Objective: Antibiotic-associated diarrhea constitutes 1 of the most frequent side effects of antimicrobial therapy with widely varying clinical presentations; however, little is known about its antibiotic-associated bloody diarrhea (AABD) form, particularly in very young children. The aim of this study was to describe the clinical, endoscopic, and histopathologic profiles of community-acquired AABD in infants. Patients and Methods: The study included 23 infants referred with bloody diarrhea that developed a few days after receiving antibiotics on an outpatient basis for watery diarrhea (18), respiratory tract infections (4), or urinary tract infection (1). Detailed clinical assessment, videosigmoidoscopy, and histopathologic examination of endoscopic biopsies were performed for all. Results: Clinically, on presentation, bloody diarrhea was acute in all except 1 patient with a prolonged course (for 25 days) and stopped in all 2 to 6 days after discontinuation of antibiotics. Fever and/or leukocytosis were present only in 8 (34.8%). Sigmoidoscopy revealed varying types of erythema (patchy, ring, diffuse) and ulcers (aphthoid, diffuse) in 18 and pseudomembranes in 5. Histopathologically, only 3 showed the characteristic mushroom-like pseudomembranes, whereas all of the other infants had nonspecific colitis. Conclusions: Community-acquired AABD is not uncommon in infants presenting with acute or chronic forms even without fever or leukocytosis. When suspected, discontinuation of antibiotics is a good policy if facilities for bacterial culture with cytotoxin assays are limited. The characteristic endoscopic or histopathologic pseudomembranes are encountered only in a small percentage (26%). Rational use of antibiotics should be adhered to particularly in cases of watery diarrhea that is mostly of viral origin.

Background: Down's syndrome (DS) patients present a high risk of developing alterations of the immune system. The increased susceptibility to bacterial and viral infection, hematologic malignancies and autoimmune disease, suggest that immunodeficiency is an integral part of DS. Little is known about the mitochondrial damage and tendency to apoptosis in peripheral T lymphocyte cells in DS individuals. Objective: to evaluate the tendency to apoptosis and mitochondrial membrane potential (ΔΨm) changes in peripheral T lymphocytes of DS children both in the presence and in the absence of acute infection. Patients and methods: The present study included thirty children had DS (all of them trisomy 21 of nondisjunction type), and thirty normal children, fifteen of each group had no evidence of acute infection and fifteen had acute infection. Potential apoptosis was measured by flow cytometry using annexin V. The ΔΨm was assessed by the retention of Rhodamine 123. Results: There was no significant difference in the percentage of CD3+ cells or potential apoptotic T lymphocytes between DS children and controls either in presence or in absence of acute infection. However, there was a significant decrease in ΔΨm in the peripheral T lymohocytes of DS children when compared to the controls. Conclusion: The function of T cells not their number is the main mechanism responsible for the impairment of the immune system in DS children. T lymphocytes in peripheral blood from DS patients do not display an increased tendency to undergo apoptosis although a significant loss of ΔΨm was found.

Background: Down's syndrome (DS) patients present a high risk of developing alterations of the immune system. The increased susceptibility to bacterial and viral infection, hematologic malignancies and autoimmune disease, suggest that immunodeficiency is an integral part of DS. Little is known about the mitochondrial damage and tendency to apoptosis in peripheral T lymphocyte cells in DS individuals. Objective: to evaluate the tendency to apoptosis and mitochondrial membrane potential (ΔΨm) changes in peripheral T lymphocytes of DS children both in the presence and in the absence of acute infection. Patients and methods: The present study included thirty children had DS (all of them trisomy 21 of nondisjunction type), and thirty normal children, fifteen of each group had no evidence of acute infection and fifteen had acute infection. Potential apoptosis was measured by flow cytometry using annexin V. The ΔΨm was assessed by the retention of Rhodamine 123. Results: There was no significant difference in the percentage of CD3+ cells or potential apoptotic T lymphocytes between DS children and controls either in presence or in absence of acute infection. However, there was a significant decrease in ΔΨm in the peripheral T lymohocytes of DS children when compared to the controls. Conclusion: The function of T cells not their number is the main mechanism responsible for the impairment of the immune system in DS children. T lymphocytes in peripheral blood from DS patients do not display an increased tendency to undergo apoptosis although a significant loss of ΔΨm was found.