Faecal glucocorticoid metabolite concentrations associated with illness, sex, age, and season in a kea Nestor notabilis population at the Cincinnati Zoo and Botanical Garden
DOI:
https://doi.org/10.19227/jzar.v10i2.654Keywords:
avian, corticosterone, faecal glucocorticoid metabolites, glucocorticoids, Kea, parrot, stressAbstract
The kea Nestor notabilis is an endangered New Zealand alpine parrot. After individuals became ill and died at the Cincinnati Zoo, it was suspected that prolonged hypothalamic-pituitary-adrenal axis activation may have precipitated illness onset. The main objective of this study was to determine if elevated concentrations of faecal glucocorticoid metabolites (fGCMs) preceded illness outbreaks. An effective protocol for extracting fGCMs from kea faeces was established, and a corticosterone enzyme immunoassay (EIA) was validated. The secondary objective was to ascertain if fGCM concentrations were impacted by sex, age, or seasonality. Samples collected over a year were analysed via EIA. fGCM concentrations in samples collected 30 days pre-symptom (PRE-SYMPT) and post-symptom (POST-SYMPT) onset were compared and found to trend higher in POST-SYMPT versus PRE-SYMPT samples (estimated marginal mean (EMM) and 95% confidence interval (CI)): 85.2, 62.7-133.1 ng/g and 58.1, 42.1-94.0 ng/g, respectively). Furthermore, POST-SYMPT values were significantly higher than those of healthy birds (NO-SYMPT) while PRE-SYMPT values did not differ (85.2, 62.7-133.1 ng/g; 53.9, 45.1-67.0 ng/g; and 58.1, 42.1-94.0 ng/g, respectively). Though not statistically significant, several trends were noted: 1) fGCM concentrations trended lower in males than females (48.5, 37.4-68.9 ng/g, and 51.0, 37.0-82.2 ng/g, respectively); 2) juvenile fGCM trended lower than that for adults (45.5, 34.1-68.2 ng/g and 54.8, 41.0-82.4 ng/g, respectively); and 3) fGCM concentrations in adult females trended higher during the breeding season (60.0, 39.5-124.3 ng/g), compared to non-breeding season (51.2, 36.2-87.2 ng/g). Contrary to the original hypothesis, fGCM concentrations in kea were not elevated prior to onset of illness.
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