: https://rumble.com/v2yp1we-ivermectin-dna-wreckage-depopulation-agent-ivm-is-mutagenic-genotoxic-and-c.html

In a study titled ‘The mutagenic effects of ivermectin in germinal cells and serum

“Effects of ivermectin on spermatocyte chromosomes: Structural aberrations: Cytological analysis of diakinesis-metaphase I spermatocytes of the treated samples revealed significant increase in chromosome aberrations over the control values.”

“Analysis of the treated samples revealed significant increase in meiotic aberrations, 33.83% vs 5.8% for the control (P < 0.001)… These findings supports the mutagenicity of IVM”

“Effects of ivermectin on spermatocyte chromosomes: … spermatocytes of the treated samples revealed significant increase in chromosome aberrations over the control values”

“The present observations pointed to the mutagenic effects of IVM. The frequency of translocation is significantly higher than that found in the control samples”

“These studies revealed high clastogenic and genotoxic potential of IVM”

“In the present work, IVM induced significant increase in the reciprocal translocation figs.of primary spermatocytes. The changes in the serum protein fractions add another warning for the mutagenicity of IVM.”

In a paper called ‘Antimutagenic Activity of Some Natural supplements on Ivermectin genotoxicity in Lymphocytes of Buffalo’ by El-makawy et al, researchers investigated the impact of garlic, L-carnitine, and wheat germ oil on the genotoxicity induced by ivermectin in buffalo lymphocyte cultures, finding that ivermectin caused a significant rise in micronuclei and chromosomal aberrations with increasing doses (full report)

“Results showed that ivermectin induced dose dependent increase in the frequencies of the binucleated lymphocytes with micronuclei as well as the number of micronuclei in lymphocytes of river buffalo”

“Ivermectin low dose caused non-significant increase in the frequency of total chromosomal aberrations in lymphocytes of river buffalo as compared to control. Whereas, in medium and high doses the frequencies of aberrant cells increased at a significant level (P ≤ 0.001) than control.”

“In addition, the numbers of binucleated lymphocytes showed dose dependent decrease than control. These results revealed that the drug has a cytotoxic effect on the number of cell divisions. As the micronuclei are small chromatin-containing bodies arising from chromosome fragmentation by breaks or deletion, the results of MN [micronuclei] formation confirmed our results of chromosomal aberrations indicating the clastogenic effects of ivermectin.”

In a study called ‘The cytogenetic potential of ivermectin on bone marrow cells of

“IVM induced high level of chromosome aberrations in somatic cells, as it is ascertained by chromosome aberration assay and micronuclei production in bone marrow cells. This study revealed high clastogenic and genotoxic potential of IVM on mice”

“The Table contains also the different types of chromosomal aberrations recorded in the examined cells. A single i.p. injection of ivermectin [200μg/kg ivermectin] resulted in a significant (P≤0.001) increase in percentage of aberrant cells”

“It is clear from the Table (II) that injection with ivermectin induced high significant increase in the frequency of the damaged cells allover the examined periods (P≤0.001).”

In a study called ‘In vitro genotoxic and cytotoxic effects of ivermectin… on Chinese hamster ovary (CHO K1 ) cells’ by Molinari et all, researchers conducted various genotoxicity and cytotoxicity assays to investigate the effects of ivermectin (IVM) and its commercial formulation ivomec® on Chinese hamster ovary (CHO K1) cells and found that Ivermectin caused DNA-strand breaks in Chinese hamster ovary cells. (Full article)

“… IVM and ivomec® … induced DNA-strand breaks revealed by SCGE [single

“Both chemicals induced DNA-strand breaks revealed by the comet assay”

“IVM and ivomec® exert both genotoxicity and cytotoxicity in mammalian cells in vitro, at least in CHO K1 cells.”

“A brief 80 min pulse-treatment of 5.0–50.0 μg/ml of IVM or 25.0 and 50.0 μ g/ml of ivomec® , resulted in a manifest level of single DNA-strand break induction.”

In a study called ‘Ivermectin Confers Its Cytotoxic Effects by Inducing AMPK/mTOR-mediated Autophagy and DNA2 Damage’ Zhang Et Al (full writeup here)

“The results indicate that IVM can induce DNA double-strand breaks in HeLa cells, and the degree of double-strand break is dependent on the concentration of IVM.”

“Ivermectin has significant ability to induce DNA oxidative damage and enhance autophagy in HeLa cells”

“As expected, we found that IVM can induce oxidative double-stranded damage in HeLa cells, indicating that IVM has potential genotoxicity to human health.”

“We conclude that IVM produces genotoxicity and cytotoxicity by inducing DNA damage and AMPK/mTOR-mediated autophagy, thereby posing a potential risk to human health.”

In a study called ‘Genotoxicity and carcinogenicity of ivermectin and amoxicillin in vivo systems’ by Aparecida de Sousa et al (full report here),

“The results revealed that IVM increased the frequency of epithelial tumor in D. melanogaster considering all evaluated concentrations”

“It was observed a dose-dependence in the frequency of MN [Micronuclei] in T. pallida considering the highest concentrations (11.42, 22.84 and 45.68 × 10−5 mM) differing statistically (p ≤ 0.05) from the negative control, evidencing a genotoxic effect of IVM”

“The results observed in D. melanogaster and T. pallida showed that IVM can increase the damage in the genetic material, leading to genetic instability.”

“Findings showed an increase in the frequency of micronuclei in T. pallida

In a study called ‘Genotoxic and cytotoxic in vitro evaluation of ivermectin… on Aedes albopictus larvae (CCL-126™) cells’ (Full paper):

“IVM… induced DNA-strand breaks enhancing both slightly damaged and damaged cells at 25–50 μg/ml IVM”

“Data indicated that IVM exerts both genotoxicity and cytotoxicity in insect cells [A. albopictus larvae CCL-126 cells] in vitro”

In a paper called ‘Comet assay to determine genetic damage by the use of ivermectin in zebu cows’ by Montes-Vergara et al, researchers explored how much DNA damage ivermectin causes in the Zebu cow.

“The values of classification of comets indicate cells with high levels of damage (grade 3: cells with high damage). The rate of DNA damage of the treatment to 1% to 3.15% was significant… The results obtained in this study demonstrate the likely genotoxic potential of the use of IVM in cattle.”

“Regardless of the IVM concentration, the presence of nuclei with DNA migration (Figure 1a and b) was observed at a percentage greater than 75% in all cells observed per plaque, demonstrating the ability of the IVM compound to produce simple chain breaks in the DNA molecule.”

The Comet classification describes how damaged the DNA of cells are. All of the control group (no treatment) measured 0 on the comet scale, indicating little if any DNA damage. Here are the comet classification results for the IVM treated cows:

“The results found in the present study constitute concrete evidence for the induction of genomic damage as exerted by IVM, using the comet assay methodology”

“In conclusion, the results suggest that the genetic damage found in the studied livestock may be associated with the use of IVM”

In a study called ‘Genotoxicity of Three Avermectins on Polypedates megacephalus Tadpoles Using the Comet Assay’ by Geng et al, some very concerning findings were noted in relation to Ivermectin’s “genotoxic effects at relatively low concentrations” in Tadpoles. (Full Paper)

“The tadpoles exposed to the lower concentrations of ABM (0.006 mg/ L) showed a significant increase in DNA damage (P < 0.05), and the tadpoles exposed to other concentrations of the three avermectins showed a highly significant increase in DNA damage (P < 0.01)”

“Our results showed clearly that avermectins caused dose dependent DNA damage on amphibian tadpoles… The three avermectins increased the DNA damage observed in the tadpoles in a dose-responsive manner. There were strong linear correlations between the DNA damages and the concentrations of the three test substances (Figure 2). The cellular distributions of DNA damages in tadpoles are shown in Figure 3. Of the tadpoles treated with increasing concentrations of the three test substances, higher proportions of cells had greater amount of DNA damage than those of the negative control”

This chart shows a dose-dependent increase in DNA damage as IVM dosing increases:

“According to these results above and our finding that avermectins can cause DNA damage in tadpoles at the concentrations below the recommended applied levels (Xu et al., 2010), we consider it possible that avermectins are carcinogenic, and confirm it has the negative impact on the development of tadpoles”

In a paper called ‘DNA damage kinetics and apoptosis in ivermectin-treated chinese hamster ovary cells’ (full report) by Molinari et al, researchers conducted an experiment using the comet assay to analyze the kinetics of DNA damage in Chinese hamster ovary cells induced by ivermectin.

“After 6 h of treatment, cell survival decreased up to 75% and 79% in IVM- and IVO-treated cultures, respectively”

“A clear increase in DNA damage was found immediately after

“For both anthelmintics, biphasic behavior in DNA damage occurred during the incubation time.”

A time-dependent increase of IVM- and IVO-induced DNA damage was observed within 0 to 3 h after pulse treatment, revealed by a progressive decrease of undamaged cells and an increase in slightly damaged and damaged cells.”

“A time-dependent increase in IVM- and IVO-induced DNA damage was observed by a progressive decrease of undamaged cells simultaneously with an increase in the frequency of slightly damaged and damaged cells within the 0–3 h post-incubation time. “

In a paper called ‘Avermectin induces the oxidative stress, genotoxicity, and immunological responses in the Chinese Mitten Crab, Eriocheir sinensis’ researchers investigated the aquatic toxicity of avermectin and its effects on E. sinensis crabs. The study found that exposure to sublethal concentrations of avermectin resulted in decreased levels of antioxidants, increased oxidative products, elevated levels of reactive oxygen species (ROS), reduced phagocytic activity, and genetic damage in the crabs, indicating significant toxic effects on the species including oxidative stress, immunological activity inhibition, and genotoxicity.

“Avermectin or its family members can induce oxidative and immunological dam-

“the 48-h and 96-h LC50 values of avermectin on E. sinensis were 1.663 mg/ L … and 0.954 mg/L”

“Avermectin induces DNA damage in haemocytes”

“a comet assay was performed to investigate the level of DNA damage under avermectin exposure. In control, most haemocytes were observed with a circular, intact nuclei, whereas different degree of comets in the exposure groups early at 24 h. More comets appeared with increase of avermectin concentration. The comet ratio and percentage of DNA in tail increased significantly at each concentration from 24 h (P< 0.05). In group of 0.48 mg/ L, the comet ratio and percentage of DNA rose about 2.7 and 4.1 fold respectively, in compari son to control at 24 h. Although there was a slight recovery at 48 or 72 h, it continued to increase at 96 h. Even in group of 0.03 mg/L, the values of both comet ratio and percentage of DNA are 3.8 and 5.0 fold higher than control at 96 h.”

“Avermectin induces MN [Micronuclei] frequency in haemocytes… An obvious increase of MN frequency was observed at high concentrations especially at 0.48 mg/L from 48h exposure. And at 96 h, there is a significant difference in concentration groups of 0.12, 0.24 and 0.48 mg/L compared to control (P< 0.05)”

“According to the results from two-way ANOVA, a significant interaction between avermectin concentration and exposure time was found for all biomarkers involved (Table 1). All bio markers investigated in this test showed a significant correlation between the concentration, exposure time and their cross combination. It indicated that both avermectin concentrations and exposure time have significant effects on the oxidative, immunological response and DNA damage in E.sinensis”

“The MN test was developed as a simple and practical in vivo cytogenetic screening method for mutagens [42]. In the present study, MN frequency increased significantly in high concentration groups from 48 h”

In a paper called ‘The Study of Genotoxic and Cytotoxic Effects and DNA Damage by Ivermectin in Bone Marrow of Male White Swiss Mice Mus musculus’ by Sadek et al, researchers evaluated the genotoxic and cytotoxic effects of Ivermectin (IVM) on the bone marrow of male white Swiss mice using various cytogenetic endpoints. The results demonstrated that IVM administration led to a significant decrease in polychromatic erythrocytes and a significant increase in micronuclei formation, indicating both anuegenic and clastogenic effects. Furthermore, the comet assay revealed significant DNA damage in bone marrow cells treated with IVM, highlighting its genotoxic and cytotoxic potential in somatic cells.

“Results of current study revealed that IVM have genotoxic and cytotoxic effects on somatic cells of male white mice.”

“Oral treatment of white mice with IVM induced a significant DNA damage in bone marrow cells, which revealed by comet assay results, the mean of damaged bone marrow cells in mice treated with doses 0.6 and 0.8 mg/ kg. b.wt. were different significantly when compared with negative control(P≤ 0.01).”

“IVM induced both anuegenic and clastogenic effects in bone marrow of male white mice, The results showed a significant increase in means of numerical chromosome aberrations (anueploidy and polyploidy) (P≤ 0.05), the highest mean of structural chromosome aberration (with and without gabs) was recorded in mice treated with 0.8 mg/ kg. b.wt. (P≤ 0.01).”

“The results showed that IVM induced significant decrease in the mean of polychromatic erythrocytes and the lowest value was recorded at the dose 0.6 mg/ kg. b.wt.(P≤ 0.01) and significant increase in the mean of micronuclei were induced by the three doses of drug (P≤ 0.01).”

In a paper called ‘Mutagenic Effects of the Combination and Its Components of Albendazole and Ivermectin in vivo and in vitro’ by Lin et al

“Albendazole and ivermectin, common antiparasitic drugs widely used in livestock production, showed mutagenic effects in some extent”

“the mice treated with ivermectin or albendazole showed higher micronucleus frequency and sperm abnormality rate.”

“The sperm abnormalities in the ivermectin single-drug group were mainly head deformities and body-tail folds… Among them, the proportion of banana head and amorphism was the highest.”

In a paper called ‘In vivo combined treatment of rats with ivermectin and aged garlic extract attenuates ivermectin-induced cytogenotoxicity in bone marrow cells’ by Khalil et al (full paper), Male Sprague Dawley rats were administered varying doses of IVM intraperitoneally, and the results indicated that high doses of IVM caused significant cytogenetic toxicity.

“IVM was found cytotoxic and mutagenic at high doses since it significantly reduced %MI [mitotic index] and increased %NA [percentage nuclear abnormalities] and %Abc [percentage chromosomal abnormalities]. These observations may be due to disturbances in the mitotic processes that lead to formation of severe CA [chromosomal aberrations] and in turn caused cell death or cease of further cell divisions.”

In a study called ‘Effect of ivermectin on male fertility and its interaction with P-glycoprotein inhibitor (verapamil) in rats’ by El-Nahas & El-Ashmawy (full report)

Ivermectin, along with a Pgp-inhibitor/ CYP3A4-inhibitor, results in a remarkable 59% increase in abnormal sperm count, while sperm motility decreases by 8% with Ivermectin alone and by 23% when combined with the Pgp-inhibitor.

Let’s look at the differences in abnormal sperm cells by category by treatment group in this series of 9 charts:

In a paper called ‘Micronuclei induction by some anthelmintic drugs in male mice’ by EL-makawy (full report)

“Contrariwise, at 72 hrs after treatment.. ivermectin induced statistically significant increase in the number of MN [Micronuclei] over the negative control”

The researchers are concerned that the veterinary dosing of livestock may pose a potential risk of dangerous exposure, which could lead to harmful “genotoxic effects on humans.”

MNPCEs stands for Micronucleated Polychromatic Erythrocytes. They are a type of abnormal cells that can be observed in the bone marrow and peripheral blood of animals, including humans, following exposure to certain genotoxic substances or conditions.

The presence of micronucleated polychromatic erythrocytes is generally considered a sign of genetic damage or chromosomal abnormalities. These cells have small additional nuclei, known as micronuclei, which contain fragments of chromosomes or whole chromosomes that were not properly incorporated into the daughter cells during cell division.

In a paper called ‘IVERMECTINAS: EVALUACIÓN DE SU EFECTO DELETÉREO

“when the comet assay was employed, both ivermectin and Ivomec® were able to induce DNA single-strand breaks in CHO-K1 and CCL-126 cells”

“Overall, the results evidence that ivermectin present a similar pattern of cytotoxic and genotoxic damage than that induced by Ivomec®.”

“Our results demonstrate that ivermectin has the ability to induce damage in the DNA molecule, at least in CHO-K1 and CCL-126 cells, but also highlight a highly cytotoxic capacity as the major deleterious effect of this antibiotic.”

“Its widespread use would seriously jeopardize the organisms that are usually treated with ivermectin including human beings.”

“DNA migration analysis was performed by measuring the length and width of the observed images. All the concentrations of both compounds tested on CHO-K1 and CCL-126 cells significantly increased the levels of DNA damage.”

“The ability to induce repair introduced DNA lesions was tested in CHO-K1 and CCL-126 cells previously exposed to 50 μg/ml ivermectin and Ivomec during a 80-min treatment pulse… Immediately after treatment with both ivermectin and Ivomect (0h) a significant increase in damaged DNA was observed in a high percentage of the cell population in both cell lines”

“The deleterious capacity exerted by both compounds was reflected in the induction of single chain breaks in the DNA from cell lines used.”

In a study from Nigeria entitled ‘Effects of Ivermectin therapy on the sperm functions of Nigerian onchocerciasis patients’, some very concerning findings were published.

“We observed significant reduction in the sperm counts and sperm motility of the patients tested. On the morphology there was significant increase in the number of abnormal sperm cells. This took the forms of two heads, double tails, white (albino) sperms and extraordinarily large heads. It is suspected that the above alterations in the already determined parameters of the patients’ sperm cells could only

“Sperm with abnormal morphology were also found to have increased after ivermectin therapy”

Here is a scatter plot of the % of sperm deemed “abnormal” before (x axis) and after (y axis) the ivermectin dosing. Points above the line indicate a higher % of abnormal sperm after the Ivermectin and points below the line indicate a lower % of abnormal sperm after Ivermectin.

“There was a significant drop in the sperm counts of the patients after their treatment with ivermectin.”

We can calculate the total motile count of each patient’s sample by multiplying the number of sperm in the sample times the percentage that were swimming properly.

In an article called ‘Increased Pathology Incidence in the Forestomach of Rats Maintained on a Diet Containing Ivermectin and Given a Single Dose of N-Methyl-N1-Nitro-N-Nitrosoguanidine’ by O’Conner et al, they observed additional cancers in mice with a small amount (2 ppm) of ivermectin in their diet given a dose of a carcinogen called N-Methyl-N1-Nitro-N-Nitrosoguanidine. From the abstract:

“No tumors or pathological lesions were observed in the forestomach of the control animals or those given ivermectin alone. However, compared to animals receiving MNNG alone, rats maintained on a diet containing ivermectin (2 ppm) and given MNNG… showed an increased number of neoplasms (9/26 vs 3/18; p = 0.30) and a statistically significant fourfold increase in the number of pathological lesions (18/26 vs 3/18; p = 0.002), which include preneoplasia in the forestomach. In all cases, the pathological lesions were more severe in the animals receiving ivermectin and MNNG, compared to those receiving MNNG alone.”

Source:  “CLASTOGENIC” – 18 Studies Highlighting Ivermectin Induced DNA Breakage and Damage

Ivermectin, WHO, UN, Merck, The World Bank & Kissinger’s World Population Plan Of Action

Pig Study Raises MAJOR Questions Of Dangers Of Combining Quercetin & Ivermectin

2 Concerning Studies: CBD & THC Enact Potent P-Glycoprotein Inhibiting Effects, Raising Very Concerning Questions About Heightened Ivermectin Toxicity For Marijuana Users

Studies Find Quercetin & Natto K2 INHIBIT P-Glycoprotein; Will This Increase Ivermectin Toxicity Susceptibility?!

Ivermectin Is Cytotoxic & Genotoxic (Damaging To Cells And DNA) & Possibly Carcinogenic (Cancer Causing)

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Ivermectin VS Sperm: 3 Disturbing Studies On Decreased Sperm Counts, Decreased Sperm Motility & Increased % Abnormal Sperm Post-Ivermectin

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Merck & Co., Inc. “35 Years: The Mectizan® Donation Program.” May 25, 2022. Merck — Mectizan Donation Program.
Useful for the 1978 Campbell proposal, 1981 human trials, Mohammed Aziz, 1987 donation decision, Roy Vagelos, and program history.

Mectizan Donation Program. “History of the Program.” The Task Force for Global Health. Accessed August 6, 2026. Mectizan Donation Program — History.
Primary program history covering Merck, WHO, William Campbell, Mohammed Aziz, West African trials, and the 1987 commitment to provide ivermectin for river blindness.

Mectizan Donation Program. “Overview.” The Task Force for Global Health. Accessed August 6, 2026. Mectizan Donation Program — Overview.
Useful for the structure of the donation program, Africa, Latin America, Yemen, lymphatic filariasis, annual treatment, and Merck’s “as much as needed, for as long as needed” commitment.

Merck & Co., Inc. “Merck Commemorates 30 Years of MECTIZAN® Donation Program Progress.” November 30, 2017. Merck — 30 Years of Mectizan.
Documents the 1987 founding of the program and its later expansion for lymphatic filariasis, including plans to reach up to an additional 100 million people annually.

World Health Organization. “Onchocerciasis.” December 4, 2025. WHO — Onchocerciasis Fact Sheet.
Key source for river blindness, Onchocerca volvulus, blackfly transmission, geographic distribution, mass drug administration, and WHO’s current ivermectin strategy. WHO states that ivermectin donated by Merck remains the core population-based treatment strategy.

Nobel Prize Outreach. “The 2015 Nobel Prize in Physiology or Medicine: Press Release.” October 5, 2015. Nobel Prize — 2015 Medicine Prize.
Official Nobel source documenting the award to William C. Campbell and Satoshi Ōmura for discoveries leading to therapies against roundworm parasites.

Nobel Prize Outreach. “The 2015 Nobel Prize in Physiology or Medicine.” 2015. Nobel Prize — Avermectin and Ivermectin Discovery.
Especially useful for the discovery chain: Ōmura’s Streptomyces cultures → Campbell’s parasite research → avermectin → modification into ivermectin → human and veterinary applications.

Ōmura, Satoshi. “A Splendid Gift from the Earth: The Origins and Impact of Avermectin.” Nobel Lecture, Karolinska Institutet, Stockholm, December 7, 2015. Satoshi Ōmura — Nobel Lecture.
An important first-person scientific history from Ōmura himself describing the origins and impact of avermectin.

Why Is Everyone Getting Explosive Diarrhea? 

Cyclospora has become one of the most difficult foodborne parasites investigated by public health officials. This episode examines how Cyclospora outbreaks are linked to fresh produce including lettuce, cilantro, basil, raspberries, herbs and packaged salad mixes, and why contaminated food can be so difficult to identify before people become sick.

It follows the process of patient interviews, stool testing, epidemiology, product sampling and traceback investigations used to reconstruct outbreaks after contaminated produce has already moved through restaurants, stores, warehouses and international supply chains. A major focus is Taylor Farms de Mexico and the repeated appearance of its Guanajuato operation in Cyclospora investigations. In 2013 a Cyclospora outbreak was traced to salad mix processed by Taylor Farms de Mexico. In 2026 epidemiology and traceback again pointed to Taylor Farms de Mexico lettuce from central Mexico.

The episode examines Guanajuato as a major agricultural region facing water scarcity, groundwater depletion, wastewater treatment challenges and the reuse of treated wastewater. It also asks what oversight actually exists for Mexican lettuce entering the United States and whether produce is routinely tested for Cyclospora before crossing the border. The investigation finds that every shipment of Mexican lettuce is not tested for Cyclospora. FDA oversight relies largely on importer verification, farm and facility inspections, preventive controls, targeted sampling and outbreak investigations rather than universal laboratory screening. FDA implemented a validated molecular detection method for Cyclospora on produce beginning around 2018 and expanded laboratory capability by training Mexican government laboratories in 2023.

The episode examines why a laboratory test can exist while contaminated produce can still move through the food supply undetected. The program also traces the scientific history of Cyclospora beginning with Richard W. Ashford’s 1979 report from Papua New Guinea and follows the parasite through years of uncertainty before it became recognized as Cyclospora cayetanensis. It explores the work of Richard W. Ashford, Graham D. F. Reid, David C. Warhurst, Robert Gilman, Ynes Ortega, Charles Sterling and other researchers, together with the Liverpool School of Tropical Medicine, the London School of Hygiene and Tropical Medicine, the Institute of Primate Research in Kenya, the World Health Organization and international tropical disease research programs. Beyond modern outbreaks, the episode traces the historical roots of sanitation and public health from nineteenth-century Europe and Bavaria through the rise of bacteriology, sewage engineering and wastewater management in the United States.

It examines how human waste, sewage sludge and today’s biosolids became incorporated into modern agriculture, how wastewater reuse developed in both the United States and Mexico, and how those practices intersect with food safety, irrigation and infectious disease prevention. The program also explores the history of biological warfare research involving diarrheal diseases during World War II and the Cold War, including Nazi Germany, the United States and later military biodefense programs. It distinguishes documented historical research into enteric diseases from the established biology of Cyclospora itself while examining how governments and scientists have long viewed foodborne illness, sanitation and gastrointestinal disease as matters of both public health and national security. Cyclospora remains unusually difficult to study.

There is still no routine laboratory culture system, no widely accepted animal model reproducing the complete human infection and no well-established human challenge model. Researchers continue to rely on naturally infected patients, molecular testing, stool examinations, epidemiological investigations and outbreak traceback. Contamination may be scattered unevenly through a field, shipment or salad mix, meaning a negative sample does not prove that the remaining produce is free of the parasite. These limitations help explain why investigators often begin with sick people and work backward toward the food, water, farm and processing facility. The episode ultimately places Cyclospora within the larger history of human feces, sanitation, sewage sludge, biosolids, wastewater reuse, agriculture, tropical medicine, epidemiology and foodborne disease. It examines how modern food production, international trade, environmental infrastructure and public health intersect to allow a microscopic parasite to travel from a contaminated field or water source to consumers hundreds or even thousands of miles away.

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September 16, 1975

April 29, 1976

August 1976

1977

Patients with prolonged diarrhea are examined, but the organism is unknown.

1978

Researchers continue observing the unusual organism in stool samples.

1979

“Occurrence of an undescribed coccidian in man in Papua New Guinea.”

Ashford describes three patients and concludes the organism is an undescribed coccidian parasite, although he cannot yet identify it precisely. This becomes the first published description of what would later be known as Cyclospora cayetanensis.

1980s

Different laboratories describe them as:

Because the organism is poorly understood, no one realizes these reports are describing the same parasite.

1993

Their work helps connect years of scattered reports into a single scientific story.

1993

Cyclospora cayetanensis.

Approximately sixteen years after the first recognized human cases in Papua New Guinea, the organism finally receives its official scientific name.

The WHO Representative Office was already operating in Port Moresby before Cyclospora was first recognized in humans. The office opened in August 1976, the first known cases appeared in 1977, additional cases followed in 1978, and Ashford published the first scientific description in 1979.

The principal researchers associated with the early discovery were:

This sequence shows that the discovery of Cyclospora was not a single event but a process that unfolded over roughly 16 years, beginning in Papua New Guinea and ending with international recognition of a new human parasite.

One of the most important lessons from military medicine is that severe diarrheal disease has historically disabled more soldiers than many weapons. Long before antibiotics, armies feared outbreaks of dysentery, cholera, typhoid, and other gastrointestinal diseases because they could incapacitate entire units.

That historical reality explains why military organizations became interested in enteric diseases—not because “explosive diarrhea” itself was viewed as a unique weapon, but because pathogens causing severe gastrointestinal illness could remove soldiers from combat.

Military planners have long recognized that diarrheal diseases can:

Modern U.S. military medical literature continues to describe diarrheal disease as one of the most common causes of lost operational effectiveness during deployments.

Nazi Germany conducted biological warfare research during World War II.

Research included:

• insect vectors

• infectious diseases

• military applications of biological agents

Documents released decades later show that the SS established an Entomological Institute at Dachau in 1942 under Heinrich Himmler. Historians examining surviving research protocols concluded the institute had an offensive biological warfare component.

The German program was much smaller than Japan’s infamous Unit 731, but it demonstrates that Nazi leadership investigated biological warfare.

There is no documented evidence that Nazi Germany produced a dedicated biological weapon whose sole purpose was to cause explosive diarrhea.

However, they did study organisms capable of causing severe gastrointestinal disease as part of broader biological warfare research.

Military interest centered on whether disease could disable enemy forces.

That is different from evidence showing an operational “explosive diarrhea weapon.”

The United States launched its offensive biological warfare program during World War II.

Major centers included:

• Camp Detrick (later Fort Detrick)

• Dugway Proving Ground

• Pine Bluff Arsenal

The program expanded greatly after the war.

Government histories show U.S. researchers investigated numerous human, animal, and plant pathogens as potential biological warfare agents before President Richard Nixon ended the offensive program in 1969 and ordered destruction of offensive stockpiles.

Yes.

But it is important to distinguish two different kinds of research.

Researchers evaluated many disease agents for military usefulness.

Some gastrointestinal pathogens were examined because they could disable troops.

The much larger body of work focused on protecting U.S. troops from naturally occurring diarrheal disease.

This includes decades of research on:

The goal was preventing outbreaks among deployed military personnel.

A soldier suffering:

is often unable to fight.

Historically this has been considered an effective way for disease—not necessarily a weapon—to reduce combat capability.

Military medicine has repeatedly documented that diarrheal illness can sideline large numbers of personnel during deployments.

Cyclospora is very different.

The parasite was first scientifically described in Papua New Guinea in 1979 by Dr. R. W. Ashford after cases observed beginning in the late 1970s.

Unlike many bacterial diarrheal diseases:

These characteristics make Cyclospora an unlikely biological warfare agent compared with organisms that spread rapidly between people.

Cyclospora presents a public health challenge because:

These characteristics complicate outbreak investigations but do not indicate intentional contamination.

Supported by documentary evidence:

✔ Nazi Germany conducted biological warfare research.

✔ The United States conducted an extensive offensive biological warfare program from World War II until 1969.

✔ Both countries studied infectious diseases with military relevance.

✔ Gastrointestinal diseases have long been recognized as capable of incapacitating armies.

✔ Modern military medicine continues extensive research on diarrheal diseases because they remain a major operational problem.

Development of modern virology laboratories and high-containment (BSL) facilities.

One thing stands out in the timeline: before the 1940s there were very few dedicated virology laboratories. The major expansion occurred after World War II, accelerated during the Cold War, expanded again after HIV, and grew rapidly after the 2003 SARS outbreak and again following COVID-19. That progression helps explain why most discussions about laboratory biosafety and possible laboratory-associated outbreaks are concentrated in the last 50 years.

…plus several others with one facility or facilities under construction, for a total of 34 countries.

1946–1967

1967–1985

1985–2000

2001–2003

These events led to a sharp increase in investment in high-containment laboratories.

2015–Present

For roughly the first 35 years of the BSL-4 era (1967–2001), only a small number of countries operated these maximum-containment laboratories. The largest worldwide expansion occurred after the 2001 anthrax attacks, after SARS in 2003, and again following COVID-19.

So, besides the United States, at least 30–35 countries have used biosolids in some form. The practice is especially widespread in Europe, Canada, Australia, New Zealand, and parts of Asia, although several countries have recently tightened restrictions or shifted away from agricultural land application because of concerns about contaminants such as PFAS and other persistent chemicals.

Late 1800s–early 1900s American and European cities rapidly built sewer systems and wastewater treatment plants. As treatment improved, they generated increasing amounts of sewage sludge.

American cities introduced technologies such as:

These processes greatly increased the volume of treated sludge that cities had to manage.

1900s–1960s Cities experimented with several disposal methods:

At this stage it was generally called sewage sludge, not biosolids.

1970s Environmental laws changed the conversation.

The U.S. banned most ocean dumping of sewage sludge and placed greater restrictions on disposal. Utilities increasingly looked to agriculture as a long-term management strategy.

1980s The wastewater industry began promoting treated sludge as a reusable product rather than simply a waste.

The term “biosolids” was developed during this period.

In 1991, the Water Environment Federation sponsored a branding effort that selected the word biosolids to distinguish treated sewage sludge meeting certain treatment standards from untreated sewage sludge.

1993 The EPA issued the federal 40 CFR Part 503 Rule, establishing national standards for land application, pathogen reduction, and metal limits.

From that point forward, “biosolids” became the standard regulatory and industry term in the United States.

So your statement is essentially correct, but I’d tighten it slightly:

American cities introduced trickling filters, sedimentation, activated-sludge treatment, chlorination, and anaerobic digestion. As wastewater treatment expanded during the early 20th century, increasing amounts of sewage sludge were produced. Cities experimented with dumping, burial, incineration, digestion, drying, and agricultural use. This evolving system became the foundation for what the United States would later rename biosolids in the early 1990s.

One important distinction is that the material existed long before the name did. The treatment processes and land application practices developed over decades, while “biosolids” is essentially a 1990s regulatory and public-relations term for treated sewage sludge that meets specified standards.

GRAS means “Generally Recognized As Safe.” It is an FDA regulatory designation for a substance used under its intended conditions—not a sanitizer itself.

Besides chlorine and peracetic acid, produce processors may also use:

Some commercial produce-wash formulations are made entirely from GRAS ingredients. For example, USDA researchers developed one antimicrobial wash whose ingredients are all classified as GRAS by the FDA.

One important point for your Cyclospora research:

Even when a sanitizer or wash uses only GRAS ingredients, that does not mean it can reliably eliminate Cyclospora from contaminated lettuce or other produce. FDA guidance emphasizes that these antimicrobial washes are mainly intended to keep the wash water from spreading contamination and may reduce surface microbes, but preventing contamination before harvest is the primary control strategy.

One detail that attracted attention during the 2026 Cyclospora outbreak involved the timing of political donations, government meetings, and FDA announcements. In 2025, Taylor Farms donated $1 million to MAGA Inc., the principal pro-Trump super PAC. Reports also stated that the company contributed more than $2 million to conservative political committees during the year.

Then, on July 16, 2026, the FDA publicly announced it was investigating a multistate Cyclospora outbreak linked to shredded iceberg lettuce served at Taco Bell. By that point, 1,644 illnesses had been identified. Investigators found that 90 percent of interviewed patients in Michigan had eaten iceberg lettuce, and the FDA said its traceback investigation had already narrowed the source to a single supplier of iceberg lettuce from Mexico, although the supplier’s name had not yet been released.

Later that same day, Taylor Farms executives met with White House and FDA officials to challenge the agencies’ handling of the outbreak investigation. On July 17, the FDA publicly identified the supplier as Taylor Farms de Mexico. The company announced it was voluntarily removing shredded iceberg lettuce from central Mexico from the market and initiated a recall. On July 18, the FDA announced that one lettuce sample associated with the investigation had tested positive for Cyclospora.

Then, on July 19, the FDA said that laboratory result was actually a false positive. However, the agency also emphasized that this did not change its overall conclusions. According to the FDA, the epidemiologic evidence and traceback investigation still pointed to Taylor Farms de Mexico’s shredded iceberg lettuce from central Mexico as the likely source of the outbreak.

One interesting historical point is that Bavaria required compulsory vaccination nearly half a century before Britain and almost 50 years before Massachusetts adopted its statewide school vaccination law. Bavaria is therefore frequently cited in histories of public health as an early pioneer in compulsory vaccination policy.

mid-to-late 1800s, many public health leaders increasingly concluded that preventing disease required more than vaccination.

The progression was roughly:

That led to a major shift in public health priorities. Cities began investing in:

In many ways, the late 1800s marked the birth of modern environmental public health.

For diseases like cholera and typhoid fever, improving water and sanitation had an enormous impact because those diseases spread through contaminated water or food.

For smallpox, however, the situation was different. Smallpox spreads primarily through close person-to-person contact and respiratory droplets, not contaminated drinking water. So cleaning up water would not have eliminated smallpox, although it greatly reduced many other infectious diseases.

So a concise historical summary would be:

After germ theory, governments increasingly realized that preventing infectious disease required not only vaccines where available, but also clean water, sewage treatment, sanitation, food safety, and hygiene.

Those investments dramatically reduced deaths from many infectious diseases, even before antibiotics became available.

The House of Wittelsbach was one of Europe’s great dynasties, and like the Habsburgs, they built influence through marriages with other royal houses. Their family tree branches across much of Europe.

Some of the major marriage and inheritance connections include:

One of the most notable examples:

The main Wittelsbach line ruled:

By the nineteenth century, Europe’s royal families had become so interconnected through marriage that many rulers were cousins. The major dynasties included:

These dynasties frequently intermarried to secure alliances, inherit territories, and strengthen political legitimacy. While the Habsburgs are often associated with the phrase “Let others wage war; you, happy Austria, marry,” the Wittelsbachs also participated extensively in this network of dynastic marriages, though they generally did not achieve the same level of continental dominance as the Habsburgs.

* Live variola (smallpox) virus research is restricted to two WHO-authorized repositories under international oversight

During all of that:

Instead, physicians relied on observation. They had seen for centuries that:

That empirical evidence was enough for Jenner’s vaccine to gain acceptance long before anyone understood why it worked.

The major scientific milestones came later:

When Bavaria passed its compulsory vaccination law in 1807, the public justification was not, “We know germs cause disease.” Rather, it was essentially:

“We know from experience that vaccinated people are far less likely to get smallpox, and smallpox kills many children.”

The policy rested on observed outcomes, not on an understanding of microbiology.

Germ theory and virology would not provide that scientific explanation until decades later.

It cannot be routinely cultured in the laboratory, and humans are the only confirmed major reservoir. Despite decades of research, many aspects of its biology remain more difficult to study than those of most bacteria, viruses, and fungi.

The most familiar examples are:

Cholera — strongly associated with sewage-contaminated water or food.

Typhoid fever — caused by Salmonella Typhi, which is shed by infected people and spreads through contaminated food or water.

Dysentery and shigellosis — spread when microscopic amounts of human feces contaminate hands, food, water, or surfaces.

Hepatitis A — transmitted through contaminated food or water or close fecal–oral contact. WHO specifically lists contaminated food and water as major transmission routes.

Polio — primarily spreads through the fecal–oral route, especially where sewage disposal and clean water systems are inadequate.

Cyclospora — human feces contaminate water, soil, or produce; the parasite must mature in the environment before it becomes infectious.

Giardiasis — commonly acquired from fecally contaminated water, food, hands, or surfaces.

Cryptosporidiosis — spreads through contaminated drinking water, pools, food, animals, and fecal contact. It is particularly difficult because the parasite is resistant to ordinary chlorine levels.

Norovirus — spreads extremely easily through contaminated food, water, hands, surfaces, vomit, and feces.

Rotavirus — a major fecal–oral diarrheal disease, especially among infants and young children.

Pathogenic E. coli infections — certain strains spread through fecally contaminated food, water, animals, or hands.

Salmonellosis — often associated with contaminated food and animals, but sanitation and hygienic food handling are central to prevention.

Intestinal worms, including roundworm, whipworm, and hookworm — strongly linked to inadequate sanitation, contaminated soil, and unsafe disposal of feces.

WHO summarizes the major group as cholera, diarrhea, dysentery, hepatitis A, typhoid, intestinal worm infections, and polio.

HIV is not considered a sanitation disease. It is transmitted through particular body fluids—principally blood, semen, vaginal and rectal fluids, and breast milk. It is not spread through sewage, drinking water, food, toilets, ordinary contact, or poor municipal sanitation.

Sanitation can still matter greatly to people with HIV because impaired immunity may make contaminated water and food more dangerous, but sanitation failure is not the route by which HIV itself spreads.

Smallpox, measles, influenza, COVID-19, tuberculosis, chickenpox, and whooping cough are mainly respiratory or close-contact diseases.

Malaria, yellow fever, dengue, Lyme disease, and West Nile virus are vector-borne diseases involving mosquitoes or ticks. Poor water management can increase mosquito breeding, but that is different from fecal contamination and sewage transmission.

Rabies is transmitted primarily through the saliva of infected animals.

Hepatitis B and hepatitis C are mainly bloodborne; hepatitis B can also spread sexually and during childbirth. Unlike hepatitis A, they are not primarily diseases of contaminated food, water, or sewage.

The core division for your topic is:

Some diseases spread because people breathe or touch an infected person. Others spread because human or animal waste enters water, food, soil, or the hands of another person.

Cyclospora belongs squarely in that second category. It is not merely a “lettuce disease.” Lettuce is one possible delivery vehicle after a sanitation failure has allowed human fecal contamination somewhere in the chain.

.

So, of the major sanitation-associated diseases on that list:

That highlights an important historical point.

For diseases where no vaccine exists, prevention relies heavily on:

One question that naturally arises when studying Cyclospora cayetanensis is whether scientists should investigate scenarios that have never been observed, such as the parasite expanding its host range beyond humans.

The answer is yes. This type of forward-looking research is a normal part of infectious disease science and public health preparedness.

Scientists generally work on three levels.

First, they document what is currently known.

For Cyclospora cayetanensis, the current evidence indicates that humans are the only confirmed natural reservoir. The parasite causes illness in humans and is primarily transmitted through food or water contaminated with human feces.

Second, scientists try to understand why current observations are true.

For Cyclospora, this includes questions such as:

These questions seek to understand the parasite’s biology rather than merely describing it.

Third, scientists project possible future scenarios.

This is where preparedness research begins.

Researchers routinely ask:

These questions are intended to reduce uncertainty before a crisis develops.

Although Cyclospora cayetanensis is widely regarded as human-specific, published scientific reviews demonstrate that researchers continue examining the possibility that animals could play a role in its ecology.

A comprehensive 2021 review evaluated every available report of Cyclospora cayetanensis in animals. The authors concluded that no confirmed natural animal reservoir has been demonstrated but emphasized that additional research is needed to determine whether animals may transport oocysts or contribute to contamination of food, water, or soil. They specifically recommended further molecular studies rather than assuming the question has been settled.

Likewise, more recent reviews continue examining host specificity and the possibility of zoonotic transmission, indicating that scientists still consider these legitimate research questions rather than closed subjects.

One misunderstanding in discussions of infectious diseases is the assumption that studying a possibility implies someone believes it is about to occur.

Scientific preparedness works differently.

Researchers often investigate events that have never happened simply because the consequences could be significant if they ever did.

Examples include:

Many of these questions were investigated years before some became major public health concerns.

Cyclospora fits within the same philosophy of preparedness, even though its biology differs substantially from respiratory viruses.

Unlike organisms such as Salmonella or E. coli, Cyclospora remains unusually difficult to study.

Major limitations include:

Federal food safety agencies have acknowledged that these limitations significantly restrict research progress and complicate outbreak investigations.

As a result, many investigators remain focused on answering basic biological questions that have already been resolved for many other foodborne pathogens.

Current evidence continues to support humans as the only confirmed natural host of Cyclospora cayetanensis.

However, the scientific literature shows that researchers continue asking questions such as:

These questions represent standard scientific inquiry rather than evidence that researchers are attempting to create a new host range.

The published literature shows that Cyclospora researchers continue investigating host specificity because important biological questions remain unanswered.

Current evidence supports humans as the only confirmed natural reservoir, but scientists continue studying animals, environmental transmission, and host biology because preparedness depends on understanding what is known, what remains uncertain, and how future changes—however unlikely—would be recognized if they occurred.

This approach is consistent with the broader philosophy of infectious disease research: study potential future risks before they become public health emergencies, while distinguishing clearly between documented evidence and hypothetical scenarios.

The legend of smallpox and its eradication as told by most textbooks and virtually the whole medical establishment goes something like this: from about the sixteenth century, Europe was ravaged by periodic epidemics of smallpox (variola major), a disease that caused pustules to erupt all over the skin and very often, in approximately a fifth of all cases, led to death. Those who survived were often scarred for life (pockmarked). Early attempts to combat it through “variolation,” i.e., inoculation of healthy adults with puss from infected individuals, proved ineffective—while those who survived this treatment were immune, the practice also served to keep the disease alive and circulating in the population.

Then, in 1796, the heroic Dr. Edward Jenner made the crucial discovery: anecdotal evidence suggested that milkmaids did not contract smallpox and Dr. Jenner surmised that contact with cattle had exposed them to cowpox (variola vaccinia), a disease that was much milder in humans. He therefore experimented with inoculating children with cowpox, and when he later exposed the same to smallpox through variolation, they proved to be immune.

The medical establishment, in the form of the Royal Society, dismissed the good Dr. Jenner, but nothing daunted, he proceeded to promote his new treatment of “vaccination” and quickly received support from enlightened doctors and statesmen, who sponsored his scheme. Thousands were vaccinated in Great Britain within a couple of years, and the treatment spread to other European countries.

Cyclospora was already trending in the wrong direction before the FoodNet surveillance change.

That’s one reason the timing has drawn attention.

What stands out is that the policy change did not occur during a period when Cyclospora was disappearing.

The published literature already described an upward trend in cases and recurring produce outbreaks.

That does not prove the surveillance change caused the 2026 outbreak. Those are separate questions. But the chronology is accurate:

The early 1980s created an environment where many explanations flourished because:

One interesting historical difference is that HIV generated numerous competing origin theories within just a few years of being recognized, whereas Cyclospora has not. Discussion around Cyclospora has focused far more on contamination pathways, food safety, sanitation, and outbreak investigation than on competing theories about the organism’s origin.

1916 — Porton Down (United Kingdom)

1943 — Fort Detrick (United States)

1949 — Sverdlovsk-19 (Soviet Union)

1954 — Plum Island Animal Disease Center (United States)

What makes Cyclospora unusual compared with the other two is not necessarily how severe it is, but where the bottleneck lies.

That’s a distinctive feature. It means outbreak investigations often rely on epidemiology and traceback after illnesses have already occurred, rather than detecting contamination in the field before food reaches consumers.

Another contrast is the transmission chain:

That environmental maturation step is one reason Cyclospora behaves differently from many other foodborne pathogens.

From a historical perspective, if you were comparing these three simply as research subjects, all have attracted sustained scientific attention, but for different reasons:

One of the easiest ways to become confused about infectious diseases is to mix together two separate questions:

Where did the organism originate? How does the organism spread once it exists?

Those are not the same question.

A scientist may debate where an organism first came from, whether it evolved naturally, was first recognized after decades of being overlooked, or even whether someone believes it originated in a laboratory. Regardless of the answer, once the organism exists outside the laboratory, it no longer has the freedom to spread however it wants. It must follow its own biology.

Lyme disease provides a useful example.

Imagine, purely as a hypothetical exercise, that someone created or discovered a new Lyme bacterium in a laboratory. Simply releasing a test tube containing the bacteria into a forest would not automatically create an epidemic.

The bacterium would first have to enter its normal biological cycle.

In other words, regardless of where the bacterium originated, it must still obey the tick-based transmission cycle.

The tick is not simply carrying the organism like dirt on its feet. It is an active biological vector that feeds on blood and moves the bacterium between animals and humans.

Imagine, again as a hypothetical exercise, that someone created or discovered Cyclospora in a laboratory. Dumping a flask containing Cyclospora into a lettuce field would not automatically create a sustained human outbreak.

Cyclospora must also follow its own biological rules.

Humans must first become infected.

Just as Lyme disease must follow the tick cycle, Cyclospora must follow the human-environment-food transmission cycle.

At first glance, it is tempting to compare lettuce to a tick because both can be associated with the transmission of disease. However, biologically they perform very different roles. A tick is a living organism that feeds on blood and participates directly in the natural transmission cycle of the pathogen it carries. Because it plays an active biological role in transmitting disease from one host to another, it is considered a biological vector. Lettuce does none of those things.

It does not become infected with Cyclospora, it does not help the parasite reproduce, and it does not alter the parasite biologically in any way. Instead, the surface of the lettuce simply becomes contaminated after mature Cyclospora oocysts are deposited on it. The lettuce then serves as a passive vehicle, carrying those oocysts until the produce is eaten. A useful way to think about the difference is this: in Lyme disease, the tick is an active biological delivery mechanism because it is part of the organism’s life cycle and transmission. In Cyclospora infections, contaminated produce serves as a passive delivery mechanism.

The lettuce is not part of the parasite’s biology; it is simply the surface that transports the infectious stage from the environment to the person who consumes it. Although both the tick and contaminated lettuce ultimately help a pathogen reach a human host, they do so through fundamentally different biological processes.

This is one of the most important concepts to understand. The origin of an organism and its transmission cycle are two separate questions. Even if someone were to propose an unusual origin for a pathogen, once that organism exists outside the laboratory, it is still governed by biology. It cannot ignore the rules of its own life cycle. Lyme disease still depends on ticks and animal reservoirs to maintain its natural transmission cycle. Cyclospora still depends on infected humans shedding oocysts, those oocysts maturing in the environment, and contamination of food or water before another person can become infected.

Every infectious organism is constrained by its own biology. It must spread according to the mechanisms that allow it to survive and reproduce. Understanding this distinction helps separate two very different scientific questions. One question asks where an organism originated. The other asks how that organism spreads once it exists. Those are related questions, but they are not the same question, and the answer to one does not automatically determine the answer to the other.

Transcript

Sam Bailey ➝ 00:00

Over and over again, we hear the media stating how many people have tested positive for COVID-19. The problem is that this makes no sense at all. Today I’m going to explain why, as we dig deeper into PCR tests once again, and have a look behind the curtain of this COVID pandemic. [music]

Sam Bailey ➝ 00:22

The purpose of using tests and clinical medicine is to distinguish between having or not having a particular condition or disease.

Sam Bailey ➝ 00:31

For example, as a patient with chest pain, having or not having a heart attack. As a woman who missed her period, pregnant or not. But a test and a condition are not the same thing. I’ve never had a woman come into my clinic and say, I think I might be positive for pregnancy. She either has a positive or negative pregnancy test and her condition as either pregnant or not pregnant.

Sam Bailey ➝ 00:54

All tests detect something. Let’s call it the object of interest and most go further and determine how much. For example, we may check the blood concentrations of glucose and cholesterol. These are direct tests, meaning the object of interest is the test, but there are many indirect tests where what is being measured as a reliable surrogate for the object of interest.

Sam Bailey ➝ 01:17

For example, when you have a heart attack, a doctor will measure an enzyme [troponin] that leaks from your damaged heart muscle cell, rather than chopping out a piece of your heart muscle to examine it under a microscope. Some tests such as home pregnancy tests are classified as positive or negative. Pregnancy tests become positive at a certain threshold of hormone [human chorionic gonadotropin] being detected in the urine, which had been reliably established over a long period of time. We use indirect tests because they are simple, safe, quick and cheap, but indirect have a caveat – before they are introduced into routine clinical practice with real patients, it is absolutely essential to determine how well they match the object of interest. There are long established scientific methods for doing this. Obviously this involves evaluating the test against the object of interest whose presence or absence is determined independently of the test.

Sam Bailey ➝ 02:13

So now that we’ve established the rules, let’s get into COVID-19. The mainstream theory is that a new virus called SARS-CoV-2 is the cause of a new disease called COVID-19. The test for SARS-CoV-2 is not for the whole virus, the complete sublight microscopic particle itself. Perhaps most familiar is this computer generated image that we see on the news. The test is supposed to detect a 1% fragment of an RNA molecule, its genome said to reside inside the virus particle. Based on its detection, a person is deemed infected with the virus SARS-CoV-2, because this tiny fragment is regarded as defecto for a hundred percent of the viruse’s RNA. It could be seen as finding a horse like hair is evidence of the horse itself. This is problematic for three reasons.

The detonator for the worldwide explosion of so-called COVID-19 PCR testing was the Corman-Drosten group paper published on 23rd of January 2020 and critically the paper was accepted for publication within 24 hours of submission, and several authors failed to declare their financial conflicts of interest with a commercial PCR test lab.

Sam Bailey ➝ 04:21

Also somewhat unusually version 1.0 of the paper protocol appeared on the WHO website nine days before the paper was even accepted for publication, but the Corman-Drosten paper was just a lab study, meaning it didn’t establish the validity of using the test in the real world. No evidence was provided about how a positive test related to the condition of COVID-19. As I’ve discussed in previous videos, this wasn’t the only problem with this paper. And on the 26th of November, 2020, a consortium of health professionals and scientists sent a reattraction request letter to Eurosurveillance outlining their multiple concerns. I believe they are still awaiting a response. Back in January, 2020, however, it was too late. And a test that had no track record was promoted to the world as the best way to diagnose COVID-19.

Sam Bailey ➝ 05:12

When the mainstream media and government scientists started telling the public that the COVID-19 PCR tests were 95% or 99% accurate, it was not made clear to the public, what that actually meant. In New Zealand for instance, the ministry of health website stated, and this is in February, 2021, that a recent laboratory study found that different COVID-19 testing kits correctly detected COVID-19 and samples more than 95% and frequently a hundred percent of the time. This statement is problematic for many reasons, including confusing COVID-19 the condition with SARS-CoV-2, the alleged virus. The RT-PCR does not test for COVID-19 in samples. And if correctly detected means accuracy, the letter cannot be determined without first evaluating the true positive and true negative rates of the RNA test for infection with SARS-Cov-2. But this has never been established. What is detected in a sample is not COVID-19. What is detected as a small piece of RNA.

Sam Bailey ➝ 06:17

So it seems likely that the ministry of health has confused the analytical specificity of the test with its diagnostic specificity for the condition. Analytical specificity in this case is how well the test can accurately detect a target RNA sequence. So if a SARS-CoV-2 RT-PCR kit has a hundred percent analytical specificity, it tells you that it never picks up the wrong RNA molecule, but you can’t get too excited because that’s like saying that your blood glucose test never picks up your blood cholesterol. What we need to know is the diagnostic specificity, which is the probability that the test will be negative when the condition is not present.

February 9, 2021 “Also somewhat unusually version 1.0 of the paper protocol appeared on the WHO website nine days before the paper was even accepted for publication” Dr Sam Bailey For example, a pregnancy test that has a hundred percent diagnostic specificity would mean we expect all non-pregnant woman to test negative. Therefore, even if a SARS-CoV-2 RT-PCR kit has a hundred percent analytical specificity, it is still meaningless as a test for viral infection without proof of the diagnostic specificity determined against the virus. And this has never been established at all. It has been amazing to see in recent times that some virologists have tuned into chemists under the spell of PCR. I was stunned to hear Australian professor of neurology, Bill Rawlinson, make the following statement last year on a broadcast: With basic science and improving diagnostics and the ability to sense a molecule, and after all a virus, is just a piece of RNA molecule.

Sam Bailey ➝ 07:48

Interestingly, after he made the statement, none of the panel of experts joining him on the broadcast, even called him out on this. Maybe this was just a slip-up on the professor’s part, but this sort of thing could be adding to the confusion. So it’s important that those of us that respect logic and the scientific method will not allow analytical specificity to be merged into diagnostic specificity, and then passed off as a valid medical practice. However, the lack of formalized clinical diagnostic criteria for COVID-19 seemed to allow the slight of hand to be hidden in plain sight. I made a video titled What is a COVID-19 Cas, in late 2020, addressing this very issue In my presentation, I show that the WHO’s official documents states that are confirmed COVID-19 case is a person with laboratory confirmation of COVID-19 infection, irrespective of clinical signs and symptoms.

This was a bad look for the WHO because it openly admitted that cases were not required to be related to disease. Just three days later, they removed the statement and published a completely revised document. While the new version looked more scientific, essentially nothing had changed as a confirmed case, could still be a person with a positive nucleic acid amplification test. So any old positive PCR will do, to edge of the smoke screen, the WHO website released another PCR update on the 20th of January, 2021, stating the assays are indicated as an aid for diagnosis.

Sam Bailey ➝ 09:27

On the 11th of November, 2020, the COVID-19 PCR tests hit some of their first major legal problems. Judges and the Lisbon court of appeal delivered some decisive rulings, including in view of current scientific evidence, this test shows itself to be unable, to determine beyond reasonable doubt that such positivity corresponds in fact, to the infection of a person by the SARS-CoV-2 virus – that I can certainly agree with. They also said the test reliability depends on the number of cycles used, which is being far too generous because no diagnostic specificity was ever established. So cycle thresholds are meaningless in this regard as well. February 9, 2021 “When the mainstream media and government scientists started telling the public that the COVID-19 PCR tests were 95% or 99% accurate, it was not made clear to the public, what that actually meant.” Dr Sam Bailey Don’t get me wrong. I’m not saying that reducing cycle threshold requirements for a positive case, wouldn’t be a good start. It’s likely that a cycle threshold of say 25 down from the 40 cycles, typically being used would result in such a dramatic decrease in cases that panicked policymakers would be forced to concede that they’ve been swept up in a PCR pandemic with regards to even 36 or 37 cycles being classified as positive for COVID-19 PCR expert.

Sam Bailey ➝ 10:33

Professor Steven Bustin stated back in April 14, 2020, it’s absolute nonsense. It makes no sense whatsoever. From his point of view, once you get above a cycle of about 35, that would be roughly equivalent to a single copy of target RNA and what a single piece of RNA, it would be absurd to conclude that a person is infected. I really encourage you to listen to Professor Bustin explaining the limits of PCR and I’ve linked his interview with the late David Crow below. The inventor of the PCR Gary Mullis had even less faith in its application for detecting infections: Separate from that. It’s just a process that’s used to make a whole lot of something out of something. That’s what it is. It’s not… It doesn’t tell you that you’re sick. And it doesn’t tell you that the thing you ended up with really was going to hurt you or anything like that. Source: A Layperson’s Guide to the PCR Based Epidemic Hoax — Dr Sam Bailey

“How much money are we talking about?”, the answer is many billions of dollars.

Some reference points:

On the company side:

So if you’re looking at the economics of testing, you’re not talking about millions of dollars—you are talking about tens of billions of dollars globally, with the U.S. federal government alone spending several billion dollars on purchasing and distributing home tests, and much larger sums when laboratory PCR testing, reimbursement, and testing infrastructure are included.

As a historical topic, it’s a fascinating one because it asks:

How large did the COVID testing industry become between 2020 and 2023?

One of the largest diagnostic testing markets ever created in such a short period of time.

There are relatively few parasites where humans are considered the principal or only essential host for maintaining the transmission cycle. Here’s a list of the best-known examples.

Now compare those with parasites that have important animal reservoirs:

Cyclospora is not unique because it is human-associated.

It is unusual because it combines several characteristics:

That combination is uncommon.

Cyclospora is first recognized in Papua New Guinea by R. W. Ashford, but it is misidentified. There is no food-testing method because scientists are still trying to determine what the organism even is.

Researchers identify Cyclospora in stool samples using microscopy and special stains. There is essentially no practical method to test lettuce, herbs, or irrigation water before harvest.

Large outbreaks associated with imported produce (especially raspberries) drive interest in detecting Cyclospora on food itself.

Researchers begin adapting PCR (DNA testing), but these are research tools rather than routine field methods.

FDA successfully detects Cyclospora in a chicken pasta salad containing fresh basil linked to an outbreak using an early laboratory method.

FDA and CDC detect Cyclospora in raspberry filling from a wedding cake associated with another outbreak.

The original FDA detection method effectively disappears because key equipment and supplies are no longer manufactured. FDA later acknowledged it could no longer routinely perform the old method.

FDA establishes its Foodborne Parasitology Research Program specifically to develop a new, more sensitive Cyclospora detection method.

The new method completes validation among FDA laboratories.

FDA adds a standardized laboratory method for detecting Cyclospora in agricultural water using dead-end ultrafiltration.

FDA continues updating the PCR method with additional produce types (romaine, basil, parsley, blueberries, blackberries, shredded cabbage, carrots, etc.) and improved PCR targets

From roughly 1979 to today—almost 50 years after Cyclospora was first described—we still do not have a routine, practical field test that growers use to certify lettuce fields are free of Cyclospora before harvest.

Instead, the advances have largely been in:

Some of the reasons are: