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riun leprae). Still others occur in individuals with underlying medical conditions that impair host defenses, allowing an opportunistic agent to become invasive (e.g., enterococci) or the acquisition of nosocomial agents (e.g., Serratia marcescens). Innovative or expanded methods for preventing nosocomial infections, with their multitude of potential specific etiologic agents, make immunization an inferior option. This list of pathogenic microorganisms excluded from consideration due to lack of scientific knowledge is not intended to be exhaustive, and the following illustration for one agent is intended to provide a rationale that would be common to several others.

Syphilis is a prominent example of an infection in the immunocompetent host that poses both a substantial disease burden and a substantial expenditure of public health resources in the United States, and against which the development of a vaccine seems unlikely in the near future. The late 1980s saw a dramatic resurgence of syphilis, especially among women (with a parallel increase in congenitally acquired infections) and among ethnic minority groups in urban areas. At least 20,000 cases of primary or secondary syphilis are reported each year, but it is estimated that only one in three or four cases is reported. Because this is a sexually transmitted infection, both the infected individual and the exposed sexual partner require counseling, diagnostic testing, treatment, and follow-up testing.

The causative agent, T. pallidum, has a complex morphology and composition. An outer membrane surrounds the endoflagella, cytoplasmic membrane, and the protoplasmic cylinder. It also is believed that T. pallidum has a glycosaminoglycan surface layer that is antiphagocytic. The organism also has more than 15 major protein constituents, some of which are covalently linked to fatty acids. The outer membrane consists of a lipid bilayer, presumably with few proteins. However, the precise cellular locations of these antigens and the identities of nonprotein constituents remain controversial.

Humoral immunity in syphilis has been studied for nearly a century. Human infection uniformly invokes immunoglobulin G (IgG) and IgM antibodies to a wide variety of T. pallidum proteins, but that infection progresses to secondary and eventually tertiary manifestations unless specific therapy is administered. Passive administration of serum from rabbits recovering from experimental infection attenuates but does not prevent infection. This finding and other evidence suggest that humoral immunity is not sufficient for the prevention of infection, and recent data indicate that cellular immune mechanisms are considerably more important. Thus, most experts conclude that despite the impressive disease burden attributable to syphilis, there is insufficient knowledge concerning mechanisms of protective immunity to T. pallidum to propose that a vaccine be developed in the near future.

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