Experimental borderline lepromatous leprosy with intraneural erythema nodosum leprosum in a mangabey monkey (Cercocebus atys).

A sooty mangabey monkey (Cercocebus atys) was inoculated with Mycobacterium leprae and developed borderline lepromatous leprosy and intraneural erythema nodosum leprosum. Previously studied mangabeys have developed only disseminated lepromatous leprosy without reactions. This case broadens the spectrum of leprosy seen in experimentally inoculated animals and further characterizes the nonhuman primate model of leprosy.

Ocular leprosy in nine-banded armadillos following intrastromal inoculation.

Leprosy shows a higher percentage of ocular involvement than any other systemic infection. In humans, the cornea is the first ocular tissue affected. Our previous studies in armadillos with naturally acquired and experimental disseminated leprosy showed that 44% had corneal infection. Mycobacterium leprae is found in armadillo burrows in Louisiana, U.S.A., and ocular abrasions may be the portal of entry for these organisms in wild armadillos. To test the cornea as a route of infection, we injected eight armadillos intrastromally with 2 x 10(6) M. leprae in 1 microliters. Two and 4 months later, the armadillos were sacrificed and their eyes processed for light- and electron-microscopy. After 2 months, M. leprae were found in histiocytes mainly in the corneal limbus, sclera and bulbar conjunctiva. At 4 months, however, there was a visible corneal leproma in one animal. Microscopically, it was found to be a histiocytic granuloma with heavy M. leprae invasion. In addition, cells were seen in the anterior chamber. Leprosy is endemic in regions where other corneal infections which compromise the epithelial barrier property are prevalent and where leprosy bacilli are found in the environment. The entry of leprosy bacilli into the cornea may produce lesions which spread posteriorly in the eye.

Histopathological changes in the eyes of mangabey monkeys with lepromatous leprosy.

Leprosy is the third leading cause of preventable blindness; however, little is known about the spread of infection to the eye. We have studied the eyes of three sooty managabey monkeys. Two were experimentally infected with Mycobacterium leprae; the third was not infected. In one of the infected animals there was histopathological evidence of lepromatous leprosy as evidenced by a chronic inflammatory infiltrate at the limbus, and detection of acid-fast bacilli in the corneal stroma, blood vessel walls, and corneal nerves. The latter were damaged as a result of the bacillary invasion. Electron microscopy revealed involvement and distortion of keratocytes with M. leprae and invasion of the corneal stroma by macrophages containing bacilli. Both infected animals showed focal collections of lymphocytes in the superficial stroma of the conjunctiva and in the ciliary body. This is the first report of the ocular manifestations of leprosy in any primate, including man, in which the duration of infection is known.

Corneal changes in nine-banded armadillos with leprosy.

Leprosy is the third leading cause of blindness worldwide; however, little is known about the ocular changes that occur during the disease process. We have studied the eyes of two nine-banded armadillos with experimental Mycobacterium leprae infection by light and electron microscopy. Both animals had been inoculated intracutaneously, one 5 years and the other 2 years previously. Light microscopy revealed invasion by acid-fast bacilli which were seen in keratocytes and mononuclear phagocytes in all layers of the corneal stroma. In both animals, large macrophage granulomas were observed in the deep stroma, which was vascularized. Acid-fast bacilli were also were found in macrophages and vascular endothelial cells. By electron microscopy, numerous bacilli were found in the keratocytes, macrophages, and Schwann cells of myelinated and unmyelinated axons, and in the endothelial cells of blood vessels. The localization of M. leprae and the presence of inflammatory cells in the ocular tissue of both animals suggest that the bacilli reach the eye by the neural and/or vascular route. One animal showed much more extensive disease and bacillary yield than the other, indicating that ocular involvement may be independent of the generalized infection. Further studies of early ocular involvement in the armadillo and other animals could help to clarify the pathogenesis of this potentially blinding infection.

Experimental leprosy in African green monkeys (Cercopithecus aethiops): a model for polyneuritic leprosy.

Three African green monkeys (Cercopithecus aethiops) were inoculated intravenously and intracutaneously with Mycobacterium leprae derived from a naturally infected mangabey monkey. All developed cutaneous lesions at inoculation sites. One developed disseminated cutaneous lesions, while the cutaneous lesions in the other two regressed and eventually disappeared. The animals were examined at necropsy five years after inoculation. All three had active leprosy infection in peripheral nerves with extensive inflammation and fibrosis. The disease histologically resembled borderline-lepromatous leprosy. These findings add a new dimension to animal models of leprosy.

Experimental leprosy in a rhesus monkey: necropsy findings.

A 6-month-old male rhesus monkey (Macaca mulatta) was inoculated intravenously and intracutaneously with Mycobacterium leprae obtained from a naturally infected mangabey monkey. The animal developed generalized lepromatous leprosy, and was killed for pathological examination 56 months after inoculation. Lesions were observed in the skin, nasal mucosa, peripheral nerves, and peripheral lymph nodes, with relative sparing of viscera. The monkey was carefully evaluated for the retrovirus STLV-III infection and was found negative. The rhesus monkey thus provides another animal model for the study of leprosy.

Experimental leprosy in the mangabey (Cercocebus atys): necropsy findings.

A mangabey monkey (Cercocebus atys) was inoculated intravenously and intracutaneously with acid-fast bacilli (AFB) from a mangabey with spontaneously acquired leprosy. It developed generalized lepromatous leprosy and died 46 months after inoculation. Necropsy revealed severe lepromatous infiltrates in the skin, nasal mucosa, peripheral nerves, and testicles. Internal organs were only minimally involved. The lesions seen at necropsy were very similar to those seen in untreated cases of human lepromatous leprosy. These findings further substantiate the mangabey monkey as a suitable animal model for the study of lepromatous leprosy.

Leprosy in a trachomatous population.

In an Egyptian leprosy hospital, 17% of 133 patients had a visual acuity of less than 3/60. Corneal opacity, phthisis bulbi, and cataract accounted for 85% of blindness. Leprosy and trachoma together produce blinding corneal opacity by exposure, leprous keratitis, and trichiasis and entropion. Inturned lids, a late result of conjunctival scarring due to childhood trachoma, were less frequent in patients with lepromatous leprosy than in patients with tuberculoid leprosy; because conjunctival scarring from trachoma depends on cell-mediated immunity, patients with lepromatous leprosy may not have had severe trachomatous scarring develop due to their lifelong abnormality in cellular immunity. In patients with leprosy, even when complicated by trachoma, simple measures to prevent or restore vision include medical treatment of leprosy, surgical correction of lid deformities, sector iridectomy for constricted pupils or central corneal opacities, and cataract extraction.