One Health, One Hive: A scoping review of honey bees, climate change, pollutants, and antimicrobial resistance.

Anthropogenic climate change and increasing antimicrobial resistance (AMR) together threaten the last 50 years of public health gains. Honey bees are a model One Health organism to investigate interactions between climate change and AMR. The objective of this scoping review was to examine the range, extent, and nature of published literature on the relationship between AMR and honey bees in the context of climate change and environmental pollutants. The review followed systematic search methods and reporting guidelines. A protocol was developed a priori in consultation with a research librarian. Resulting Boolean search strings were used to search Embase® via Ovid®, MEDLINE®, Scopus®, AGRICOLA™ and Web of Science™ databases. Two independent reviewers conducted two-stage screening on retrieved articles. To be included, the article had to examine honey bees, AMR, and either climate change or environmental pollution. Data, in accordance with Joanna Briggs Institute guidelines, were extracted from relevant articles and descriptively synthesized in tables, figures, and narrative form. A total of 22 articles met the inclusion criteria, with half of all articles being published in the last five years (n = 11/22). These articles predominantly investigated hive immunocompetence and multi-drug resistance transporter downregulation (n = 11/22), susceptibility to pests (n = 16/22), especially American foulbrood (n = 9/22), and hive product augmentation (n = 3/22). This review identified key themes and gaps in the literature, including the need for future interdisciplinary research to explore the link between AMR and environmental change evidence streams in honey bees. We identified three potential linkages between pollutive and climatic factors and risk of AMR. These interconnections reaffirm the necessity of a One Health framework to tackle global threats and investigate complex issues that extend beyond honey bee research into the public health sector. It is integral that we view these "wicked" problems through an interdisciplinary lens to explore long-term strategies for change.

Parenterally fed neonatal piglets have a low rate of endogenous arginine synthesis from circulating proline.

Parenterally fed neonatal piglets cannot synthesize sufficient arginine to maintain arginine status, presumably due to the intestinal atrophy that occurs with parenteral feeding. Parenteral feeding-induced atrophy can be reduced by the infusion of glucagon-like peptide 2 (GLP-2). GLP-2 infusion was hypothesized to increase the rate of endogenous arginine synthesis from proline, the major arginine precursor, in parenterally fed piglets receiving an arginine-deficient diet. Male piglets, fitted with jugular vein catheters for diet and isotope infusion, and femoral vein catheters for blood sampling (d 0), were allocated to a continuous infusion of either GLP-2 (n = 5; 10 nmol x kg(-1) x d(-1)) or saline (n = 5) for 7 d. Piglets received 2 d of a complete diet, followed by 5 d of an arginine-deficient [0.60 g x kg(-1) x d(-1)] diet. Piglets received primed, constant infusions of [guanido-(14)C]arginine to measure arginine flux (d 6) and [U-(14)C]proline (d 7) to measure proline conversion to arginine. Plasma arginine concentrations and arginine fluxes indicated a similar whole-body arginine status. Piglets receiving GLP-2 showed improvements in intestinal variables, including mucosal mass (P < 0.01) and villus height (P < 0.001), and a greater rate of arginine synthesis (micromol x kg(-1) x h(-1)) from proline (11.6 vs. 6.3) (P = 0.03). Mucosal mass (R(2) = 0.71; P = 0.002) and villus height were correlated (R(2) = 0.66; P = 0.004) with arginine synthesis. This study was the first to quantitate arginine synthesis in parenterally fed neonates and showed that although GLP-2 infusion increased arginine synthesis in a manner directly related to mucosal mass, this increased arginine synthesis was insufficient to improve whole-body arginine status in piglets receiving a low arginine diet.

Coadministration of ornithine and alpha-ketoglutarate is no more effective than ornithine alone as an arginine precursor in piglets enterally fed an arginine-deficient diet.

Simultaneous administration of alpha-ketoglutarate and ornithine, in a 1:2 molar ratio, may improve the effectiveness of ornithine as an arginine precursor in neonatal piglets by shifting ornithine metabolism away from oxidation and toward the synthesis of arginine and other metabolically important compounds. To study this proposed mechanism, enterally fed piglets were allocated to receive 1 of 4 diets for 5 d: an arginine-deficient [1.2 mmol/(kg . d) arginine] diet (basal), or the basal diet supplemented with either alpha-ketoglutarate [4.6 mmol/(kg x d)] (+alpha-KG), ornithine [9.2 mmol/(kg x d)] (+Orn), or both ornithine and alpha-ketoglutarate (+alpha-KG/+Orn, molar ratio 1:2). Primed, constant infusions of [1-(14)C]ornithine given both intragastrically and intraportally were used to measure ornithine kinetics and determine the role of first-pass intestinal metabolism in ornithine metabolism. Whole body arginine and glutamate kinetics were measured using a primed, constant intragastric infusion of [guanido-(14)C]arginine and [3,4-(3)H]glutamate. The diets did not affect plasma arginine or ammonia concentrations, arginine flux, or arginine synthesis from ornithine. Therefore, arginine synthesis was not increased by the simultaneous infusion of ornithine and alpha-ketoglutarate. Piglets that received dietary ornithine had a 2-fold greater rate of proline synthesis from ornithine (P < 0.05) and oxidized a greater (P < 0.05) portion of the infused ornithine than piglets in the basal and +alpha-KG groups. Overall, ornithine addition to an arginine deficient diet had a greater effect on ornithine and arginine metabolism than the addition of alpha-ketoglutarate. First-pass intestinal metabolism was critical for ornithine synthesis and conversion to other metabolites but not for ornithine oxidation.