Host-Pathogen Interactions in Chronic Prostatitis Revisited

J Dimitrakov,1 A Casadevall2

Department of Urology and Nephrology,, Higher Medical Institute, Plovdiv,, Bulgaria and 2Division of Infectious Diseases, Department of Medicine, and Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY

Background Existing concepts of virulence and pathogenicity are inadequate because they do not account for the full complexity of microbial pathogenesis in hosts with and without impaired immunity. The generally used definition of a pathogen as a microbe that causes disease in a host seems inadequate in some patients with chronic prostatitis (CP), because some microbes do not cause clinically evident disease in all hosts and vice versa, some commensal microorganisms (like coagulase-negative staphylococcus) might be involved in some prostatitis cases (Nickel JC, 1992).

Object To better define the host-pathogen interactions in chronic prostatitis patients.

Proposal The Casadevall-Pirofski Classification (1999): A damage-response continuum to define microbial pathogenesis. Class 1: pathogens that cause damage only in situations of weak immune responses. Class 2: pathogens that cause damage either in hosts with weak immune responses or in the setting of normal immune responses. Class 3: pathogens that cause damage in the setting of appropriate immune responses and produce damage at both ends of the continuum of immune responses. Class 4: pathogens that cause damage primarily at the extremes of both weak and strong immune responses. Class 5: pathogens that cause damage across the spectrum of immune responses, but damage can be enhanced by strong immune responses. Class 6: microorganisms that can cause damage only in conditions of strong immune responses.

Conclusion By merging the concepts that the host response contributes to pathogen-mediated damage and the classical view that pathogens have distinct characteristics that define their virulence, the damage-response classification permits a new approach to host-pathogen interactions in chronic prostatitis that is not constrained by pathogen-and/or host-centered views of microbial pathogenesis.