Peripheral Neural Involvement in Cutaneous Leishmaniasis

Abstract

Peripheral neural involvement in cutaneous leishmaniasis has recently been recognized. A man presented with several tender hyperesthetic skin nodules. Histopathologic examination confirmed the diagnosis of cutaneous leishmaniasis. Of most interest was the presence of a striking lymphohistocytic inflammatory infiltrate around and within cutaneous nerves in addition to demonstrable leishmania organisms in the perineural space. This observation led to a detailed histopathologic evaluation of leishmanial skin lesions that developed in 13 mice after subcutaneous injection with leishmania major promastigotes. Varying degrees of neural involvement was noted in skin lesions from nine animals. In some lesions, in addition to inflammatory cells in the nerves, organisms were demonstrable within probable schwann cells. Three pathologic stages of dermal neural involvement were identified, namely, an early, intermediate, and late stage, depending on the severity of damage; however no correlation was found between the pathologic stage and the duration of the leismanial skin lesion of a specific animal.

Leishmanial antigens in the diagnosis of active lesions and ancient scars of American tegumentary leishmaniasis patients

“…In addition, amastigotes were found in dermal nerves in 3 out 12 active lesions in which the neural pattern was detected. These findings could be related to the fact that cutaneous ulcer is painless (Kubba et al 1987, Satti et al 1989. Neural structures were not found in the dense connective tissue of scar lesions.…”

Contribution of spinal cord glial cells to L. amazonensis experimental infection-induced pain in BALB/c mice

“…Thus, stimulus was not capable of inducing the same alterations in the contralateral side as in the ipsilateral side to the stimulus. No ulcerative lesions were observed during the experiments, which are important to allow studying the nociceptive phase of disease [2, 9, 13]. Furthermore, L. amazonensis infection did not alter ipsilateral ATF3 mRNA expression in DRG cells at the 30th day post-infection indicating no neuronal lesion in contrast with neuropathic pain conditions such as CCI of the sciatic nerve.…”