Autotransporters but not pAA are critical for rabbit colonization by Shiga toxin-producing Escherichia coli O104:H4.
The outbreak of diarrhoea and haemolytic uraemic syndrome that occurred in Germany in 2011 was caused by a Shiga toxin-producing enteroaggregative Escherichia coli (EAEC) strain. The strain was classified as EAEC owing to the presence of a plasmid (pAA) that mediates a characteristic pattern of aggregative adherence on cultured cells, the defining feature of EAEC that has classically been associated with virulence. Here we describe an infant rabbit-based model of intestinal colonization and diarrhoea caused by the outbreak strain, which we use to decipher the factors that mediate the pathogen's virulence. Shiga toxin is the key factor required for diarrhoea. Unexpectedly, we observe that pAA is dispensable for intestinal colonization and development of intestinal pathology. Instead, chromosome-encoded autotransporters are critical for robust colonization and diarrhoeal disease in this model. Our findings suggest that conventional wisdom linking aggregative adherence to EAEC intestinal colonization is false for at least a subset of strains.
1] Division of Infectious Diseases, Brigham & Women's Hospital, Boston, Massachusetts 02115, USA [2] Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA [3] HHMI, Boston, Massachusetts 02115, USA.
Diana
D
Munera
1] Division of Infectious Diseases, Brigham & Women's Hospital, Boston, Massachusetts 02115, USA [2] Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA [3].
Jennifer M
JM
Ritchie
1] Division of Infectious Diseases, Brigham & Women's Hospital, Boston, Massachusetts 02115, USA [2] Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA [3] HHMI, Boston, Massachusetts 02115, USA.
Stavroula K
SK
Hatzios
Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Rod
R
Bronson
Department of Genetics and Genomic Sciences, Mount Sinai School of Medicine, New York, New York 10029, USA.
Gang
G
Fang
Department of Genetics and Genomic Sciences, Mount Sinai School of Medicine, New York, New York 10029, USA.
Eric E
EE
Schadt
1] Division of Infectious Diseases, Brigham & Women's Hospital, Boston, Massachusetts 02115, USA [2] Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA [3] HHMI, Boston, Massachusetts 02115, USA.
Brigid M
BM
Davis
1] Division of Infectious Diseases, Brigham & Women's Hospital, Boston, Massachusetts 02115, USA [2] Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA [3] HHMI, Boston, Massachusetts 02115, USA.
Matthew K
MK
Waldor
D000818:Animals; D002352:Carrier Proteins / Q000502:physiology*; D003967:Diarrhea / Q000378:metabolism / Q000382:microbiology / Q000503:physiopathology; D004195:Disease Models, Animal; D004927:Escherichia coli Infections / Q000378:metabolism / Q000382:microbiology / Q000503:physiopathology; D029968:Escherichia coli Proteins / Q000502:physiology*; D005260:Female; D007422:Intestines / Q000382:microbiology / Q000473:pathology; D008297:Male; D010802:Phylogeny; D010957:Plasmids / Q000502:physiology*; D011817:Rabbits; D054323:Shiga-Toxigenic Escherichia coli / Q000235:genetics* / Q000472:pathogenicity*
D002352:Carrier Proteins; D029968:Escherichia coli Proteins