Intestinal pathogen clearance in children with severe acute malnutrition is unrelated to inpatient morbidity.

Christian J Versloot, Suzanna Attia, Céline Bourdon, Susan E Richardson, Isabel Potani, Robert H J Bandsma, Wieger Voskuijl

Journal: Clinical nutrition ESPEN 2019;24():109-113

PMID: 29576347

Abstract

BACKGROUND & AIMS

Children with Severe Acute Malnutrition (SAM) often suffer from diarrhea, which is associated with increased mortality. The contribution of intestinal bacteria, parasites and viruses to morbidity such as diarrhea in SAM remains poorly understood. To evaluate their association with clinical outcomes, we detected stool pathogens in children with SAM at hospital admission and after clinical stabilization prior to discharge.

METHODS

15 intestinal pathogens, fecal calprotectin and C-reactive protein (CRP) were determined at admission and after clinical stabilization in children aged 8-59 months (n = 47) hospitalized in Malawi for complicated SAM. Differences in fecal pathogens, intestinal and systemic inflammation, and clinical outcomes between time points were evaluated using the Wilcoxon Signed-Rank test or Wilcoxon rank-sum test.

RESULTS

On admission pathogens were present in nearly all children and after clinical stabilization many were cleared with only 55% of children still harboring a pathogen (89% vs. 55%, p = 0.001). Nosocomial infections were infrequent. The pathogens Giardia lamblia and Shigella spp. were most likely to persist. After clinical stabilization, fecal calprotectin was higher in children harboring a pathogen (median (IQR): 383 mg/kg (903-149 mg/kg) vs 140 mg/kg (300-71 mg/kg), p = 0.03). CRP did not correlate with fecal calprotectin levels nor was it associated with pathogen detection. Presence of stool pathogens was not associated with clinical outcomes such as diarrhea.

CONCLUSIONS

Fecal pathogens were very common and cleared in most children with complicated SAM treated with antibiotics. The presence of stool pathogens after stabilization was associated with increased intestinal inflammation but not with clinical outcomes. (http://www.isrctn.com/ISRCTN13916953).

Copyright © 2018 European Society for Clinical Nutrition and Metabolism. Published by Elsevier Ltd. All rights reserved.

Address: Physiology and Experimental Medicine, Peter Gilgan Centre for Research and Learning, The Hospital for Sick Children, Toronto, ON, Canada; University of Groningen, University Medical Center Groningen, Department of Pediatric Gastroenterology, Hepatology, and Nutrition, Groningen, The Netherlands.; Division of Gastroenterology, Hepatology, and Nutrition, The Hospital for Sick Children, Toronto, ON, Canada.; Physiology and Experimental Medicine, Peter Gilgan Centre for Research and Learning, The Hospital for Sick Children, Toronto, ON, Canada.; Division of Microbiology, The Hospital for Sick Children, Toronto, ON, Canada.; Department of Paediatrics and Child Health, College of Medicine, University of Malawi, Blantyre, Malawi.; Physiology and Experimental Medicine, Peter Gilgan Centre for Research and Learning, The Hospital for Sick Children, Toronto, ON, Canada; University of Groningen, University Medical Center Groningen, Department of Pediatric Gastroenterology, Hepatology, and Nutrition, Groningen, The Netherlands; Division of Gastroenterology, Hepatology, and Nutrition, The Hospital for Sick Children, Toronto, ON, Canada; Centre for Global Child Health, The Hospital for Sick Children, Toronto, ON, Canada.; Department of Paediatrics and Child Health, College of Medicine, University of Malawi, Blantyre, Malawi; Global Child Health Group, Emma Children's Hospital, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands. Electronic address: [email protected].
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