A 46-year-old man was bitten by a dog in Mall; anti-rabies vaccination
was incomplete. Three months later he was admitted to hospital with f
ever and diarrhea. Human immunodeficiency virus (HIV) serology was pos
itive and CD4 count was 70/mm(3). His status worsened rapidly with con
fusion hydrophobia and hypersialorrhea. Despite anti-rabies serotherap
y and vaccination, he died suddenly 12 days after admission. Immunoflu
orescence on cerebral tissue samples established rabies encephalitis.
Neuropathology showed mild encephalitis with occasional Babes nodules
and rare perivascular mononuclear cuffs, Intraneuronal Negri inclusion
bodies were remarkably diffuse and abundant. They were clearly demons
trated by immunocytochemistry and electron microscopy, Apoptotic neuro
ns were identified in the brain stem and hippocampus in the vicinity o
f inflammatory foci, In contrast, apoptosis could not be demonstrated
in non-inflammatory areas, even where Negri bodies were numerous. Ther
e was no associated HIV encephalitis or opportunistic infection, The o
ccurrence of rabies encephalitis in AIDS represents a random associati
on, but is probably not exceptional as rabies is endemic in many count
ries and the AIDS epidemic is spreading worldwide, In this case, altho
ugh the incubation duration and clinical presentation were comparable
to those in classical rabies, the T-cell-mediated immunosuppression ma
y account for the weak inflammatory reaction and unusually abundant vi
ral multiplication, This observation confirms that all those at risk f
or rabies, particularly immunocompromised patients, should receive com
plete anti-rabies treatment including vaccines and specific immunoglob
ulins, as soon as possible after infection.