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Bacillary dysentery is an invasive infectious disease of the human colon. At least three genetic loci on the chromosome and a huge plasmid have been implicated in its pathogenesis. Results obtained from molecular genetic studies, mainly of the genes, virG, virF and kcpA are discussed.
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An outbreak of bacillary dysentery in 1978 affecting 928 persons, most of whom were living in the village of St-Jacques, PQ, is described. An epidemiologic study suggested the water supply as the source of the infection, and it was established that the water carried by the municipal aqueduct was contaminated by feces containing the causal agent, Shigella sonnei. This epidemic, the largest mentioned in he Canadian medical literature, demonstrates how contagious this infection is.
The development of acute bacillary dysentery was followed in 23 patients involved in two outbreaks and in three sporadic, mutually unrelated cases. Repeated cultivations performed at 2-day intervals for 10 days yielded 386 identifiable strains of "opportune intestinal flora". Escherichia coli colicinogenic activity is one of the significant factors of gastrointestinal tract protection. The period of shigella excretion is significantly reduced (p less than 0.02) if an appropriate colicinogenic E. coli strain is present. Analysis of the results suggested a working hypothesis of differentiated approach to bacillary dysentery treatment in outbreaks. In the absence of a suitable colicinogenic flora neomycin therapy should be administered since it does not damage the natural colonizing flora (bacteroids, bifidobacters, aerobic lactobacilli); in the presence of a suitable colicinogenic flora, no antibiotic should be used as this would abolish the coli-flora.
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The Shigella bacteria cause bacillary dysentery, which remains a significant threat to public health. The genus status and species classification appear no longer valid, as compelling evidence indicates that Shigella, as well as enteroinvasive Escherichia coli, are derived from multiple origins of E.coli and form a single pathovar. Nevertheless, Shigella dysenteriae serotype 1 causes deadly epidemics but Shigella boydii is restricted to the Indian subcontinent, while Shigella flexneri and Shigella sonnei are prevalent in developing and developed countries respectively. To begin to explain these distinctive epidemiological and pathological features at the genome level, we have carried out comparative genomics on four representative strains. Each of the Shigella genomes includes a virulence plasmid that encodes conserved primary virulence determinants. The Shigella chromosomes share most of their genes with that of E.coli K12 strain MG1655, but each has over 200 pseudogenes, 300 approximately 700 copies of insertion sequence (IS) elements, and numerous deletions, insertions, translocations and inversions. There is extensive diversity of putative virulence genes, mostly acquired via bacteriophage-mediated lateral gene transfer. Hence, via convergent evolution involving gain and loss of functions, through bacteriophage-mediated gene acquisition, IS-mediated DNA rearrangements and formation of pseudogenes, the Shigella spp. became highly specific human pathogens with variable epidemiological and pathological features.
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