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Genomic Features of the 2015 Elizabethkingia Outbreak

JUN 01, 2017 | NICOLA M. PARRY, BVSC, MRCVS, MSC, DIPACVP
The 2015-2016 Elizabethkingia outbreak in the Midwest was caused by a single strain of Elizabethkingia anophelis that represents a new sublineage of E. anophelis and has unique genomic regions. 
 
Amandine Perrin and Elise Larsonneur, from the Pasteur Institute, Paris, France, Ainsley C. Nicholson, from the Centers for Disease Control and Prevention, Atlanta, Georgia, and colleagues published the results of their study in Nature Communications.
 
“Strikingly, the outbreak isolates show an accelerated evolutionary rate and an atypical mutational spectrum,” the authors wrote.
 
A deadly outbreak of infections caused by E. anophelis began in the Midwest in November 2015, affecting Wisconsin, Illinois, and Michigan. This was the largest documented outbreak of this rare bacterial infection, and the only one which was predominantly community-associated.
 
“The unique magnitude and setting of the Wisconsin outbreak and its elusive source prompted us to explore the genomic features of the outbreak strain, and compare them to other Elizabethkingia strains,” the authors wrote.
 
The investigators analyzed 69 isolates of the bacterium from the Wisconsin outbreak and 45 comparative strains of E. anophelis. and other Elizabethkingia species, and found that the outbreak was caused by a new sublineage of E. anophelis.
 
All but 3 of the isolates originated from a single ancestor. Analysis of the isolates also showed that the outbreak was highly dynamic, with an increased evolutionary rate and a unique spectrum of mutations.
 
To examine the genomic characteristics of the outbreak strain, the investigators analyzed the entire set of protein families in E. anophelis genomes (the pan-genome). They found that the pan-genome contained 8808 protein families, whereas the outbreak strains encompassed only 3637 of these. According to the authors, the core-genome of the outbreak isolates also represented 97% of the average number of proteins per genome, and 94% of the outbreak pan-genome. This highlights the striking genetic similarity of the outbreak isolates, compared with the diversity within the entire bacterial species, the authors stressed.
 
The investigators also discovered a defective DNA repair mutY gene in the outbreak strain, caused by insertion of an integrative and conjugative element (ICE). ICEs are mobile genetic elements found in most bacteria and play a key role in adaptation of their host organism.
 
This change probably contributed to both the speed of evolution of the outbreak strain and its adaptability, the authors say.
 
They also performed antimicrobial susceptibility testing and showed that the outbreak isolates were resistant to most beta-lactam antibiotics, as well as to aminoglycosides, chloramphenicol, fosfomycin, tetracycline, and vancomycin. In contrast, however, the outbreak isolates were susceptible to quinolones, trimethoprim-sulfamethoxazole, and rifampicin. 
 
Based on the mutation involved in the outbreak strain, the investigators hypothesize that the outbreak strain could once again switch back to a functional mutY sequence and recover its ability to repair DNA. This reversible switch could, therefore, have important implications for the future survival and possible resurgence of the Wisconsin outbreak strain. 
 
“We, therefore, urge healthcare and public health systems to establish a laboratory based surveillance for Elizabethkingia infections, and to be particularly vigilant for a possible re-emergence of the unique E. anophelis strain that caused the Wisconsin outbreak,” the authors concluded.
 
Dr. Parry graduated from the University of Liverpool, England in 1997 and is a board-certified veterinary pathologist. After 13 years working in academia, she founded Midwest Veterinary Pathology, LLC where she now works as a private consultant. She is passionate about veterinary education and serves on the Indiana Veterinary Medical Association’s Continuing Education Committee. She regularly writes continuing education articles for veterinary organizations and journals, and has also served on the American College of Veterinary Pathologists’ Examination Committee and Education Committee.
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