Bubonic plague

EVOLUTIONARY ANALYSIS OF THE BUBONIC PLAGUE

Introduction and Mechanisms for Pathogenicity: The bubonic plague is a potentially lethal infection that is caused by the bacteria Yersinia pestis. The term bubonic plague is often used as being synonymous with the plague, but it is actually used to refer to the specific part of the disease that affects the lymphatic system of the organism (Schoenstadt 2006). The lymphatic system works closely in accordance with the immune system (Williams 1974). Therefore the bacterium species responsible for the bubonic plague has the ability to resist responses such as antibody production and phagocytosis. It can even reside in phagocytes long enough to reproduce (Schoenstadt 2006). Bubonic plague is a disease most common in rats, but by using the rat flea (Xenopsylla cheopis) as a vector, other organisms can easily become a victim of the bacterial infection. When a rat flea resides on an already infected rodent, the bacteria collects in the gut of the flea. Once the original host succumbs to the bacterial infection, the flea then searches for a new host. Proteins encoded by the genome of Y. pestis inhibit the infected fleas feeding system, causing it to regurgitate the blood back into the host along with the pathogen (Sebbane 2008). A single bite from a flea is enough to transfer the bacteria to the host and invade its bodily systems.

Symptoms and Proximate Causes of the Symptoms: The most prominent sign of this bacterial disease is the swelling and tenderness of the lymph nodes found in the neck, armpit, and groin areas of the body (Kugler 2008). These swellings are referred to as buboes and occur due to the bacteria multiplying within the lymphatic system. Symptoms of an infection show up within two days of bacterial inhabitation of the hosts body (Schoenstadt 2006). Bubonic plague can cause discoloration all around the body, as a result of hemorrhages and ruptured capillaries that occur right under the skin. Patients experience excruciating pain in the skin, which is actually because of the skin decomposing (Kugler 2008). Other symptoms include fever, headache, chills, vomiting and diarrhea, the latter two which may even contain blood. The six-day period in which the plague manifests itself in the host organism is known as the plague incubation period. If left untreated during this stage, the bubonic plague will progress to produce septicemia, which is the bacterial invasion of the bloodstream. Septicemia will produce severe effects on the cardiac system, such as a rapid increase the heart rate. Yersinia pestis will also spread to the lung, causing pneumonic plague and inflammation of the lungs. This in turn induces heavy breathing and respiratory failure. A rare, but still fatal effect is when the bacteria invade tissues and fluid surrounding the brain, leading to meningitis. The bubonic plague and all consequential diseases that stem from it have the potential to bring death upon the host organism (Schoenstadt 2006).

History of Evolution and Outbreaks of the Disease: Yersinia pestis, is a gram-negative bacterium that, after the use of molecular technology, was recognized to stem from another species of bacilli, the Yersinia pseudotuberculosis (Chain 2004). Through history, there are three pandemics that have been caused by the bubonic plague. Careful studies reveal that although the bacterium causes the same symptoms in ancient and modern plagues, Yersinia pestis can divided into three biovars, each corresponding to a pandemic. Biovar Antiqua is thought to correspond to the very first recorded pandemic during the 6th century A.D. in the Byzantine Empire under the rule of Justinian I. This pandemic was known as the Plague of Justinian, since the emperor himself contracted the disease, and continued to occur in waves throughout the 8th century claiming as many as 100 million lives. The second, and perhaps most well-known pandemic, was the Black Death that swept across Europe in the 14th century, claiming over a fourth of Europes population. This is caused by Biovar Mediaevalis and was thought to have been brought over from Central Asia along trade routes. Waves of this pandemic continued all the way into the 19th century. The third and final pandemic, as well as modern day plague outbreaks, are results of Biovar Orientalis, a plague that spread from China all the way into India and then the rest of Asia, claiming lives for almost a whole century. The spread of the plague was primarily due to shipping and trade between the countries around Asia. The differences in the three biovars are attributed to their abilities to ferment glycerol and reduce nitrates; Orientalis cannot do either of the two functions, Mediaevalis can only ferment glycerol, but Antiqua has the ability to do both (Achtman 2004).

Ecology of the Disease: Most known cases of the bubonic plague today occur in countries that display low levels of sanitation practices and are usually underdeveloped. Both rural and urban areas of these countries have problems with rat infestation, thereby increasing the chances of bubonic plague outbreaks. This includes regions in Russia, the Middle East, Asia, Africa, Central and South America (Kugler 2008, Stenseth 2006). Cases in North America, Europe and Australia are usually unheard of, about ten to fifteen cases are reported from the southwest regions of the United States each year (Center for Disease Control 2001). Much of the drop in rates of the bubonic plague can be attributed to the increased control of the rodent population, specifically flea-ridden rats and more advanced sanitation practices. Drop in rates can also be accredited to the emergence of new drugs that can effectively combat the bacteria. Patients that are infected with the disease will most likely survive if treated with antibiotics such as tetracyclines (Kugler 2008). The bubonic plague has troubled the human population time and time again, and continues to do so in some areas to this date.

Bibliography

Achtman, Mark et al. 2004. Microevolution and History of the Plague Bacillus, Yersinia Pestis. Proceedings of the National Academy of Sciences of the United States of America 101: 17837-17842.

Center for Disease Control. 2001. CDC Plague Home Page. http://www.cdc.gov/ncidod/dvbid/plague/ (November 19th, 2009).

Chain, P.S. G. et al. 2004. Insights into the Evolution of Yersinia pestis through Whole-Genome Comparison with Yersinia pseudotuberculosis. Proceedings of the National Academy of Sciences of the United States of America 101: 13826-13831.

Kugler, Mary. 2008. Bubonic Plague still exists in some parts of the world. http://rarediseases.about.com/cs/bubonicplague/a/111602.htm (November 19th, 2009).

Schoenstadt, Arthur. 2006. Bubonic plague symptoms. http://plague.emedtv.com/bubonic-plague/bubonic-plague-symptoms.html (November 17th. 2009).

Sebbane, Florent et al. 2008. The Yersinia pestis caf1M1A1 Fimbrial Capsule Operon Promotes Transmission by Flea Bite in a Mouse Model of Bubonic Plague. American Society for Microbiology 77: 1222-1229

Stenseth, Nils et al. 2006. Plague Dynamics are Driven by Climate Variation. Proceedings of the National Academy of Sciences of the United States of America 103: 13110-13115.

Williams, James E. et al. 1974. Antibody and Resistance to Infection with Yersinia pestis in the Progeny of Immunized Rats. The Journal of Infectious Diseases 129: S72-S77

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