ABSTRACT
Aim: There is lack of information on the severity of diarrheal disease with etiology. Thus the study aimed to compare the etiology of under-five children with moderate-to-severe disease (MSD) and mild disease (MD). Study Design: Diarrheal disease surveillance. Place and Duration of Study: Mirzapur Kumudini Hospital, Tangail, rural Bangladesh, January 2010 – December 2011. Methodology: Overall, 2,324 under-5 diarrhea children were enrolled in the hospital who came from the demographic surveillance system (DSS) catchment area. Whole stool samples were collected from each enrolled child to detect rotavirus, Shigella, ETEC and V. cholerae. Information on socio-demographic and clinical characteristics was also collected. Results: Among all the study children, 1,098 (47%) were aged 0-11 months; 789 (34%) were 12-23 months, and 437 (19%) were 24-59 months. Rotavirus (33%) was mainly responsible for diarrhea amongst children under-5 and 90% of them were less than 2 years. Shigella represented 14%; of which, 45% were 24-59 months old. However, ETEC and V. cholerae represented only 3% and 2% respectively. Shigella was the most commonly detected pathogen (27%) for MSD followed by rotavirus (16%). Conversely, rotavirus (43%) was responsible for MD. MSD were most likely to be infected with Shigella flexneri [OR-9.81; 95% CI (6.38, 15.18)] and Shigella sonnei [6.29; (3.67, 10.87)] compared to their counterparts with MD. In logistic regression analysis, Shigella was responsible for a 2.25 times higher risk for MSD. Children with Shigella were 3.28 times at higher risk for bloody stool and 2.45 times more likely to have fever. However, rotavirus diarrhea was more likely to be presented with vomiting (OR-2.46) and fever (OR-1.28), and Vibrio cholerae, most often with watery diarrhea (OR-4.35). None of the clinical features were significantly associated with ETEC. Conclusion: Shigella was the leading pathogen that was detected most often in MSD, whereas rotavirus was often associated with MD.
ABSTRACT
Shigella dysenteriae type 1 causes devastating epidemics in developing countries with high case-fatality rates in all age-groups. The aim of the study was to compare host immune responses to epidemic (T2218) and endemic strains of S. dysenteriae type 1. Shigellacidal activity of serum from rabbits immunized with epidemic or endemic strains, S. dysenteriae type 1-infected patients, and healthy adult controls from Shigellaendemic and non-endemic regions was measured. Immunogenic cross-reactivity of antibodies against Shigella antigens was evaluated by Western blot analysis. Oxidative burst and phagocytic responses of monocytes and neutrophils to selected S. dysenteriae type 1 strains were assessed by flow cytometry. Rabbit antisera against epidemic strain were less effective in killing heterologous bacteria compared to endemic antisera (p=0.0002). Patients showed an increased serum shigellacidal response after two weeks of onset of diarrhoea compared to the acute stage (3-4 days after onset) against their respective homologous strains; the response against T2218 and heterologous endemic S. dysenteriae type 1 strains was not significant. The serum shigellacidal response against all the S. dysenteriae type 1 strains was similar among healthy controls from endemic and non-endemic regions and was comparable with the acute stage response by patients. Compared to endemic strains of S. dysenteriae type 1, T2218 was significantly resistant to phagocytosis by both monocytes and neutrophils. No obvious differences were obtained in the induction of oxidative burst activity and cathelicidin-mediated killing. Cross-reactivity of antibody against antigens present in the epidemic and endemic strains showed some differences in protein/peptide complexity and intensity by Western blot analysis. In summary, epidemic T2218 strain was more resistant to antibody-mediated defenses, namely phagocytosis and shigellacidal activity, compared to endemic S. dysenteriae type 1 strains. Part of this variation may be attributed to the differential complexity of protein/peptide antigens.