Bacteria not only develop resistance to antibiotics; they also can pick it up from their rivals.

In a recent publication in Cell Reports, researchers from Biozentrum at the University of Basel in Switzerland have demonstrated that some bacteria inject a toxic cocktail into their competitors that causes cell lysis and death. Then, by integrating the released genetic material, which may also carry drug resistance genes, the predator cell can acquire antibiotic resistance.

The frequent use of antibiotics leads to an increasingly rapid spread of resistance, the university said, and hospitals are a particular hot spot for this. Patients not only introduce a wide variety of pathogens that may already be resistant, but due to the use of antibiotics to combat infections, hospitals also may be a place where antimicrobial resistance can develop and be transferred from pathogen to pathogen.

One of these typical hospital germs is Acinetobacter baumannii. The bacterium is also known as the "Iraq bug" because multi-drug-resistant bacteria of this species caused severe wound infections in American soldiers during the Iraq war.

Gene exchange

The emergence and spread of multi-drug resistance could be attributed to, among other things, the special skills of certain bacteria. First, they combat their competitors by injecting them with a mix of toxic proteins — so-called effectors — using the type VI secretion system (T6SS), a poison syringe. Second, they are able to uptake and reuse the released genetic material.

Professor Marek Basler's team at Biozentrum has now identified five differently acting effectors in the model organism Acinetobacter baylyi, a close relative of the Iraq bug.

"Some of these toxic proteins kill the bacterial competition very effectively but do not destroy the cells," Basler explained. "Others severely damage the cell envelope, which leads to lysis of the attacked bacterium and, hence, the release of its genetic material."

The predator bacteria take up the released DNA fragments. If these fragments carry certain drug resistance genes, the specific resistance can be conferred upon the new owner, the researcher said. As a result, the antibiotic is no longer effective, and the bacterium can reproduce largely undisturbed.

Pathogens with such abilities are a major problem in hospitals, because they may accumulate resistance to many antibiotics through contact with other resistant bacteria, thus becoming multi-drug resistant. In the worst case, antibiotic treatments are no longer effective, and nosocomial infections with multi-drug-resistant pathogens become a deadly threat to patients.

"The T6SS, as well as a set of different effectors, can also be found in other pathogens, such as those which cause pneumonia or cholera," Basler said.

Interestingly, not all effectors are sufficient to kill the target cell, as many bacteria have developed or acquired antitoxins — so-called immunity proteins.

"We have also been able to identify the corresponding immunity proteins of the five toxic effectors in the predator cells. For the bacteria, it makes absolute sense to produce not only a single toxin but a cocktail of various toxins with different effects," Basler explained. “This increases the likelihood that the rivals can be successfully eliminated and, in some cases, also lysed to release their DNA.”

New environmental niches

Antibiotics and antimicrobial resistance have existed for a long time. They developed through the coexistence of microorganisms and enabled bacteria to defend themselves against enemies or to eliminate competitors, the university said. This is one of the ways bacteria can conquer and colonize new environmental niches.

With the use of antibiotics in medicine, however, the natural ability to develop resistance has become a problem, presenting researchers with the challenge of continually developing new antibiotics and slowing down the spread of drug resistance.