Smokers provide a home for the bacteria that now makes people with cystic fibrosis sick
Explain how I am. Smoking habits have been found to be harmful since the early 1900s - not for smokers or their families, but for people with cystic fibrosis.
Cystic fibrosis is an inherited disease that makes the mucous membranes of sufferers thick and sticky. Their lungs are a breeding ground for bacteria that the immune system of healthy people easily defeats. people with cystic fibrosis often take antibiotics to prevent lung infections, but antibiotics do not kill everything. A bacterium called Mycobacterium abscessus (M. abscessus) is resistant to many common medications and has become an epidemic in the cystic fibrosis community in recent decades.

A few years ago, scientists began studying how to do this. The plague was caused by analyzing the genome of M. abscessus collected from people around the world, and researchers have tracked the bacteria's spread over the past century. They found that before the 1950s—before medical advances allowed people with cystic fibrosis to survive infancy—M. cysts had already spread worldwide and were an ancient enemy of public health. The lungs of smokers created a reservoir in which the pathogen could live and reproduce, a reservoir that rapidly overflowed when people with cystic fibrosis began to live to adulthood.

The unexpectedly required sequence of the complete genomes of thousands of M. "There are abscess strains from all over the world, and scientists who were not involved in the study say the hard work has paid off," said Wagard Elulm, an infectious disease researcher. . "This article is really interesting," said Variety Hill, a molecular epidemiologist at the University of Edinburgh at the Norwegian Institute of Public Health. "Really beautiful and really thoughtful." ADVERTISEMENTS: The infected become infected. When exposed to contaminated soil or water. That changed five years ago, when a team led by infectious disease researchers led by Julian Barkhill and Anders Floto showed that M. abscessus can be transmitted from one person with cystic fibrosis to another — and that cystic fibrosis treatment centers were the epicenter of transmission. /p > people treated at the CF center to find out the extent of diversity and whether this genetic diversity is associated with pathogenicity. They believed that each infected person transmitted the pathogen independently from the environment, so the genome would be significantly different. Instead, many of the genomes were similar or even identical. "We were really surprised that there was so much evidence that these patients passed it on to each other," Barkhill said. Hospital Some of the genomes were so similar that they were taken from the environment, but so different that they came directly from other people in the center. So where did they come from?

Larger Study

"The answer to every question is always more data." His team sequenced the genomes of M. abscessus strains isolated from more than 1,000 people around the world — some with cystic fibrosis, others with other types of lung damage — to understand how the pathogen spreads.

Equipped with a boat. "You're making what is essentially a family tree," says Hill, who uses similar techniques to track the spread of viruses. Genetically similar bacteria, such as how siblings occupy the same branches of the family tree. Knowing that the M. abscessus genome makes new mutations almost every now and then allows researchers to add dates to the tree. M. abscessus began to mutate rapidly, resulting in a dense network of branches. This time is associated with the establishment of cystic fibrosis treatment centers, which allow people with cystic fibrosis to live and interact with each other since childhood. "You're creating a place for the bacteria to live in -- that place in the lung of people with cystic fibrosis -- as well as a transmission pathway," Barkhill said. What's good for people with cystic fibrosis is good for Mycobacterium abscess, so it stands to reason that the pathogen grew in the middle of the century. Researchers wonder why M. Abscessus spread before modern treatment for cystic fibrosis was available, when most sufferers die at a young age? He was also susceptible to M. abscess, and coincidentally, his colleagues published a study showing that tobacco-associated cancer cells had specific gene mutations. Barkale wondered if he could detect the same mutations in M. Abscessus.

“I didn't really think it would work,” he said. Because the mutation signature is linked to smoking, his lab had to analyze hundreds of genomes to make sure the signatures they found were real evidence of tobacco exposure, not just accidents. Each genome contains more than a dozen Moby-Dick characters containing databases of DNA, so the computer program written by the researchers took several days to process all the data. But, in the end, the signature of the tobacco boom shone through the genetic noise. The team felt they had convincing evidence that smokers carried M. abscess.

This study is the first time researchers have used mutation analysis to identify the environments in which a pathogen lives. “I wasn't immediately convinced that what they were saying was something they could prove. But this mutation spectrum analysis is actually very convincing," Hill said. This is a precedent.” He suspects this study will encourage other microbiologists to do similar analyzes. When researchers realized that M. abscess can spread among people with cystic fibrosis, they changed the mindset of health care providers. A new study on prevention shows Diseases that the risk of transmission is greater. But knowledge creates options. “The more we can identify [ways] of transmission, the more we can stop it.” Sima is a freelance science writer in Somerville, Massachusetts. When he's not writing, he enjoys cycling in the city Learn photography and practice taekwondo. Why doesn't Apple Touch return an ID to iPhone?

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