My personal journey to understanding that our microbial friends were having problems began on July 9, 1977. This date is well remembered – that’s when I first heard the name of the microbe Campylobacter, which literally gave rise to the cause of my life. I was a new graduate student at the infectious diseases Department at the University of Colorado medical center in Denver.

That morning, I was asked to examine a 33-year-old patient who had arrived at the hospital a few days earlier. He was suffering from a high fever and disorientation. Spinal puncture determined his meningitis-a serious inflammation of the nervous system. The doctors sent blood and cerebrospinal fluid samples to the Microbiology lab to determine if it was a bacterial infection, and if so, to find out which one. While the tests were being prepared, the patient was prescribed antibiotics because he looked terrible. The doctors thought that if you do not immediately give a large dose of drugs, he will die. And they were right.

Tests have shown the presence of the slow-growing bacteria Campylobacter fetus, an organism that no one in the hospital has ever heard of. That’s why they called me and gave me nine days to find out what was going on.

Campylobacter is a genus of spiral-shaped bacteria. Like small corkscrews, they, thanks to their shape, penetrate through the jelly-like mucus, which covers the walls of the gastrointestinal tract. But why does the species have such a strange name-fetus? (In biology, each organism is defined first by the genus name, in this case – Campylobacter, and then – species, in this case – fetus. There are many species and subspecies in each genus. People, for example, – Homo sapiens: genus Homo, species sapiens.) Digging through the medical literature, I found that the microbe got a strange name because it infected pregnant sheep and cows causing miscarriage. In humans, it is extremely rare. How our patient contracted it is a mystery. After all, a city dweller, a musician.

After we learned the name of the “culprit“, picked up the appropriate antibiotics for treatment, and two weeks later the young man recovered. I, meanwhile, had to give a lecture at a clinical conference, and I decided to choose the Campylobacter theme. It’s great to talk about a rare infection that no one really knows about. At the same time, there was hope that no one would notice my beginner ignorance.

Reading about Campylobacter fetus, I soon found out that she has a “cousin” – Campylobacter jejuni (in Latin – “jejunum”). Literature was not very much, but it was possible to find out that people affected by the bacteremia (the presence of bacteria in the blood), and most often causes diarrhea. Two almost identical organisms behave quite differently in our body. Why one remains in the intestine where he was, in fact, the place, and the other runs away like a ninja in the circulatory system?

Over the next few years, moving from teaching staff to Centers for disease control and prevention and back again (Colorado state University and Vanderbilt University), I’ve become a real expert on “the bacteria that I love” and discovered some secrets that explain Houdini’s dexterity.

From this point of view, fetus played an important role in the evolution of my vanishing microbiome hypothesis by teaching a fundamental lesson: I learned how bacteria can survive in their carriers. Yes, they cause diseases, but, as it became clear later, we live in micro-organisms that use a variety of similar tools to hide from the immune system. Usually they do not harm, even on the contrary-protect. In their business, bacteria use countless tricks, honed by millions of years of trial and error. And can either help or harm the carrier depending on the circumstances. This idea we will consider in more detail.

The fetus, in particular, told me about the disguise – how microorganisms acquire the ability to avoid the host system. And 99.9 % of all bacteria, including the one with the blood substances, but the one with the blood gets into the bloodstream, putting on a kind of “invisible mantle“. However, even it can fall into the prisoner cells of the healthy liver. But if it is not cleaned out of the blood of a person with a liver disease (later I learned that the very young patient was a chronic alcoholic), it can lead to meningitis.

While I was in the early 80’s he worked with C. fetus and C. jejuni, opened their cousin, oddly enough, in the stomach. Then it was called “gastric Campylobacter-like organism” (“GKPO”), and now – Helicobacter pylori.

As it turned out, she has a considerable set of tricks and, like Jekyll and Hyde, can either harm us or protect. I have been chasing this organism for twenty-eight years with faith (and hope to prove) that it can become a guiding star in solving the mystery of the “plague of modernity”.

Our first meeting took place in October 1983 at the Second international conference on Campylobacter infections in Brussels. There I met Dr. Barry Marshall, a young doctor from Australia, who opened the GKPO and said that he causes gastritis and stomach ulcers. Nobody believed him. At that time, they “knew” that they are caused by stress and excess gastric juice. I, too, was skeptical about this idea and, of course, immediately realized that the scientist discovered a new bacterium. But, as for me, convincing evidence that it causes an ulcer, was not provided.

Only two years later, when other scientists confirmed the connection of the microbe with gastritis and peptic ulcer disease, I decided to see if I could contribute to the study of gastrointestinal TRACT (in 1989, the bacterium was renamed Helicobacter pylori, finding that it is separate from Campylobacter species). They are relatives about the same distance as the lion (Pantera leo) and the domestic cat (Felis catus): there are some similarities, but the differences are quite large, due to which they can be attributed to different genera. My laboratory has developed a blood test for this microbe and showed that if it lives in your body, then you have a natural protection against it.

But doctors declared war on pylori not for life, but for death, prescribing antibiotics for any gastric discomfort. Their motto was the phrase “Good H. pylori a dead H. pylori”. I, too, belonged to this camp almost ten years.

However, by the mid-nineties changed his mind. Evidence has begun to accumulate that pylori is part of the normal microflora of our gut {10} and plays a huge role in health. Only by abandoning the dogma that proclaimed “gastritis is bad”, it was possible to re-evaluate the biology of this bacterium. Yes, it spoils the lives of some adults, but later we learned that it is very useful for children. Destroying it can do more harm than good.

A great achievement of Marshall and his research partner Robin Warren was the clinical studies that showed that the destruction of H. pylori with the help of antibiotics cures ulcer. Others confirmed and expanded observations. For this discovery, scientists received the Nobel prize in physiology or medicine in 2005.

In 2000, I went to new York University and set up a laboratory there to find out what this ancient bacterium was doing in our stomachs and what the consequences were. In fourteen years, there has been a great deal of evidence that the disappearance of this venerable microbe may have been one of the causes of the current epidemics. And then pylori led me to a broader study of the human microbiome as a whole.

There’s a lot of fuss in my lab right now. We are working on more than twenty projects – observing how antibiotics act on microbes and their carriers, conducting experiments on both mice and humans. In a typical animal experiment, we give them drugs in drinking water and compare them to those who don’t. Research begins very early, sometimes even before the birth of a baby. Then we give to grow up and monitor the conditions and changes: how thick they become, how the liver works, how immunity is produced in the intestine, how the bones grow, what happens to hormones and the brain.

This is a very interesting work, because in each of the areas we see changes caused by antibiotics, and at an early stage of life. It became clear that infancy is a key window of vulnerability. At a very young age, there are critical periods of growth, and our experiments show: the loss of friendly intestinal bacteria at this stage of development leads to obesity – at least in mice. We also conduct research on social development and celiac disease. We have a lot of ideas about how to apply this data about mice to humans. The main goal is to help recover from the damage, including the development of strategies for the return of the disappeared microbes. A key step in all these strategies is to reduce the dosage and frequency of antibiotics in children, and the sooner this happens, the better.

My Odyssey, which began almost thirty-seven years ago, after the very patient with meningitis, convinced me that now – the most important stage of my career. Years of work as an infectious disease doctor and scientific experiments helped to form their own point of view on the”plague of modernity”. I didn’t expect this to happen. But as if pushing, work carried me through valleys and mountains and oceans of scientific medical research. It also led to new ideas about the changing modern life, which I want to share with you. Today’s” plague ” is not the one that took the lives of my father’s sisters, but no less deadly.

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