Yersinia pestis (Y. pestis; formerly Pasteurella pestis) is a gram-negative, non-motile, coccobacillus bacterium without spores. It is related to pathogens Yersinia enterocolitica, and Yersinia pseudotuberculosis, from which it evolved. Yersinia pestis is responsible for the disease plague, which caused the Plague of Justinian and the Black Death, one of the deadliest pandemics in recorded history. Plague takes three main forms: pneumonic, septicemic, and bubonic. Y. pestis is a facultative anaerobic parasitic bacterium that can infect humans primarily via its host the Oriental rat flea (Xenopsylla cheopis), but also through aerosols and airborne droplets for its pneumonic form. As a parasite of its host, the rat flea, which is also a parasite of rats, Y. pestis is a hyperparasite.

Y. pestis was discovered in 1894 by Alexandre Yersin, a Swiss/French physician and bacteriologist from the Pasteur Institute, during an epidemic of the plague in Hong Kong. Yersin was a member of the Pasteur school of thought. Kitasato Shibasaburō, a Japanese bacteriologist who practised Koch's methodology, was also engaged at the time in finding the causative agent of the plague. However, Yersin actually linked plague with a bacillus, initially named Pasteurella pestis; it was renamed Yersinia pestis in 1944.

Between one thousand and two thousand cases of the plague are still reported to the World Health Organization every year. With proper antibiotic treatment, the prognosis for victims is much better than before antibiotics were developed. Cases in Asia increased five- to sixfold during the time of the Vietnam War, possibly due to the disruption of ecosystems and closer proximity between people and animals. The plague is now most commonly found in the Democratic Republic of the Congo, Madagascar, and Peru. The plague also has a detrimental effect on non-human mammals; in the United States, these include the black-tailed prairie dog and the endangered black-footed ferret.

Y. pestis is a non-motile coccobacillus, a facultative anaerobic bacterium with bipolar staining (giving it a safety pin appearance) that produces an antiphagocytic slime layer. Similar to other Yersinia species, it tests negative for urease, lactose fermentation, and indole. The species grows best in temperatures of 28–30 °C (82.4-86 °F), and at a pH of 7.2–7.6, but can live in a large temperature and pH range. It dies very rapidly if exposed to UV light, dried out, or exposed to temperatures higher than 40°C (104°F). There are 11 species in the Yersinia genus, and three of them cause human diseases. The other two are Yersinia pseudotuberculosis and Yersinia enterocolitica, infections by either of these are usually acquired from ingesting contaminated food or water.

Several complete genome sequences are available for various strains and subspecies of Y. pestis: strain KIM (of biovar Y. p. medievalis), and strain CO92 (of biovar Y. p. orientalis, obtained from a clinical isolate in the United States). In 2006 the genome sequence of a strain of biovar Antiqua was completed. Some strains are non-pathogenic, such as that of strain 91001, whose sequence was published in 2004.

Like Y. pseudotuberculosis and Y. enterocolitica, Y. pestis is host to the plasmid pCD1. It also hosts two other plasmids, pPCP1 (also called pPla or pPst) and pMT1 (also called pFra), that are not carried by the other Yersinia species. pFra codes for a phospholipase D that is important for the ability of Y. pestis to be transmitted by fleas. pPla codes for a protease, Pla, that activates plasmin in human hosts and is a very important virulence factor for pneumonic plague. Together, these plasmids and a pathogenicity island called HPI encode several proteins that cause the pathogenesis for which Y. pestis is famous. Among other things, these virulence factors are required for bacterial adhesion and injection of proteins into the host cell, invasion of bacteria in the host cell (via a type-III secretion system), and acquisition and binding of iron harvested from red blood cells (by siderophores). Y. pestis is thought to be descended from Y. pseudotuberculosis, DNA studies have found that the two are 83% similar, which is high enough to be considered the same species. In 1981 it was proposed that Y. pestis be reclassified as a subspecies of Y. pseudotuberculosis, but the Judicial Commission of the International Committee on Systematic Bacteriology declined to do this because the course of Y. pestis disease is so different than that of Y. pseudotuberculosis, which usually causes a mild diarrhea, that reclassification would generate confusion.

A comprehensive and comparative proteomics analysis of Y. pestis strain KIM was performed in 2006. The analysis focused on growth under four different sets of conditions that were designed to model flea and mammal hosts.

Numerous bacterial small noncoding RNAs have been identified to play regulatory functions. Some can regulate the virulence genes. Some 63 novel putative sRNAs were identified through deep sequencing of the Y. pestis sRNA-ome. Among them was Yersinia-specific (also present in Y. pseudotuberculosis and Y. enterocolitica) Ysr141 (Yersinia small RNA 141). Ysr141 sRNA was shown to regulate the synthesis of the type III secretion system (T3SS) effector protein YopJ. The Yop-Ysc T3SS is a critical component of virulence for Yersinia species. Many novel sRNAs were identified from Y. pestis grown in vitro and in the infected lungs of mice suggesting they play role in bacterial physiology or pathogenesis. Among them, sR035 is predicted to pair with the SD region and transcription initiation site of a thermo-sensitive regulator ymoA, and sR084 is predicted to pair with fur, ferric uptake regulator.