Neuropathies can result directly from various bacterial and viral infections, as well as from an indirect or parainfectious autoimmune response to the infection (Table 17-1). Parainfectious neuropathies (e.g., Guillain–Barré syndrome associated with various infections and vasculitis associated with hepatitis) are discussed in detail in other chapters.
TABLE 17-1.INFECTIOUS AGENTS ASSOCIATED WITH NEUROPATHIES ||Download (.pdf) TABLE 17-1.INFECTIOUS AGENTS ASSOCIATED WITH NEUROPATHIES
Leprosy is caused by the acid-fast bacteria Mycobacterium leprae. Leprosy is the most common cause of peripheral neuropathy in Southeast Asia, Africa, and South America. The main route of transmission is felt to be from person-to-person spread via nasal droplets. The bacteria is very slow growing with an incubation period that can vary between 2 and 40 years, customarily between 5 and 7 years.1
There is a spectrum of clinical manifestations ranging from tuberculoid leprosy at one end to lepromatous leprosy on the other end of the spectrum, with borderline leprosy in between based upon the Ridley–Joplin classification (Table 17-2).1–5 The World Health Organization (WHO) introduced a simpler classification based on the number of skin lesions to help guide treatment: multibacillary (six more skin lesions) and paucibacillary (fewer than six skin lesions) leprosy.1 In general, lepromatous leprosy is always multibacillary, and tuberculoid leprosy is usually paucibacillary; borderline leprosy can be either multibacillary or paucibacillary. The clinical manifestations of the disease are determined by the immunological response of the host to the infection. In tuberculoid leprosy, the cell-mediated immune response is intact.1–5 Thus, there are focal, circumscribed inflammatory responses to the bacteria within the affected areas of skin and nerves. The resulting skin lesions appear as well-defined, scattered hypopigmented patches and plaques with raised, erythematous borders (Figs. 17-1 and 17-2). Cutaneous nerves are often affected, resulting in a loss of sensation in the center of these skin lesions. Cooler regions of the body (e.g., face and limbs) are more susceptible than warmer regions such as the groin or axilla. In addition, the ulnar nerve at the medial epicondyle, the median nerve at the distal forearm, the peroneal nerve at the fibular head, the sural nerve, the greater auricular nerve, and the superficial radial nerve at the wrist are common sites of involvement and become encased with granulomas, leading to mononeuropathy or mononeuropathy multiplex. These nerves are thickened and often palpable.
TABLE 17-2.CLINICAL, LABORATORY, IMMUNOLOGICAL, AND HISTOPATHOLOGICAL ...