A study of factors associated with intestinal immunoglobulin A in children with diarrhoea only and those with diarrhoea and malnutrition
A cross sectional study was undertaken to determine the role of intestinal immunoglobulin A (IgA) in prevention from, or limitation of diarrhoea disease among normal, malnourished and human immunodeficiency virus (HIV) seropositive children. stools were collected from children aged less than 5 years old, from which total IgA was determined by radial immunodifusion and specific IgA by Enzyme-linked immunosorbent assay (ELISA). Intestinal parasites were identified by wet preparation and microscopy. Enteric bacteria namely Salmonella, Shigella, Escherichia coli and Campylobacter were isolated by culture on selective media then identified by biochemical tests and slide agglutination serotyping. Rotavirus was determined by ELISA test. Human immunodeficiency virus was determined by an ELISA screening test and confirmed by Western Blot. Peripheral blood was collected from the children for determination of T-helper (CD4) and T-suppressor (CD8) lymphocytes by flow cytometry and phagocytic activity by killed Candida albicans yeast cells. A total of 55h children ~ere included in the stUdy, mean aqe 11.5 months, standard deviation 14.8 months and range 5 days to 60 months. Malnourished children had diarrhoea of longer duration (p=O.OOl) and more severity (p<0.04) than those well nourished. Similar results have been reported in other studies. Apart from total IgA which was higher in marasmic children (p=O.Ol), specific IgA levels, phagocytic activity and T-Iymphocyte counts were independent of nutritional status. While there was no association between severity of diarrhoea and either total IgA, T-Iymphocytes or phagocytic activity, Rotavirus specific IgA (p = 0.05) and EPEe 086A:K61 (p = 0.01) was significantly higher in mild compared to severe diarrhoea. It is therefore probable that prolonged and severe diarrhoea in malnutrition may be a result of impaired immune system. There was a trend for increased total IgA levels (p=0.2) and T-helper cell count (p=0.06) in breast fed children compared to those mixed fed or bottle fed. Breast feeding may provide a direct localized protective function in the gut or via primed T-cells which regulate committed B-cells to produce IgA. When the presence of specific IgA was compared with enteric pathogens, children had diarrhoea caused by different organisms other than the one they had intestinal IgA antibody to (p<0.05). This suggests that intestinal IgA may have a protective role to play in the host's resistance to diarrhoea disease. The occurrence of enteropathogens in neonates suggest that passive immunity may be inadequate. Total IgA, (p=O.3) and phagocytic activity, (p=O .1) were reduced, though not significantly in HIV seropositive children. The occurrence of enteropathogens was independent of HIV serostatus and CD4 cell depletion. Absolute CD4 lymphocyte counts were low in HIV seropositive children with severe diarrhoea (p=O.Ol). This suggests that CD4 lymphocytes may have a role to play in limiting severity of diarrhoea in HIV infection. Children of HIV seroposi tive mothers had prolonged diarrhoea than those of HIV seronegative mothers (p=O.06) regardless of their HIV status, and diarrhoea was more common among those aged less than six months (p=O.02, Odds ratio=4. 75). Probably HIV infection prevents passive transfer of maternal immunity. The r-esuLt.s cf this st.udy suggest that the presence of intestinal IgA may have a role to play in protection against diarrhoea in both normal and malnourished children. The role of passive transfer of maternal immunity in HIV seropositive mothers needs further investigation.