It is a facultative anaerobic organism that can infect humans primarily via the Oriental rat flea (Xenopsylla cheopis), but also through airborne droplets for its pneumonic form.

Kitasato Shibasaburō, a Japanese bacteriologist who practised Koch's methodology, was also engaged at the time in finding the causative agent of the plague.

Cases in Asia increased five- to six-fold during the time of the Vietnam War, possibly due to the disruption of ecosystems and closer proximity between people and animals.

The plague also has a detrimental effect on non-human mammals;[8] 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.

[18] pPla codes for a protease, Pla, that activates plasmin in human hosts and is a very important virulence factor for pneumonic plague.

[19] Together, these plasmids, and a pathogenicity island called HPI, encode several proteins that cause the pathogenesis for which Y. pestis is famous.

[23] 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.

Several proteins then contribute to the maintenance of the bacteria in the flea digestive tract, among them the hemin storage system and Yersinia murine toxin (Ymt).

[32] While in the insect vector, proteins encoded by hemin storage system genetic loci induce biofilm formation in the proventriculus, a valve connecting the midgut to the esophagus.

[35] Aggregation in the biofilm inhibits feeding, as a mass of clotted blood and bacteria forms (referred to as "Bacot's block" after entomologist A.W.

Ingested blood is pumped into the esophagus, where it dislodges bacteria lodged in the proventriculus, which is regurgitated back into the host circulatory system.

Y. pestis expresses a plasmin activator that is an important virulence factor for pneumonic plague and that might degrade on blood clots to facilitate systematic invasion.

The YopO, YopH, YopM, YopT, YopJ, and YopE are injected into the cytoplasm of host cells by T3SS into the pore created in part by YopB and YopD.

[38] The injected Yops limit phagocytosis and cell signaling pathways important in the innate immune system, as discussed below.

[40] In macrophages, YopH has been shown to dephosphorylate p130Cas, Fyb (FYN binding protein) SKAP-HOM and Pyk, a tyrosine kinase homologous to FAK.

YopT is a cysteine protease that inhibits RhoA by removing the isoprenyl group, which is important for localizing the protein to the cell membrane.

People can be exposed by coming into contact with an infected animal (dead or alive), or inhaling infectious droplets that a sick dog or cat has coughed into the air.

[49][50] A formalin-inactivated vaccine was available in the United States for adults in 1993[51] at high risk of contracting the plague until removal from the market by the Food and Drug Administration.

[53] A systematic review by the Cochrane Collaboration found no studies of sufficient quality to make any statement on the efficacy of the vaccine.

Though both investigators reported their findings, a series of confusing and contradictory statements by Kitasato eventually led to the acceptance of Yersin as the primary discoverer of the organism.

[citation needed] In 1898, French scientist Paul-Louis Simond (who had also come to China to battle the Third Pandemic) discovered the rat–flea vector that drives the disease.

[65] A site in Sweden was the source of the DNA evidence and trade networks were proposed as the likely avenue of spread rather than migrations of populations.

[66] The Y. pestis bacterium has a relatively large number of nonfunctioning genes and three "ungainly" plasmids, suggesting an origin less than 20,000 years ago.

[68] In 2021, researchers found a 5,000-year-old victim of Y. pestis, the world's oldest-known, in hunter-gatherer remains in the modern Latvian and Estonian border area.

[8] In September 2009, the death of Malcolm Casadaban, a molecular genetics professor at the University of Chicago, was linked to his work on a weakened laboratory strain of Y. pestis.

[76] On November 3, 2019, two cases of pneumonic plague were diagnosed at a hospital in Beijing's Chaoyang district, prompting fears of an outbreak.

The patient was a middle-aged man with fever, who had complained of difficulty breathing for some ten days, accompanied by his wife with similar symptoms.

[78] In July 2020, officials increased precautions after a case of bubonic plague was confirmed in Bayannur, a city in China's Inner Mongolia autonomous region.

According to China's Global Times, a second suspected case was also investigated, and a level 3 alert was issued, in effect until the end of the year.