Antibiotic-resistant Acinetobacter baumannii bacteria acquired* antibiotic sensitivity after exposure to bacteriophages. It was discovered that, in an attempt to evade the bacteriophages, the bacteria mutated in a way that made them vulnerable to antibiotics.

Antibiotic resistance in pathogenic bacteria is one of the most serious problems in modern healthcare. Doctors most frequently encounter severe antibiotic-resistant infections caused by bacterial species such as Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter sp. (collectively known as ESKAPE). The development of new antibiotics capable of combating these "superbugs" is progressing very slowly, so scientists are actively seeking alternative antibacterial therapy methods. One of the most studied and readily available today is bacteriophages.

Scientists from Monash University in Melbourne studied the effects of various bacteriophages on antibiotic-resistant strains of A. baumannii and isolated two bacteriophages specific to this bacterium—ΦFG02 and ΦCO01. However, the experiment revealed that some A. baumannii strains were resistant to bacteriophages. This phage resistance was found to be caused by a mutation that deprived the bacteria of their surface capsule, to which phages attach before penetrating the bacterial cell. Without the capsule, phages are unable to attach and infect the bacteria. However, this same capsule also acts as a barrier to various antibiotics, rendering A. baumannii immune to most antibiotics. Therefore, by mutating to protect against bacteriophages, the bacteria regain their sensitivity to antibiotics. Experiments showed that in the presence of phage ΦFG02, the bacteria became 16 times more sensitive to ceftazidime and twice as sensitive to other beta-lactams and ciprofloxacin. Phage ΦCO01 restored A. baumannii's sensitivity to minocycline, cefepem, and ampicillin.

Another interesting effect of phages was discovered: mutant bacteria became susceptible to the complement system (an element of the nonspecific immune response in mammals). As a result, in experiments on mice infected with phage-resistant strains of A. baumannii , infection with bacteriophages led to a reduction in bacterial numbers in affected tissues after just 8-12 hours: by an order of magnitude in the presence of ΦFG02 and by two orders of magnitude in the presence of ΦCO01. In other words, the bacteriophages made the bacteria more vulnerable to the mouse immune defense.

*Gordillo Altamirano F, Forsyth JH, Patwa R et al. Bacteriophage-resistant Acinetobacter baumannii are resensitized to antimicrobials. Nat Microbiol, Published: 11 January 2021. https://doi.org/10.1038/s41564-020-00830-7