The genome of Shigella dysenteriae strain Sd1617 comparison to representative strains in evaluating pathogenesis

Vongsawan, Ajchara A.; Kapatral, Vinayak; Vaisvil, Benjamin; Burd, Henry; Serichantalergs, Oralak; Venkatesan, Malabi M.; Mason, Carl J.

doi:10.1093/femsle/fnv011

Cited by 6 publications

(4 citation statements)

References 46 publications

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“…Single-nucleotide polymorphisms (SNPs) were detected by mapping short-read sequences against Sd1 reference genomes: Sd197 17 , which was isolated during an outbreak in China in the 1950s, and Sd1617 18 , which was isolated in Guatemala during the 1968-1969 epidemic. Maximum likelihood (ML) phylogenetic analysis was performed on 14,677 (mapping against Sd197) and 15,752 (mapping against Sd1617) chromosomal SNPs, which were randomly distributed over the non-repetitive nonrecombinant core genome (85.6% of the Sd197 chromosome, Supplementary Information).…”

Section: Textmentioning

confidence: 99%

“…Among the 149 isolates bearing the SRL-PAI, only two showed a partial deletion of the SRL-PAI, resulting in a loss of the antibiotic resistance cluster (i.e., the SRL sensu stricto). This structure is therefore quite stable over time, particularly in a bacterium containing hundreds of ISs 17,18 . This 66-kb element encodes resistance to ampicillin, streptomycin, chloramphenicol and tetracycline, with no more resistance than the previously circulating large plasmids.…”

Section: Lineage II Contained Mostly Isolates Collected In Europe Betmentioning

confidence: 99%

“…Sd1 strain Sd19717 was used as the reference genome. A second Sd1 genome Sd161718 was used as a second reference genome, to confirm the population structure found withSd197. Short-read sequences from the following six Sd1 genomes published by Rohmer et al 2 were downloaded from the ENA and included in this study: 2735 (USA, 1974, SRR765065), 91R17 (Guatemala, 1991, SRR765098), 91R14 (Guatemala, 1991, SRR765104), DH03 (Central African Republic, 1996, SRR765110), DH05 (Central African Republic, 1996, SRR765112), and DH06 (Central African Republic, 1996, SRR765113).…”

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confidence: 99%

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Global phylogeography and evolutionary history of Shigella dysenteriae type 1

Njamkepo¹,

Fawal²,

Tran-Dien³

et al. 2016

Nat Microbiol

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Together with plague, smallpox and typhus, epidemics of dysentery have been a major scourge of human populations for centuries(1). A previous genomic study concluded that Shigella dysenteriae type 1 (Sd1), the epidemic dysentery bacillus, emerged and spread worldwide after the First World War, with no clear pattern of transmission(2). This is not consistent with the massive cyclic dysentery epidemics reported in Europe during the eighteenth and nineteenth centuries(1,3,4) and the first isolation of Sd1 in Japan in 1897(5). Here, we report a whole-genome analysis of 331 Sd1 isolates from around the world, collected between 1915 and 2011, providing us with unprecedented insight into the historical spread of this pathogen. We show here that Sd1 has existed since at least the eighteenth century and that it swept the globe at the end of the nineteenth century, diversifying into distinct lineages associated with the First World War, Second World War and various conflicts or natural disasters across Africa, Asia and Central America. We also provide a unique historical perspective on the evolution of antibiotic resistance over a 100-year period, beginning decades before the antibiotic era, and identify a prevalent multiple antibiotic-resistant lineage in South Asia that was transmitted in several waves to Africa, where it caused severe outbreaks of disease.

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Section: Textmentioning

confidence: 99%

Section: Lineage II Contained Mostly Isolates Collected In Europe Betmentioning

confidence: 99%

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Global phylogeography and evolutionary history of Shigella dysenteriae type 1

Njamkepo¹,

Fawal²,

Tran-Dien³

et al. 2016

Nat Microbiol

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“…The characteristics of the master cell bank of the S. dysenteriae Type 1 1617 strain used were confirmed by (i) slide agglutination test to show it agglutinated with S. dysenteriae Type 1 specific sera; (ii) plaque assay to show that it invaded intracellularly by forming hollow plaques in LLC‐MK2 cells; (iii) stability assay to show that it was stable by having > 80% of single‐well‐isolated virulent colonies present after three consecutive sub‐cultures on Congo Red agar plates. Our previous studies have determined that the optimal challenge dose for an 80% attack rate of shigellosis is 2 × 10 9 CFUs .…”

Section: Non‐human Primatesmentioning

confidence: 99%

Controlling the cytokine storm in severe bacterial diarrhoea with an oral Toll‐like receptor 4 antagonist

et al. 2015

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SummaryShigella dysenteriae causes the most severe of all infectious diarrhoeas and colitis. We infected rhesus macaques orally and also treated them orally with a small and non-absorbable polypropyletherimine dendrimer glucosamine that is a Toll-like receptor-4 (TLR4) antagonist. Antibiotics were not given for this life-threatening infection. Six days later, the clinical score for diarrhoea, mucus and blood was 54% lower, colon interleukin-8 and interleukin-6 were both 77% lower, and colon neutrophil infiltration was 75% less. Strikingly, vasculitis did not occur and tissue fibrin thrombi were reduced by 67%. There was no clinical toxicity or adverse effect of dendrimer glucosamine on systemic immunity. This is the first report in non-human primates of the therapeutic efficacy of a small and orally bioavailable TLR antagonist in severe infection. Our results show that an oral TLR4 antagonist can enable controlled resolution of the infectionrelated-inflammatory response and can also prevent neutrophil-mediated gut wall necrosis in severe infectious diarrhoeas.

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