Editorial commentary: the new Acinetobacter equation: hypervirulence plus antibiotic resistance equals big trouble.

Acinetobacter baumannii is well known to clinicians as a cause of healthcareassociated infections [1]. Although biochemically indistinguishable from A. baumannii, Acinetobacter pittii and Acinetobacter nosocomialis are more recently described species that may also cause healthcare-associated infection and form part of the A. baumannii “complex.” The typical antibiotic-resistance phenotype of A. baumannii and related species in most hospitals is now one of resistance to carbapenems and numerous other antibiotic classes. In many cases, A. baumannii is extensively drug resistant (XDR), implying susceptibility to only 1 or 2 antibiotic classes. XDR A. baumannii is typically clonal, with about 50% of cases worldwide being part of the international clonal complex II [1]. Although frequently causing colonization of the respiratory tract, clinically significant infections are seen, especially in compromised patients. While mortality attributable to XDR A. baumannii certainly occurs, mortality is often a result of underlying disease. Acinetobacter baumannii is rightly described as generally being a low-virulence organism. The significance of the report by Jones and colleagues in this issue of Clinical Infectious Diseases [2] lies in its demonstration of healthcare-associated A. baumannii infections being due to highly virulent pathogens,with consequentdeath of patients with relatively minor underlying disease (Table 1). In this report, 6 patients from the northwestern United States who died from healthcare-associated XDR A. baumannii infections are described. Two clades are described—one belonging to the geographically widespread international clonal complex II (and sequence type 2) and the other belonging to the relatively uncommon sequence type 10. The rarity of this second clade, which predominated in the outbreak, is indicated by its unique pulsed-field gel electrophoresis pattern among 1800 A. baumannii isolates in the Walter Reed Army Institute of Research collection. The clade was extensively drug resistant, with 21 antibiotic-resistance genes being detected. Worse still, representative isolates of this clade were highly virulent in a mouse model and possessed a unique combination of virulence genes. This included a novel gene cluster encoding enzymes for protein glycosylation, which is a process known to play a key role in virulence determinants such as biofilm formation or capsule production. Jones and colleagues should be commended for their multifaceted approach to the outbreak investigation, including comparative genomics and animal models of virulence to complement the clinical and microbiological data. The application of whole genome sequencing not only