The first clear-cut description of a virus-nerve cell interaction was made by Adelchi Negri in 1903 with the detection of cytoplasmic bodies (Negri bodies) in subsets of neurons in the brain from rabies-infected animals. A biographical sketch of Negri is given here; he was born in Perugia, Italy, in 1875 and died in Pavia in 1912. In 1900 Negri became assistant to Camillo Golgi, who encouraged him to study rabies-infected brains with histological techniques. The report of intraneuronal bodies described by Negri as specific for rabies stimulated an intense debate both concerning their diagnostic value and their nature. The diagnostic value was finally determined in a study by Negri's wife, Lina Negri-Luzzani, in 1913, while the viral nature of the bodies had to await the introduction of electron microscopy and immunohistochemistry. However, the true significance of the Negri bodies is still mysterious, since they only develop in subsets of infected neurons and occur mainly after infection with wild, so-called 'street', virus strains and not after infection with strains passaged in the laboratory, so-called 'fixed' strains.
A very brief review of the literature on the clinicopathological aspects of leprosy is given; mainly through references. The salient features of the two main types of leprosy--tuberculoid and lepromatous--are presented in a Table. The surgical and pathological findings are briefly described and the pathogenesis of involvement of the facial nerve (a motor nerve) is discussed. On the basis of (i) the severe histopathologic changes (degeneration) of the most distal part of the zygomatic branch of the facial nerve (innervating the orbicularis oculi), with sparing of the roots of all branches and the trunk of the nerve; (ii) the concurrent loss of cutaneous sensations in the territory of the maxillary division of the trigeminal nerve (the region of the zygoma and the lower eyelid); and (iii) the close approximation or even anastomoses occurring between the ultimate branches of these two nerves, it is postulated that paralysis of orbicularis oculi occurs secondarily to the sensory nerve damage, i.e. due to spread of infection from the sensory branches of the trigeminal to the motor branches of the facial nerve. The surgical and pathological findings of the nerves in the arm, especially the ulnar and the median and their branches are described, in tuberculoid and lepromatous leprosy. The forms of nerve degeneration, the occasional axon regeneration, and the role of the Schwann cell in harbouring the bacilli, are illustrated. The lysosomal enzyme activity in the Schwann cells of nerve fibres, particularly of unmyelinated fibres which preferentially phagocytose the M. leprae, and their role, albeit not very successful, in degrading the bacilli and controlling the infection, are also stressed, through light and electronmicrographs. The constellation of secondary factors of the terrain operating to produce further damage to primarily diseased nerves, is discussed. These factors include indirect compression from unyielding fibroosseous tissues, minor traumata, stretching of the nerves, and their exposure to lower temperatures in subcutaneous tissues.
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