Pseudomonas aeruginosa: Attack of the “epidemic clones”: How a harmless bacterium caused half a million deaths a year | Health and well-being

It took bacteria 200 years, just a microsecond on the human timeline. Pseudomonas aeruginosa They have gone from being harmless microbes that inhabited ponds, streams and plants to one of the greatest infectious threats on the planet. The bacilli, which cause more than 500,000 deaths a year, are now blacklisted by the World Health Organization as a “high priority” pathogen due to their resistance to antibiotics and widespread distribution around the world. The investigation is published Thursday in the journal The science mapped the genomic journey of this species of bacteria and found that P. aeruginosa They take advantage of the immunological defect in cystic fibrosis patients to survive and continue their existence.

“Over the last 200 years or so, some individual bacteria, which we call clones, have managed to absorb new genes and become more capable of infecting humans. These clones then expanded and spread around the world. The most likely date for the spread of the first clone is around 1890, although the confidence interval is wide,” explains scientist Andres Floto, professor of respiratory biology at the University of Cambridge and author of the study. To these family tree branches P. aeruginosa that have spread around the world, the authors call them “epidemic clones.” The study identified about 21 viruses that are responsible for more than 50% of all infections caused by P. aeruginosa on the planet. “They are probably the main causes of antibiotic resistance and mortality,” the researcher muses in an email response.

That malignant tumor that P. aeruginosa It is relatively young. Having studied the family tree of this species, the authors cautiously suggest that the starting point of this whole phenomenon is the end of the 18th century. “It is unlikely that before that date they would have posed a significant threat to human health,” agrees Flotho.

Since the early 19th century, the researcher notes, “these epidemic clones have been appearing more frequently.” The authors believe that each of them experienced at least one corresponding population increase between 1850 and 2000. “They have arisen randomly around the world, but they seem to be expanding with increasing frequency. For example, from 1900 to 1950, six epidemic clones arose; and between 1950 and 2000, 12 appeared,” Floto illustrates.

These phenomena of global expansion among humans, according to the scientist, continue to occur with increasing frequency: “We are seeing more and more epidemic clones appearing and spreading around the world, which we think may be related to air pollution and built-up density.” The authors suggest that the spread of these more aggressive families of bacteria has accelerated with urban overcrowding, a product of migratory movements to large cities during industrialization: there was a breeding ground for densely populated areas and increased pollution, leading to greater susceptibility to infections and greater ease of spread of these infectious conditions.

Today P. aeruginosa They have become opportunistic pathogens. This means that they do not harm healthy people, but they cause pulmonary and systemic infections in people with a weakened immune system. For example, people with chronic obstructive pulmonary disease (COPD) or cystic fibrosis. Infections caused by these bacteria have been reported in patients admitted to hospitals (nosocomial infections) and in community settings. “This issue is at the forefront of all health authorities,” explains Bruno González-Zorn, director of the Antimicrobial Resistance Unit at the Complutense University of Madrid and an adviser to the World Health Organization (WHO) in this area: “It is very important. It has an extraordinary ability to adapt to many ecosystems, and what worries us is the level of antibiotic resistance and the number of patients it kills each year.”

By analysing almost 10,000 samples of the microorganism from people, animals and the environment, Cambridge researchers were able to trace the microorganism’s family history. P. aeruginosabut they also identified a mechanism of bacterial tolerance that may be key to understanding their resilience. In samples from cystic fibrosis patients, the scientists found that macrophages, the immune cells responsible for engulfing and destroying harmful microorganisms, were unable to eliminate harmful microorganisms. P. aeruginosa: These clones were able to survive inside macrophages and establish a persistent infection.

The scientists believe that the ability of some of the epidemic clones to survive in macrophages is a combination of the bacteria’s genetics (they have identified the gene involved) and a glitch in the body’s defenses in people with cystic fibrosis. “The bacteria take advantage of this immunological defect to infect this group of patients,” Floto says.

More dangerous and effective

During this succession of generations infecting people, these bacteria evolved, adapting through mutations in their DNA to become more effective at infecting the lungs and more virulent in fighting the scourge of antibiotics. Another finding of these researchers is that these multiple stages of adaptation to the lungs and subsequent transmission to another person occur differently for the bacteria that infect patients with cystic fibrosis compared with the bacilli that infect people without the disease. “The bacteria become increasingly specialized, and some clones continue to transmit between patients with cystic fibrosis, while other clones transmit between patients without the disease. But these specialized bacterial clones lose the ability to transmit from patients with cystic fibrosis to patients without it, and vice versa,” he says.

María del Mar Tomas, a microbiologist at the University Hospital Complex of A Coruña and a representative of the Spanish Society of Infectious Diseases and Clinical Microbiology (SEIMC), emphasizes the importance of this study, in which she was not involved, to deepen our knowledge of the mechanisms of bacterial tolerance and resistance. These molecular systems help the bacillus survive stress. “This is very important because these are global mechanisms that are activated in any stressful situation for bacteria, such as starvation or taking an antibiotic. And this could become a therapeutic target for the development of new treatments.” González-Zorn says in the same vein: “This is a relevant study because it allows us to understand the evolutionary trajectory of bacteria and how they manage to develop strategies that cause disease. “If we know these mechanisms, we can develop strategies to contain these bacteria.”

The authors, for their part, warn that their findings highlight “the importance of global surveillance and prevention of cross-contamination to avoid the emergence of future epidemic clones.” “We have indications that epidemic clones will become increasingly adapted to human lungs and will become increasingly resistant to antibiotics if they are allowed to continue this cycle of infection, adaptation and transmission,” warns Floto.

Given the speed at which epidemic clones emerge, the researcher urges us to actively seek them out to prevent their spread, and to quickly detect bacteria in the lungs to eradicate them as quickly as possible. In this sense, although there are control measures to prevent infection P. aeruginosa In cystic fibrosis, the scientist reminds us that his results show that transmission between people “also occurs very frequently in people without cystic fibrosis,” which makes us think about how to protect these other risk groups.

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