Abstract

Entomopathogenic nematodes (EPNs) are small worms whose ecological behaviour consists to invade, kill insects and feed on their cadavers thanks to a species-specific symbiotic bacterium belonging to any of the genera Xenorhabdus or Photorhabdus hosted in the gastro-intestinal tract of EPNs. The symbiont provides a number of biological functions that are essential for its EPN host including the production of entomotoxins, of enzymes able to degrade the insect constitutive macromolecules and of antimicrobial compounds able to prevent the growth of competitors in the insect cadaver. The question addressed in this study was to investigate whether a mammalian pathogen taxonomically related to Xenorhabdus was able to substitute for or “hijack” the symbiotic relationship associating Xenorhabdus and Steinernema EPNs. To deal with this question, a laboratory experimental model was developed consisting in Galleria mellonella insect larvae, Steinernema EPNs with or without their natural Xenorhabdus symbiont and Yersinia pseudotuberculosis brought artificially either in the gut of EPNs or in the haemocoel of the insect larva prior to infection. The developed model demonstrated the capacity of EPNs to act as an efficient reservoir ensuring exponential multiplication, maintenance and dissemination of Y. pseudotuberculosis.

Highlights

  • Entomopathogenic nematodes (EPNs) are microscopic soil worms exclusively feeding on insect preys

  • We show that Y. pseudotuberculosis can be successfully transmitted by the EPN carrier inside an insect larva in which it persists and multiplies

  • Nalidixic-acid resistant (NalR) bacteria were obtained in three consecutive steps by plating 107 to 109 CFU per agar plate supplemented with increasing concentrations of Nalidixic acid (5μg/ml; 20μg/ml; 50μg/ml)

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Summary

Introduction

Entomopathogenic nematodes (EPNs) are microscopic soil worms exclusively feeding on insect preys. MW8B, 7 independent Galleria mellonella infection experiments were conducted with a Y. pseudotuberculosis GFPmut2-labelled strain (4N1G strain) (Table 2).

Results
Conclusion
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