Acinetobacter spp. are Gram-negative bacteria that have become one of the most difficult pathogens to treat. The species A.
baumannii, largely unknown 30 years ago, has risen to prominence particularly because of its ability to cause infections in immunocompromised
patients. It is now a predominant pathogen in many hospitals as it has acquired resistance genes to virtually all antibiotics capable
of treating Gram-negative bacteria, including the fluoroquinolones and the cephalosporins. Some members of the species have accumulated
these resistance genes in large resistance islands, located in a "hot-spot" within the bacterial chromosome. The only conventional
remaining treatment options were the carbapenems. However, A. baumannii possesses an inherent class D β-lactamase gene (blaOXA-51-like)
that can have the ability to confer carbapenem resistance. Additionally, mechanisms of carbapenem resistance have emerged that derive
from the importation of the distantly related class D β-lactamase genes blaOXA-23 and blaOXA-58. Although not inducible, the expression of
these genes is controlled by mobile promoters carried on ISAba elements. It has also been found that other resistance genes including the
chromosomal class C β-lactamase genes conferring cephalosporin resistance are controlled in the same manner. Colistin is now considered
to be the final drug capable of treating infections caused by carbapenem-resistant A. baumannii; however, strains are now being isolated
that are resistant to this antibiotic as well. The increasing inability to treat infections caused by A. baumannii ensures that this
pathogen more than ranks with MRSA or Clostridium difficile as a threat to modern medicine.