Leprosy is a disease that poorly understood by many health care professionals. Although there is some knowledge of the mechanism, transmission, and treatment of the disease, there are many questions that still remain. The following paper attempts to provide some background information on what is known about leprosy and then attempts to investigate certain aspects of the disease that are unknown. A description of the classification, mechanism of infection, transmission, distribution, and treatment of the disease will be provided. After reviewing the background material, a great deal of questions may arise as to how exactly this disease is spread from person to person and what conditions promote infection. For example, one may wish to investigate the following:

It is interesting to note that leprosy does not affect the nerves of the central nervous system. Why is this the case? This is because M. leprae specifically attacks the myelinating Schwann cells which facilitate the entry of the bacilli into the nerve. Since Schwann cells are the primary targets for this microorganism, it does not affect the nerves of the central nervous system because Schwann cells are found only in the peripheral nervous system.

Although researchers have not yet reached definitive conclusions about this mode of transmission, this seems to be the most probable method. Also, the skin has been another portal of entry and exit of the disease. Untreated patients shed large numbers of bacteria from lesions or ulcers, or otherwise injured skin (van Beers et al, 1996). There is no evidence that the bacilli can penetrate intact skin, therefore, the skin of the recipient must be broken or injured as well. There has also been evidence that arthropods could possibly play a role in the transmission, however, the evidence is seen as circumstantial (van Beers et al, 1996).

The main mechanism for infecting the peripheral nerves is that M. leprae binds to the G-domain of the a2 chain of the basal lamina sheath of the Schwann-cell axon unit. Binding to the surface of the nerve leads to internalization of the bacilli and establishment of Schwann cell infection (Weinstein et al, 1999). Schwann cells infected by the M. leprae lose their ability to maintain normal axonal contact and support, resulting is rapid disintegration of the myelin sheath (Weinstein et al, 1999). The degradation of the myelin sheath results in the calicification and permanent loss of neural function.

2) Why is leprosy so prevalent in some parts of the world (i.e. India) but not in others?

#1 - http://who.int/lep/disease/Microbiology/transmis.htm

It would seem logical that once a person living in an area contracts the disease, other living in close proximity are bound to contract it as well. Van Beers et al (1996) indicate that the risk of contracting leprosy from a household member can be five to ten times higher than not living with an infected person, especially if the infected person carries mulitbacillary leprosy. On the other hand, Klaster et al (1993) indicate that infection in endemic populations is widespread and not just restricted to household contacts. Whether a single group of people can be held accountable for the widespread infection of this disease remains questionable. The spread of the disease most likely involves many factors, such as the ones discuss in the above India example. The spread of infection involves a complex association of many factors and it is difficult to determine the importance of each factor.

Some common words found in the essay are:
Van Beers, Jacobson Krahenbuhl, Jacobosn Krahenbuh, Mechanism Infection, Bhattacharya Sehgal, Armaeur Hansen, Transmission Leprosy, Leprosy Leprosy, , Microbiology Letters, et al, van beers, van beers et, beers et, beers et al, et al 1996, al 1996, leprosy difficult, leprosy prevalent, krahenbuhl 1999, schwann cells, jacobson krahenbuhl 1999, mdt effective, stages disease, de wit myl,
Approximate Word count = 3293
Approximate Pages = 13 (250 words per page double spaced)