Journal Article > ResearchFull Text
Nat Microbiol. 21 March 2016; Volume 1 (Issue 4); DOI:10.1038/nmicrobiol.2016.27
Njamkepo E, Fawal N, Tran-Dien A, Hawkey J, Strockbine N, et al.
Nat Microbiol. 21 March 2016; Volume 1 (Issue 4); DOI:10.1038/nmicrobiol.2016.27
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.
Journal Article > ResearchAbstract Only
Science. 10 November 2017; Volume 358 (Issue 6364); 785-789.; DOI:10.1126/science.aad5901
Weill FX, Domman D, Njamkepo E, Tarr C, Rauzier J, et al.
Science. 10 November 2017; Volume 358 (Issue 6364); 785-789.; DOI:10.1126/science.aad5901
The seventh cholera pandemic has heavily affected Africa, although the origin and continental spread of the disease remain undefined. We used genomic data from 1070 Vibrio cholerae O1 isolates, across 45 African countries and over a 49-year period, to show that past epidemics were attributable to a single expanded lineage. This lineage was introduced at least 11 times since 1970, into two main regions, West Africa and East/Southern Africa, causing epidemics that lasted up to 28 years. The last five introductions into Africa, all from Asia, involved multidrug-resistant sublineages that replaced antibiotic-susceptible sublineages after 2000. This phylogenetic framework describes the periodicity of lineage introduction and the stable routes of cholera spread, which should inform the rational design of control measures for cholera in Africa.
Journal Article > ResearchFull Text
Trans R Soc Trop Med Hyg. 1 December 2006; Volume 100 (Issue 12); DOI:10.1016/j.trstmh.2006.02.007
Bercion R, Accou-Demartin M, Recio C, Massamba PM, Frank T, et al.
Trans R Soc Trop Med Hyg. 1 December 2006; Volume 100 (Issue 12); DOI:10.1016/j.trstmh.2006.02.007
Shigella dysenteriae type 1 (Sd1) represents a particular threat in developing countries because of the severity of the infection and its epidemic potential. Antimicrobial susceptibility testing and molecular subtyping by pulsed-field gel electrophoresis (PFGE) and plasmid profiling (PP) of Sd1 isolates collected during two dysentery outbreaks (2013 and 445 cases of bloody diarrhoea) in Central African Republic (CAR) during the period 2003-2004 were reported. Eleven Sd1 comparison strains (CS) acquired by travellers or residents of Africa (n=10) or Asia (n=1) between 1993 and 2003 were also analysed. The 19 Sd1 isolates recovered from CAR outbreaks were multidrug resistant, although susceptible to quinolones and fluoroquinolones. Molecular subtyping by PFGE was more discriminatory than PP. The PFGE using XbaI and NotI restriction enzymes indicated that the two outbreaks were due to two different clones and also revealed a genetic diversity among the CS recovered from outbreak or sporadic cases between 1993 and 2003. This study was the result of a fruitful collaboration between field physicians and microbiologists. The data collected will serve as the basis for establishing long-term monitoring of Sd1 in CAR.