Microbiome
Antibiotics hurt bee gut and survival
Open access · cc by · source: Europe PMC
Tetracycline shrinks the honeybee gut microbiome and elevates mortality after hive return.
Study at a glance
- Design
- Animal / in-vitro — Worker honeybees fed tetracycline; 16S community and survival vs germ-free controls
- N
- Cup cages of 30 bees × 15 replicates per condition; 16S profiles n≈14–15 per arm — no single primary N
- Population
- Worker honeybees with conventional or germ-free guts
- Outcome
- Core gut microbiota disruption and mortality after tetracycline
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
Four of eight core gut species dropped; elevated mortality in treated bees; germ-free bees did not show the same antibiotic mortality spike.
Methodology
Fed worker bees tetracycline, quantified 16S community size/composition, and tracked survival in hive vs lab recovery conditions.
Limitations
Does not test every antibiotic class or all hive stressors.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
Bacterial bile-salt enzymes can change host bile acids and weight-related phenotypes in models.
Selective bacterial bile-salt hydrolases can change host bile-acid chemistry and weight-related phenotypes in colonization models—evidence that specific microbial enzymes, not only community membership lists, can matter for host physiology.
Scope note — different host — honey bees, not mammalian colonization models
Limits the claim's scope: a different population, assay, or outcome.
Human observational and MR studies do not automatically generalise to bee antibiotic/pesticide disruptions or to enzyme-focused colonization experiments. Animal and insect systems test different host–microbe questions; they limit how far a human association travels rather than falsifying it.
Evidence for the claim as stated.
Severe COVID tracks plasma markers of barrier leak and microbial translocation.
Multi-omic plasma profiling linked severe COVID-19 to higher tight-junction permeability markers and bacterial/fungal product translocation versus milder disease/controls.
Scope note — antibiotic–microbiota mortality work — not a COVID barrier assay
Limits the claim's scope: a different population, assay, or outcome.
Antibiotics can perturb gut communities with host-cost consequences in model systems.
Antibiotic exposure perturbs gut microbiota and elevates mortality in the cited experimental setting—evidence that community disruption is not neutral for the host.
Evidence for the claim as stated.
Acute viral severity markers, antibiotic perturbation experiments, and chronic microbiota–disease associations should not be collapsed into one “leaky gut causes X” claim.
Evidence for the claim as stated.
The same chemistry can count bacterial 16S templates rather than a host mRNA. Tetracycline-fed worker bees were scored for 16S community size and composition: four of eight core gut species dropped, and treated bees showed elevated mortality that germ-free bees did not match. That is a community-load experiment, not a host gene-expression time course.
Evidence for the claim as stated.
qPCR is not one experiment. Cod heat-shock QPCR and aphid miRNA RT-PCR quantify candidate transcripts after a screen; chicken defensin RT-PCR confirms that predicted genes are expressed; bee work quantifies 16S community size. Treating those as interchangeable 'expression papers' hides whether the template is host mRNA, a miRNA, or bacterial DNA.
Evidence for the claim as stated.
Experimental perturbations shift 16S profiles and, in bees, survival. In-hive pesticides altered hundreds of bacterial OTUs and ITS fungi in foragers and brood; tetracycline dropped four of eight core bee-gut species and raised mortality, a spike not seen in germ-free bees given the same antibiotic.
Evidence for the claim as stated.
Observational blooming and experimental knockdown are not the same evidence. B. dorei rises before autoimmunity in a birth cohort; bee antibiotics and pesticides are assigned exposures with community and (for tetracycline) survival readouts. The first cannot support 'kill this taxon to prevent T1D'; the second still does not prove that every OTU shift causes colony collapse.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
Human observational and MR studies do not automatically generalise to bee antibiotic/pesticide disruptions or to enzyme-focused colonization experiments. Animal and insect systems test different host–microbe questions; they limit how far a human association travels rather than falsifying it.
Acute viral severity markers, antibiotic perturbation experiments, and chronic microbiota–disease associations should not be collapsed into one “leaky gut causes X” claim.
qPCR is not one experiment. Cod heat-shock QPCR and aphid miRNA RT-PCR quantify candidate transcripts after a screen; chicken defensin RT-PCR confirms that predicted genes are expressed; bee work quantifies 16S community size. Treating those as interchangeable 'expression papers' hides whether the template is host mRNA, a miRNA, or bacterial DNA.
- Supports · Atlantic cod heat-shock gene responses
- Supports · Pea aphid miRNAs and plasticity
- Supports · Chicken β-defensin gene cluster
Observational blooming and experimental knockdown are not the same evidence. B. dorei rises before autoimmunity in a birth cohort; bee antibiotics and pesticides are assigned exposures with community and (for tetracycline) survival readouts. The first cannot support 'kill this taxon to prevent T1D'; the second still does not prove that every OTU shift causes colony collapse.
- Supports · B. dorei rises before T1D autoimmunity
- Supports · Pesticides reshape honey bee gut microbes
History
When this study was placed
Dated entries from the concept change log — when this paper was added or removed as support, challenge, or qualifier on a claim.
Placed as a scope qualifier on Microbiome
Selective bacterial bile-salt hydrolases can change host bile-acid chemistry and weight-related phenotypes in colonization models—evidence that specific microbial enzymes, not only community membership lists, can matter for host physiology.
Placed as supporting evidence on Microbiome
Human observational and MR studies do not automatically generalise to bee antibiotic/pesticide disruptions or to enzyme-focused colonization experiments. Animal and insect systems test different host–microbe questions; they limit how far a human association travels rather than falsifying it.
Related papers in this topic
Same topic cluster — not a recommendation engine.