Maternal gestational cortisol and testosterone are associated with trade-offs in offspring sex and number in a free-living rodent (Urocitellus richardsonii).

The adaptive manipulation of offspring sex and number has been of considerable interest to ecologists and evolutionary biologists. The physiological mechanisms that translate maternal condition and environmental cues into adaptive responses in offspring sex and number, however, remain obscure. In mammals, research into the mechanisms responsible for adaptive sex allocation has focused on two major endocrine axes: the hypothalamic pituitary adrenal (HPA) axis and glucocorticoids, and the hypothalamic pituitary gonadal (HPG) axis and sex steroids, particularly testosterone. While stress-induced activation of the HPA axis provides an intuitive model for sex ratio and litter size adjustment, plasma glucocorticoids exist in both bound and free fractions, and may be acting indirectly, for example by affecting plasma glucose levels. Furthermore, in female mammals, activation of the HPA axis stimulates the secretion of adrenal testosterone in addition to glucocorticoids (GCs). To begin to untangle these physiological mechanisms influencing offspring sex and number, we simultaneously examined fecal glucocorticoid metabolites, free and bound plasma cortisol, free testosterone, and plasma glucose concentration during both gestation and lactation in a free-living rodent (Urocitellus richardsonii). We also collected data on offspring sex and litter size from focal females and from a larger study population. Consistent with previous work in this population, we found evidence for a trade-off between offspring sex and number, as well as positive and negative correlations between glucocorticoids and sex ratio and litter size, respectively, during gestation (but not lactation). We also observed a negative relationship between testosterone and litter size during gestation (but not lactation), but no effect of glucose on either sex ratio or litter size. Our findings highlight the importance of binding proteins, cross-talk between endocrine systems, and temporal windows in the regulation of trade-offs in offspring sex and number

DNA sequencing confirms meningeal worm (Parelaphostrongylus tenuis) and muscle worm (Parelaphostrongylus andersoni) in white-tailed deer (Odocoileus virginianus): Implications for moose (Alces alces) management

In North America, some moose populations are declining, and meningeal worm (Parelaphostrongylus tenuis) infections may be contributing. Moose are aberrant hosts for meningeal worm and develop severe pathology whereas white-tailed deer (WTD) are definitive hosts that experience minimal pathology and spread parasite larvae into the environment. Analyses of harvested WTD heads confirmed meningeal worm in Western Manitoba, Canada including in areas where moose have experienced population declines and are currently of management concern. The prevalence of larval meningeal worm from WTD feces in these areas are unknown, particularly because the dorsal-spined larvae (DSL) are morphologically indistinguishable from muscle worm (Parelaphostrongylus andersoni). To assess transmission risk of DSL, we investigated the spatial and temporal variation of prevalence in WTD feces from four areas (two with historical moose population declines and two without) sampled across two summers. We predicted higher prevalence of DSL in areas where moose are of management concern and surveys have shown higher meningeal worm prevalence in WTD heads. Further, we expected to only recover meningeal worm, as muscle worm has only been reported from caribou in more northern areas of Manitoba. We collected WTD feces by transect sampling, used the Baermann technique to obtain larvae, and sequenced partial cytochrome oxidase 1 and internal transcribed spacer 2 genes to confirm species identity. Zero-inflated models revealed that DSL prevalence did not differ temporally but was higher in areas where moose are of management concern. Genetic analyses revealed that meningeal worm and muscle worm were both present in Western Manitoba and co-occurred in three areas. Our results reveal novel insights into the geographic distribution of muscle worm and emphasize the importance of DNA sequencing for DSL identification. We suggest that concern for moose populations is warranted given the increased risk of parasite infection in some management areas

Reproductive parameters for female Richardson’s ground squirrels during the 2013 breeding season.

‡<p>Sex ratio shown as median and interquartile range.</p><p>Physiological measurements were accompanied by reproductive data for focal females only (n = 15), however reliable reproductive data was available for between 44 and 65 females in the larger study area, depending on the variable.</p><p>Reproductive parameters for female Richardson’s ground squirrels during the 2013 breeding season.</p

Physiological parameters for 21 female Richardson’s ground squirrels through the breeding season.

Θ<p>Mean ± standard error: total plasma cortisol, bound cortisol.</p>‡<p>Median and interquartile range: Free cortisol, FGMs, plasma testosterone, and plasma glucose.</p>∞<p>FGMs not significantly different using Tukey post-hoc contrasts.</p><p>Means (± SEM) or median and interquartile range, plus overall results of linear mixed effects model and <i>P</i>-values, number of observations for each model are shown. For tests with significant overall differences, superscript letters indicate significant differences using post-hoc Tukey contrasts (<i>P</i><0.05).</p><p>Physiological parameters for 21 female Richardson’s ground squirrels through the breeding season.</p

Relationship between bound maternal gestational cortisol (A) and glucose (B) during gestation and sex ratio.

<p>Both graphs show multiple points for each individual, accounted for using mixed effects models with individual identity as a random factor. The relationship between bound cortisol and sex ratio was significant (<i>P</i> = 0.030), while glucose was not correlated with sex ratio in this study (<i>P</i> = 0.836).</p

Relationship between total maternal gestational cortisol (A) and testosterone (B) and litter size.

<p>Both graphs show multiple points for each individual, accounted for using mixed effects models with maternal identity as a random factor (<i>P</i><0.05 for both).</p