The plague is a commonly known infectious disease with a brutal past. Dubbed the Black Death of Europe during 1348, the plague is responsible for the demise of nearly two-thirds of Europeís population. (5) The Plague made a vast presence nearly a millennium prior to the Black Death. In the years 541-544 BC, the Justinian plagues killed 20-25% of Europe's population in a pandemic affecting many continents (1). It is believed to have originated in East Africa and then traveled down the Nile to Europeís main port, Alexandria. It then traveled to Central and South Asia, Arabia, North Africa and much of Southern Europe. Constantinople, the central trading port of the Mediterranean estimated 40% died between 541 and 542 BC.(3 )However the plague existed in years much earlier. Descriptions of an epidemic prior to the Justinian plagues are described in the Bible among the Palestinians in 1320BC (1). During this time very little was know about the etiology of the plague and many believed it was an act of vengeance of the gods, supernatural powers or by heavenly disturbance. (4)
In 1894 the third pandemic began in Canton and Hong Kong (1). It was in Hong Kong that Yersin and Kitasoto discovered the Plagueís etiologic agent. This discovery took place after bipolar staining organisms were cultured from swollen lymph nodes, blood, lungs, livers and spleens of dead patients. These isolated cultures were then inoculated into a variety of laboratory animals that died days later. The same bacilli were then cultured from these animals. After confusing statements and questions from Kitasoto, Yersin became the microbe primary discoverer, and it took the name Yersinia pestis. Yersin noted that rats were not only affected by the plague during the human epidemics, but also preceding them. The locals knew the disease as the disease of the rats. (4)
Yersinia pestis is a non-motile, non-acid, non-sporeforming, gram-negative cocco bacillus, facultative anaerobe measuring 1.5 by .75 microns. Sunlight, high temperatures, and desiccation potentially damage the microbe. (1) Virulence factors include a capsule covering the microbe to resist phagocytosis. It also includes fibrinolysin to dissolve clots, coagulase to coagulate fibrinogen and other factors such as calcium dependence, endotoxin, lysosomal enzyme resistance and V and W antigens. (2 & 7) Diagnostic tests include bipolar staining, growth on selective media, culture on MacConkeyís agar or EMB, fluorescent antibody, no gas TSI and serology. (2)
Plague reservoirs are commonly rodent fleas. It can be transmitted between rodents and other animals via fleas, cannibalism or contaminated soil. Wild plague exists in natural foci independent of humans. Domestic plague is associated with rodents living with humans and can produce epidemics in both human and animal populations. Foci are dynamic and change in response to landscape, climate and rodent migration. Humans become susceptible indirectly from a flea's bite that travels to them after the death of an infected rodent in search of food. This often occurs when humans live among infected rodents. Seldom is the disease transmitted from one infected human to another via human fleas. The microbe can also penetrate through skin lesions and openings in the pores after one handling, cutting, and skinning the meat of infected rodents. (1)
The plague exists in three forms; bubonic, pneumonic, and septicemic plague. Bubonic plague is the most common form of the plague and has an incubation period of about 6 days. (6) Symptoms include fever, chills, large swollen lymph nodes (buboes), headache, abdominal pain, weakness, malaise and others including stupor. (2) Pneumonic plague occurs when Y. pestis infects the lungs. Breathing in microbes suspended in droplets can transmit this form. It has an incubation period of about 2 days and is the rarest and most fatal form. Pneumonic plague can also occur as a secondary disease to bubonic or septicemic plague. (1) Symptoms of pneumonic plague include fever, headache, difficulty breathing, chest pain and sometimes bloody or watery sputum. (6) Septicemic plague can occur as complications of pneumonic or bubonic plague otherwise it is caused in the same manner as bubonic except buboes do not develop. (6) Symptoms include fever, chills, prostration, abdominal pain, bleeding into skin and other organs and shock.
Treatment used to reduce the chance of death must be taken with 24 hours. Antibiotics such as tetracycline, chloramphenicol, or an effective sulfonamide may be taken in the event of exposure. (4) If there is slight suspicion treatment must be immediate and it should no be prolonged for lab confirmation. (1) Streptomycin is the most affective antibiotic, particularly for pneumonic plague. (1) Chloramphenicol is a suitable for treatment of bubonic and septicemic plague. Public health officials are carrying out four techniques in order to maintain prevention. These techniques include environmental management, public health education and vaccines. Environmental management is primarily obtained by controlling the rat populations in rural or urban areas in which the threats of outbreaks are typically exist. This entails close surveillances of human and rat plague cases and the use of an effective insecticide when outbreaks occur. Public health education includes preventive measures: eliminating food and shelter for rodents in and around the home, surveillance of plague activity in rodent populations, use of effective insecticides and flea control of pets. Vaccines are available worldwide and are moderately to highly reactogenic. However they do not protect against primary pneumonic plague. (1) The vaccine USP is manufactured by Greer Laboratories and is shipped refrigerated in 20ml vials and should be stored a 2-8 degrees C. Those that should be vaccinated include; workers encountering y. pestis in the lab or field and those working in areas or with animals infected with the plague. (4)
Though the plague is most common in Europe and in Eastern civilizations, it has occurred in the United States especially in the western states. High-risk groups in the US include those exposed to rodent fleas, wild rodents or animals in enzootic areas. Most cases occur in CA, CO, NM and AZ. Highest rates are in Native Americans especially Navajo and hunters, hikers, camper, veterinarians, those with infected cats and those traveling to areas with infected animals. (4) It is highly recommended that Americans traveling outside to eastern or developing countries be vaccinated against Y. pestis.
References
1. "Plague Manual: Epidemiology, Distribution, Surveillance and Control". 1999. Dennis, David T. Dr. May 1,2002 http://www.who.int/emcdocuments/plague/docs/whocdscsredc992a.pdf
2. "Y. pestis". 9 April 1999. unknown. May 5, 2002 http://www.medinfo.ufl.edu/year2/mmid/bms5300/bugs/yerpest.html.
3. "TED Case Studies: The Role of Transmitting the Black Death'. Thomas, Richard. 1997 May. May 5,2002 http://www.american.edu/projects/mandala/TED/BUBONIC.HTM#r1
4. "Natural History" 22 June 2001.unknown. May 5,2002. http://www.cdc.gov/ncidod/dvbid/plague/history.htm
5. "Plague and Public Health in Renaissance Europe". Institute for Advanced Technology in the Humanities. 28 Oct.1997. May 5,2002.http://jefferson.village.virginia.edu/osheim/plaguein.html
6."Facts About Pneumonic Plague". Unknown. 14, Oct. 2001. April 29,2002 http://www.bt.cdc.gov/DocumentsApp/FactSheet/Plague/About.asp
7.Tortora. ìMicrobiology, An Introductionî. San Francisco: Benjamin Cummings, 2001.