ArticlePLoS neglected tropical diseases2014
Noma affected children from Niger have distinct oral microbial communities based on high-throughput sequencing of 16S rRNA gene fragments.
Article in PLoS neglected tropical diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 30 citations in OpenAlex.
- Periodontitis and Periodontal Conditions in Systemically Healthy Children and Adolescents.Journal of clinical periodontology · 2026Review
- Shotgun metagenomic analysis of the oral microbiomes of children with noma.PLoS neglected tropical diseases · 2026Article
- Nonparametric Testing of Body Mass Index as a Predictor of Severe Noma: Assessing Potential Association.The American journal of tropical medicine and hygiene · 2024Article
- Noma (cancrum oris): A scoping literature review of a neglected disease (1843 to 2021).PLoS neglected tropical diseases · 2021Article
- Noma (cancrum oris): An unresolved global challenge.Periodontology 2000 · 2019Review
- Risk factors for diagnosed noma in northwest Nigeria: A case-control study, 2017.PLoS neglected tropical diseases · 2018Article
- Noma in an HIV infected patient in Guinea-Bissau: a case report.Infection · 2017Article
- Bacterial Community Associated with Healthy and Diseased Pacific White Shrimp (Frontiers in microbiology · 2017Article
- Unraveling Core Functional Microbiota in Traditional Solid-State Fermentation by High-Throughput Amplicons and Metatranscriptomics Sequencing.Frontiers in microbiology · 2017Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We aim to understand the microbial ecology of noma (cancrum oris), a devastating ancient illness which causes severe facial disfigurement in>140,000 malnourished children every year. The cause of noma is still elusive. A chaotic mix of microbial infection, oral hygiene and weakened immune system likely contribute to the development of oral lesions. These lesions are a plausible entry point for unidentified microorganisms that trigger gangrenous facial infections. To catalog bacteria present in noma lesions and identify candidate noma-triggering organisms, we performed a cross-sectional sequencing study of 16S rRNA gene amplicons from sixty samples of gingival fluid from twelve healthy children, twelve children suffering from noma (lesion and healthy sites), and twelve children suffering from Acute Necrotizing Gingivitis (ANG) (lesion and healthy sites). Relative to healthy individuals, samples taken from lesions in diseased mouths were enriched with Spirochaetes and depleted for Proteobacteria. Samples taken from healthy sites of diseased mouths had proportions of Spirochaetes and Proteobacteria that were similar to healthy control individuals. Samples from noma mouths did not have a higher abundance of Fusobacterium, casting doubt on its role as a causative agent of noma. Microbial communities sampled from noma and ANG lesions were dominated by the same Prevotella intermedia OTU, which was much less abundant in healthy sites sampled from the same mouths. Multivariate analysis confirmed that bacterial communities in healthy and lesion sites were significantly different. Several OTUs in the Orders Erysipelotrichales, Clostridiales, Bacteroidales, and Spirochaetales were identified as indicators of noma, suggesting that one or more microbes within these Orders is associated with the development of noma lesions. Future studies should include longitudinal sampling of viral and microbial components of this community, before and early in noma lesion development.
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