Distinct Salmonella Enteritidis lineages associated with enterocolitis in high-income settings and invasive disease in low-income settings.

Feasey NA1,2,3,4, Hadfield J2, Keddy KH5,6, Dallman TJ7, Jacobs J8,9, Deng X10,11, Wigley P4, Barquist Barquist L12, Langridge GC2, Feltwell T2, Harris SR2, Mather AE2, Fookes M2, Aslett M2, Msefula C3,13, Kariuki S14, Maclennan CA2,15, Onsare RS14, Weill FX16, Le Hello S16, Smith AM5, McClelland M17,Desai P17, Parry CM1,18,19, Cheesbrough J20, French N4, Campos J21, Chabalgoity JA22, Betancor L22, Hopkins KL23, Nair S7, Humphrey TJ24, Lunguya O25,26, Cogan TA27, Tapia MD28, Sow SO29, Tennant SM28, Bornstein K28, Levine MM28, Lacharme-Lora L4, Everett DB4, Kingsley RA2,30, Parkhill J2,Heyderman RS3,31, Dougan G2, Gordon MA3,4, Thomson NR2,18.

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Abstract

An epidemiological paradox surrounds Salmonella enterica serovar Enteritidis. In high-income settings, it has been responsible for an epidemic of poultry-associated, self-limiting enterocolitis, whereas in sub-Saharan Africa it is a major cause of invasive nontyphoidal Salmonella disease, associated with high case fatality. By whole-genome sequence analysis of 675 isolates of S. Enteritidis from 45 countries, we show the existence of a global epidemic clade and two new clades of S. Enteritidis that are geographically restricted to distinct regions of Africa. The African isolates display genomic degradation, a novel prophage repertoire, and an expanded multidrug resistance plasmid. S. Enteritidis is a further example of a Salmonella serotype that displays niche plasticity, with distinct clades that enable it to become a prominent cause of gastroenteritis in association with the industrial production of eggs and of multidrug-resistant, bloodstream-invasive infection in Africa.