Degree Type


Date of Award


Degree Name

Doctor of Philosophy


Veterinary Microbiology and Preventive Medicine

First Advisor

Michael J. Wannemuehler


The pathogenesis of disease caused by Serpulina hyodysenteriae was examined by (1) determining the susceptibilities of inbred murine strains to lesion development, (2) examining the ability of S. hyodysenteriae endotoxin and lipopolysaccharide (LPS) preparations to induce tumor necrosis factor (TNF), and (3) investigating the contributions of secondary bacteria to S. hyodysenteriae-induced pathogenesis in gnotobiotic mice. Of all inbred murine strains tested, C3H strains of mice appeared most susceptible to lesion development after S. hyodysenteriae challenge. C3H/HeJ mice, being LPS-hyporesponsive, were less susceptible to lesion development than LPS-responsive C3H/HeN. S. hyodysenteriae endotoxin preparations were active in increasing serum TNF activity in vivo in mice. Sera from pigs treated with S. hyodysenteriae endotoxin or LPS preparations exhibited much less TNF activity than sera from pigs treated with LPS from Escherichia coli or Salmonella typhimurium;Secondary bacteria appear to contribute a dynamic role to the pathogenesis of the disease; treating conventional mice with oral antibiotics prevented lesion formation even with high levels of colonizing S. hyodysenteriae. Additionally, a defined diet is described which, through presumed changes in gut microflora, increases susceptibility of mice to development of lesions after S. hyodysenteriae challenge. Gnotobiotic mice were monoassociated with S. hyodysenteriae or with S. innocens for protracted incubation times. A difference noted histologically between the two groups was that pathogenesis S. hyodysenteriae invaded the lamina propria of the cecum, whereas the non-pathogenic S. innocens did not. Severe combined immunodeficient (SCID) mice were experimentally challenged with S. hyodysenteriae; SCID mice developed similar gross cecal lesions, but, histologically, the lamina propria cellular infiltrate was characterized by high numbers of neutrophils. Since SCID mice are lacking in functional T or B lymphocytes, this might suggest that inflammatory cytokines are being produced in the cecal lamina propria of infected mice, primarily by macrophages.



Digital Repository @ Iowa State University,

Copyright Owner

Stuart Kent Nibbelink



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File Size

176 pages