Abstract
Plague is a vector-borne disease caused by Yersinia pestis. Transmitted by fleas from rodent reservoirs, Y. pestis emerged <6000 years ago from an enteric bacterial ancestor through events of gene gain and genome reduction. It is a highly remarkable model for the understanding of pathogenic bacteria evolution, and a major concern for public health as highlighted by recent human outbreaks. A complex set of virulence determinants, including the Yersinia outer-membrane proteins (Yops), the broad-range protease Pla, pathogen-associated molecular patterns (PAMPs), and iron capture systems play critical roles in the molecular strategies that Y. pestis employs to subvert the human immune system, allowing unrestricted bacterial replication in lymph nodes (bubonic plague) and in lungs (pneumonic plague). Some of these immunogenic proteins as well as the capsular antigen F1 are exploited for diagnostic purposes, which are critical in the context of the rapid onset of death in the absence of antibiotic treatment (less than a week for bubonic plague and <48 h for pneumonic plague). Here, we review recent research advances on Y. pestis evolution, virulence factor function, bacterial strategies to subvert mammalian innate immune responses, vaccination, and problems associated with pneumonic plague diagnosis.
Highlights
Plague is a vector-borne illness transmitted by fleas to a variety of wildlife rodents, which represent natural reservoirs for the disease in a wide range of habitats around the world [1]
Plague has impacted the history of humankind through several pandemics that have initially spread from Central Asia to Africa
In the 21st century, plague is present in Asia, Africa and America [5], and recent outbreaks in Uganda [6], China [7], Democratic Republic of Congo [8], and Madagascar [9, 10] remind that plague is still a major public health concern
Summary
Plague is a vector-borne illness transmitted by fleas to a variety of wildlife rodents, which represent natural reservoirs for the disease in a wide range of habitats around the world [1]. The plasminogen activator Pla, a key virulence factor responsible for the fulminant lung infection specific of Y. pestis, was carried by Gok, LNBA, 0.PE2, and 0.PE7 lineages in its ancestral form (I259), which has been associated with reduced bacterial dissemination in mammals [20] This suggests that these strains may have had a limited flea-borne transmissibility and a reduced invasiveness within the host [13, 15]. Many Y. pestis strains attenuated by genetic engineering are immunogenic and confer protection, but none was brought to the clinical evaluation phases Another molecular vaccine, patented by the University of Chicago and called V10, is composed of a shorter V antigen only, and provided 100% protection against bubonic and pneumonic plague to mice and Cynomolgus macaques [115]. Automated identification systems are more and more often used in the laboratories: they are fast and can efficiently identify a large variety of bacteria; misidentifications of Y. pestis have been reported [132]; a reference laboratory must always confirm the taxonomic assignation
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