New research says that an aggressive type of flesh-eating infection that spreads in one’s body and devours the tissues can be carried on by multiple groups of microbes, not by only one kind of bacteria.
Only Functioning as a Couple
Known as ‘polymicrobial’ diseases originated from collaborating parasites, bacteria, viruses, or fungi have been studied by pathologists for a long time now, but until recently, necrotizing fasciitis was believed to be a single germ’s job.
That ended up not being so. A number of years back, a patient was identified with an infection created by two strains functioning as one. To discover how the germs were causing it, in the new research, scientists infected mice with mutant strains of the bacteria known as Aeromonas hydrophila and discovered that they were, as thought, collaborating as one.
“One of the strains produces a toxin that breaks down muscle tissue and allows the other strain to migrate into the blood system and infect the organs,” bacteriologist Rita Colwell, from the University of Maryland Institute for Advanced Computer Studies said.
Any one of multiple bacteria can be the cause of this aggressive disease. The most common is Streptococcus pyogenes, but also types of taphylococcus, Klebsiella, and Aeromonas are involved.
As a matter of fact, it was a particular case of A. hydrophila infection that made Colwell and her colleagues analyze the matter more deeply. The team genetically observed the microbes from necrotic tissues in an immunocompromised patient and discovered that two separate lineages were the cause of the disease.
The findings of the way the two strains collaborate are based on previous work. Previous research of the samples of isolated microbe showed that neither of the strains, dubbed NF1 and NF2, were able to produce infection when separated. But combined, their separate abilities to either seek or kill made a fantastic couple.
Knowing How the Strains Function
To better understand this peculiar combination and its effects, the researchers exchanged the genes between NF1 and NF2 in the latest analyze. This made each strain behave a bit more like its team-mate rather than its usual self; these mutants were then tested on mice to observe their pathology.
The researchers found that the original, non-mutant NF1 strains could not move distances after it contaminated a wound, as it has no ability to devour the surrounding flesh. However, as soon as its half NF2 came along, it could move, as the second strain broke down the tissue to make way.
Moreover, NF1 ultimately killed its team-mate, injecting it with bacteria-murdering chemicals to make sure it could devour all the resources by itself and stay in the place for longer, as well. Knowing precisely how each strain function, could generate a path towards developing certain drugs that make sure all strains are disabled and eliminated to completely treat the deadly infection.
Rapid intervention via heavy-hitting doses of drugs and surgical removal of dead tissue is frequently crucial if the patient has chances of survival, but it only functions if all bits of the infection is eliminated. Even then, survival can be as low as 66 percent, and numerous patients remain with serious deformities.
This research was published in PNAS.