through the upper respiratory tract. Older research suggested the skin as the main route of transmission, but recent research has increasingly favored the respiratory route. Transmission occurs through inhalation of bacilli present in upper airway secretion. Leprosy is not sexually transmitted and is not spread through pregnancy to the unborn child. The majority (95%) of people who are exposed to M. leprae do not develop leprosy; casual contact such as shaking hands and sitting next to someone with leprosy does not lead to transmission. People are considered non-infectious 72 hours after starting appropriate multi-drug therapy. Two exit routes of M. leprae from the human body often described are the skin and the nasal mucosa, although their relative importance is not clear. Lepromatous cases show large numbers of organisms deep in the dermis, but whether they reach the skin surface in sufficient numbers is doubtful. Leprosy may also be transmitted to humans by armadillos, although the mechanism is not fully understood. Genetics {| class="wikitable" style="float: right; margin-left:15px; text-align:center" |- ! Name ! Locus ! OMIM ! Gene |- | LPRS1 | 10p13 | | |- | LPRS2 | 6q25 | | PARK2, PACRG |-' | LPRS3 | 4q32 | | TLR2|- | LPRS4 | 6p21.3 | | LTA|- | LPRS5 | 4p14 | | TLR1|- | LPRS6 | 13q14.11 | | |} Not all people who are infected or exposed to M. leprae develop leprosy, and genetic factors are suspected to play a role in susceptibility to an infection. Cases of leprosy often cluster in families and several genetic variants have been identified. In many people who are exposed, the immune system is able to eliminate the leprosy bacteria during the early infection stage before severe symptoms develop. A genetic defect in cell-mediated immunity may cause a person to be susceptible to develop leprosy symptoms after exposure to the bacteria. The region of DNA responsible for this variability is also involved in Parkinson's disease, giving rise to current speculation that the two disorders may be linked at the biochemical level. Mechanism Most leprosy complications are the result of nerve damage. The nerve damage occurs from direct invasion by the M. leprae bacteria and a person's immune response resulting in inflammation. The molecular mechanism underlying how M. leprae produces the symptoms of leprosy is not clear, but M. leprae has been shown to bind to Schwann cells, which may lead to nerve