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7NEWS
03-06-2025
- Health
- 7NEWS
Gene mutation found in the bacterium behind the Black Death helped plague conquer the world, scientists say
One of the bleakest periods in medieval Europe was the plague pandemic known as the Black Death, which killed at least 25 million people in just five years. But the disease didn't stop there. The plague adapted to keep its hosts alive longer, so it could spread farther and keep infecting people for centuries, and researchers now say they've discovered how. The disease is caused by the bacterium Yersinia pestis, which has been circulating among human populations for at least 5000 years. The pathogen has fueled three major plague pandemics since the first century AD, and though its deadliest years appear to be behind us, plague hasn't disappeared. Cases still occur a few times a year in Asia, South America and the United States and more commonly in parts of Africa, according to the Cleveland Clinic, and can be treated with antibiotics. Scientists are still searching for answers about how Y. pestis evolved and dispersed, but recent analysis of ancient and modern Y. pestis samples revealed how plague managed to persist among humans for hundreds of years after pandemic waves petered out. After an initial period of high infection rates and rapid mortality — killing infected people within three days — changes to just one gene in the bacterium produced new strains that were less deadly and more transmissible, according to research published Thursday in the journal Science. Those weakened strains eventually went extinct; the dominant lineage of today's Y. pestis is the deadlier variety, the study authors reported. However, these findings about historic instances of Y. pestis adaptation could provide important clues to help scientists and physicians manage modern plague outbreaks. Trio of outbreaks Plague's most common form is bubonic plague, which causes painful swelling in lymph nodes and spreads among people through bites from fleas hitchhiking on infected rats. An outbreak of bubonic plague from 1347 to 1352 in Europe famously killed about 30 to 50 per cent of the continent's population. But the earliest known bubonic plague outbreak — the Plague of Justinian — took hold in the Mediterranean Basin and lasted from AD 541 to AD 544. Another plague outbreak emerged in China in the 1850s and sparked a major epidemic in 1894. Scientists view modern plague cases as part of this third pandemic. For the new study, scientists collected ancient samples of Y. pestis from human remains dating back to about 100 years after the appearance of the first and second plague pandemics, sampling remains from Denmark, Europe and Russia. After reconstructing the genomes of these plague strains, they compared them with older, ancient strains that dated back to the start of plague pandemics. The researchers also examined more than 2700 genomes of modern plague samples from Asia, Africa, and North and South America. One of the study coauthors, Jennifer Klunk, is a product scientist at Daciel Arbor Biosciences, a biotechnology company in Michigan that provided synthetically created molecules for the experiments, but there was no financial gain associated with the research. The researchers found that their newly reconstructed genomes from 100 years into the first two plague pandemics had fewer copies of a gene called pla, which has been recognised for decades as one of the factors that made plague so deadly, according to the study's co-lead author Ravneet Sidhu, a doctoral student in the McMaster Ancient DNA Centre at McMaster University in Ontario, Canada. Pla encodes an enzyme that interacts with host proteins, 'and one of the functions that it carries out is in breaking down blood clots,' Sidhu told CNN. This ability helps Y. pestis spread into the host's lymph nodes, where it replicates before attacking the rest of the body. 'Not every function of this gene is fully known,' Sidhu added. However, prior studies by other researchers linked pla to severity of illness caused by both bubonic and pneumonic plague — an airborne form of the disease that affects the lungs, she said. While the reconstructed strains showed fewer copies of the pla gene, the scientists were still uncertain whether that would directly affect how deadly the disease could be. So they tested strains of reduced-pla bubonic plague on mice, and found that survival rates for this type of plague were 10 to 20 per cent higher in those experiment subjects than in mice infected with Y. pestis that had a normal amount of the pla gene. It also took the reconstructed bubonic strain about two days longer to kill its hosts. 'The paper presents a strong argument that depletion, but not total loss, of Pla (the enzyme produced by the pla gene) is part of the evolution of the plague pathogen and may help explain the decline of plague in the second pandemic commonly known as the Black Death,' said Deborah Anderson, a professor of veterinary pathobiology at the University of Missouri's College of Veterinary Medicine. Anderson, who was not involved in the new research, investigates the virulence of plague, and these findings could shed light on transmission patterns in modern cases, she told CNN in an email. 'Our laboratory studies the flea-rodent cycle and we have collaborators who conduct field research in areas that experience annual or occasional plague outbreaks in the wild,' Anderson said. 'There are nearly 300 rodent species that can transmit Yersinia pestis, and today, burrowing rodents such as prairie dogs or ground squirrels are considered key animal hosts that experience outbreaks of disease,' she added. 'After reading this paper, we will pay closer attention to Pla in the future to see if there continues to be a role for its expression in driving the explosive outbreaks of plague in the animal populations.' 'Epidemic burnout' Mathematical models suggested how this might have played out in human populations centuries ago, leading to an 'epidemic burnout' about 100 years after a bubonic plague outbreak. In a pandemic's early stages, infections were swift, and death came quickly for both rats and humans. Over time, as dense rat populations thinned out, selective pressures favoured the emergence of a less deadly strain of Y. pestis, with fewer copies of the pla gene. Rat hosts infected with this new strain would have a little more time to carry the disease, potentially enabling them to infect more rats — and more people. 'They suggest a model that can be readily pursued in the laboratory that may help explain the spread of plague today in the wild,' Anderson said. These weaker strains of the disease eventually sputtered out and went extinct. In the modern samples, the researchers found just three examples of strains with reduced pla genes, from Vietnam: one from a human subject and two from black rats (Rattus rattus). 'We've been able to do this really cool interdisciplinary study between the modern and ancient data and marry these things that have been happening throughout (the plague's) long evolutionary history,' Sidhu said. 'It could be interesting to see how future researchers continue to try and bridge that gap between the modern third pandemic and those first and second ancient pandemics, to see other similarities. Because there aren't a lot of ancient pathogens that we have as much data on, as we do for Yersinia pestis.' One of the unusual features of plague pandemics is their persistence, and understanding how Y. pestis changed its infection patterns and survived over time could shed light on the adaptive patterns of modern pandemics such as COVID-19, she added. 'Even if we aren't experiencing it to the amount that we were in 2020 or 2021, the pathogen is in the background — still evolving and persisting.'
CNN
03-06-2025
- Health
- CNN
Gene mutation found in the bacterium behind the Black Death helped plague conquer the world, scientists say
One of the bleakest periods in medieval Europe was the plague pandemic known as the Black Death, which killed at least 25 million people in just five years. But the disease didn't stop there. The plague adapted to keep its hosts alive longer, so it could spread farther and keep infecting people for centuries, and researchers now say they've discovered how. The disease is caused by the bacterium Yersinia pestis, which has been circulating among human populations for at least 5,000 years. The pathogen has fueled three major plague pandemics since the first century AD, and though its deadliest years appear to be behind us, plague hasn't disappeared. Cases still occur a few times a year in Asia, South America and the United States and more commonly in parts of Africa, according to the Cleveland Clinic, and can be treated with antibiotics. Scientists are still searching for answers about how Y. pestis evolved and dispersed, but recent analysis of ancient and modern Y. pestis samples revealed how plague managed to persist among humans for hundreds of years after pandemic waves petered out. After an initial period of high infection rates and rapid mortality — killing infected people within three days — changes to just one gene in the bacterium produced new strains that were less deadly and more transmissible, according to research published Thursday in the journal Science. Those weakened strains eventually went extinct; the dominant lineage of today's Y. pestis is the deadlier variety, the study authors reported. However, these findings about historic instances of Y. pestis adaptation could provide important clues to help scientists and physicians manage modern plague outbreaks. Plague's most common form is bubonic plague, which causes painful swelling in lymph nodes and spreads among people through bites from fleas hitchhiking on infected rats. An outbreak of bubonic plague from 1347 to 1352 in Europe famously killed about 30% to 50% of the continent's population. But the earliest known bubonic plague outbreak — the Plague of Justinian — took hold in the Mediterranean Basin and lasted from AD 541 to AD 544. Another plague outbreak emerged in China in the 1850s and sparked a major epidemic in 1894. Scientists view modern plague cases as part of this third pandemic. For the new study, scientists collected ancient samples of Y. pestis from human remains dating back to about 100 years after the appearance of the first and second plague pandemics, sampling remains from Denmark, Europe and Russia. After reconstructing the genomes of these plague strains, they compared them with older, ancient strains that dated back to the start of plague pandemics. The researchers also examined more than 2,700 genomes of modern plague samples from Asia, Africa, and North and South America. One of the study coauthors, Jennifer Klunk, is a product scientist at Daciel Arbor Biosciences, a biotechnology company in Michigan that provided synthetically created molecules for the experiments, but there was no financial gain associated with the research. The researchers found that their newly reconstructed genomes from 100 years into the first two plague pandemics had fewer copies of a gene called pla, which has been recognized for decades as one of the factors that made plague so deadly, according to the study's co-lead author Ravneet Sidhu, a doctoral student in the McMaster Ancient DNA Centre at McMaster University in Ontario, Canada. Pla encodes an enzyme that interacts with host proteins, 'and one of the functions that it carries out is in breaking down blood clots,' Sidhu told CNN. This ability helps Y. pestis spread into the host's lymph nodes, where it replicates before attacking the rest of the body. 'Not every function of this gene is fully known,' Sidhu added. However, prior studies by other researchers linked pla to severity of illness caused by both bubonic and pneumonic plague — an airborne form of the disease that affects the lungs, she said. While the reconstructed strains showed fewer copies of the pla gene, the scientists were still uncertain whether that would directly affect how deadly the disease could be. So they tested strains of reduced-pla bubonic plague on mice, and found that survival rates for this type of plague were 10 to 20 percent higher in those experiment subjects than in mice infected with Y. pestis that had a normal amount of the pla gene. It also took the reconstructed bubonic strain about two days longer to kill its hosts. 'The paper presents a strong argument that depletion, but not total loss, of Pla (the enzyme produced by the pla gene) is part of the evolution of the plague pathogen and may help explain the decline of plague in the second pandemic commonly known as the Black Death,' said Dr. Deborah Anderson, a professor of veterinary pathobiology at the University of Missouri's College of Veterinary Medicine. Anderson, who was not involved in the new research, investigates the virulence of plague, and these findings could shed light on transmission patterns in modern cases, she told CNN in an email. 'Our laboratory studies the flea-rodent cycle and we have collaborators who conduct field research in areas that experience annual or occasional plague outbreaks in the wild,' Anderson said. 'There are nearly 300 rodent species that can transmit Yersinia pestis, and today, burrowing rodents such as prairie dogs or ground squirrels are considered key animal hosts that experience outbreaks of disease,' she added. 'After reading this paper, we will pay closer attention to Pla in the future to see if there continues to be a role for its expression in driving the explosive outbreaks of plague in the animal populations.' Mathematical models suggested how this might have played out in human populations centuries ago, leading to an 'epidemic burnout' about 100 years after a bubonic plague outbreak. In a pandemic's early stages, infections were swift, and death came quickly for both rats and humans. Over time, as dense rat populations thinned out, selective pressures favored the emergence of a less deadly strain of Y. pestis, with fewer copies of the pla gene. Rat hosts infected with this new strain would have a little more time to carry the disease, potentially enabling them to infect more rats — and more people. 'They suggest a model that can be readily pursued in the laboratory that may help explain the spread of plague today in the wild,' Anderson said. These weaker strains of the disease eventually sputtered out and went extinct. In the modern samples, the researchers found just three examples of strains with reduced pla genes, from Vietnam: one from a human subject and two from black rats (Rattus rattus). 'We've been able to do this really cool interdisciplinary study between the modern and ancient data and marry these things that have been happening throughout (the plague's) long evolutionary history,' Sidhu said. 'It could be interesting to see how future researchers continue to try and bridge that gap between the modern third pandemic and those first and second ancient pandemics, to see other similarities. Because there aren't a lot of ancient pathogens that we have as much data on, as we do for Yersinia pestis.' One of the unusual features of plague pandemics is their persistence, and understanding how Y. pestis changed its infection patterns and survived over time could shed light on the adaptive patterns of modern pandemics such as Covid-19, she added. 'Even if we aren't experiencing it to the amount that we were in 2020 or 2021, the pathogen is in the background — still evolving and persisting.' Mindy Weisberger is a science writer and media producer whose work has appeared in Live Science, Scientific American and How It Works magazine. She is the author of 'Rise of the Zombie Bugs: The Surprising Science of Parasitic Mind Control' (Hopkins Press).
Yahoo
29-05-2025
- General
- Yahoo
How the bubonic plague has survived for centuries
The catastrophic loss of life at the hands of a single bacterium during the 14th century remains one of human history's most devastating events. Yersinia pestis–the bacterium that causes bubonic plague–managed to survive for centuries by adjusting its severity and the length of time it takes to kill its hosts. Despite that virulence, some forms of plague did ultimately die out. Now, scientists have documented the way that one single gene in Yersinia pestis made it so adaptable. The findings are described in a study published May 29 in the journal Science. [ Related: Bubonic plague discovered in ancient Egyptian mummy DNA. ] According to the Cleveland Clinic, there are three types of plague. Which type that you have depends on where in your body Yersinia pestis ends up. Bubonic plague infects the lymph nodes, septicemic plague is in the blood, and pneumonic plague affects the lungs. Yersinia pestis itself is a bacterium with some deep historical roots and has caused three major pandemics in recorded human history. The Plague of Justinian in the mid-500s is the first recorded plague pandemic in human history. It is named for Justinian I, the Byzantine emperor at that time, and it devastated the Mediterranean region. Mortality estimates vary between 25 million and 100 million deaths. It killed roughly 40 percent of Constantinople's (now Istanbul) population, which was the most important center of cultural and political life in the world. at the time. It eventually led to the second plague pandemic–the Black Death in the 14th century. The Black Death is still the deadliest pandemic in recorded human history, killing 30 to 50 percent of the population in Europe, Western Asia, and Africa. The disease re-emerged in several waves over more than 500 years and persisted in that form until 1840. The third plague pandemic began in China in 1855 and continues today. Antibiotics have significantly helped treat the disease, but its impacts are still felt in parts of Madagascar and the Democratic Republic of Congo, where cases are regularly reported. Strains of the original Justinian plague went extinct after 300 years of wreaking havoc on European and Middle Eastern populations. The strains that caused the Black Death emerged from infected rodents before it broke into two major lineages. One of these two lineages is the ancestor of the present-day strains, while the other strain re-emerged over centuries in Europe and went extinct by the early 19th century. 'This is one of the first research studies to directly examine changes in an ancient pathogen, one we still see today, in an attempt to understand what drives the virulence, persistence and/or eventual extinction of pandemics,' Hendrik Poinar, a study co-author and molecular evolutionary geneticist and biological anthropologist at McMaster University in Canada, said in a statement. In the new study, the team used hundreds of samples from ancient and modern plague victims. They screened the samples for a gene known as pla. This gene helps Yersinia pestis move through the body's immune system undetected by the lymph nodes before it spreads to the rest of the body. The genetic analysis revealed that its copy number–the total number of pla genes found in the bacterium–actually decreased in the later plague outbreaks. This decreased mortality by about 20 percent, while increasing the length of infection. The hosts typically lived longer before they died. These studies were performed in mice models of bubonic plague, according to the team. When the pla gene was in its original, high copy number, the disease was much more virulent. It killed all of its hosts and did so much quicker. Additionally, the team also pinpointed a similarity between the trajectories of both modern and ancient strains. These strains independently evolved similar reductions in the pla gene during the later stages of the first and second plague pandemics and in three samples from the third pandemic that were uncovered in present day Vietnam. In both the Justinian plague from the 500s and the Black Death, the evolutionary change occurred approximately 100 years after the first outbreaks. The team believes that when the gene copy number dropped and the infected rats lived longer, the rodents could spread infection farther. This spread helped ensure the pathogen's reproductive success. 'The reduction of pla may reflect the changing size and density of rodent and human populations,' explained Poinar. 'It's important to remember that plague was an epidemic of rats, which were the drivers of epidemics and pandemics. Humans were accidental victims.' Due to their high numbers and proximity to humans, the black rats in cities likely acted as 'amplification hosts.' Since these black rats are highly susceptible to Yersinia pestis themselves, the pathogen needed the rat populations to stay high enough to supply new hosts for Yersinia pestis to persist and allow the natural pandemic cycle to continue. [ Related: DNA from plague victims' teeth may unravel the origin of Black Death. ] However, the strains of plague that did not have the pla gene eventually went extinct. This likely reflects another shift that occurred in the host-pathogen relationship within their environment. When the team searched for signs of pla gene depletion in samples of the third plague pandemic preserved in a large collection at the Institut Pasteur in Paris, they found three contemporary strains with the pla depletion. The diminished virulence that the pathogen evolved in response to more of its hosts dying potentially caused these earlier plague pandemics to fizzle out. 'Thanks to our international collaborators who monitor local epidemics of plague worldwide, we were able to find the unique bacterial samples used for this project, akin to finding of three rare needles in a haystack,' Javier Pizarro-Cerdá, a study co-author and microbiologist who specializes in plague at the Institut Pasteur, said in a statement. Despite this evolution, most of the strains circulating in some countries in Africa, South America, and Asia are more virulent. 'Today, the plague is a rare disease, but one that remains a public health concern and serves as a model for gaining a broad understanding of how pandemics emerge and become extinct,' said Javier Pizarro-Cerdá. 'This example illustrates the balance of virulence a pathogen can adopt in order to spread effectively from one host to another.'
