Yersinia pestis is a Gram‑negative, non‑motile coccobacillus within the family Enterobacteriaceae and is the causative agent of plague. It primarily infects rodents and is transmitted between mammals by the bite of infected fleas. Human infections occur when contaminated flea saliva enters through a bite wound or when infectious droplets are inhaled, resulting in bubonic, septicemic or pneumonic plague.
Pathogenic cycle and virulence factors
The enzootic cycle of *Y. pestis* involves its replication in the midgut of fleas feeding on bacteremic rodents. At ambient temperatures the bacterium produces a biofilm that blocks the flea proventriculus, causing repeated feeding attempts and regurgitation of bacteria into new hosts. Upon entering a mammalian host, *Y. pestis* rapidly expresses a temperature‑regulated antiphagocytic capsule composed of F1 antigen and synthesizes a type III secretion system that injects Yersinia outer proteins (Yops) into host immune cells, blocking phagocytosis and cytokine production. Additional virulence factors include the plasminogen activator protease Pla, which facilitates dissemination by degrading fibrin, and the high‑pathogenicity island encoding siderophores for iron acquisition. Three plasmids (pYV, pFra/pMT1 and pPla/pPCP1) collectively encode many of these determinants. The ability to transition between flea and mammalian environments underscores its adaptability and high virulence.
Clinical forms and historical importance
Bubonic plague, the most common form, presents after an incubation period of 2–7 days with sudden fever, chills and painful, swollen lymph nodes (buboes) near the bite site. If untreated, bacteria may spread to the bloodstream causing septicemic plague, characterized by disseminated intravascular coagulation, shock and high mortality. Pneumonic plague results from inhalation of infectious aerosols or secondary spread from septicemia to the lungs; it manifests as rapidly progressive pneumonia and is highly transmissible between humans. Prompt treatment with aminoglycosides or doxycycline dramatically reduces mortality, and supportive public health measures such as vector control, surveillance of rodent populations and prophylactic antibiotics for contacts are essential. Historically, *Y. pestis* was responsible for the Plague of Justinian and the Black Death in 14th‑century Europe, which decimated populations and altered social structures. Although modern sanitation and antibiotics have curtailed large outbreaks, plague remains endemic in parts of Africa, Asia and the western United States, emphasizing the need for ongoing vigilance.
*Yersinia pestis* exemplifies a highly adapted zoonotic pathogen that utilizes flea vectors and a suite of virulence factors to cause fulminant disease in humans. Understanding its ecology and pathogenesis informs both historical perspectives and modern control strategies.
Related Terms: Plague, Zoonosis, Flea, Bubonic plague, Type III secretion system