The Leper's Curse

The Leper's Curse, a photo by firoze shakir photographerno1 on Flickr.

Beggars at the Maha Kumb

From Wikipedia, the free encyclopedia

Leprosy, also known as Hansen's disease (HD), is a chronic disease caused by the bacteria Mycobacterium leprae and Mycobacterium lepromatosis.[1][2] Named after physician Gerhard Armauer Hansen, leprosy is primarily a granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract; skin lesions are the primary external sign.[3] Left untreated, leprosy can be progressive, causing permanent damage to the skin, nerves, limbs and eyes. Contrary to folklore, leprosy does not cause body parts to fall off, although they can become numb or diseased as a result of secondary infections; these occur as a result of the body's defenses being compromised by the primary disease.[4][5] Secondary infections, in turn, can result in tissue loss causing fingers and toes to become shortened and deformed, as cartilage is absorbed into the body.[4][5][6]
Leprosy has affected humanity for over 4,000 years,[7] and was recognized in the civilizations of ancient China, Egypt and India.[8] In 1995, the World Health Organization (WHO) estimated that between 2 and 3 million people were permanently disabled because of leprosy at that time.[9] In the past 20 years, 15 million people worldwide have been cured of leprosy.[10] Although the forced quarantine or segregation of patients is unnecessary in places where adequate treatments are available, many leper colonies still remain around the world in countries such as India (where there are still more than 1,000 leper colonies),[10] China,[11] Romania,[12] Egypt, Nepal, Somalia, Liberia, Vietnam,[13] and Japan.[14] Leprosy was once believed to be highly contagious and was treated with mercury — all of which applied to syphilis, which was first described in 1530. It is possible that many early cases thought to be leprosy could have actually been syphilis.[15]
The age-old social stigma[16] associated with the advanced form of leprosy lingers in many areas, and remains a major obstacle to self-reporting and early treatment. Effective treatment for leprosy appeared in the late 1930s with the introduction of dapsone and its derivatives. Leprosy bacilli resistant to dapsone soon evolved and, due to overuse of dapsone, became widespread. It was not until the introduction of multidrug therapy (MDT) in the early 1980s that the disease could be diagnosed and treated successfully within the community.[17]
MDT for multibacillary leprosy consists of rifampicin, dapsone, and clofazimine taken over 12 months. Dosages adjusted appropriately for children and adults are available in all primary health centres in the form of blister packages.[17] Single dose MDT for single lesion leprosy consists of rifampicin, ofloxacin, and minocycline. The move toward single-dose treatment strategies has reduced the prevalence of disease in some regions, since prevalence is dependent on duration of treatment. World Leprosy Day was created to draw awareness to leprosy and its sufferers.
Mycobacterium leprae


Mycobacterium leprae, one of the causative agents of leprosy. As acid-fast bacteria, M. leprae appear red when a Ziehl-Neelsen stain is used.
Main article: Mycobacterium leprae
Mycobacterium leprae and Mycobacterium lepromatosis are the causative agents of leprosy. M. lepromatosis is a relatively newly identified mycobacterium isolated from a fatal case of diffuse lepromatous leprosy in 2008.[2][3]
An intracellular, acid-fast bacterium, M. leprae is aerobic and rod-shaped, and is surrounded by the waxy cell membrane coating characteristic of Mycobacterium species.[30]
Due to extensive loss of genes necessary for independent growth, M. leprae and M. lepromatosis are obligate pathogens, and unculturable in the laboratory, a factor that leads to difficulty in definitively identifying the organism under a strict interpretation of Koch's postulates.[2][31] The use of non-culture-based techniques such as molecular genetics has allowed for alternative establishment of causation.
While the causative organisms have to date been impossible to culture in vitro, it has been possible to grow them in animals. Charles Shepard, chairman of the United States Leprosy Panel, successfully grew the organisms in the footpads of mice in 1960. This method was improved with the use of congenitally athymic mice (nude mice) in 1970 by Joseph Colson and Richard Hilson at St George's Hospital, London.
A second animal model was developed by Eleanor E. Storrs at the Gulf South Research Institute. Dr Storrs had worked on the nine-banded armadillo for her PhD, because this animal had a lower body temperature than humans and might therefore be a suitable animal model.[32] The work started in 1968 with material provided by Waldemar F. Kirchheimer at the United States Public Health Leprosarium in Carville, Louisiana.[33] These experiments proved unsuccessful, but additional work in 1970 with material provided by Chapman H. Binford, medical director of the Leonard Wood Memorial, was successful. The papers describing this model led to a dispute of priority. Further controversy was generated when it was discovered that wild armadillos in Louisiana were naturally infected with leprosy.
Naturally occurring infection also has been reported in non-human primates including the African chimpanzee, sooty mangabey, and cynomolgus macaque.

en.wikipedia.org/wiki/Leprosy