A clade B strain of Acinetobacter baumannii (AB) was tied to a healthcare-associated outbreak that led to six patient deaths. Clade B is characterized by extensive drug resistance. It is also hypervirulent, and experts warn it warrants continued investigation and increased surveillance.

Crystal L. Jones, MD, from the Walter Reed Army Institute of Research in Silver Spring, Maryland, and colleagues published their outbreak report online March 29 in Clinical Infectious Diseases. The outbreak investigation included clinical and microbiological data as well as comparative genomics and animal models of virulence.
Instead of using the more common multilocus sequence typing (MLST) assay, the investigators used a polymerase chain reaction (PCR) assay for clade B strains. “The [MLST] assay is useful for epidemiologic surveillance, especially if all that they have available is MLST for genetic fingerprinting… but it can’t distinguish this strain/clade from other closely related strains,” explained senior author Emil P. Lesho, MD, also from Walter Reed Army Institute, in an email to Medscape Medical News.

AB is a known cause of healthcare-associated infections. There have been previous reports of higher-virulence healthcare-associated AB isolates. The clade B strain is noteworthy because it is not only highly virulent but also very resistant to antibiotics.

“[Acinetobacter] is usually not a high-virulence pathogen, in that it mainly affects patients who are substantially immune compromised and very sick. It is unusual to see a strain that is very resistant and very virulent,” explained Dr Lesho.

“A key finding of our work was that AB strains that are genetically closely related may show significant differences in virulence, suggesting that small genomic changes can profoundly affect virulence. To our knowledge, this is the first report leveraging comparative genomics, animal models, and a surveillance network with isolate repository to characterize an emerging clade of [extensively drug-resistant]-AB associated with a fatal outbreak in patients not severely immunocompromised,” the authors write.

In an accompanying editorial, David L. Paterson, MD, PhD, and Patrick N.A. Harris, MD, from the University of Queensland Centre for Clinical Research in Brisbane, Australia, agree that the significance of the outbreak report lies in the fact that AB infection killed patients who had relatively minor underlying disease. The study also suggests that assumptions about AB pathogenicity may be misplaced.
“Our current understanding of A. baumannii pathogenicity is primarily based on mutagenesis studies using reference strains ATCC 19606 and ATCC 17978, which were isolated over 50 years ago. Considering the ease with which A. baumannii can alter its genetic structure and acquire resistance or virulence determinants, these models of AB pathogenesis may have limited clinical relevance,” write Dr Jones and colleagues.

The investigators propose that the potential virulence gene structures may provide insights into path-adaptation and evolutionary relationship of the clade B strain. They also report that the host response to the pathogen is a driver of virulence and outcomes.