Contributions to the Bacteriology of Leprosy
I. The Diphtheroid in Leprosy
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Clinical and Pathological Aspects of Human African Trypanosomiasis (T. B. Gambiense) with Particular Reference to Reactive Arsenical Encephalopathy
L. Haller
L. Haller
WHO/TDR Programme, Tryprespro, Daloa, Ivory Coast, Africa
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H. Adams
H. Adams
Department of Neuropathology, Southern General Hospital, Glasgow G51 4TF, Scotland
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F. Merouze
F. Merouze
Rural Health Sector, Daloa, Ivory Coast, Africa
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A. Dago
A. Dago
Department of Pathology, CHU Treichville, Abidjan, Ivory Coast, Africa
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Fourteen of 330 patients treated with melarsoprol (Mel B) for human African trypanosomiasis (HAT) developed a severe reactive arsenical encephalopathy (RAE). Six of these cases were fatal and postmortem examination was performed on 5 patients. Symptoms of “sleeping sickness” were compared with symptoms after treatment with arsenicals and the subsequent onset of RAE. There are 3 characteristic syndromes of RAE: convulsive status associated with acute cerebral edema, rapidly progresive coma without convulsions, and acute nonlethal mental disturbances without neurological signs. Three subjects revealed hypoxic brain damage with acute cerebral edema, and multiple hemorrhages of brain stem in those comatose. The pathology of the underlying HAT (chronic perivascular inflammation and plasma cytic infiltration of the brain) and the pathology of the RAE (characterized by acute vasculitis) are distinct. RAE occurs in the first as well as in the second stage (CNS involvement) of trypanosomiasis but the reason for this is unclear; an exclusive toxicity of the drug, or a Herxheimer reaction are possible but seem unlikely. Both clinical and laboratory findings point rather to a drug-related, delayed immune response.
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