Transferable Plasmid-Mediated Resistance to Streptomycin in Clinical Isolate of Yersinia pestis

Guiyoule, Annie; Gerbaud, Guy; Buchrieser, Carmen; Galimand, Marc; Rahalison, Lila; Chanteau, Suzanne; Courvalin, Patrice; Carniel, Élisabeth

doi:10.3201/eid0701.010106

Cited by 216 publications

(173 citation statements)

References 13 publications

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“…In 1995, two strains isolated from patients in different regions of Madagascar were found to have acquired two genetically unrelated antibiotic resistant plasmids [26,34]. These plasmids could be readily transmissible to other Y. pestis strains under laboratory conditions.…”

Section: -Emergence Of New Ribotypesmentioning

confidence: 99%

From the recent lessons of the Malagasy foci towards a global understanding of the factors involved in plague reemergence

et al. 2005

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-Re-emergence of human cases of plague after decades of silence does not necessarily mean that plague foci are re-emerging. Most often, Yersinia pestis bacteria have been maintained and circulating at low levels in the rodent populations. It seems therefore more appropriate to speak in terms of expansion or regression phases for sylvatic rodent plague foci and to reserve the term reemergence for human cases. From the analysis of well-documented human plague cases in Madagascar, we underline the causes of re-emergence that can be generalized to most world foci, and can help define environments at risk where the threat of new emergence lurks. In all recent plague outbreaks, usually more than one risk factor was at the origin of the re-emergence. The reduction or discontinuance of surveillance and control, as well as poverty and insalubrity are the main factors in the re-emergence of human cases, allowing increased contacts with infected rodents and fleas. Environment changes (i.e. climatic changes, deforestation, urbanization) induce changes in flea and rodent populations by (i) extension of rodent habitats (for example by replacing forests by steppes or farmlands); (ii) modifications in population dynamics (possible outbreaks due to an increase of available food resources); but also, (iii) emergence of new vectors, reservoirs and new Y. pestis genotypes. Numerous and spontaneous genomic rearrangements occur at high frequencies in Y. pestis, which may confer selective advantages, enhancing the ability of Y. pestis to survive, to be transmitted to new hosts, and to colonize new environments. Therefore, any environmental change should be taken as a warning signal and active surveillance programs should be initiated.

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Section: -Emergence Of New Ribotypesmentioning

confidence: 99%

From the recent lessons of the Malagasy foci towards a global understanding of the factors involved in plague reemergence

et al. 2005

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“…pestis containing conjugative plasmids that encode high-level resistance to multiple antibiotics have been isolated from human patients in Madagascar (Galimand et al 1997;Guiyoule et al 2001). The source of these newly acquired plasmids is unknown, but conjugative plasmid transfer among bacteria can occur at high frequency within a dense, multicellular biofilm (Hausner and Wuertz 1999;Molin and Tolker-Nielsen 2003).…”

Section: Host Interfacementioning

confidence: 99%

Yersinia pestis Biofilm in the Flea Vector and Its Role in the Transmission of Plague

Hinnebusch¹,

Erickson²

2008

Current Topics in Microbiology and Immunology

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Transmission by fleabite is a relatively recent evolutionary adaptation of Yersinia pestis, the bacterial agent of bubonic plague. To produce a transmissible infection, Y. pestis grows as an attached biofilm in the foregut of the flea vector. Biofilm formation both in the flea foregut and in vitro is dependent on an extracellular matrix (ECM) synthesized by the Yersinia hms gene products. The hms genes are similar to the pga and ica genes of Escherichia coli and Staphylococcus epidermidis, respectively, that act to synthesize a poly-β-1,6-N-acetyl-dglucosamine ECM required for biofilm formation. As with extracellular polysaccharide production in many other bacteria, synthesis of the Hms-dependent ECM is controlled by intracellular levels of cyclic-di-GMP. Yersinia pseudotuberculosis, the food-and water-borne enteric pathogen from which Y. pestis evolved recently, possesses identical hms genes and can form biofilm in vitro but not in the flea. The genetic changes in Y. pestis that resulted in adapting biofilm-forming capability to the flea gut environment, a critical step in the evolution of vector-borne transmission, have yet to be identified. During a flea bite, Y. pestis is regurgitated into the dermis in a unique biofilm phenotype, and this has implications for the initial interaction with the mammalian innate immune response.

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“…The recommended antibiotic of choice for treatment of human plague is streptomycin (14), but with the emergence of streptomycin-resistant strains and the limited availability of streptomycin, reliance on this drug for the treatment of plague has decreased (4,15). Doxycycline, chloramphenicol, gentamicin, and ciprofloxacin are recommended for treatment of plague and are more commonly used today (4,14), although inhibitory in vitro ␤-lactams and sulfas may not be effective in vivo (6).…”

Section: Discussionmentioning

confidence: 99%

In Vitro Efficacy of Antibiotics Commonly Used To Treat Human Plague against Intracellular Yersinia pestis

Wendte¹,

Ponnusamy²,

Reiber

et al. 2011

Antimicrob Agents Chemother

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Transferable Plasmid-Mediated Resistance to Streptomycin in Clinical Isolate of Yersinia pestis

Cited by 216 publications

References 13 publications

From the recent lessons of the Malagasy foci towards a global understanding of the factors involved in plague reemergence

From the recent lessons of the Malagasy foci towards a global understanding of the factors involved in plague reemergence

Yersinia pestis Biofilm in the Flea Vector and Its Role in the Transmission of Plague

In Vitro Efficacy of Antibiotics Commonly Used To Treat Human Plague against Intracellular Yersinia pestis

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