Yersinia pestis

From MicrobeWiki, the student-edited microbiology resource

A Microbial Biorealm page on the genus Yersinia pestis


Higher order taxa

Kingdom: Eubacteria

Phylum: Proteobacteria

Class: Gamma Proteobacteria

Order: Enterobacteriale

Genus: Yersinia


Yersinia pestis

Description and significance

Yersinia pestis was discovered in Hong Kong in 1894 by a Swiss physician Alexandre Yersin, who was a student of the Pasteur school of thought. He linked Y. pestis to the bubonic plauge, an epidemic that ravaged Europe during the 1300s. The organism was isolated during a outbreak in Hong Kong, a new geographical region for the organism that has been seen in Europe and Africa.

Yersinia pestis is a rod shaped gram-negative bacteria that can also have a spherical shape. It is also covered by a slime envelope that is heat labile. When the bacteria is in a host, it is nonmotile (incapable of self-propelled movement), but when isolated it is motile.

It is very important to have the genome sequenced for Y. pestis because this organism is capable of causing very fatal diseases. Since scientists were able to sequence the genome, they now have information of how diseases caused by this pathogenic bacteria are developed and also the evolutionary history of the bacteria. Having the genome sequenced also means that they are able to determine other species that are related to yersinia pestis which can prevent future outbreaks.

Genome structure

Yersinia pestis has three sub species in which only two have been sequenced, strain KIM and strain CO92. Each strain consists of one chromosome. Strain KIM consists of 4,600,755 base pairs and has a circular chromosome. This strain is also related with the black plague. Strain CO92 has 4,653,728 base pairs and contains three plasmids (pMT1, pCD1 and pPCP1) of 96.2 kilobases (kb), 70.3 kb and 9.6 kb. Strain KIM also carries these plasmids. These plasmids along with a pathogenicity island called HPI, create a protein that causes the pathogenicity of the organism. These factors are important for adhesion and injection of proteins into the host cell, invasion of the bacteria and binding of iron from red blood cells. The genome has many insertion sequences and many G-C base pair differences, which means frequent recombination. Many of the genes have been acquired from other bacteria and viruses. Strain CO92 also consists of 4,012 protein-coding genes and 150 pseudogenes.

A recent study compared both these strains to show that one of these strains may have evolved from the other throughout the years.

Cell structure and metabolism

Yersinia pestis is a rod shaped gram-negative bacteria that can also have a spherical shape. It is also covered by a slime envelope that is heat labile. When the bacteria is in a host, it is nonmotile (incapable of self-propelled movement), but when isolated it is motile.

Y. pestis uses aerobic respiration and anaerobic fermentation to produce and consume hydrogen gas for energy.


Yersinia pestis interacts mainly with rodents such as rats and fleas. Through these carriers, Yersinia pestis is able to invade human cells and create diseases. Yersinia pestis are not rich in nuterients and can grow at temperatures ranging from about 26 celcius to 37 elcius.


Y. pestis causes diseases through a bite of an infected rat or flea, but can also be transmitted by air. Fleas can become infected by taking the blood of other infected animals. Y. pestis grows in the midgut and eventually blocks the proventriculus, starving the flea for blood. The insects attempt to feed more often but end up giving back infected blood into the wound of the bite.

Symptons include:

  • Sudden onset of high fever
  • The classic sign is a smooth, painful swelling of a lymph gland(s), called a buboe. The most common area is the groin, but swollen glands may also occur in the armpits or neck. Pain may occur in the area before the swelling.
  • Chills
  • General discomfort or ill feeling (malaise)
  • Muscular pain
  • Severe headache
  • Seizures

The major defense against Y pestis infection is the development of specific anti-envelope (F1) antibodies, which serve as opsonins for the virulent organisms, allowing their rapid phagocytosis and destruction while still within the initial infectious locus. The immune mechanism against this disease is extremely complex and involves a combination of humoral and cellular factors. The host is immune to virulent rechallenge, the inoculum being eliminated as though the organisms were completely avirulent. Killed Y. pestis vaccines induce some measure of host protection, although it is less effective.

Yersinia pestis infections must be diagnosed quickly due to the high virulence of these organisms. Death from pneumonic plague can occur in as little as 24 hours after the first appearance of clinical symptoms.

Yersinia pestis can be killed by mild heat (55°C) and by treatment with 0.5 percent phenol for 15 minutes. It is susceptible to sulfadiazine, streptomycin, tetracycline, and chloramphenicol in vitro.

Application to Biotechnology

This organism does not provide any enzymes or proteins for biotechnology.

Current Research

Enter summaries of the most recent research here--at least three required


[Sample reference] Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "Palaeococcus ferrophilus gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". International Journal of Systematic and Evolutionary Microbiology. 2000. Volume 50. p. 489-500.

Edited by student of Rachel Larsen