The recent emergence of plague: A process of felonious evolution

被引:29
作者
Brubaker, RR [1 ]
机构
[1] Michigan State Univ, Dept Microbiol & Mol Genet, E Lansing, MI 48824 USA
关键词
D O I
10.1007/s00248-003-1022-y
中图分类号
Q14 [生态学(生物生态学)];
学科分类号
071012 ; 0713 ;
摘要
Yersinia pestis, the causative agent of bubonic plague, evolved from closely related Yersinia pseudotuberculosis within the past 20,000 years, an event that corresponds to the end of the last ice age and distribution of Homo sapiens throughout the world. Y. pseudotuberculosis causes chronic but generally mild enteropathogenic infections whereas plague is the most devastating acute disease experienced by mankind. The very recent evolution of plague from its progenitor assures close genomic homogeneity between the two species and thus high probability that disparities in DNA sequence mediate dramatic differences in symptoms of infection. The purpose of this minireview is to define salient distinctions between the genomes of Y. pestis and Y. pseudotuberculosis and to equate unique functions to respective acute and chronic mechanisms of virulence. The significance of these processes is then related to the procedures the organisms use to survive when between hosts (i.e., the flea vector colonized by Y. pestis and natural environments including soil and water in the case of Y. pseudotuberculosis). Next, an attempt is made to order the various mutational events that caused the recent emergence of Y. pestis as a distinct species. Finally, selective pressures such as predatory soil nematodes are considered that possibly influenced the early evolution of those yersiniae now pathogenic to humans.
引用
收藏
页码:293 / 299
页数:7
相关论文
共 76 条
[31]   MUTATION TO RHAMNOSE UTILIZATION IN PASTEURELLA-PESTIS [J].
ENGLESBERG, E .
JOURNAL OF BACTERIOLOGY, 1957, 73 (05) :641-648
[32]   PLASMIDS IN YERSINIA-PESTIS [J].
FERBER, DM ;
BRUBAKER, RR .
INFECTION AND IMMUNITY, 1981, 31 (02) :839-841
[33]   ANALYSIS OF THE PESTICIN RECEPTOR FROM YERSINIA-PESTIS - ROLE IN IRON-DEFICIENT GROWTH AND POSSIBLE REGULATION BY ITS SIDEROPHORE [J].
FETHERSTON, JD ;
LILLARD, JW ;
PERRY, RD .
JOURNAL OF BACTERIOLOGY, 1995, 177 (07) :1824-1833
[34]   LOSS OF THE PIGMENTATION PHENOTYPE IN YERSINIA-PESTIS IS DUE TO THE SPONTANEOUS DELETION OF 102 KB OF CHROMOSOMAL DNA WHICH IS FLANKED BY A REPETITIVE ELEMENT [J].
FETHERSTON, JD ;
SCHUETZE, P ;
PERRY, RD .
MOLECULAR MICROBIOLOGY, 1992, 6 (18) :2693-2704
[35]   THE PIGMENTATION LOCUS OF YERSINIA-PESTIS KIM6+ IS FLANKED BY AN INSERTION-SEQUENCE AND INCLUDES THE STRUCTURAL GENES FOR PESTICIN SENSITIVITY AND HMWP2 [J].
FETHERSTON, JD ;
PERRY, RD .
MOLECULAR MICROBIOLOGY, 1994, 13 (04) :697-708
[36]   Common themes in microbial pathogenicity revisited [J].
Finlay, BB ;
Falkow, S .
MICROBIOLOGY AND MOLECULAR BIOLOGY REVIEWS, 1997, 61 (02) :136-+
[37]  
FRIESEN HG, 1995, MRC COMMUNIQUE, V21, P2
[38]   Reevaluation of the virulence phenotype of the inv yadA double mutants of Yersinia pseudotuberculosis [J].
Han, YW ;
Miller, VL .
INFECTION AND IMMUNITY, 1997, 65 (01) :327-330
[39]   High-frequency RecA-dependent and -independent mechanisms of Congo red binding mutations in Yersinia pestis [J].
Hare, JM ;
McDonough, KA .
JOURNAL OF BACTERIOLOGY, 1999, 181 (16) :4896-4904
[40]   Independent acquisition and insertion into different chromosomal locations of the same pathogenicity island in Yersinia pestis and Yersinia pseudotuberculosis [J].
Hare, JM ;
Wagner, AK ;
McDonough, KA .
MOLECULAR MICROBIOLOGY, 1999, 31 (01) :291-303