leprae

leprosy Hansen Disease Indonesian From Wikipedia, the free encyclopedia Pending changes displayed on the page iniBelum Review Jump to: navigation, search Hansen Disease Classification and external resources A 24-year-old man suffering from leprosy. ICD-10 A30. ICD-9030 OMIM 246 300 DiseasesDB 8478 MedlinePlus 001 347 eMedicine med/1281 derm/223 neuro/187 MESH C01.252.410.040.552.386 Hansen's disease or Morbus Hansen's disease formerly known as leprosy or leprosy is a chronic infectious disease before, known only caused by the bacteria Mycobacterium leprae, [1] to find the bacteria Mycobacterium lepromatosis by the University of Texas in 2008, [2] which causes a type of leprosy endemic in Mexico and the Caribbean, more specifically known as diffuse lepromatous leprosy. [3] While the bacterium Mycobacterium leprae was discovered by a Norwegian scientist named Gerhard Henrik Armauer Hansen in 1873 as a pathogen that causes a disease that has long been known as leprosy. Currently, leprosy is referred to as Hansen's disease, not only to appreciate the hard work of its inventor, but also because the word leprosy and the flat has a very negative connotation, so the naming of a more neutral applied to reduce the social stigma that is not supposed to be suffered by leprosy patients. [ 4] This disease is a type of granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract, and skin lesions are a sign that can be observed from outside. [5] If left untreated, leprosy can be progressive, causing damage to the skin, nerves, member motion, and eye. Unlike the myths that circulate in society, leprosy does not cause the release of the body which is so easy, such as severe tzaraath. Table of contents [Hide]

    * 1 History
    * 2 The characteristics
    * 3 Causes
    * 4 Pathophysiology
    * 5 Treatment
    * 6 Epidemiology
          o 6.1-risk group
          o 6.2 Global Situation
    * 7 See also
    * 8 References
          o 8.1 Further reading
    * 9 External links
[Edit] History It is said that leprosy has been attacking humans since 300 BC, and has been known by the ancient Chinese civilization, ancient Egypt, and India. [6] In 1995, the World Health Organization (WHO) estimates that there are two to three million people are permanently disabled because of leprosy. [7] Although the isolation or separation of patients with community needs and perceived less unethical, some groups of patients can still be found in various parts of the world, like India and Vietnam. Effective treatment of leprosy was found in akir the 1940s with the introduction of dapsone and its derivatives. However, the bacterium that causes leprosy gradually become resistant to dapsone and become increasingly spread. This occurs until the discovery multiobat treatment in the early 1980s and the disease was able to be handled again. [Edit] Characteristics Skin lesions on the thigh. Clinical manifestations of leprosy is very diverse, but mainly on the skin, nerves, and mucous membranes. [8] Patients with this disease can be grouped again into 'tuberculoid leprosy (UK: paucibacillary), lepromatous leprosy (multibacillary Hansen's disease), or multibacillary leprosy ( borderline leprosy). Multibacillary leprosy, with intermediate severity, is the most common form. There are skin lesions that resemble tuberculoid leprosy but more numerous and irregular; large part to disrupt the entire limb, and peripheral nerve disorder with weakness and loss of taste stimuli. This type is unstable and can become like lepromatous leprosy or tuberculoid leprosy. Tuberculoid leprosy is characterized by one or more macular hypopigmentation of skin and the part that does not taste (anesthetic). Multibacillary Hansen's disease associated with lesions, nodules, plaques symmetrical skin, thickened dermis, and the development of the nasal mucosa causing blockage of the nose (nasal congestion) and epistaxis (nose bleed), but the detection of nerve damage is often late. Not in line with the myth or belief that there is, this disease does not cause decomposition of the body. According to the old study by Paul Brand, noted that the powerlessness felt the stimuli on the motion often causes sores or lesions. Today, leprosy can also cause problems in people with AIDS. [9] [Edit] Causes The main article for this section are: Mycobacterium leprae Mycobacterium leprae. Package multiobat therapy. Mycobacterium leprae is the cause of leprosy. [5] An acid-resistant bacteria M. leprae is also an aerobic bacteria, gram positive, rod-shaped, and the cell membrane dikelilimgi by candle that is a hallmark of Mycobacterium species. [10] M. leprae can not be cultured in the laboratory. [11] [Edit] Pathophysiology The exact mechanism of transmission is unknown. Several hypotheses have been advanced as a close contact and transmission from the air. [12] Apart from humans, animals can tekena leprosy is the armadillo, chimpanzee, and crab-eating monkeys. [13] There is evidence that not all people infected by the bacteria M. leprae suffering from leprosy, and presumed genetic factors also come into play, after a through study and observation in the group of leprosy disease in certain families. Not yet known is also why it can happen that different types of leprosy in each individual. [14] The insufficiency of nutritional factors are also believed to be the causative factor. The disease is often believed that the transmission is caused by contact between infected and healthy people. [15] In a study of incidence, the rate of infection to contacts lepromatous leprosy varied from 6.2 per 1000 per year in Cebu, Philippines [16] to 55 , 8 per 1000 per year in South India. [17] Two exit of M. leprae from the human body are the skin and nasal mucosa. It was proved that lepromatous cases show adnaya number of organisms in the dermis. However still can not be proved that the organism can move to the skin surface. Although there are reports that ditemukanya acid-resistant bacteria in the skin epithelium deskuamosa, Weddel et al reported that they found no acid-resistant bacteria in the epidermis. [18] In a recent study, Job et al found a number of M. large leprae in the superficial keratin layer of skin in lepromatous leprosy patients. These form a prediction that the organism could exit through the sweat glands. [19] The importance of the nasal mucosa has been proposed by Schaffer in 1898. [20] The number of bacteria from nasal mucosal lesions in lepromatous leprosy, according to Shepard, between 10,000 to 10,000,000 bacteria. [21] Pedley reported that the majority of lepromatous patients showed the existence of bacteria in the secretions their noses. [22] Davey and Rees indicated that nasal secretions from lepromatous patients to produce 10 million organisms per day. [23] The entrance of M. leprae into the human body is still a question mark. It is estimated that the skin and upper respiratory tract into the gate of entry of bacteria. Rees and McDougall have been successfully tried transmission of leprosy through aerosols in mice suppressed immune system. [24] The report also raised with the successful trials on mice with bacterial exposure at the breathing hole. [25] Many scientists who believe that the respiratory tract is the most feasible route to the gate of entry of bacteria, although opinions on the skin can not be removed. The incubation period of leprosy surely can not be raised. Some researchers tried to measure the period of incubation. Minimum incubation period reported is a few weeks, based on the existence of leprosy cases in young infants. [26] The maximum incubation period reported for 30 years. It is reported based on observations on war veterans who had been exposed in endemic areas and then move into non-endemic areas. In general, it was agreed, that the average incubation period of leprosy is 3-5 years. [Edit] Treatment Until the development of dapsone, rifampin, and clofazimine in the 1940s, there is no effective treatment for leprosy. However, dapsone is only bactericidal drugs (exterminator bacteria) that lemih against M. leprae. The use of dapsone single cause bacterial populations become resistant. {There are 1960s, dapsone is not used anymore. The search for anti-leprosy drug that is better than dapsone, clofazimine and rifampicin finally discovered in the 1960s and 1970s. [27] Drug therapy multiobat leprosy. Then, Shantaram Yawalkar and colleagues to formulate a combination therapy using rifampicin and dapsone, to outsmart the immune bacteria. [28] multiobat and combination therapy of three drugs on the first time recommended by the WHO Expert Committee in 1981. This method became standard treatment multiobat. Three of these drugs are not used as a single agent to prevent bacterial immunity or resistance. Therapies on pretty expensive, so it is quite difficult to get into the endemic countries. In 1985, leprosy remains a public health problem in 122 countries. At the World Health Assembly (WHA) in Geneva 44th, 1991, passed a resolution to remove leprosy as a public health problem in 2000, and strive to be compressed into 1 case per 100,000. WHO is mandated to develop strategies for the elimination of leprosy. WHO Working Group report on Chemotherapy of Leprosy in 1993 recommended two types of therapy and standard multiobat. [29] The first is the treatment for 24 months for lepromatous leprosy with rifampicin, clofazimine, and dapsone. The second is 6 months of treatment for tuberculoid leprosy with rifampicin and dapsone. Since 1995, the WHO provides leprosy terapoi drug package for free in endemic countries, through the Ministry of Health. This strategy will bejalan until the end of 2010. Multiobat treatment is still effective and the patient no longer infected in the first month of usage. [6] This method is safe and easy. period of usage has been listed on the packaging of drugs. [6] [Edit] Epidemiology Distribution of world leprosy in 2003. Worldwide, two to three million people are estimated to suffer from leprosy. [7] India is the country with the largest number of patients, followed by Brazil and Myanmar. In 1999, the incidence of leprosy du world estimated 640,000, in 2000, 738,284 cases were identified. In 1999, 108 cases occurred in the United States. In 2000, WHO made a list of 91 countries are endemic leprosy. 70% of the world's cases are in India, Myanmar, and Nepal. In 2002, 763,917 cases are found worldwide, and according to the WHO in the year, 90% of the world's leprosy cases found in Brazil, Madagascar, Mozambique, Tanzania and Nepal. [Edit] risk group High-risk group exposed to leprosy is living in endemic areas with poor conditions such as inadequate bedding, no clean water, poor nutrition, and the inclusion of other diseases such as HIV that can suppress the immune system. Men have affected the level of leprosy two times higher than women. [Edit] Global Situation Table 1: Prevalence in early 2006, and trend discovery of new cases in 2001-2005, not including in Europe Prevalence Areas listed (rate/10, 000 pop.) New cases are discovered in Beginning 2006 2001 2002 2003 2004 2005 Africa 40,830 (0.56) 39,612 48,248 47,006 46,918 42,814 American 32,904 (0.39) 42,830 39,939 52,435 52,662 41,780 Southeast Asia 133,422 (0.81) 668,658 520,632 405,147 298,603 201,635 Eastern Mediterranean 4,024 (0.09) 4,758 4,665 3,940 3,392 3,133 Western Pacific 8,646 (0.05) 7,404 7,154 6,190 6,216 7,137 Total 219,826 763,262 620,638 514,718 407,791 296,499