Lori Carpenter - The Plague February 23, 2014

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1 Lori Carpenter - The Plague February 23, 2014 Causative Agent Plague is caused by Yersinia pestis, a gram-negative, facultatively anaerobic, nonendospore forming, pleomorphic rod that is a member of the Enterobacteriaceai family of bacteria. It is motile when isolated from the environment, but becomes non-motile once inside its mammalian host. The plague has been referred to by many names, with the most common being, the Black Death, the great pestilence, and the bubonic plague (4). Yersinia was named in honor of Alexander Yersin, a Swiss-born scientist who isolated the bacteria in the year 1894 (4). Historical significance The origin of the term plague is derived from the Greek word plegei for blow and the Latin plungere meaning lament. These together refer to the overwhelming pestilence caused by the disease. The plague has created multiple epidemic and three great pandemics, dating back as early as Old Testament Biblical times and also described in Homer s Iliad during the Trojan War (4). Outbreaks of the plague have proven explosive in nature, invariably lethal, and devastating. (1). The Justinian plague was known as the first pandemic, occurring during B.C. It is believed to have originated in Egypt, but it later spread throughout the Mediterranean and Middle East. Over 100 million people succumbed to the plague in around 60 years time. Reportedly up to 10,000 people a day died in the city of Constantinople as a result (4). The second pandemic, also called the Black Plague, began in 1347 and resulted from the introduction of plague infested rats arrived at the ports of Sicily, unknowingly brought by traders from central Asia. During this time, sanitation was poor and rat population within the cities was high. The bites from infected fleas caused subcutaneous hemorrhage and gangrenous extremities that became black as the tissues died. Unfortunately, the cause and treatment for the plague were not known; by the year 1350, approximately one-fourth of Europe s population and one-third of the world s population became victims of the Black Death, around million people (4). Rats transported on ships to Africa, Asia, and South America caused the third pandemic in the 1860s. The plague later spread to Hong Kong in the 1890s and made its way to the United States via the port in San Francisco in Epidemics appeared 1 P age The Plague

2 sporadically over the next fifty years until it was discovered that the pesticide DDT stopped its spread (4). Since that time, the plague has been observed in rural and semi-rural areas of the western United States, usually in semi-arid upland forests and grasslands where multiple types of rodent species are involved (2). A) B) C) A) Y. pestis bacteria morphology (9). B) The Plague of Ashdod as painted by Angelo Caroselli (7). C) Reported cases of plague in the United States as reported by the Center of Disease Control from (2). Epizootiology and Public Health The plague has a world-wide epidemiology and is capable of affecting people at all times of year of any age. As with any infectious agent, children, the elderly, and those who are immunocompromised are most susceptible (4). Currently, about 10 cases of the plague are reported annually in the United States, and 300 worldwide. Between 1990 and 1995 significantly more cases were documented, around 13,000. Each of the following countries contributed more than 100 cases during this time: China, Congo, India, Madagascar, Mozambique, Myanmar, Peru, Tanzania, Uganda, Vietnam, and Zimbabwe (4). D) D) Map provided by the Center of Disease Control of reported plague cases from the years (2). 2 P age The Plague

3 Pathogenesis Y. pestis has the capability to produce a lipopolysaccharide endotoxin, coagulase, fibrinolysin, and virulence plasmids, all of which contribute to its extreme pathogenesis. The plasmids have many functions, including coding for adhesions, various secretions, an outer membrane protein plasminogen activator, and proteins contained in the capsule. Adhesions on the capsule make the bacterium very sticky and able to attach easily to cells. The secretion system simultaneously injects proteins into the host macrophages and neutrophils that trigger cell death. Protein plasminogen activators prohibit blood coagulation and further activation in the complement coagulation cascade. Capsular proteins, namely, plasmid, enhance the invading bacterium s resistance to being phagocytized by the host s immune system (4). Transmission Transmission of the plague occurs through contact with infected wild or domestic animals or other humans. More than 200 mammals are reported as being capable reservoirs. These hosts are typically asymptomatic and spread the disease quickly to other mammals who become referred to as amplifying hosts. Examples of amplifying hosts of the plague are the brown rat, black rat, ground squirrel, wood rat, chipmunk, prairie dog, and rabbit (4). Scientists believe that plague bacteria circulate at low rates within populations of certain rodents without causing excessive death. These infected animals and their fleas become long-term reservoirs for the bacteria and is referred to as the plague enzootic cycle (1). The vector responsible for transmission of Y. pestis from reservoir host to amplifying host and finally, to people, is the flea. More than 1500 species of flea are able to transmit the plague, with the most common culprit being the oriental rat flea, Xenopsylla cheopis. Bacteria multiply in the flea s gut after ingesting a blood meal from an infected host. The bacteria begin to accumulate so that the flea is unable to swallow the clotted blood, which is now blocking its esophagus. When it attempts to feed, the flea will regurgitate this infectious material into successive bite wounds it makes, thus further transmitting the disease. Fleas prefer their natural hosts for feeding; however, a hungry flea will attempt to obtain a blood meal from less-preferential species if these natural hosts are not available (4). An epizootic occurs when species besides the flea s regular host becomes infected. Humans become more at risk during this time. Epizootics are more likely to occur in the southwestern United States during cool summers that follow wet winters (2). The plague becomes transmitted to humans in four different ways: a bite from an infected flea, the handling of skins and meats of amplifying hosts, inhalation of aerosols, or by a bite wound from a cat who had previously fed on infected carcasses (2),(4). 3 P age The Plague

4 E) E) Various methods of transmission of Yersenia pestis (6). Symptomology Clinical signs in cats and dogs include fever as high as 106 F, pneumonia, and lymphadenitis (4). Human disease can manifest itself in three ways, depending on the form of the plague contracted. Patients with exposure to bubonic plague will exhibit buboes, or enlarged lymph nodes, a high fever, lethargy, and chills. Sometimes a papular rash on the hands and feet is observed, as is hepatomegaly and splenomegaly. Incubation period for the bubonic plague is between 2 and 6 days. The second form of the plague is referred to as septicemic plague. Those affected develop fever, chills, abdominal pain, bleeding into the skin and other organs, and shock. This particular type of plague is associated with a very high mortality rate as a result of the systemic shock experienced by the patient. The subcutaneous bleeding may lead to necrosis and gangrene of infected tissue. These patients that present to the hospital in shock may display hypothermia, tachycardia, tachypnea, and hypotension. The most contagious form of the disease, pneumonic plague, is spread by aerosol droplets. They will develop chest pain, a productive cough, and dyspnea (4). 4 P age The Plague

5 Disease progression Once a person or animal is bitten by an infected flea, thousands of bacteria are inoculated into the skin. The bacteria then migrate to the host s lymph nodes where they are phagocytized by neutrophils and monocytes. Neutrophils are usually able to eliminate the bacteria, but Y. pestis thrives in macrophages and continues to multiply. Plague bacteria destroy the macrophages, are released into the blood stream, and further spread to distant organs (4). Bubonic plague can progress into septicemic plague once the bacteria relocate from the lymphatics into blood circulation. If the bacteria become lodged in the lungs, either from direct inhalation, or by circulatory transport, it is deemed pneumonic plague (4). Pneumonic plague can further progress to hemorrhagic pneumonia (1). The only way the plague is spread person to person is by aerosol droplets. This method of transmission has not been observed in the United States since 1924, but can still be seen in developing countries (2). Diagnosis Early clinical diagnosis is essential as disease progression is extremely rapid (1). Diagnosis of the plague can be confirmed by Wayson staining, media culture, or by lymph node aspirates. Blood and serum cultures can be examined for antibody detection and flea material inspected by fluorescent antibody testing to encourage antigen expression. In humans, a direct immunoflurorescence test of fluid serves as a positive disease indicator (4). Treatment If a person is believed to have been exposed to the plague, the patient should be immediately isolated and local health departments notified. Once diagnosis is confirmed, antibiotics such as streptomycin, chloramphenicol, or gentamicin should be begun as quickly as possible (4),(5). In cats, the disease is lethal and rapid. Both streptomycin and tetracycline can help stop disease progression, and should be given for five days after the animal appears to normalize, thus preventing successive relapse (4),(5). Cats will usually present with high fever, sneezing, coughing, and nasal discharge. Some may have a draining sore below the jaw. Dogs, however, are usually asymptomatic and are known to recover (7). Both human and animals with diagnosis of the plague should be quarantined for a minimum of three days after beginning antibiotic therapy (5). 5 P age The Plague

6 Studies are inconclusive if immunity exists after plague recovery (5). Management and Control Invariably, attempts to eliminate wild rodent plague are costly and unproductive. The most effective method of prevention is controlling rat populations and limiting human exposure (4). The Center of Disease Control recommends that field workers in endemic areas receive the plague vaccine, as well as laboratory personnel who are routinely exposed to Y. pestis. Flea control products to kill flea eggs, larva, and adult fleas help to minimize flea populations on household pets and thus reduce human contact with contaminated fleas (4), Good sanitation practices of environmental sanitation could limit the spread of disease. This includes removal of food sources sought by common reservoirs, rodent-proofing homes and warehouses, and use of chemical insecticides to kill both fleas and rodents (4). As with any other infectious disease, the best method of prevention and control is public education. 6 P age The Plague

7 Bibliography 1. Barron, Samuel. Medical Microbiology Web - Accessed February 23, Center for Disease Control. Plague - Last updaded, June Accessed February 23, Cole, Stewart T. Nature. Bacterial genomics: A plague o' both your hosts. Volume 413, October, Web. Accessed February 23, Rominch, Janet Amundson. Understanding Zoonotic Diseases. Canada: Delmar Learning Corporation, p Print. 5. New York State Department of Health - Web. Accessed February 23, Web. Accessed February 23, Texas Department of State Health Services - Basic Fact Sheet Plague in Animals, Zoonosis Control Division - Last updated, January 27, Web. Accessed February 23, Web. Accessed February 23, P age The Plague