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ARS Home » Plains Area » Manhattan, Kansas » Center for Grain and Animal Health Research » ABADRU » Research » Publications at this Location » Publication #283436
Title: Pathogenicity and virulence

Author
item McVey, David
item CZUPRYNSKI, CHARLES - University Of Wisconsin

Submitted to: Book Chapter
Publication Type: Book / Chapter
Publication Acceptance Date: 9/10/2012
Publication Date: 7/1/2013
Citation: Mcvey, D.S., Czuprynski, C. 2013. Pathogenicity and virulence. Book Chapter. Veterinary Microbiology, 3rd Edition:491-500. ISBN:978-0-470-95949-7

Interpretive Summary:

Technical Abstract: Many pathogenic microorganisms are host-specific in that they parasitize only one or a few animal species. For example, the cause of equine strangles, Streptococcus equi subspecies equi, is essentially limited to infection of horses. Others—certain Salmonella serotypes, for example—have a broad host range. The basis for this difference in host specificity often is incompletely understood, but it may in part be related to the need for specific attachment devices between host (receptors) and parasite (adhesins). Some agents infect several host species with varying effects. For example, the plague bacillus Yersinia pestis behaves as a commensal parasite in many, small rodent species but causes fatal disease in rats and humans. Evolutionary pressure may have produced some of these differences. For instance, Coccidioides immitis, a saprophytic fungus that requires no living host, infects cattle and dogs with equal ease; yet it produces no clinical signs in cattle but frequently causes progressive fatal disease in dogs. Potential pathogens also vary in their effects on different tissues in the same host. The Escherichia coli strains that are commensals in the intestine can cause severe disease in the urinary tract and peritoneal cavity. Some microorganisms that are commensals in one habitat may be pathogenic in the same, or some other, habitat that is pathologically altered or otherwise compromised. For example, oral streptococci, which occasionally enter the bloodstream, may colonize a damaged heart valve and initiate bacterial endocarditis. In the absence of such a lesion, however, the Streptococci would not colonize and would be cleared uneventfully by the innate immune system. Similarly, the frequent translocation of intestinal bacteria across the intestinal mucosa, and Into the vascular channels, normally leads to their clearance by innate and adaptive defense mechanisms. In immuno-deficient hosts, however, such entrance may lead to fatal septicemia.