TY - JOUR
T1 - Evolution of Burkholderia pseudomallei in recurrent melioidosis.
AU - Hayden, Hillary S.
AU - Lim, Regina
AU - Brittnacher, Mitchell J.
AU - Sims, Elizabeth H.
AU - Ramage, Elizabeth R.
AU - Fong, Christine
AU - Wu, Zaining
AU - Crist, Eva
AU - Chang, Jean
AU - Zhou, Yang
AU - Radey, Matthew
AU - Rohmer, Laurence
AU - Haugen, Eric
AU - Gillett, Will
AU - Wuthiekanun, Vanaporn
AU - Peacock, Sharon J.
AU - Kaul, Rajinder
AU - Miller, Samuel I.
AU - Manoil, Colin
AU - Jacobs, Michael A.
PY - 2012
Y1 - 2012
N2 - Burkholderia pseudomallei, the etiologic agent of human melioidosis, is capable of causing severe acute infection with overwhelming septicemia leading to death. A high rate of recurrent disease occurs in adult patients, most often due to recrudescence of the initial infecting strain. Pathogen persistence and evolution during such relapsing infections are not well understood. Bacterial cells present in the primary inoculum and in late infections may differ greatly, as has been observed in chronic disease, or they may be genetically similar. To test these alternative models, we conducted whole-genome comparisons of clonal primary and relapse B. pseudomallei isolates recovered six months to six years apart from four adult Thai patients. We found differences within each of the four pairs, and some, including a 330 Kb deletion, affected substantial portions of the genome. Many of the changes were associated with increased antibiotic resistance. We also found evidence of positive selection for deleterious mutations in a TetR family transcriptional regulator from a set of 107 additional B. pseudomallei strains. As part of the study, we sequenced to base-pair accuracy the genome of B. pseudomallei strain 1026b, the model used for genetic studies of B. pseudomallei pathogenesis and antibiotic resistance. Our findings provide new insights into pathogen evolution during long-term infections and have important implications for the development of intervention strategies to combat recurrent melioidosis.
AB - Burkholderia pseudomallei, the etiologic agent of human melioidosis, is capable of causing severe acute infection with overwhelming septicemia leading to death. A high rate of recurrent disease occurs in adult patients, most often due to recrudescence of the initial infecting strain. Pathogen persistence and evolution during such relapsing infections are not well understood. Bacterial cells present in the primary inoculum and in late infections may differ greatly, as has been observed in chronic disease, or they may be genetically similar. To test these alternative models, we conducted whole-genome comparisons of clonal primary and relapse B. pseudomallei isolates recovered six months to six years apart from four adult Thai patients. We found differences within each of the four pairs, and some, including a 330 Kb deletion, affected substantial portions of the genome. Many of the changes were associated with increased antibiotic resistance. We also found evidence of positive selection for deleterious mutations in a TetR family transcriptional regulator from a set of 107 additional B. pseudomallei strains. As part of the study, we sequenced to base-pair accuracy the genome of B. pseudomallei strain 1026b, the model used for genetic studies of B. pseudomallei pathogenesis and antibiotic resistance. Our findings provide new insights into pathogen evolution during long-term infections and have important implications for the development of intervention strategies to combat recurrent melioidosis.
UR - http://www.scopus.com/inward/record.url?scp=84866149966&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0036507
DO - 10.1371/journal.pone.0036507
M3 - Article
C2 - 22615773
AN - SCOPUS:84866149966
VL - 7
SP - e36507
JO - PLoS ONE
JF - PLoS ONE
SN - 1932-6203
IS - 5
ER -