Skip to content
PaperFren

Microbiome

Pesticides reshape honey bee gut microbes

Kakumanu ML, Reeves AM, Anderson TD, et al. · Frontiers in microbiology · 2016

Open access · cc by · source: Europe PMC

In-hive pesticide exposures change honey bee gut bacterial and fungal community composition.

Study at a glance

Design
Animal / in-vitro — In-hive pesticide exposures across sites; 16S and ITS pyrosequencing of foragers and brood
N
N=24 · 24 sequenced samples (4 treatments × 3 sites × 2 bee types), each pooled from five bees
Population
Honey bees (Apis mellifera) exposed to in-hive pesticides
Outcome
Gut bacterial and fungal community composition under pesticide treatments

Structured fields used in claim comparison tables when every cited study has a complete layer.

Key findings

Hundreds of bacterial OTUs and altered relative abundances under pesticide treatments versus controls; core taxa include Firmicutes/proteobacteria lineages.

Methodology

Exposed bees to in-hive pesticides across sites, then pyrosequenced 16S and ITS amplicons from foragers and brood.

Limitations

Does not prove every abundance shift causes colony collapse; sequencing is compositional.

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.

  • SupportsMicrobiomeconcept

    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.

  • 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.

  • Marker-gene 16S and shotgun metagenomes answer different questions in this set. HMP biogeography and the bee pesticide paper are amplicon community maps (the bee paper adds ITS); the infant diet paper sequences stool metagenomes and host mRNA. Treating every 'microbiome sequencing' paper as 16S genus tables hides the extra functional genes the infant paper actually uses.

    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.

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.

  1. 2026-09-14

    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.