[The plague reviewed by way of molecular biology]

The aetiology of plague was first discovered during the third pandemic of the disease occurring in Hong Kong in 1894. After Alexandre Yersin had identified the causal agent (Y. Pestis), Paul-Louis Simond proved the flea's role as vector. These discoveries were of prime importance for the subsequent development of efficient means for fighting plague as well as for preventive and curative treatments and vaccines. Vaccination brought about a sharp decrease in plague mortality and morbidity. However, the disease has never been eradicated. It is still prevalent in various Asian, African and American countries and is among the re-emerging diseases at the present time. The genetic basis of transmission mechanisms and pathogenicity of the bacillus are only beginning to be understood. We now know that the attenuation of the EV76 strain used by Girard and Robic as an anti-plague vaccine in Madagascar is due to the spontaneous excision of a large chromosomal DNA fragment of 102 kb, a part of which contains a group of genes implicated in the pathogenicity and appropriately called high pathogenicity island. These mechanisms of flea bacillus transmission are also beginning to be known. Two bacterial loci participating in the blocking of the ectoparasite's proventriculus have been identified. One is situated next to the high pathogenicity island on the unstable 102 kb chromosomal fragment, the other--on the large 95 kb plasmid specific to Y. pestis. The molecular basis of the bacillus' acquisition of multi-resistance to antibiotics have likewise recently been characterised. However, although Y. pestis is one of the most pathogenic micro-organisms of the bacterial world, the mechanisms responsible for this high level of pathogenecity have still not been identified. This is well worth noting, since a certain number of genes acting as pathogenicity factors in other species are present but altered in Y. pestis. Plague still withholds many secrets.