Where did the intestinal inflammation come from?

In 1859, a judge sentenced a London doctor, Thomas Smethurst, to death by hanging for the murder of his beloved, forty-three-year-old Isabella banks. The woman died of diarrhea and a fever that looked suspiciously like poisoning, and doctors said they found traces of arsenic in her feces.

However, no poison was found during the second examination. A subsequent autopsy showed a large number of ulcers and scars in the woman’s colon, which served as evidence not of a violent death, but of a prolonged illness.

“Such acute inflammation of the colon, whatever its origin, can in itself lead to death,” wrote Samuel Wilkes, the doctor who performed the autopsy. Smethurst was pardoned by the Queen, but was later convicted again — for bigamy. (He was already married when he married Isabella banks.)

Meanwhile, Wilkes called the disease that banks suffered from a simple ulcerative colitis. Although there have been at least two previous descriptions of a similar disease (accompanied by inflammation and scarring for no apparent reason), historians generally consider Wilkes ‘ detailed description of the disease to be the first confirmed case of inflammatory bowel disease.

At the end of the nineteenth century, the spread of the disease accelerated markedly, especially in London and Dublin. Between 1883 and 1908, more than three hundred patients with intestinal inflammation, which causes debilitating pain, were admitted to London hospitals. At the time, treatments for the disease included large amounts of sour milk, opium, and enemas with antiseptics such as boric acid and silver nitrate. Almost half of the patients (141 people) died from this disease.

During the first decades of the twentieth century, there were new reports of unexplained cases of intestinal inflammation in France, Germany, and Italy. In 1909, when the microbial theory was already recognized, scientists held a meeting at the Royal society of London to discuss this strange and often fatal disease that occurs when there are no obvious causes. They are used to dealing with cases of infectious dysentery, intestinal tuberculosis, and various intestinal tumors, but where does the inflammation come from in the absence of infection?

According to the first descriptions, this disease affected a disproportionately large proportion of the upper classes — “well-off, well-fed people with excellent health”, as the London doctor William Allchin said. Of course, this pattern was in direct contrast to the spread of infectious diseases such as cholera and typhoid, which often occurred in malnourished people living in cramped, dirty conditions.

Then in 1932, Burrill Bernard Krohn presented his work at the American medical Association conference in New Orleans. He described in this work “inflammation that causes chronic necrosis and scarring” — an inflammatory process that leads to thinning of tissues, scarring and intestinal spasm. The fourteen patients (all Jews) were mostly young and in the Prime of life. Kron called this ailment terminal ileitis (inflammation of the ileum), and then regional ileitis. (The ileum is the last segment of the small intestine about three meters long.) Over time, gastroenterologists started calling this disease Crohn’s disease.

Weinstock believed that the accelerated spread of inflammatory bowel diseases among the upper classes after the industrial revolution occurred simultaneously with the loss of parasites (it should be noted that this occurred in the same population group in which the number of cases of hay fever first increased sharply). The preponderance of Jews from new York among patients with Crohn’s disease also pointed to helminths-or the absence of them. In the United States, new York became the first major city to restore order by providing residents with drinking water, organizing garbage collection, sewage treatment, and paving streets. Weinstock suggested that dietary restrictions (avoiding pork and treating meat with salt) reduced the number of Jewish contacts with parasites to a greater extent than in all other population groups. And the newfound prosperity (even such simple things as shoes were of great importance) further limited the infection with helminths.

In other parts of the country, helminth infection remained fairly common for much of the twentieth century. In the case of a sixth of the autopsies performed in the late 30s, cysts of spiral Trichinella (Trichinella spiralis) were found-a terrible helminth that chews through the muscles and brain, which enters the human body as a result of consuming raw or undercooked pork. However, in the 60s, Trichinella was found in only 4.2% of autopsies. (Today, the centers for disease control and prevention records no more than 25 cases of trichinosis per year, mostly in hunters who eat undercooked Cougar and bear meat.)

Of course, Trichinella was not the most common helminth in the United States. In 1909, when employees of the newly created Rockefeller Foundation went to destroy hookworms in the South-Eastern regions of the country, parasites were found in about 40% of the children examined. Employees paid for by the Foundation spread out across the southern United States to teach people how to build and use latrines during rural fairs. Dig a hole away from streams, wells, and other water sources. Cover it when not in use. Fill the sump with earth. If necessary, fill in the hole, dig a new one, and move the restroom to a new location.

Hookworm control measures, based mainly on awareness-raising, have been extremely effective. In the 1910s, 61% of Florida residents had hookworm. In 30 years this figure has decreased almost two times — up to 34%. In the 50s, the prevalence of infection with these helminths decreased by another half — to 18%. Other States have seen similar improvements. The prevalence of hookworm in South Carolina dropped from 37% in the 10s to 24% two decades later. (In the late ‘ 80s, only 2% of southern residents showed signs of helminth infection.)

Still, it was some time before the Americans were completely free of helminths. According to some estimates, at the end of world war II, about a third of the inhabitants of North America and Europe (residents of industrialized countries, supposedly at the forefront of civilization) were carriers of helminths. Many children (60 to 80%) on both continents had pinworms, the main symptom of which (anal itching) was so harmless compared to the symptoms of other helminths that it was often ignored during health campaigns.

“It is impossible to survive a war without being overwhelmed and oppressed by the number of parasites in the world,” said parasitologist Norman Stoll in a 1947 speech that is now considered a classic. For greater effect, Stoll calculated the total weight of microscopic eggs laid by giant roundworms in the bodies of 335 million infected inhabitants of China per year. He estimated that this weight would reach 18,000 tons, which is about the same as the weight of a hundred very large blue whales.

By the middle of the twentieth century, we had already invented airplanes and automobiles, mastered the secrets of atomic energy, and were ready for the beginning of the space age. However, despite all these outstanding achievements, the parasites continued to infect people in the United States and around the world. Progress in the eradication of parasites has been erratic. In some localities, they existed for decades after disappearing elsewhere. In fact, it is this very uneven process of destroying parasites that, in Wainstock’s view, has largely helped explain the equally uneven prevalence of inflammatory bowel diseases.

African-Americans remained infected with helminths longer than whites, which was a consequence of complex race relations in the country. The same thing happened to other national minorities who were disadvantaged, such as the Cherokee who lived on a reservation in North Carolina. Belonging to the white race did not always protect against infection with helminths. In 1965, a survey of residents of poor Clay County in Kentucky found helminths in two-thirds of those surveyed. Poverty, which at the beginning of the twentieth century protected against inflammatory bowel diseases, created highly favorable conditions for helminths.

In General, this pattern was the opposite of the spread of inflammatory bowel diseases in the United States. After Dr. Kron first described the disease in new York, it spread beyond its borders. At first, intestinal inflammation affected white residents of the North-Eastern regions of the country. (President John F. Kennedy, who was born into a wealthy Massachusetts family, suffered terribly from colitis throughout his adult life.) Ten years later, white southerners noticed an increase in the prevalence of this disease. In the 70s, more cases of intestinal inflammation were reported among black residents of the Northern and southern States. And in the 90s, native Americans who left their reservations began to suffer from this disease more often. However, those who remained on reservations had relatively few inflammatory bowel diseases. Weinstock estimates that about a decade after a community got rid of helminths, there was an increase in cases of inflammatory bowel disease.

A large gap in the Weinstock hypothesis occurred in the part of the so-called “global South”. He knew that helminth infections were widespread in Africa, South America, and South Asia, but there was very little data on the prevalence of inflammatory bowel diseases in these regions. What did this apparent lack of data mean — a real lack of data or limited diagnostic capabilities? Weinstock and Elliott started asking this question at various conferences. They found that African and Asian doctors often study in Europe and North America. These doctors knew the symptoms of inflammatory bowel diseases and simply did not observe these symptoms in those populations where there were not only many cases of helminth infection, but also many cases of malaria, dysentery and other infectious diseases.

In fact, in 1988, more than 130 years after Samuel Wilkes described Isabella banks ‘ ulcerative colitis, a doctor in Soweto, South Africa, registered the “first 46 patients” treated there for ulcerative colitis. He also noted that these patients are from Johannesburg, not rural areas. In addition, they mostly belonged to the “higher educated class” and to “categories of the population with higher education”.

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