We report a 68-year-old man who received an IV inoculation of WBCs for an indium radionuclide scan containing 600 to 700 tissue culture infectious doses of human immunodeficiency virus type 1 (HIV-1) from an HIV-1-infected individual. The recipient immediately received zidovudine, then was switched to dideoxyinosine and interferon-alpha, but died of hepatorenal syndrome and hepatic encephalopathy 15 days later. HIV-1 cultures were positive from the recipient's blood on day 14 but not days 0, 1, and 8. At autopsy, cultures of parietal lobe isolated HIV-1. HIV-1 nucleic acid was present in several brain areas, but not in several other organs, by two independent laboratories using the polymerase chain reaction. The brain showed mild perivascular cuffing and a mild lymphocytic meningitis, but there was no evidence of glial nodules, giant cells, or white matter abnormalities. HIV-1 pg41 viral antigen was seen by immunoperoxidase staining in rare infiltrating cells within perivascular and subpial spaces. Thus, HIV-1 was isolated from brain 15 days after mistaken HIV-1 inoculation and 1 day after virus was first recovered from blood.
A year-long prospective study of 152 Bangladeshi children with mild to moderate protein-calorie malnutrition related nutritional status and cellular immune defects to morbidity due to diarrheal, respiratory, and febrile diseases. In children older than 36 mo, wasting correlated with skin test anergy to three recall antigens and with inability to initiate hypersensitivity to dinitrochlorobenzene. In this older age group, anergy was associated with a 58% increased attack rate and an 83% increased duration of diarrheal diseases but not with febrile or respiratory infections. In stepwise regression analysis, this anergy effect was independent of the small negative impact of poorer nutritional status on morbidity. Ninety-three percent of diarrheal illnesses lasting at least 14 d were among anergic children. Cellular immune incompetence, indicated by anergy of unknown etiology, is associated with increased diarrheal morbidity and may promote the vicious cycle of repeated infections and deteriorating nutritional status.
The severity of diarrhea and nutritional status were measured in a prospective study of 97 patients hospitalized with cholera in Dacca, Bangladesh. Ninety-five percent of both adults and children were below their respective medians in weight as related to height; greater than 15% of each group showed second-degree protein-calorie malnutrition. Duration of diarrhea, but no volume of stool per hour, was prolonged by 30%-70% in those adults and children suffering from more severe malnutrition. The increased stool loss was unrelated to antibiotic usage, to presence of intestinal parasites, or to the refeeding diet given. It is suggested that the prolongation of diarrhea represents the continued effect of cholera toxin that is irreversibly bound to intestinal mucosal cells, the replacement of which would be retarded under conditions of poor nutrition.
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