Drosophila melanogaster Natural Variation Affects Growth Dynamics of Infecting Listeria monocytogenes

Alejandra Guzmán Hotson1, David S Schneider2

  • 1Department of Microbiology and Immunology, Stanford University, California 94305-5124.

G3 (Bethesda, Md.)
|October 7, 2015
PubMed

Insights

Host genetics influence Listeria monocytogenes growth dynamics, impacting both maximal growth rate and plateau. These pathogen parameters correlate with host survival and could drive host evolution.

Area of Science:

  • Microbiology and immunology
  • Evolutionary biology
  • Genetics

Background:

  • Listeria monocytogenes is a significant human pathogen.
  • Drosophila melanogaster serves as a model organism for studying host-pathogen interactions.
  • Understanding pathogen growth kinetics is crucial for infection modeling.

Purpose of the Study:

  • To investigate the kinetics of Listeria monocytogenes growth in a Drosophila melanogaster infection model.
  • To determine the impact of host genetic variation on pathogen growth parameters.
  • To explore the relationship between pathogen growth and host survival.

Main Methods:

  • Utilizing a Listeria monocytogenes/Drosophila melanogaster infection model.
  • Analyzing pathogen growth using logistic kinetics to determine maximal growth rate and growth plateau.
  • Assessing the influence of host genotype on pathogen growth parameters and host survival.

Main Results:

  • Listeria monocytogenes exhibits logistic growth kinetics in the infection model.
  • Host genetic variation independently affects pathogen maximal growth rate and growth plateau.
  • Both growth rate and plateau correlate with host survival.
  • Pathogen growth parameters are sensitive to initial infectious dose in a host genotype-dependent manner.

Conclusions:

  • Host genetics play a critical role in shaping pathogen growth dynamics.
  • Pathogen growth rate and plateau are potential drivers of host evolutionary adaptation.
  • Experimental outcomes in host-pathogen studies can be influenced by initial infectious dose and host genotype interactions.