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Viruses that infect bacteria can cause drug-resistant superbugs to evolve by inserting their genes into bacterial DNA, a new study suggests.
The bacteria attack virus, called phages, act like parasites in that they depend on their hosts for survival. Viral parasites often kill their microbial hosts after infiltrating their DNAsaid lead author of the study, Vaughn Cooper, director of the Center for Evolutionary Biology and Medicine at the University of Pittsburgh School of Medicine. But sometimes phages creep into the bacterial genome and then lie down, slyly altering the bacteria’s behavior, Cooper said.
For example, the virus can induce the bacteria to secrete toxins that kill nearby phages, so the virus can keep its new host to itself. But now, a new study, published Friday, July 16 in the journal Science Advances, suggests that phages may also help their bacterial hosts develop resistance against antibiotic treatments.
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In the new study, the team focused on Pseudomonas aeruginosa, a type of bacteria that is one of the main causes of nosocomial infections and is often resistant to several drugs. In particular, bacterial infection often affects people with immune systemswhether it’s because of conditions like cystic fibrosis or drugs that suppress the immune system, like steroids.
Knowing that P. aeruginosa can be so difficult to kill, the team wondered how the different strains of the microbe compare to each other and what makes the superior strains so effective at triggering a difficult-to-treat infection. “If you have six different strains of Pseudomonas aeruginosa, who wins? ”Cooper said.
The team approached this question by introducing six different strains of P. aeruginosa in pig burns. Soon two of the six strains had completely taken over, leading to the extinction of the others. “It happened extremely quickly, within days,” Cooper said.
These two “winning” strains produced small colonies of wrinkled-looking bacteria that came together in biofilms – clusters of bacterial cells which secrete a viscous substance which protects them both from the host’s immune system and from phage attacks. The presence of biofilms and small wrinkled cell colonies has been associated with slower healing and poorer clinical outcomes, compared to infections that lack these qualities, Cooper said.
In this case, the winning strains showed “hyperbiofilm formation”, well beyond any biofilm formation observed in the competing strains.
The slime from the biofilm protects bacteria from the host’s immune system, as the immune cells have a hard time getting lodged on the large matrix and engulfing the bacteria inside. The phages also integrate into this protective matrix and release chemicals to fight off other nearby phages, again, to keep their bacterial hosts to themselves.
In addition, when bacteria begin to produce biofilms, their metabolism slows down and their cells divide more slowly; this can interfere with the effects of antibiotics, as many work by causing cells to short circuit during cell division, Previously reported live science.
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The two winning strains of P. aeruginosa did not immediately produce biofilms upon entering pigs, but rather entered this viscous protective state over time. To find out why, the team zoomed in on the winning strains’ DNA.
They compared the genetic sequence of the winning strains with their ancestors – the versions of those same strains that were first introduced into pig wounds – to see if any mutations occurred when the bacteria divided in the pigs. animals. They also compared the genetic sequences of the winning strains with those of the losing strains.
Instead of finding small mutations scattered throughout the DNA, the team found that entirely new segments of DNA had been added to the genomes of the winning strains. They identified these “foreign” pieces of DNA as belonging to phages, viruses that infect bacteria. And in fact, the phages in question first penetrated the pig’s wounds on the DNA of the losing bacterial strains.
In other words, once inside the wound, these phages jumped out of their original host bacteria and made their way into the winner. P. aeruginosa strains. In fact, the cells sampled from the winning strains each had about one to four segments of new phage DNA added to their genetic codes.
Specifically, a phage has inserted its genetic material into a gene called retS, an important switch that turns biofilm production on and off. When activated, retS acts as a stop switch and suppresses biofilm production; but once the phage infiltrated this gene into the winning strains, retS could no longer be activated and biofilm production was unleashed.
The team put a normal version of retS back into the winning strains, to see if biofilm production would stop again, and they did. This suggested that, yes, the phage-related gene changes had caused the bacteria to produce biofilms and likely helped the winning strains dominate where the losing strains failed.
This discovery suggests that, at the onset of infections, phages could jump between bacterial strains, passing superpowers until an insect emerges victorious and, as in this case, endowed with antibiotic resistance. That said, it’s not clear how often people get infected with multiple strains of bacteria at once, so the question arises as to how often these types of exchanges occur, Cooper said. Either way, the study suggests that phages may play a key role in bacterial evolution and the increase in treatment-resistant insects.
But not all phages are bad – viruses could offer a smart strategy to eliminate superbugs when all other treatments fail. Phages can kill bacteria by opening up the microbes from within; viruses do this after multiplying inside bacteria. So when the bacterial cell divides, new copies of the phage spread.
“With the increase in antibiotic resistance, the field has become interested in reusing these viruses as antibiotics themselves,” Cooper said. To achieve this ambition, scientists will need to better understand how phages infect their bacterial hosts and which phage genes help kill hosts. And since a given phage typically only infects a single species or strain of bacteria, developing phage-based drugs that work against many superbugs could present a challenge, he said.
“Most of the genes in phages are basically black matter for us, ”so the field has a long way to go, Cooper said.
Originally posted on Live Science.
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