Pathophysiology Of The Bubonic Plague Term Paper

Pathophysiology Of The Bubonic shame - Term Paper ExampleOf these the most common form in bubonic iniquity (WHO, 2011) and this pull up stakes be discussed in this essay. Pathogenesis Yersinia pestis is an anerobic facultative gram-negative intracellular boron (Dufel, 2009). The organism is mainly transmitted from horde to human beings through bite of a vector. The host is usually rodent and vector is flea. Other sources of infection are close contact with body fluids or tissues contaminated or infected with the organism and ambition of aerosolized bacteria. There are 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 overwhelm human lice and ticks. there are certain rodents that are resistant to infection like deer mice and woods rates. These however form an enzootic represent in which the baci llus 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 vernal 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 fish are resistant to the disease (Dufel, 2009). Virulent plague-causing organism survive in soil, grains, animal carcasses, flea feces, dried impassiveness and buried bodies (Ayyadurai et al, 2008). 80- 85 percent cases are bubonic form (Dufel, 2009). Bubonic plague is caused by testimony 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 famishm ent and to 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 accordingly invades the lymphoid tissue near the site of bite, producing bubos which are nothing but lymph nodes that have become necrotic, aggravate 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 in deposited in the vasculature. In this condition, there occurs early dissemination 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 seve ral countries in the world like Africa, Asia, the Americas and the former Soviet Union. According to WHO (2011), in 2003, 9 countries report 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