---
title: "Gut and Nasal Microbiome Trajectories Predict Respiratory Disease Severity in Calves"
id: "biorxiv-21-gut-and-nasal-microbiome-trajectories-shape-respiratory-disease-severity-in"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-21-gut-and-nasal-microbiome-trajectories-shape-respiratory-disease-severity-in"
content_type: "clinical_feed_article"
specialty: "Infectious Disease"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.10.16.759607v1?rss=1"
published_at: "2026-10-17T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Gut and Nasal Microbiome Trajectories Predict Respiratory Disease Severity in Calves
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-21-gut-and-nasal-microbiome-trajectories-shape-respiratory-disease-severity-in
- **Specialty:** [Infectious Disease](https://medichelpline.com/clinical-feed/infectious-disease.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.10.16.759607v1?rss=1)
- **Published At:** 2026-10-17T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- Investigators experimentally inoculated 28 calves with **Mycoplasma bovis**, **bovine coronavirus**, and **influenza D virus**; half the cohort received metaphylactic **tilmicosin**. - The study team classified longitudinal clinical courses into mild, moderate, and severe phenotypes using unsupervised clustering of health scores. - Severe disease associated with higher and more persistent nasal **influenza D virus** loads, but pathogen burden alone did not explain inter-individual variability in outcomes. - Calves treated with **tilmicosin** developed substantially milder disease despite comparable measured pathogen loads and showed lower markers of systemic inflammation. - Neither nasal nor faecal microbiota diversity consistently explained severity across animals; diversity metrics alone were not predictive. - The cohort that later developed severe BRDC had a more homogeneous nasal microbiota prior to infection, suggesting pre-existing community structure may affect susceptibility. - The strongest disease-associated microbial signatures appeared in the faecal microbiota; antibiotic-induced gut dysbiosis correlated with severity, specific intestinal taxa, systemic inflammation, and faecal **short-chain fatty acid (SCFA)** profiles. - **Chlamydia** abundance was strongly associated with disease severity in the dataset, while other gut taxa linked to inflammatory biomarkers and SCFA concentrations. - Authors proposed a holobiont-driven model for **Bovine respiratory disease complex (BRDC)** in which interactions among pathogens, host inflammatory responses, and microbiota functions determine clinical severity. - The preprint status and the absence of peer review are documented; the report did not provide detailed dosing regimens, full taxa lists beyond highlighted associations, or all sampling-time specifics in the abstract.
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Maverick Monie--Ibanes 1 INRAE; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Maverick%2BMonie--Ibanes%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Monie--Ibanes%20M&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AMaverick%2BMonie--Ibanes%2B) Thomas Peyret 2 ENVT * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Thomas%2BPeyret%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Peyret%20T&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AThomas%2BPeyret%2B) Guenaelle Derolez 2 ENVT * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Guenaelle%2BDerolez%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Derolez%20G&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AGuenaelle%2BDerolez%2B) Marie Corbin 2 ENVT * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Marie%2BCorbin%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Corbin%20M&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AMarie%2BCorbin%2B) Florence Mompart 1 INRAE; 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* [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Mariette%2BDucatez%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Ducatez%20M&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AMariette%2BDucatez%2B) * [ORCID record for Mariette Ducatez](http://orcid.org/0000-0001-9632-5499 "Open in new tab") Nuria Mach 1 INRAE; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Nuria%2BMach%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Mach%20N&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ANuria%2BMach%2B) * [ORCID record for Nuria Mach](http://orcid.org/0000-0002-8001-6314 "Open in new tab") * For correspondence: nuria.mach@inrae.fr * [Abstract](https://www.biorxiv.org/content/10.64898/2026.10.16.759607v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5880694/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.10.16.759607v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5880694/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.10.16.759607v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5880694/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.10.16.759607v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5880694/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.10.16.759607v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5880694/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Bovine respiratory disease complex (BRDC) is a multifactorial syndrome resulting from interactions among pathogens, host responses, and environmental stressors. However, substantial variation in disease severity persists among animals exposed to similar infectious challenges. To assess the contribution of the respiratory and gut microbiota to BRDC severity, we experimentally inoculated 28 calves with Mycoplasma bovis, bovine coronavirus (BCoV), and influenza D virus (IDV), with half receiving metaphylactic tilmicosin. Clinical trajectories were classified into mild, moderate, and severe phenotypes using unsupervised clustering of longitudinal health scores. Severe BRDC was associated with higher and more persistent nasal IDV loads, yet pathogen burden alone failed to explain the marked inter-individual variability in clinical outcomes. Tilmicosin-treated calves developed substantially milder disease despite comparable pathogen loads, coinciding with lower systemic inflammation, suggesting that host-pathogen interactions, rather than pathogen replication alone, influenced disease severity. Neither nasal nor faecal microbiota diversity consistently explained BRDC severity. However, calves that later developed severe disease displayed a more homogeneous nasal microbiota before infection, indicating that early microbial community structure may influence susceptibility. In contrast, the strongest disease-associated microbial signatures were observed in the faecal microbiota. Gut antibiotic-induced dysbiosis revealed associations between BRDC severity, specific intestinal bacterial taxa, systemic inflammation, and faecal short-chain fatty acid (SCFA) profiles. Notably, Chlamydia was strongly associated with disease severity, while several other taxa were linked to inflammatory biomarkers and SCFA concentrations. Collectively, these findings support a holobiont-driven model of BRDC in which disease severity emerges from interactions among pathogens, host inflammatory responses, and microbiota-associated functions. The stronger associations observed in the intestinal microbiota, along with links between gut bacteria, SCFAs, and disease outcomes, provide evidence for a functional gut-lung axis in calves and highlight microbial metabolism as a potential target for strategies to improve respiratory health and reduce antibiotic use. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared European Union’s Horizon Europe Project, 101136346 Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a [CC-BY-NC-ND 4.0 International license](http://creativecommons.org/licenses/by-nc-nd/4.0/). bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. [Donate
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