Epidemiological evidence suggests that there is acquired immunity to shigellosis; however, it is species- and subtype-specific. Endemic shigellosis is primarily a childhood disease, although introduction of a new strain into a population results in disease in all age groups (Keusch, 1982). The best evidence for type-specific immunity comes from trials using live streptomycin-dependent shigella vaccine strains in a large community field study in Yugoslavia (Mel et al., 1968). In this study, two groups of subjects received different vaccine strains. The overall rate of shigellosis did not differ between the groups, but each group was protected only against the strains included in the vaccine it received. This finding is supported by experimental vaccine studies in volunteers, which demonstrate serotype-specific protection when challenged with the same strain (Dupont et al., 1972). These findings indicate that antibacterial immunity is involved. Although patients develop antibodies to the homologous somatic O antigens of the infecting strain, primarily of the IgM isotype, there is no evidence that this serum antibody is protective.

Patients with shigellosis also develop IgM-neutralizing serum antibody to the shigella toxin. Current evidence indicates, however, that serum-neutralizing antibody is not protective against oral challenge with the organism (Keusch, 1982). Indeed, parenteral immunization of Rhesus monkeys with toxoid resulting in high serum antitoxin titers does not protect against clinical shigellosis following oral bacterial challenge (McIver et al., 1977).

Shigellas are worldwide in distribution, but the prevalence of different species varies from country to country. For unexplained epidemiological reasons, S. dysenteriae 1, which was the predominant worldwide isolate for the first 30 years after its discovery in 1898, was replaced by S. flexneri in the years before World War II. For the past 2 decades, S. sonnei has become the dominant organism in the industrialized nations, while S. flexneri has persisted in the developing countries, punctuated by outbreaks of epidemic dysentery due to S. dysenteriae 1 (Keusch, 1982). Because the more virulent species are more prevalent in developing countries, where malnutrition, poor hygiene, and lack of medical care are also widespread, morbidity and mortality are considerably more severe.

The disease burden estimates for shigella are shown in Table D-15.1. The derivation of the number of acute cases is described in Appendix C.