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Behind the Worm Attacks Feathers Ada Apa? Genesis in 2011 is similar to caterpillars attack that occurred in 2009, recorded two stricken city this caterpillar attack, bandung and Lamongan. Early events in bandung, tgl 26-March-2009, Silkworm attack on New Setrasari Happened First in Bandung, Citizens Housing Setrasari Elite Feather Worm Attacked result, Attack Worm Feather, People Got to the hotel refugees [Image] Bandung - So many caterpillars that attack the houses of citizens, even down to the bedroom, there are people who are displaced to the hotel. Number of caterpillars that had attacked thousands of elite housing, Complex Setrasari, precisely on Jalan Raya Setrasari Kulon since Thursday (26/03/2009). Angi (35), the owner of a house in Jalan Raya Setrasari Kulon No. 26 B, admitted his family were forced to flee to the hotel because it was not bear caterpillars attacked. "Last night our family was forced to stay at the hotel. Sometime later we were amused as well as caterpillars have reached the room, "he said when met at his residence on Saturday (03/28/2009). According to the caterpillars were crawling on the wall of the house, yard, even into the bedroom. "The most Fridays. Mat in front of my house that color brown change color black. Pas caterpillars studied were all, "he said with a shudder. "At first my child happy, because she loves animals. But over time so horrified, too. I have brooms, but still there. In fact, I collect up to a jar, "he continued. Angi told homeowners that are behind his house was angry because jemurannya many caterpillars. "At first he thought the caterpillar was from my home. And the wall behind his house that was adjacent to vacant land. Well it happened to fit the clothesline, "said Angi.Ribuan caterpillars that attack several residents came home from twenty Kaliki Trees growing on vacant land.
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وراء الهجمات دودة الريش ابا ادا؟
سفر التكوين في عام 2011 هو مماثل للهجوم على اليرقات التي وقعت في 2009 ، سجلت اثنين من المدينة المنكوبة هذا الهجوم كاتربيلر ، وباندونغ وامونجان. الأحداث في وقت مبكر في باندونغ ، tgl 26 آذار / مارس 2009 ، دودة القز الهجوم على Setrasari جديد حدث في الأولى ، باندونغ المواطنون الإسكان Setrasari نتيجة الريشة النخبة هجوم دودة ، هجوم دودة الريشة ، وحصلت على الناس للاجئين الفندق
[صورة]
باندونغ -- اليرقات حتى ان الكثير من الهجوم على منازل المواطنين ، بانخفاض حتى الى غرفة النوم ، وهناك الناس الذين شردوا إلى الفندق. عدد اليرقات التي هاجمت آلاف من المساكن النخبة ، Setrasari مجمع ، وتحديدا على Setrasari جالان Kulon راية منذ يوم الخميس (26/03/2009). اعترف انجي (35) ، صاحب منزل في Setrasari جالان راية Kulon ب 26 رقم ، أجبر عائلته على الفرار الى الفندق لأنه لم يكن يتحمل اليسروع تعرضت لهجوم. "الليلة الماضية اضطرت عائلتنا على البقاء في الفندق. في وقت لاحق ونحن مسليا وكذلك اليرقات وصلت إلى غرفة" ، وقال انه عندما التقى في مقر اقامته يوم السبت (2009/3/28). وفقا لاليسروع والزحف على جدار المنزل ، والفناء ، حتى في غرفة النوم. "إن معظم أيام الجمعة. بساط أمام بيتي أن اللون البني لون تغيير السوداء. اليسروع باس درس كانوا جميعا" ، وقال انه مع قشعريرة. "في البداية طفلي سعيدة ، لأنها تحب الحيوانات ، ولكن مع مرور الوقت حتى روعت أيضا. لدي مكانس ، ولكن لا يزال هناك ، في الواقع ، أنا جمع ما يصل الى جرة" ، وتابع. وقال انجي أصحاب المنازل التي تكون خلف منزله كان غاضبا اليسروع jemurannya لأن الكثير. "في البداية كان يعتقد ان كاتربيلر كان من بيتي ، وعلى الحائط وراء منزله الذي كان بالقرب من الأراضي الشاغرة. حسنا ما حدث لتناسب حبل الغسيل" ، وقال اليسروع Angi.Ribuan هذا الهجوم العديد من السكان وجاءت البداية من الأشجار Kaliki العشرين تزايد على الأراضي الشاغرة.
Rabu, 18 Mei 2011
Dietro il Worm Attacca Ada Feathers Apa? Genesis nel 2011 è simile ad attaccare bruchi che si sono verificati nel 2009, registrò due città colpita questo attacco bruco, Bandung e Lamongan. I primi eventi in Bandung, TGL 26-Marzo-2009, attacco di bachi da seta a New Setrasari Happened primo a Bandung, Cittadini Housing Setrasari risultato Elite Feather Attaccato Worm, Worm Attack Feather, la gente ha i rifugiati hotel [Image] Bandung - Così molti bruchi che attaccano le case dei cittadini, anche verso la camera da letto, ci sono persone che sono sfollate per l'hotel. Numero di bruchi che aveva attaccato migliaia di alloggi elite, Complesso Setrasari, proprio sulla Jalan Raya Setrasari Kulon dal Giovedi (26/03/2009). Angi (35), il proprietario di una casa in Jalan Raya Setrasari Kulon n. 26 B, ha ammesso la sua famiglia furono costretti a fuggire per l'hotel, perché non era orso bruchi attaccato. "La scorsa notte la nostra famiglia è stata costretta a rimanere in albergo. Qualche tempo dopo eravamo divertiti così come bruchi hanno raggiunto la stanza", ha detto quando ha incontrato nella sua residenza il Sabato (2009/03/28). Secondo i bruchi sono stati strisciare sul muro della casa, giardino, persino in camera da letto. "Il più venerdì. Mat di fronte alla mia casa, che cambiano colore marrone colore nero. Bruchi Pas studiato erano tutti", ha detto con un brivido. "All'inizio il mio bambino felice, perché lei ama gli animali. Ma nel corso del tempo così inorridita, anche. Ho scope, ma ancora lì. In realtà, io raccogliere fino a un vaso", ha continuato. Angi ha detto proprietari di case che si trovano dietro la sua casa era arrabbiato perché bruchi jemurannya molti. "In un primo momento pensava che il bruco è stata dalla mia casa. E il muro dietro la sua casa che era adiacente a terreni liberi. Beh, è successo a montare il bucato", ha detto che l'attacco di bruchi Angi.Ribuan molti residenti tornato a casa da venti Kaliki alberi che crescono su terreni liberi.
Kamis, 05 Mei 2011
Behind the Worm Attacks Feathers Ada Apa?
Genesis in 2011 is similar to caterpillars attack that occurred in 2009, recorded two stricken city this caterpillar attack, bandung and Lamongan. Early events in bandung, tgl 26-March-2009, Silkworm attack on New Setrasari Happened First in Bandung, Citizens Housing Setrasari Elite Feather Worm Attacked result, Attack Worm Feather, People Got to the hotel refugees
[Image]
Bandung - So many caterpillars that attack the houses of citizens, even down to the bedroom, there are people who are displaced to the hotel. Number of caterpillars that had attacked thousands of elite housing, Complex Setrasari, precisely on Jalan Raya Setrasari Kulon since Thursday (26/03/2009). Angi (35), the owner of a house in Jalan Raya Setrasari Kulon No. 26 B, admitted his family were forced to flee to the hotel because it was not bear caterpillars attacked. "Last night our family was forced to stay at the hotel. Sometime later we were amused as well as caterpillars have reached the room, "he said when met at his residence on Saturday (03/28/2009). According to the caterpillars were crawling on the wall of the house, yard, even into the bedroom. "The most Fridays. Mat in front of my house that color brown change color black. Pas caterpillars studied were all, "he said with a shudder. "At first my child happy, because she loves animals. But over time so horrified, too. I have brooms, but still there. In fact, I collect up to a jar, "he continued. Angi told homeowners that are behind his house was angry because jemurannya many caterpillars. "At first he thought the caterpillar was from my home. And the wall behind his house that was adjacent to vacant land. Well it happened to fit the clothesline, "said Angi.Ribuan caterpillars that attack several residents came home from twenty Kaliki Trees growing on vacant land.
Genesis in 2011 is similar to caterpillars attack that occurred in 2009, recorded two stricken city this caterpillar attack, bandung and Lamongan. Early events in bandung, tgl 26-March-2009, Silkworm attack on New Setrasari Happened First in Bandung, Citizens Housing Setrasari Elite Feather Worm Attacked result, Attack Worm Feather, People Got to the hotel refugees
[Image]
Bandung - So many caterpillars that attack the houses of citizens, even down to the bedroom, there are people who are displaced to the hotel. Number of caterpillars that had attacked thousands of elite housing, Complex Setrasari, precisely on Jalan Raya Setrasari Kulon since Thursday (26/03/2009). Angi (35), the owner of a house in Jalan Raya Setrasari Kulon No. 26 B, admitted his family were forced to flee to the hotel because it was not bear caterpillars attacked. "Last night our family was forced to stay at the hotel. Sometime later we were amused as well as caterpillars have reached the room, "he said when met at his residence on Saturday (03/28/2009). According to the caterpillars were crawling on the wall of the house, yard, even into the bedroom. "The most Fridays. Mat in front of my house that color brown change color black. Pas caterpillars studied were all, "he said with a shudder. "At first my child happy, because she loves animals. But over time so horrified, too. I have brooms, but still there. In fact, I collect up to a jar, "he continued. Angi told homeowners that are behind his house was angry because jemurannya many caterpillars. "At first he thought the caterpillar was from my home. And the wall behind his house that was adjacent to vacant land. Well it happened to fit the clothesline, "said Angi.Ribuan caterpillars that attack several residents came home from twenty Kaliki Trees growing on vacant land.
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
* 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
lepra
Penyakit Hansen
Dari Wikipedia bahasa Indonesia, ensiklopedia bebas
| Penyakit Hansen | ||
| Klasifikasi dan bahan-bahan eksternal | ||
 | ||
|---|---|---|
| Seorang pria berusia 24 tahun yang menderita kusta. | ||
| ICD-10 | A30. | |
| ICD-9 | 030 | |
| OMIM | 246300 | |
| DiseasesDB | 8478 | |
| MedlinePlus | 001347 | |
| eMedicine | med/1281 derm/223 neuro/187 | |
| MeSH | C01.252.410.040.552.386 | |
Penyakit ini adalah tipe penyakit granulomatosa pada saraf tepi dan mukosa dari saluran pernapasan atas; dan lesi pada kulit adalah tanda yang bisa diamati dari luar.[5] Bila tidak ditangani, kusta dapat sangat progresif, menyebabkan kerusakan pada kulit, saraf-saraf, anggota gerak, dan mata. Tidak seperti mitos yang beredar di masyarakat, kusta tidak menyebabkan pelepasan anggota tubuh yang begitu mudah, seperti pada penyakit tzaraath.
Daftar isi[sembunyikan] |
[sunting] Sejarah
Konon, kusta telah menyerang manusia sejak 300 SM, dan telah dikenal oleh peradaban Tiongkok kuna, Mesir kuna, dan India.[6] Pada 1995, Organisasi Kesehatan Dunia (WHO) memperkirakan terdapat dua hingga tiga juta jiwa yang cacat permanen karena kusta. [7] Walaupun pengisolasian atau pemisahan penderita dengan masyarakat dirasakan kurang perlu dan tidak etis, beberapa kelompok penderita masih dapat ditemukan di berbagai belahan dunia, seperti India dan Vietnam.Pengobatan yang efektif terhadap penyakit kusta ditemukan pada akir 1940-an dengan diperkenalkannya dapson dan derivatnya. Bagaimanapun juga, bakteri penyebab lepra secara bertahap menjadi kebal terhadap dapson dan menjadi kian menyebar. Hal ini terjadi hingga ditemukannya pengobatan multiobat pada awal 1980-an dan penyakit ini pun mampu ditangani kembali.
[sunting] Ciri-ciri
Kusta multibasiler, dengan tingkat keparahan yang sedang, adalah tipe yang sering ditemukan. Terdapat lesi kulit yang menyerupai kusta tuberkuloid namun jumlahnya lebih banyak dan tak beraturan; bagian yang besar dapat mengganggu seluruh tungkai, dan gangguan saraf tepi dengan kelemahan dan kehilangan rasa rangsang. Tipe ini tidak stabil dan dapat menjadi seperti kusta lepromatosa atau kusta tuberkuloid.
Kusta tuberkuloid ditandai dengan satu atau lebih hipopigmentasi makula kulit dan bagian yang tidak berasa (anestetik).
Kusta lepormatosa dihubungkan dengan lesi, nodul, plak kulit simetris, dermis kulit yang menipis, dan perkembangan pada mukosa hidung yang menyebabkan penyumbatan hidung (kongesti nasal) dan epistaksis (hidung berdarah) namun pendeteksian terhadap kerusakan saraf sering kali terlambat.
Tidak sejalan dengan mitos atau kepercayaan yang ada, penyakit ini tidak menyebabkan pembusukan bagian tubuh. Menurut penelitian yang lama oleh Paul Brand, disebutkan bahwa ketidakberdayaan merasakan rangsang pada anggota gerak sering menyebabkan luka atau lesi. Kini, kusta juga dapat menyebabkan masalah pada penderita AIDS.[9]
[sunting] Penyebab
Artikel utama untuk bagian ini adalah: 
[sunting] Patofisiologi
Mekanisme penularan yang tepat belum diketahui. Beberapa hipotesis telah dikemukakan seperti adanya kontak dekat dan penularan dari udara. [12] Selain manusia, hewan yang dapat tekena kusta adalah armadilo, simpanse, dan monyet pemakan kepiting.[13] Terdapat bukti bahwa tidak semua orang yang terinfeksi oleh kuman M. leprae menderita kusta, dan diduga faktor genetika juga ikut berperan, setelah melalui penelitian dan pengamatan pada kelompok penyakit kusta di keluarga tertentu. Belum diketahui pula mengapa dapat terjadi tipe kusta yang berbeda pada setiap individu. [14] Faktor ketidakcukupan gizi juga diduga merupakan faktor penyebab.Penyakit ini sering dipercaya bahwa penularannya disebabkan oleh kontak antara orang yang terinfeksi dan orang yang sehat.[15] Dalam penelitian terhadap insidensi, tingkat infeksi untuk kontak lepra lepromatosa beragam dari 6,2 per 1000 per tahun di Cebu, Philipina[16] hingga 55,8 per 1000 per tahun di India Selatan.[17]
Dua pintu keluar dari M. leprae dari tubuh manusia diperkirakan adalah kulit dan mukosa hidung. Telah dibuktikan bahwa kasus lepromatosa menunjukkan adnaya sejumlah organisme di dermis kulit. Bagaimanapun masih belum dapat dibuktikan bahwa organisme tersebut dapat berpindah ke permukaan kulit. Walaupun terdapat laporan bahwa ditemukanya bakteri tahan asam di epitel deskuamosa di kulit, Weddel et al melaporkan bahwa mereka tidak menemukan bakteri tahan asam di epidermis. [18] Dalam penelitian terbaru, Job et al menemukan adanya sejumlah M. leprae yang besar di lapisan keratin superfisial kulit di penderita kusta lepromatosa. Hal ini membentuk sebuah pendugaan bahwa organisme tersebut dapat keluar melalui kelenjar keringat. [19]
Pentingnya mukosa hidung telah dikemukakan oleh Schäffer pada 1898.[20] Jumlah dari bakteri dari lesi mukosa hidung di kusta lepromatosa, menurut Shepard, antara 10.000 hingga 10.000.000 bakteri.[21] Pedley melaporkan bahwa sebagian besar pasien lepromatosa memperlihatkan adanya bakteri di sekret hidung mereka.[22] Davey dan Rees mengindikasi bahwa sekret hidung dari pasien lepromatosa dapat memproduksi 10.000.000 organisme per hari.[23]
Pintu masuk dari M. leprae ke tubuh manusia masih menjadi tanda tanya. Saat ini diperkirakan bahwa kulit dan saluran pernapasan atas menjadi gerbang dari masuknya bakteri. Rees dan McDougall telah sukses mencoba penularan kusta melalui aerosol di mencit yang ditekan sistem imunnya. [24] Laporan yang berhasil juga dikemukakan dengan pencobaan pada mencit dengan pemaparan bakteri di lubang pernapasan. [25] Banyak ilmuwan yang mempercayai bahwa saluran pernapasan adalah rute yang paling dimungkinkan menjadi gerbang masuknya bakteri, walaupun demikian pendapat mengenai kulit belum dapat disingkirkan.
Masa inkubasi pasti dari kusta belum dapat dikemukakan. Beberapa peneliti berusaha mengukur masa inkubasinya. Masa inkubasi minimum dilaporkan adalah beberapa minggu, berdasarkan adanya kasus kusta pada bayi muda.[26] Masa inkubasi maksimum dilaporkan selama 30 tahun. Hal ini dilaporan berdasarkan pengamatan pada veteran perang yang pernah terekspos di daerah endemik dan kemudian berpindah ke daerah non-endemik. Secara umum, telah disetujui, bahwa masa inkubasi rata-rata dari kusta adalah 3-5 tahun.
[sunting] Pengobatan
Sampai pengembangan dapson, rifampin, dan klofazimin pada 1940an, tidak ada pengobatan yang efektif untuk kusta. Namun, dapson hanyalah obat bakterisidal (pembasmi bakteri) yang lemih terhadap M. leprae. Penggunaan tunggal dapson menyebabkan populasi bakteri menjadi kebal. {ada 1960an, dapson tidak digunakan lagi.Pencarian terhadap obat anti kusta yang lebih baik dari dapson, akhirnya menemukan klofazimin dan rifampisin pada 1960an dan 1970an. [27]
Obat terapi multiobat kusta.
Terapi di atas lumayan mahal, maka dari itu cukup sulit untuk masuk ke negara yang endemik. Pada 1985, kusta masih menjadi masalah kesehatan masyarakat di 122 negara. Pada Pertemuan Kesehatan Dunia (WHA) ke-44 di Jenewa, 1991, menelurkan sebuah resolusi untuk menghapus kusta sebagai masalah kesehatan masyarakat pada tahun 2000, dan berusaha untuk ditekan menjadi 1 kasus per 100.000. WHO diberikan mandat untuk mengembangkan strategi penghapusan kusta.
Kelompok Kerja WHO melaporkan Kemoterapi Kusta pada 1993 dan merekomendasikan dua tipe terapi multiobat standar.[29] Yang pertama adalah pengobatan selama 24 bulan untuk kusta lepromatosa dengan rifampisin, klofazimin, dan dapson. Yang kedua adalah pengobatan 6 bulan untuk kusta tuberkuloid dengan rifampisin dan dapson.
Sejak 1995, WHO memberikan paket obat terapoi kusta secara gratis pada negara endemik, melalui Kementrian Kesehatan. Strategi ini akan bejalan hingga akhir 2010.
Pengobatan multiobat masih efektif dan pasien tidak lagi terinfeksi pada pemakaian bulan pertama.[6] Cara ini aman dan mudah. jangka waktu pemakaian telah tercantum pada kemasan obat.[6]
[sunting] Epidemiologi
Pada 1999, insidensi penyakit kusta du dunia diperkirakan 640.000, pada 2000, 738.284 kasus ditemukan. Pada 1999, 108 kasus terjadi di Amerika Serikat. Pada 2000, WHO membuat daftar 91 negara yang endemik kusta. 70% kasus dunia terdapat di India, Myanmar, dan Nepal. Pada 2002, 763.917 kasus ditemukan di seluruh dunia, dan menurut WHO pada tahun itu, 90% kasus kusta dunia terdapat di Brasil, Madagaskar, Mozambik, Tanzania dan Nepal.
[sunting] Kelompok berisiko
Kelompok yang berisiko tinggi terkena kusta adalah yang tinggal di daerah endemik dengan kondisi yang buruk seperti tempat tidur yang tidak memadai, air yang tidak bersih, asupan gizi yang buruk, dan adanya penyertaan penyakit lain seperti HIV yang dapat menekan sistem imun. Pria memiliki tingkat terkena kusta dua kali lebih tinggi dari wanita.[sunting] Situasi global
| Tabel 1: Prevalensi pada awal 2006, dan tren penemuan kasus baru pada 2001-2005, tidak termasuk di Eropa | ||||||
| Daerah | Prevalensi terdaftar (rate/10,000 pop.) | Kasus baru yang ditemukan pada tahun | ||||
|---|---|---|---|---|---|---|
| Awal 2006 | 2001 | 2002 | 2003 | 2004 | 2005 | |
| Afrika | 40.830 (0.56) | 39.612 | 48.248 | 47.006 | 46.918 | 42.814 |
| Amerika | 32.904 (0.39) | 42.830 | 39.939 | 52.435 | 52.662 | 41.780 |
| Asia Tenggara | 133.422 (0.81) | 668.658 | 520.632 | 405.147 | 298.603 | 201.635 |
| Mediterania Timur | 4.024 (0.09) | 4.758 | 4.665 | 3.940 | 3.392 | 3.133 |
| Pasifik Barat | 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 |
| Tabel 2: Prevalensi dan Penemuan | ||||||
| Negara | Prevalensi terdaftar (rate/10,000 pop.) | Penemuan kasus baru (rate/100,000 pop.) | ||||
|---|---|---|---|---|---|---|
| Awal 2004 | Awal 2005 | Awal 2006 | Selama 2003 | Selama 2004 | Selama 2005 | |
 Brasil | 79.908 (4.6) | 30.693 (1.7) | 27.313 (1.5) | 49.206 (28.6) | 49.384 (26.9) | 38.410 (20.6) |
 Republik Demokratik Kongo | 6.891 (1.3) | 10.530 (1.9) | 9.785 (1.7) | 7.165 (13.5) | 11.781 (21.1) | 10.737 (18.7) |
 Madagaskar | 5.514 (3.4) | 4.610 (2.5) | 2.094 (1.1) | 5.104 (31.1) | 3.710 (20.5) | 2.709 (14.6) |
 Mozambik | 6.810 (3.4) | 4.692 (2.4) | 4.889 (2.5) | 5.907 (29.4) | 4.266 (22.0) | 5.371 (27.1) |
 Nepal | 7.549 (3.1) | 4.699 (1.8) | 4.921 (1.8) | 8.046 (32.9) | 6.958 (26.2) | 6.150 (22.7) |
 Tanzania | 5.420 (1.6) | 4.777 (1.3) | 4.190 (1.1) | 5.279 (15.4) | 5.190 (13.8) | 4.237 (11.1) |
| Total | 112.092 | 60.001 | 53.192 | 80.707 | 81.289 | 67.614 |
Tabel 1 menunjukkan penemuan kasus secara global menurun sejak 2001. Tabel 2 menunjukkan situasi kusta pada enam negara utama.
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