Neurocysticercosis: parasitology, clinical presentation, diagnosis, and recent advances in management.
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Biomedical subjects
Publications and source records attributed to G C Cook.
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Gastrointestinal helminths (nematodes, trematodes and cestodes) constitute some of the most common and important infective agents of mankind and are responsible for much morbidity and some mortality. Whereas many symptoms and signs are confined to the intestine and less often the associated digestive organs, systemic manifestations are also numerous; this applies especially to indigenous populations of developing 'Third World' countries. Using a clinical classification these organisms can be broadly separated into those involving the small-intestine and those which have a colo-rectal distribution; of the former, a minority has been causally related to intestinal malabsorption. Clearly, however, not all gastrointestinal helminths are associated with disease and it is important to be able to separate these two groups; when present at high concentration and especially in infants and children some of the least pathogenic are not, however, entirely asymptomatic. Maintenance of a high 'index of suspicion' is necessary and this applied especially to 'western' populations in whom rapid and extensive travel to areas of the world with substandard sanitation and contaminated food and water supplies is now common; first evidence of infection in them may result from serious clinical complications. Recent advances have focussed on treatment, and especially the introduction of the benzimidazole compounds (especially albendazole) for nematode, and praziquantel for cestode, infections. Treatment of strongyloidiasis remains, however, unsatisfactory. Mass elimination of gastrointestinal helminths in developing 'Third World' countries remains a major challenge.
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Differential absorption of D-xylose and 3-O-methyl-D-glucose, and unmediated intestinal permeation of lactulose and L-rhamnose has been investigated in 14 patients with diarrhoea following tropical exposure and in 16 healthy control subjects. Five had malabsorption of fat, D-xylose and B12 ('tropical malabsorption' (TM) group), and that was absent or minimal in the others ('tropical diarrhoea' (TD) group). After combined ingestion of the four test sugars in iso-osmolar solution a marked depression in plasma D-xylose concentration (with a slow rise) occurred in all of the TM group; the TD group did not differ significantly from the controls. In contrast, 3-O-methyl-D-glucose absorption was similar in all three groups. Urine analysis demonstrated that intestinal permeation of lactulose was increased and that of rhamnose decreased in the TM group compared with the controls. Ingestion as a hyperosmotic solution further enhanced abnormal lactulose permeation in the TM group. Although some of the TD group showed one or the other of these changes, discrimination of the TM group from the TD and control groups was improved when results were expressed as lactulose/rhamnose differential permeation ratios, especially when using a hyperosmotic stress. Similar abnormalities have previously been demonstrated in untreated gluten-induced enteropathy (coeliac disease). The magnitude of the absorption defects demonstrated in TM are more severe than would be anticipated from the jejunal mucosal abnormalities alone; this suggests that there is probably significant pathology in the distal small intestine (including the ileum) in TM.
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Typhoid fever is still a major problem in developing Third World countries where socioeconomic conditions and standards of hygiene are still well below standard. Prophylaxis is far from satisfactory. However, recent developments using live oral vaccines are encouraging. Specific treatment for the disease consists of chloramphenicol or co-trimoxazole; amoxycillin and ampicillin are inferior agents but are of value in several situations because their potential toxic effects are less marked. Most other agents also have drawbacks or are relatively ineffective. In the severely toxic patient, corticosteroids seem to affect prognosis favourably. Of the many other acute complications of typhoid fever, ileal perforation is the most serious; there is still controversy concerning the respective roles of conservative and surgical management, but it is clear that individual cases must be assessed on their merit. Amoxycillin, because it is very rapidly absorbed and produces very high blood concentrations, is probably the best antibiotic for the carrier state.
Hypochlorhydria by compromising the defence mechanisms of the upper gastrointestinal tract predisposes to intestinal bacterial and parasitic infections. Achlorhydria predisposes to anaerobic colonization of the small intestine; colonization is far greater than in normal subjects even with partial neutralization of their gastric acidity after a meal. The best evidence for increased incidence of specific bacterial infection in the presence of achlorhydria relates to the nontyphoid salmonelloses. There is also strongly suggestive evidence in cholera. Among parasitic infections, the most impressive evidence relates to giardiasis and strongyloidiasis. In some instances, the infections themselves may also cause hypochlorhydria. Longitudinal studies are required. Whether patients receiving H2-receptor antagonists are unduly vulnerable to gastrointestinal infections is unclear. The importance of hypochlorhydria in 'Third World' populations, in whom gastrointestinal infections are extremely common, especially in infancy, is, at present, also impossible to evaluate.
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Postinfective tropical malabsorption (TM; tropical sprue) starts with an acute intestinal infection (bacterial, viral, or parasitic) which can affect predominantly the small or the large intestine. Miscellaneous invasive pathogens cause subsequent enterocyte damage affecting the entire small intestine and, to a lesser extent, the colon. Enteroglucagon, a tropic hormone, is then liberated and reaches a high plasma concentration. Small-intestinal stasis results. Further bacterial colonisation (in the lumen and also at the enterocyte surface) is encouraged. Continuing enterocyte damage is worsened by coexistent folate depletion, which is initiated at the onset of disease; body stores of folate reach a low concentration by 3 or 4 months. The cycle continues until the bacterial overgrowth is eliminated with an antibiotic (eg, tetracycline), or mucosal integrity recovers (hastened by oral folic-acid supplements), or both.
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