01777nas a2200253   4500000000100000008004100001260001200042653002300054653001200077653001500089653003000104653002000134100001500154700002000169700000900189700001400198700001600212245010600228856007300334300001200407490000600419520108400425022001401509       2020                            d  c10/202010aHansen’s disease10aleprosy10aneuropathy10aperipheral nervous system10askin appendages1 aGranger DL1 aRosado-Santos H1 aLo T1 aFlorell S1 aShimwella R00aFunctional Impairment of Skin Appendages Due to Peripheral Nerve Involvement by Mycobacterium leprae.  uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7566401/pdf/ofaa419.pdf  aofaa4190 v73 a<p>In the earliest stage of  infection, bacteria parasitize fine fiber twigs of autonomic peripheral nerves supplying efferent impulses to appendages of the skin. This obligate intracellular pathogen invades Schwann cells, the glial cells of peripheral nerves. Intracellular events inhibit Schwann cell physiology in complex ways, which include demyelination and dedifferentiation. Ultimately, axons embraced by their surrounding dysfunctional glia are damaged by poorly understood mechanisms. Loss of nerve conduction impairs the functions of skin appendages including hair growth, sebaceous gland secretion, sweating, and skin pigmentation. At the clinical level, these changes may be subtle and may precede the more obvious anesthetic skin lesions associated with Hansen's disease. Recognizing the early signs of skin appendage malfunction may aid in diagnosis leading to initiation of antimycobacterial treatment. Effective therapy administered early during infection may prevent irreversible peripheral nerve destruction, the presage for morbid complications of leprosy.</p>  a2328-8957