Host-induced epidemic spread of the cholera bacterium.
The factors that enhance the transmission of pathogens during epidemic spread are ill defined. Water-borne spread of the diarrhoeal disease cholera occurs rapidly in nature, whereas infection of human volunteers with bacteria grown in vitro is difficult in the absence of stomach acid buffering. It is unclear, however, whether stomach acidity is a principal factor contributing to epidemic spread. Here we report that characterization of Vibrio cholerae from human stools supports a model whereby human colonization creates a hyperinfectious bacterial state that is maintained after dissemination and that may contribute to epidemic spread of cholera. Transcriptional profiling of V. cholerae from stool samples revealed a unique physiological and behavioural state characterized by high expression levels of genes required for nutrient acquisition and motility, and low expression levels of genes required for bacterial chemotaxis.
Merrell
D Scott
DS
Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
Butler
Susan M
SM
Qadri
Firdausi
F
Dolganov
Nadia A
NA
Alam
Ahsfaqul
A
Cohen
Mitchell B
MB
Calderwood
Stephen B
SB
Schoolnik
Gary K
GK
Camilli
Andrew
A
D000818:Animals; D000831:Animals, Newborn; D001459:Bangladesh / Q000453:epidemiology; D002633:Chemotaxis; D002771:Cholera / Q000453:epidemiology / Q000635:transmission*; D005243:Feces / Q000382:microbiology*; D005618:Fresh Water / Q000382:microbiology; D005744:Gastric Acid / Q000378:metabolism; D020869:Gene Expression Profiling; D015964:Gene Expression Regulation, Bacterial; D005798:Genes, Bacterial / Q000235:genetics; D006801:Humans; D051379:Mice; D020411:Oligonucleotide Array Sequence Analysis; D012329:RNA, Bacterial / Q000235:genetics / Q000378:metabolism; D014734:Vibrio cholerae / Q000235:genetics* / Q000254:growth & development / Q000302:isolation & purification / Q000502:physiology*
D012329:RNA, Bacterial