Yersinia pestis Brandon Tucker
Yersinia pestis is a gram negative, rod-shaped, facultative anaerobic bacterium, known for causing the plague. Y. pestis was first discovered by a French-born Swiss bacteriologist named Alexander Yersin in 1894. Yersin stumbled upon this bacterium while in China studying a plague epidemic there. However, before then, Y. pestis has been wreaking havoc throughout human history.
Figure 1 “Scanning Electron Micrograph of Yersinia pestis
During the 6th century AD Y. pestis infected the world for 50 years killing upwards of a hundred million people. In the 14th century the Black Plague, believed to be an outbreak of the Bubonic Plague caused by Y. pestis, killed 25% of the European population. Even now, in the present day, Y. pestis is the major cause of plague around the world.
There are two cycles to the plague: Sylvatic Cycle and Urban Cycle. The Sylvatic Cycle is pre-human infection. Y. pestis, during this cycle, starts out in wild rodents which are then bit by fleas. The fleas will transfer the plague between the wild rodents until that population is dead. This cycle continues on in this fashion until either all the rodents are dead, or the fleas find a new food source, usually domestic rats. Once a domestic rat gets bitten, or another domestic animal, the Urban Cycle starts. The start of this cycle is similar to the Sylvatic cycle, where the fleas will bite one domestic animal and then spread it to the next. During this cycle is when humans get infected. If a flea that carries Y. pestis happens to bite a human then that human is infected. While in the human, there are two different ways the plague can manifest itself: the Bubonic Plague or Pneumonic Plague.
The Bubonic Plague after about 2 to 7 days will cause a painful bubo, a swelling of the lymph nodes usually in the groin. A fever and gangrene in the extremities typically accompany the bubo. The appearance of gangrene is what gave the plague the nickname “The Black Death.” While in the nodes, Y. pestis avoids the immune system, and replicates, causing the lymph nodes to swell. The nodes will get hot, tender, and then they will start to bleed excessively. As the plague develops, the bacteria move into the blood stream. Without treatment, death by endotoxic shock will occur in about 50 to 75% of all patients. If the bacteria move into the lungs, Pneumonic Plague develops. Unlike Bubonic Plague, Pneumonic Plague; however, does not require a vector, but can instead be transmitted from human to human. Pneumonic Plague has an incubation time of about 2 to 3 days, and starts with a fever, a general feeling of not being well, and tightness of the chest. If left untreated, the patient will develop a cough, produce high levels of sputum, their skin will turn blue, and then 99% of patients will die. The common treatment of the plague is Streptomycin which lowers the mortality rate to 10 to 20%.
Figure 2 “Life Cycle of Yersinia pestis”
The reason why Y. pestis is so successful is because of their elusiveness to the host’s immune system and their ability to suppress it. Y. pestis produces two anti-phagocytic antigens, F1 antigen and VW antigen. These antigens are both required for virulence and are only produced when the organism grows at 37oC temperatures, which explains why fleas, whose body temperatures are lower than that, can act as a vector. Y. pestis can also resist phagocytosis by injecting macrophages and immune cells with YOPS (Yersinia Outer Proteins). The YOPS are able to create pours in the cell, allowing more YOPS to get into the cytoplasm and limit phagocytosis.
The plague is still prevalent in some parts of the world, including America. Although there aren’t many outbreaks of human infection in America, there are rodents in the southwestern parts of America that are infected with it. For us to be able to control Y. pestis the rodent and flea populations need to be controlled. People who are at high risk can get a temporary vaccine to help protect against an infection. If a person does get infected, though, quick and aggressive treatment is required. Because of the high mortality rate and the ease of infection, Y. pestis is considered to be a very likely candidate for being weaponized by terrorists to use in bioterrorism and biological warfare.
Figure 3 “Scanning electron microscope picture of Yersinia pestis in the foregut of a flea vector.”
Arnold, Paul. “How Does Yersinia Pestis Attack and Spread?” Bright Hub: The Hub for Bright Minds. Sep 24, 2009. Bright Hub Inc. Feb 16, 2010. <http://www.brighthub.com/science/genetics/articles/50016.aspx>
Catlin, Kristen. “Yersinia Pestis.” American Society for Microbiology. 5/12/2003. American Society for Microbiology. Feb 16, 2010. <http://www.microbelibrary.org/Infectious%20Disease/details.asp?id=1423&Lang=>
Figure 1: Meckes, Oliver. “Yersinia pestis.” Britannica Online Encyclopedia. Researches, Inc. Feb 16, 2010. < http://www.britannica.com/EBchecked/topic-art/48203/75880/Scanning-electron-micrograph-of-Yersinia-pestis-the-bacterium-responsible-for>
Figure 2: Public Health Image Library. “Yersinia Pestis.” American Society for Microbiology. 5/12/2003. Centers for Disease Control and Prevention. Feb 16, 2010. <http://www.microbelibrary.org/microbelibrary/files/ccImages/Articleimages/cdcphil/Yersinia%20pestis%20fig3.jpg>
Figure 3: US Federal Government. “How Does Yersinia Pestis Attack and Spread?” Bright Hub: The Hub for Bright Minds. Sep 24, 2009. Bright Hub Inc. Feb 16, 2010. <http://www.brighthub.com/science/genetics/articles/50016.aspx?image=26367 >
*Disclaimer - This report was written by a student participaring in a microbiology course at the Missouri University of Science and Technology. The accuracy of the contents of this report is not guaranteed and it is recommended that you seek additional sources of information to verify the contents.
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