The armadillo as a model for peripheral neuropathy in leprosy.

Leprosy (also known as Hansen's Disease) is a chronic infectious disease caused by Mycobacterium leprae that primarily targets the peripheral nervous system; skin, muscle, and other tissues are also affected. Other than humans, nine-banded armadillos (Dasypus novemcinctus) are the only natural hosts of M. leprae, and they are the only laboratory animals that develop extensive neurological involvement with this bacterium. Infection in the armadillo closely recapitulates many of the structural, physiological, and functional aspects of leprosy seen in humans. Armadillos can be useful models of leprosy for basic scientific investigations into the pathogenesis of leprosy neuropathy and its associated myopathies, as well as for translational research studies in piloting new diagnostic methods or therapeutic interventions. Practical and ethical constraints often limit investigation into human neuropathies, but armadillos are an abundant source of leprotic neurologic fibers. Studies with these animals may provide new insights into the mechanisms involved in leprosy that also might benefit the understanding of other demyelinating neuropathies. Although there is only a limited supply of armadillo-specific reagents, the armadillo whole genomic sequence has been completed, and gene expression studies can be employed. Clinical procedures, such as electrophysiological nerve conduction testing, provide a functional assessment of armadillo nerves. A variety of standard histopathological and immunopathological procedures including Epidermal Nerve Fiber Density (ENFD) analysis, Schwann Cell Density, and analysis for other conserved cellular markers can be used effectively with armadillos and will be briefly reviewed in this text.

A comparison of the expression of NGFr, PGP 9.5 and NSE in cutaneous lesions of patients with early leprosy using immunohistochemistry.

We examined the immunohistochemical expression of the neuronal proteins NGFr, PGP 9.5, and NSE in cutaneous lesions of patients with early leprosy and in the skin of normal individuals. PGP 9.5- and NSE-immunoreactive nerve fibers were decreased in the skin of leprosy patients. This reduction was topographically unrelated to the early leprosy infiltrate. However, no difference in the expression of NGFr was found between the leprosy patient and normal groups. It was shown that there is a selective alteration in the expression of neuronal proteins in early leprosy lesions which seems to be unrelated to the inflammatory infiltrate in the initial stages of leprosy. Pathogenic mechanisms other than inflammation, which are intrinsic to the Mycobacterium leprae-nerve relationship, may thus contribute to the nerve damage in leprosy neuropathy.