Data from: The enemy within: how does a bacterium inhibit the foraging aptitude and risk management behavior of Allenby’s gerbils?

Microbes inhabiting multi-cellular organisms have complex, often subtle
effects on their hosts. Gerbillus andersoni allenbyi are
commonly infected with the Mycoplasma haemomuris-like bacteria,
which may cause mild nutrient (choline, arginine) deficiencies. However,
are there more serious ecological consequences of infection such
as effects on foraging aptitudes and risk management? We tested
alternatives: 1) nutrient compensation hypothesis, does nutrient
deficiency induce infected gerbils to make up for the shortfall by
foraging more and taking greater risks? or 2) lethargy
hypothesis, do sick gerbils forage less, and are they compromised in their
ability to detect predators or risky microhabitats? We compared the
foraging and risk management behavior of infected and non-infected
gerbils. We experimentally infected gerbils with the bacteria, which
allowed us to compare between non-infected, acutely infected (peak
infection loads), and chronically infected (low infection loads)
individuals. Our findings supported the lethargy
hypothesis over the nutrient compensation
hypothesis. Infected individuals incurred dramatically
elevated foraging costs, including less efficient foraging, diminished
“quality” of time spent vigilant, and increased owl predation.
Interestingly, gerbils that were chronically infected (lower bacteria
load) experienced larger ecological costs than acutely infected
individuals (i.e. peak infection loads). This suggests that the
debilitating effects of infection occur gradually, with a progressive
decline in the quality of time gerbils allocated to foraging and
managing risk. These increased long-term costs of infection
demonstrate how small direct physiological costs of infection can
lead to large indirect ecological costs. The indirect ecological costs of
this parasite appear much greater than the direct physiological costs.