Following the marked decrease of rabies cases among domestic animals in the US in the 1940s and 1950s, indigenously acquired rabies among humans decreased to fewer than two cases per year in the 1960s and 1970s and fewer than one case per year during the 1980s. ^1,2 In 1950, for example, 4,979 cases of rabies were reported among dogs and 18 were reported among human populations; in 1989, 160 cases were reported among dogs and one was reported among humans. Thus, the likelihood of human exposure to a rabid domestic animal has decreased greatly; however, the many possible exposures that result from frequent contact between domestic dogs and humans continue to be the basis of most antirabies treatments. ^1,3

Rabies among wild animals - especially skunks, raccoons, and bats - has become more prevalent since the 1950s accounting for > 85% of all reported cases of animal rabies every year since 1976. ^1,2 Rabies among animals occurs throughout the continental US; only Hawaii remains consistently rabies-free. Wild animals now constitute the most important potential source of infection for both humans and domestic animals in the US. In much of the rest of the world, including most of Asia, Africa, and Latin America, the dog remains the major species with rabies and the major source of rabies among humans. Nine of the 13 human rabies deaths reported to CDC from 1980 through 1990 appear to have been related to exposure to rabid animals outside of the US. ^{1,4 - 10}

Although rabies among humans is rare in the US, every year approximately 18,000 persons receive rabies pre-exposure prophylaxis and an additional 10,000 receive postexposure prophylaxis. Appropriate management of persons possibly exposed to rabies depends on the interpretation of the risk of infection. Decisions about management must be made immediately. All available methods of systemic prophylactic treatment are complicated by occasional adverse reactions, but these are rarely severe. ^{1,11 - 15}

Data on the efficacy of active and passive rabies immunization have come from both human and animal studies. Evidence from laboratory and field experience in many areas of the world indicates that postexposure prophylaxis combining local wound treatment, passive immunization, and vaccination is uniformly effective when appropriately applied. ^{1,16 - 21}

Although no postexposure vaccine failures have occurred in the US during the 10 years that HDCV has been licensed, seven persons have contracted rabies after receiving postexposure treatment with both HRIG and HDCV outside the US. An additional six persons have contracted the disease after receiving postexposure prophylaxis with other cell culturederived vaccines and HRIG or ARS (equine antirabies serum). However, in each of these cases, there was some deviation from the recommended postexposure treatment protocol. ^{1,22 - 24} Specifically, patients who contracted rabies after postexposure prophylaxis did not have their wounds cleansed with soap and water or other antiviral agents, did not receive their rabies vaccine injections in the deltoid area (i. e., vaccine was administered in the gluteal area), or did not receive passive vaccination around the wound site. ¹

Rabies antibody provides passive protection when given immediately to individuals exposed to rabies virus. ^25,26 Rabies Immune Globulin (Human) [RIG( H)] of adequate potency 27 was used in conjunction with Rabies Vaccine of duck embryo origin. ^27,28 When a globulin dose of 20 IU/kg of rabies antibody was given simultaneously with the first dose of vaccine, levels of passive rabies antibody were detected 24 hours after injection in all individuals. There was minimal or no interference with the immune response to the initial and subsequent doses of vaccine, including booster doses.

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