@article{e34cb077d7ad453eb1b538de04779b97,
title = "The incremental value of repeated induced sputum and gastric aspirate samples for the diagnosis of pulmonary tuberculosis in young children with acute community- acquired pneumonia",
abstract = "Background. Mycobacterium tuberculosis (Mtb) contributes to the pathogenesis of childhood acute community-acquired pneumonia in settings with a high tuberculosis burden. The incremental value of a repeated induced sputum (IS) sample, compared with a single IS or gastric aspirate (GA) sample, is not well known. Methods. Two IS samples were obtained for Mtb culture from children enrolled as cases in the Pneumonia Etiology Research for Child Health (PERCH) study in South Africa. Nonstudy attending physicians requested GA if pulmonary tuberculosis was clinically suspected. We compared the Mtb yield of 2 IS samples to that of 1 IS sample and GA samples. Results. Twenty-seven (3.0%) culture-confirmed pulmonary tuberculosis cases were identified among 906 children investigated with IS and GA samples for Mtb. Results from 2 IS samples were available for 719 children (79.4%). Of 12 culture-confirmed pulmonary tuberculosis cases identified among children with ≥2 IS samples, 4 (33.3%) were negative at the first IS sample. In head-to-head comparisons among children with both GA and IS samples collected, the yield of 1 GA sample (8 of 427; 1.9%) was similar to that of 1 IS sample (5 of 427, 1.2%), and the yield of 2 GA samples (10 of 300; 3.3%) was similar to that of 2 IS samples (5 of 300; 1.7%). IS samples identified 8 (42.1%) of the 19 culture-confirmed pulmonary tuberculosis cases that were identified through submission of IS and GA samples. Conclusions. A single IS sample underestimated the presence of Mtb in children hospitalized with severe or very severe pneumonia. Detection of Mtb is enhanced by combining 2 IS with GA sample collections in young children with acute severe pneumonia.",
keywords = "Child, Gastric aspirate, Induced sputum, Tuberculosis, Yield",
author = "Moore, {David P.} and Higdon, {Melissa M.} and Hammitt, {Laura L.} and Christine Prosperi and DeLuca, {Andrea N.} and {Da Silva}, Pedro and Baillie, {Vicky L.} and Adrian, {Peter V.} and Azwifarwi Mudau and Knoll, {Maria Deloria} and Feikin, {Daniel R.} and Murdoch, {David R.} and O'Brien, {Katherine L.} and Madhi, {Shabir A.}",
note = "Funding Information: Supplement sponsorship. This article appears as part of the supplement “Pneumonia Etiology Research for Child Health (PERCH): Foundational Basis for the Primary Etiology Results,” sponsored by a grant from the Bill & Melinda Gates Foundation to the PERCH study of Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland. Funding Information: Financial support. This work is supported by the Bill & Melinda Gates Foundation (grant 48968 to the International Vaccine Access Center, Department of International Health, Johns Hopkins Bloomberg School of Public Health). Funding Information: Potential conflict of interest. M. D. K. has received funding for consultancies from Merck, Pfizer, and Novartis, and grant funding from Merck. L. L. H. has received grant funding from Pfizer and GlaxoSmithKline (GSK). S. A. M. has received honoraria for advisory board participation from Bill & Melinda Gates Foundation (BMGF), Pfizer, Medimmune, and Novartis and institutional grants from GSK, Novartis, Pfizer, Minervax, and BMGF and has served on the speakers bureau for Sanofi Pasteur and GSK. K. L. O. has received grant funding from GSK and Pfizer and participates on technical advisory boards for Merck, Sanofi Pasteur, PATH, Affinivax, and ClearPath. All other authors: No reported conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed. Publisher Copyright: {\textcopyright} The Author 2017.",
year = "2017",
doi = "10.1093/cid/cix099",
language = "English (US)",
volume = "64",
pages = "S309--S316",
journal = "Clinical Infectious Diseases",
issn = "1058-4838",
publisher = "Oxford University Press",
}