As the name suggests, you really don't want infection with meat dishes. The frightening affliction can make your body's tissues work faster, and new research confirms that this type of attack is caused not only by one type of bacteria, but also by a whole cartel of microbes.
So-called "polymicrobial" diseases caused by co-operation with parasites, bacteria, viruses or fungi have been on the pathologists' radar for years, but until recently, necrotizing fascism was thought to be the work of a germ.
It turned out not to be the case. Several years ago, a patient was diagnosed with an infection consisting of two types that function as one. In a new study, researchers infected mice with mutant strains of the bacterium to find out how the bacteria did it. Aeromonas hydrophilia, and found that they really did get along.
"One of the compounds creates a toxin that breaks down muscle tissue and allows the other virus to migrate into the bloodstream and infect the organs," says bacteriologist Rita Colwell of the Institute for Advanced Computer Studies at the University of Maryland.
Any of the numerous bacteria can be responsible for this terrible disease. Streptococcus pyogenes is the most common, but species of Staphylococci, Klebsiella, and Aeromonas often involved.
In fact, it was a specific case of A. hydrophilic an infection that caught the attention of Colwell and her colleagues. The team genetically examined microbes from necrotic tissues in an immunocompromised patient, finding the culprits of the two different vines.
Their discovery of how the two types do the job relies on previous work. In previous studies of isolated microbe specimens, researchers have found that none of the compounds – simply called NF1 and NF2 – can cause a bad infection per se. But in combination, their individual ability to seek or destroy has made them a serious duo.
The information about their cooperation seemed to lie in the types of genes that these species possessed. Researchers have found that NF1 has a unique type of secretion system, for example, which has helped the agent gain an advantage over other bacteria and survive immune attacks more easily.
While NF2 did not have the opportunity to wipe out competitors, it was instead armed with a toxin called exoA that eliminated the important reading tasks in our own cells, effectively killing them with a heart attack.
To get to the end, in a recent study, researchers exchanged genes between NF1 and NF2, making each act a little more like his teammate than usual. These mutant species were then tested on mice to monitor their pathology.
The team discovered that the original, non-mutant NF1 strains could not move very far after entering the wound, unable to break down the surrounding meat. As soon as his comrade NF2 arrived he could move, with the second tissue wound up to clear the path.
As a result, NF1 eventually reinforced its team-mate at the back, injecting it with chemicals that kill bacteria to ensure it can eat all the resources by itself and stick around for longer.
Knowing exactly how each load works can provide a pathway to the development of targeted drugs that will ensure that all types of surplus are activated to fully treat the devastating infection.
Quick intervention through large doses of antibiotics and surgical removal of dead tissue is often vital if the patient is to survive at all, but only if all traces of the infection are taken care of. Even then, survival can be as high as 66 percent, and patients often remain with severe deformities.
"We are thrilled by this very elegant detective work," says Colwell.
"We now have the opportunity, through metagenomics, to identify individual infectious agents involved in polymicrobial infections. With these powerful new methods we can determine how microbes work together, whether they are bacteria, viruses or parasites."
This research was published in PNAS.