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BACTERIAL PATHOGENICITY |

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*Department of Microbiology & Infectious Diseases,
Department of Pathology & Laboratory Medicine, University of Calgary and
Calgary Laboratory Services, Calgary, Canada
Corresponding author: Dr A. P. Gibb (e-mail: a.p.gibb{at}ed.ac.uk). Present address: Department of Medical Microbiology, Medical School, Teviot Place, Edinburgh EH8 9AG, UK.
Received 31 May 2001; accepted 5 June 2001.
Abstract
Yersinia enterocolitica is a bacterium capable of growth at 4°C in donated blood and has been responsible for many deaths following transfusion. Interaction of Y. enterocolitica with blood cells is of interest in understanding the mechanisms of survival and growth in blood. The closely related organism Y. pseudotuberculosis is known to invade platelets and cause platelet aggregation by a mechanism that involves expression of the chromosomal inv gene. Yersinia isolates were made to express green fluorescent protein (GFP) and their interaction with platelets was studied by flow cytometry. Y. enterocolitica did not cause platelet aggregation or activation, not even when grown at 22°C to maximise inv expression. Attachment of Y. enterocolitica O:9 to platelets occurred with virulence plasmid-bearing (pYV+) strains grown at 37°C but not with pYV- strains nor with strains grown at 22°C. Y. pseudotuberculosis containing inv did cause platelet activation and aggregation when grown at 22°C, as has been shown before, but also showed enhanced attachment to platelets when grown at 37°C. Electron microscopy studies confirmed that inv-expressing Y. pseudotuberculosis invaded platelets but Y. enterocolitica attached only to the outer surface of platelets. Interaction of Y. enterocolitica O:9 with platelets provided a modest protection against bacterial killing by human serum. Interaction of Y. enterocolitica O:9 with platelets does not lead to platelet invasion or activation, and is mediated through plasmid-coded factors, not inv.
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