Ultrastructure of leprous phlebitis.

An ultrastructural study on vein biopsies from six lepromatous leprosy patients was carried out. The results showed that a) the lumen-lining bacillated cells were endothelial in origin due to the presence of specific Weibel-Palade endothelial cell granules; b) endothelial cells released Mycobacterium leprae into the lumen by exophagocytosis; c) M. leprae were able to grow and multiply in the endothelial and smooth muscle cells; and d) smooth muscle cells did not show any evidence of reaction due to the presence of M. leprae in their cytoplasm.

An electron microscopic study of the small cutaneous vessels in lepromatous leprosy.

The small dermal vessels play an important role for the propagation of Mycobacterium leprae. Bacteria can multiply in the endothelial cells as well as in the pericytes and can enter the blood stream from the endothelial cells and the interstitial space from the pericytes. M. leprae can be phagocytosed by blood monocytes.

Electron microscopic findings of the peripheral nerve lesions of nude mice inoculated with M. leprae.

Peripheral nerve lesions of nude mice inoculated with Mycobacterium leprae were examined from 1 year to 1 year and 8 months post-inoculation. Leprosy bacilli and intracytoplasmic foamy structures were found in the perineurial cells, endothelial cells of capillaries, Schwann cells, and axons of the myelinated nerve fibers inside the lepromas of foot pads. In the proximal portion of the sciatic nerve, bacilli were found chiefly in the macrophages of the endoneurial space. Bacilli were not found in the perineurial cells of the sciatic nerves. Marked fibrosis, hypertrophy or degeneration of Schwann cells, demyelination, axonal damage or irreversible destruction of nerve architecture were not observed clearly. Therefore, it is thought that nude mice inoculated with M. leprae are suitable models for the study of the early peripheral nerve lesions of lepromatous leprosy.

Vascular changes in nerves in experimental leprosy--an ultrastructural study.

Ultrastructural observations made on the blood vessels of nerves in CBA/J mice with experimentally produced M. leprae infection revealed cytoplasmic filamentous structures along with large sized vacuoles in the endothelial cells and reduplication of peripericytal basement membranes in the 6-9 months of infection. In animals with late infection of 9-15 months duration, the endothelial cells presented foamy appearance caused by an increase in the number of vacuoles. These findings are suggestive of degenerative changes in the endothelial cells probably due to circulation of noxious substance in the blood stream.

Ultrastructure of skin in erythema nodosum leprosum.

The ultrastructural changes observed in erythema nodosum leprosum lesions were gross damage to blood vessels, particularly the endothelial cells, and deposition of immune complexes in vessel walls. Infiltrating cells and alteration of the ground substance formed a constant feature of the reaction. These changes are characteristic of an immune complex reaction.

Ultrastructural changes in blood vessels of peripheral nerves in leprosy neuropathy. I. Tuberculoid and borderline-tuberculoid leprosy patients.

Radial or superficial peroneal nerve biopsies of 6 patients with tuberculoid or borderline-tuberculoid leprosy and 6 control nerve biopsies were examined by electron microscopy. Endoneurial blood vessels showed histopathology in all the leprosy patients. Changes, in particular, involved the basement membrane in postcapillary venules and venules. Multilayered parellel basement membranes, with collagen and ground substance, formed a thick coat ("hyaline zone") around the vessels. It is suggested that the zone inhibits passage of nutrients and metabolites and, thus, contributes to or is the main cause of the local destruction of (unmyelinated) nerve fibres and the lack of nerve fibre regeneration observed in this type of leprosy. The perivascular zone, presumably, is produced by pericytes in response to defects in the "blood-nerve barrier" of endoneurial vessels. In granulomata of leprosy skin lesions, a perivascular zone was not present. The endothelium of endoneurial vessels, in affected nerves, generally was normal. Occasionally, however, gaps and fenestrations were seen and there were histological indications that leakage of blood plasma had occurred through the gaps and through the basement membrane of the endothelium. Occlusion of endoneurial vessels was found only in the oldest patient and the degeneration of nerve fibres generally observed thus is considered not to be caused by ischaemia. Histopathology in epi-and perineurial vessels was definitely less pronounced than in endoneurial vessels.