RESUMEN
Although the roles played by systemic tumour necrosis factor (TNF) and interleukin 1beta (IL-1beta), and their upregulation of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and E-selectin, in the pathogenesis of human cerebral malaria (CM) are well established, the role of local cytokine release, in the brain, remains unclear. Immunohistochemistry was therefore used to compare the expression of ICAM-1, VCAM-1, E-selectin, IL-1beta, TNF and transforming growth factor beta (TGF-beta) at light-microscope level, in cryostat sections of cerebral, cerebellar and brainstem tissues collected, post-mortem, from Ghanaian children. Among the 21 children investigated were 10 cases of CM, five of severe malarial anemia (SMA), one of purulent bacterial meningitis (PBM), two of non-central-nervous-system infection (NCNSI) and three children who had no infection (NI) when they died. Parasitised erythrocytes were detected in all of the sections from the cases of fatal malaria (CM and SMA), and sequestered leucocytes were present in most of the sections from the CM cases (but none of the sections from the SMA cases). Significantly elevated vascular expression of all three adhesion molecules investigated was detected in the brains of the 15 cases of fatal malaria and one of the cases of NCNSI (a child with Salmonella septicaemia), and in the malaria cases this showed highly significant co-localization with the areas of erythrocyte sequestration. In terms of the levels of expression of ICAM-1, VCAM-1 and E-selectin, there were, however, negligible differences between the CM and SMA cases. Although TGF-beta showed intravascular and perivascular distribution in all the subjects, its expression was most intense in the PBM case and the CM group. Only in the sections from the PBM and CM cases did TNF and IL-1beta show prominent brain parenchymal staining, in addition to the intravascular and perivascular staining seen in all subjects. The highest observed expression of each of the six antigens studied was in the cerebellar sections of the malaria cases. Endothelial activation in the brain therefore appears to be a feature of fatal malaria and Salmonella sepsis, and in cases of fatal malaria is closely associated with leucocyte sequestration. In the present study, IL-1beta and TNF were only up-regulated in the brains of children with neurodegenerative lesions, whereas TGF-beta was present in all cases.
Asunto(s)
Moléculas de Adhesión Celular/análisis , Citocinas/análisis , Malaria Cerebral/metabolismo , Anemia/metabolismo , Niño , Preescolar , Selectina E/análisis , Eritrocitos/parasitología , Femenino , Humanos , Inmunohistoquímica/métodos , Lactante , Molécula 1 de Adhesión Intercelular/análisis , Interleucina-1/análisis , Leucocitos Mononucleares/parasitología , Malaria Cerebral/mortalidad , Masculino , Meningitis Bacterianas/metabolismo , Factor de Crecimiento Transformador beta/análisis , Molécula 1 de Adhesión Celular Vascular/análisisRESUMEN
Human rotavirus (HRV) infection and its seasonal distribution was studied over a 12-month period in Ghana. A total of 561 stool samples, 447 diarrhoea stools and 114 non-diarrhoea stools (controls), were obtained from children attending three polyclinics in Accra. Rotavirus was detected during 10 of the 12 months and showed a seasonal trend. It was high during the relatively cool dry months and low during the wet season. Peaks of infection were in February (26.2%) and September (24.5%). HRV was detected in 67 of 447 of the diarrhoea stools (15.0%) and in eight of 114 controls (7.0%). The HRV isolation rate was highest (20.2%) in the under-18-months age group. The RNA electropherotype of the HRV isolates was predominantly (83.6%) of the long type. Non-group A HRV was detected in 14.9% of the HRV-positive samples.