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Infection and Immunity, February 2001, p. 1120-1126, Vol. 69, No. 2
MRC Microbiology and Gut Biology Group,
University of Dundee, Dundee, United Kingdom
Received 1 August 2000/Returned for modification 8 September
2000/Accepted 23 October 2000
Clostridium septicum is responsible for several
diseases in humans and animals. The bacterium is capable of a simple
kind of multicellular behavior known as swarming. In this
investigation, environmental and physiologic factors affecting growth
and swarm cell formation in C. septicum were studied over a
range of dilution rates (D = 0.02 to 0.65 h
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.2.1120-1126.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Toxin Synthesis and Mucin Breakdown Are Related to
Swarming Phenomenon in Clostridium septicum
1) in glucose-limited, glucose-excess, and mucin-limited
chemostats. Cellular differentiation was observed at low specific
growth rates, irrespective of the carbon and energy source, showing
that swarming occurred in response to nutrient depletion. Differential
expression of virulence determinants was detected in swarm cells.
Hemolysin was secreted by short motile rods but not swarm cells,
whereas in cultures grown with glucose, only swarm cells formed DNase, hyaluronidase, and neuraminidase. However, neuraminidase and, to a
lesser degree, hyaluronidase were induced in short motile rods in
mucin-limited cultures. Both swarm cells and short rods were cytotoxic
to Vero cells. Mucin was chemotaxic to C. septicum, and
large amounts of mucin-degrading enzymes (
-galactosidase, N-acetyl
-glucosaminidase, glycosulfatase, and
neuraminidase) were produced. Synthesis of these enzymes was catabolite
regulated. In chemostat experiments, glycosulfatase secretion occurred
only in swarm cells at low dilution rates in mucin-limited cultures. Determinations of oligosaccharide utilization demonstrated that N-acetylglucosamine, galactose, and
N-acetylgalactosamine were the main carbon sources for
C. septicum in mucin. Neuraminic acid was not assimilated,
showing that neuraminidase does not have a direct nutritional function
in this pathogen.
*
Corresponding author. Mailing address: MRC Microbiology
and Gut Biology Group, Level 6, Ninewells Hospital and Medical School, Dundee, DD1 9SY, Scotland, United Kingdom. Phone: 44-1382-496250. Fax:
44-1382-633952. E-mail: g.t.macfarlane{at}dundee.ac.uk.
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