#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

Within-Host Evolution of in Four Cases of Acute Melioidosis


Little is currently known about bacterial pathogen evolution and adaptation within the host during acute infection. Previous studies of Burkholderia pseudomallei, the etiologic agent of melioidosis, have shown that this opportunistic pathogen mutates rapidly both in vitro and in vivo at tandemly repeated loci, making this organism a relevant model for studying short-term evolution. In the current study, B. pseudomallei isolates cultured from multiple body sites from four Thai patients with disseminated melioidosis were subjected to fine-scale genotyping using multilocus variable-number tandem repeat analysis (MLVA). In order to understand and model the in vivo variable-number tandem repeat (VNTR) mutational process, we characterized the patterns and rates of mutations in vitro through parallel serial passage experiments of B. pseudomallei. Despite the short period of infection, substantial divergence from the putative founder genotype was observed in all four melioidosis cases. This study presents a paradigm for examining bacterial evolution over the short timescale of an acute infection. Further studies are required to determine whether the mutational process leads to phenotypic alterations that impact upon bacterial fitness in vivo. Our findings have important implications for future sampling strategies, since colonies in a single clinical sample may be genetically heterogeneous, and organisms in a culture taken late in the infective process may have undergone considerable genetic change compared with the founder inoculum.


Vyšlo v časopise: Within-Host Evolution of in Four Cases of Acute Melioidosis. PLoS Pathog 6(1): e32767. doi:10.1371/journal.ppat.1000725
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1000725

Souhrn

Little is currently known about bacterial pathogen evolution and adaptation within the host during acute infection. Previous studies of Burkholderia pseudomallei, the etiologic agent of melioidosis, have shown that this opportunistic pathogen mutates rapidly both in vitro and in vivo at tandemly repeated loci, making this organism a relevant model for studying short-term evolution. In the current study, B. pseudomallei isolates cultured from multiple body sites from four Thai patients with disseminated melioidosis were subjected to fine-scale genotyping using multilocus variable-number tandem repeat analysis (MLVA). In order to understand and model the in vivo variable-number tandem repeat (VNTR) mutational process, we characterized the patterns and rates of mutations in vitro through parallel serial passage experiments of B. pseudomallei. Despite the short period of infection, substantial divergence from the putative founder genotype was observed in all four melioidosis cases. This study presents a paradigm for examining bacterial evolution over the short timescale of an acute infection. Further studies are required to determine whether the mutational process leads to phenotypic alterations that impact upon bacterial fitness in vivo. Our findings have important implications for future sampling strategies, since colonies in a single clinical sample may be genetically heterogeneous, and organisms in a culture taken late in the infective process may have undergone considerable genetic change compared with the founder inoculum.


Zdroje

1. CharpentierC

NoraT

TenaillonO

ClavelF

HanceAJ

2006 Extensive recombination among human immunodeficiency virus type 1 quasispecies makes an important contribution to viral diversity in individual patients. J Virol 80 2472 2482

2. NoraT

CharpentierC

TenaillonO

HoedeC

ClavelF

2007 Contribution of recombination to the evolution of human immunodeficiency viruses expressing resistance to antiretroviral treatment. J Virol 81 7620 7628

3. ShankarappaR

MargolickJB

GangeSJ

RodrigoAG

UpchurchD

1999 Consistent viral evolutionary changes associated with the progression of human immunodeficiency virus type 1 infection. J Virol 73 10489 10502

4. ShrinerD

RodrigoAG

NickleDC

MullinsJI

2004 Pervasive genomic recombination of HIV-1 in vivo. Genetics 167 1573 1583

5. SmithEE

BuckleyDG

WuZ

SaenphimmachakC

HoffmanLR

2006 Genetic adaptation by Pseudomonas aeruginosa to the airways of cystic fibrosis patients. Proc Natl Acad Sci U S A 103 8487 8492

6. ChengAC

CurrieBJ

2005 Melioidosis: epidemiology, pathophysiology, and management. Clin Microbiol Rev 18 383 416

7. PeacockSJ

SchweizerHP

DanceDA

SmithTL

GeeJE

2008 Management of accidental laboratory exposure to Burkholderia pseudomallei and B. mallei. Emerg Infect Dis 14 e2

8. PuthuchearySD

ParasakthiN

LeeMK

1992 Septicaemic melioidosis: a review of 50 cases from Malaysia. Trans R Soc Trop Med Hyg 86 683 685

9. PearsonT

GiffardP

Beckstrom-SternbergS

AuerbachR

HornstraH

2009 Phylogeographic reconstruction of a bacterial species with high levels of lateral gene transfer. BMC Biology In press

10. HoldenMT

TitballRW

PeacockSJ

Cerdeno-TarragaAM

AtkinsT

2004 Genomic plasticity of the causative agent of melioidosis, Burkholderia pseudomallei. Proc Natl Acad Sci U S A 101 14240 14245

11. SimSH

YuY

LinCH

KaruturiRK

WuthiekanunV

2008 The core and accessory genomes of Burkholderia pseudomallei: implications for human melioidosis. PLoS Pathog 4 e1000178 doi:10.1371/journal.ppat.1000178

12. NiermanWC

DeShazerD

KimHS

TettelinH

NelsonKE

2004 Structural flexibility in the Burkholderia mallei genome. Proc Natl Acad Sci U S A 101 14246 14251

13. TuanyokA

LeademBR

AuerbachRK

Beckstrom-SternbergSM

Beckstrom-SternbergJS

2008 Genomic islands from five strains of Burkholderia pseudomallei. BMC Genomics 9 566

14. TumapaS

HoldenMT

VesaratchavestM

WuthiekanunV

LimmathurotsakulD

2008 Burkholderia pseudomallei genome plasticity associated with genomic island variation. BMC Genomics 9 190

15. U'RenJM

SchuppJM

PearsonT

HornstraH

FriedmanCL

2007 Tandem repeat regions within the Burkholderia pseudomallei genome and their application for high resolution genotyping. BMC Microbiol 7 23

16. PearsonT

U'RenJM

SchuppJM

AllanGJ

FosterPG

2007 VNTR analysis of selected outbreaks of Burkholderia pseudomallei in Australia. Infect Genet Evol 7 416 423

17. LimmathurotsakulD

WuthiekanunV

ChantratitaN

WongsuvanG

ThanwisaiA

2007 Simultaneous infection with more than one strain of Burkholderia pseudomallei is uncommon in human melioidosis. J Clin Microbiol 45 3830 3832

18. MaharjanB

ChantratitaN

VesaratchavestM

ChengA

WuthiekanunV

2005 Recurrent melioidosis in patients in northeast Thailand is frequently due to reinfection rather than relapse. J Clin Microbiol 43 6032 6034

19. SwaminathanB

BarrettTJ

HunterSB

TauxeRV

2001 PulseNet: the molecular subtyping network for foodborne bacterial disease surveillance, United States. Emerg Infect Dis 7 382 389

20. VoglerAJ

KeysC

NemotoY

ColmanRE

JayZ

2006 Effect of repeat copy number on variable-number tandem repeat mutations in Escherichia coli O157:H7. J Bacteriol 188 4253 4263

21. GirardJM

WagnerDM

VoglerAJ

KeysC

AllenderCJ

2004 Differential plague-transmission dynamics determine Yersinia pestis population genetic structure on local, regional, and global scales. Proc Natl Acad Sci U S A 101 8408 8413

22. VoglerAJ

KeysCE

AllenderC

BaileyI

GirardJ

2007 Mutations, mutation rates, and evolution at the hypervariable VNTR loci of Yersinia pestis. Mutat Res 616 145 158

23. U'RenJM

HornstraH

PearsonT

SchuppJM

LeademB

2007 Fine-scale genetic diversity among Burkholderia pseudomallei soil isolates in northeast Thailand. Appl Environ Microbiol 73 6678 6681

24. LevinsonG

GutmanGA

1987 Slipped-strand mispairing: a major mechanism for DNA sequence evolution. Mol Biol Evol 4 203 221

25. FeilEJ

LiBC

AanensenDM

HanageWP

SprattBG

2004 eBURST: inferring patterns of evolutionary descent among clusters of related bacterial genotypes from multilocus sequence typing data. J Bacteriol 186 1518 1530

26. PittTL

TrakulsomboonS

DanceDA

2007 Recurrent melioidosis: possible role of infection with multiple strains of Burkholderia pseudomallei. J Clin Microbiol 45 680 681

27. HertDG

FredlakeCP

BarronAE

2008 Advantages and limitations of next-generation sequencing technologies: a comparison of electrophoresis and non-electrophoresis methods. Electrophoresis 29 4618 4626

28. ChouDW

ChungKM

ChenCH

CheungBM

2007 Bacteremic melioidosis in southern Taiwan: clinical characteristics and outcome. J Formos Med Assoc 106 1013 1022

29. VidyalakshmiK

ShrikalaB

BharathiB

SuchitraU

2007 Melioidosis: an under-diagnosed entity in western coastal India: a clinico-microbiological analysis. Indian J Med Microbiol 25 245 248

30. ChierakulW

WinothaiW

WattanawaitunechaiC

WuthiekanunV

RugtaenganT

2005 Melioidosis in 6 tsunami survivors in southern Thailand. Clin Infect Dis 41 982 990

31. WongsuvanG

LimmathurotsakulD

WannapasniS

ChierakulW

TeerawattanasookN

2009 Lack of correlation of Burkholderia pseudomallei quantities in blood, urine, sputum and pus. Southeast Asian J Trop Med Public Health 40 781 784

32. SamIC

SeeKH

PuthuchearySD

2009 Variations in ceftazidime and amoxicillin-clavulanate susceptibilities within a clonal infection of Burkholderia pseudomallei. J Clin Microbiol 47 1556 1558

33. WuthiekanunV

LimmathurotsakulD

WongsuvanG

ChierakulW

TeerawattanasookN

2007 Quantitation of B. Pseudomallei in clinical samples. Am J Trop Med Hyg 77 812 813

34. AshdownLR

1979 An improved screening technique for isolation of Pseudomonas pseudomallei from clinical specimens. Pathology 11 293 297

35. de LamballerieX

ZandottiC

VignoliC

BolletC

de MiccoP

1992 A one-step microbial DNA extraction method using “Chelex 100” suitable for gene amplification. Res Microbiol 143 785 790

36. GodoyD

RandleG

SimpsonAJ

AanensenDM

PittTL

2003 Multilocus sequence typing and evolutionary relationships among the causative agents of melioidosis and glanders, Burkholderia pseudomallei and Burkholderia mallei. J Clin Microbiol 41 2068 2079

37. PearsonT

OkinakaRT

FosterJT

KeimP

2009 Phylogenetic understanding of clonal populations in an era of whole genome sequencing. Infect Genet Evol 9 1010 1019

38. ColmanRE

VoglerAJ

LowellJL

GageKL

MorwayC

2009 Fine-scale identification of the most likely source of a human plague infection. Emerg Infect Dis 15 1623 1625

Štítky
Hygiena a epidemiológia Infekčné lekárstvo Laboratórium

Článok vyšiel v časopise

PLOS Pathogens


2010 Číslo 1
Najčítanejšie tento týždeň
Najčítanejšie v tomto čísle
Kurzy

Zvýšte si kvalifikáciu online z pohodlia domova

Získaná hemofilie - Povědomí o nemoci a její diagnostika
nový kurz

Eozinofilní granulomatóza s polyangiitidou
Autori: doc. MUDr. Martina Doubková, Ph.D.

Všetky kurzy
Prihlásenie
Zabudnuté heslo

Zadajte e-mailovú adresu, s ktorou ste vytvárali účet. Budú Vám na ňu zasielané informácie k nastaveniu nového hesla.

Prihlásenie

Nemáte účet?  Registrujte sa

#ADS_BOTTOM_SCRIPTS#