Pathophysiology Of The Bubonic Plague Term Paper

Pathophysiology Of The Bubonic Plague - Term Paper ExampleOf these the most earthy form in bubonic plague (WHO, 2011) and this will be discussed in this essay. Pathogenesis Yersinia pestis is an anerobic facultative gram-negative intracellular atomic number 5 (Dufel, 2009). The organism is mainly transmitted from emcee to tender-hearted beings through bite of a vector. The host is usually rodent and vector is flea. Other sources of transmission ar close contact with body fluids or tissues contaminated or infected with the organism and inhalation of aerosolized bacteria. There be more than 200 different rodents and these serve as hosts. the vector flea is Xenopsylla cheopis (Dufel, 2009). So far, about 30 different species of flea have been identified (Dufel, 2009). Other carriers of plague causing bacillus include human lice and ticks. there ar certain rodents that are resistant to infection like deer mice and wood rates. These however form an enzootic stage in which the bacil lus survives long-term. Sometimes, the fleas transfer the pathogenic bacteria to animals that are susceptible to the disease like ground squirrels. Whenever large number of host animals die, the hungry fleas search new sources of food. This is the epizootic stage and this stage helps spread of organisms to newer territory. When human beings are infected from wild animals, a sylvtic stage occurs. Most carnivores are resistant to the disease, but they can act as transfer vectors. Birds, reptiles, hoofed animals and look for are resistant to the disease (Dufel, 2009). Virulent plague-causing organism survive in soil, grains, animal carcasses, flea feces, dried sputum and buried bodies (Ayyadurai et al, 2008). 80- 85 percent cases are bubonic form (Dufel, 2009). Bubonic plague is caused by deposition of the bacillus in the skin because of the bite of flea. The bacillus proliferates in the esophagus of the flea, preventing the entry of food into the stomach, This causes starvation and t o overcome this, the flea starts sucking blood. In the process of swallowing, recoiling of the distended bacillus-packed esophagus occurs, thus depositing bacillus into the skin of the victim. The bacillus then invades the lymphoid tissue near the site of bite, producing bubos which are nothing but lymph nodes that have become necrotic, inflamed and hemorrhagic due to pathophysiology of the disease. Untreated bubonic plague can eventually lead to bacteremia and septicaemia. The bacillus has the capacity to seed every organ, including the liver, lungs, spleen, kidneys and even the meninges. The most virulent form of plague is the pneumonic plague. This occurs when the bacilli get deposited in the vasculature. In this condition, there occurs early dispersal and no bubo formation is seen. Such a pathology is seen when the bite occurs in regions of high vascularity like tonsils, pharynx and oral mucosa (Dufel, 2009). Epidemiology The disease is endemic in several countries in the world like Africa, Asia, the Americas and the former Soviet Union. According to WHO (2011), in 2003, 9 countries reported 2118 cases and 182 deaths. 98.7% of those cases and 98.9% of those deaths were reported from Africa. The distribution of plague endemicity depends on the geographical distribution of the natural foci of infection, the small animals and fleas (WHO, 2011). Bubonic plague has occurred as several epidemics in the world. The first recorded epidemic was during the 6th century in the