We examined the need for new in vivo avian toxicity testing for three common industrial chemicals (1,2 dichloropropane, 1,1,2-trichloroethane and triphenyl phosphate) based on estimated avian exposures using fugacity and multimedia fate models for current conditions of use compared to hazard information including existing in vivo test data for the chemicals and analogs, interspecies correlation estimates and results from hundreds of acute avian dietary toxicity studies. The data indicated that acute avian toxicity is not likely to be observed below 10 ppm in the diet for any chemical with the exception of those with a specific mode of toxic action. Modeling indicated low exposure potential for terrestrial birds to any of the three chemicals, with estimated dietary concentration of less than 0.001 ppm. Despite uncertainty associated with the underlying data sources, the four order of magnitude gap between potential exposure and a minimum hazard threshold suggests that additional avian in vivo testing would not generate valuable data. However, a weight of evidence approach for integrating data is necessary to engender greater confidence among government decision-makers in cases where data from a particular in vivo study is not expected to improve risk decision-making and an existing data gap can remain unfilled.

Organisms adapt to daily and seasonal environmental changes to maximise their metabolic and reproductive fitness. For seasonally breeding animals, photoperiod is considered the most robust cue to drive these changes. It, however, does not explain the interannual variations in different seasonal phenotypes. Several studies have repeatedly shown the influence of ambient temperature on the timing of different seasonal physiologies including the timing of migration, reproduction and its associated behaviours, etc. In the present review, we have discussed the effects of changes in ambient temperature on different seasonal events in endotherms with a focus on migratory birds as they have evolved to draw benefits from distinct but largely predictable seasonal patterns of natural resources. We have further discussed the physiological and molecular mechanisms by which temperature affects seasonal timings. The primary brain area involved in detecting temperature changes is the hypothalamic preoptic area. This area receives thermal inputs via sensory neurons in the peripheral ganglia that measure changes in thermoregulatory tissues such as the skin and spinal cord. For the input signals, several thermal sensory TRP (transient receptor potential ion channels) channels have been identified across different classes of vertebrates. These channels are activated at specific thermal ranges. Once perceived, this information should activate an effector function. However, the link between temperature sensation and the effector pathways is not properly understood yet. Here, we have summarised the available information that may help us understand how temperature information is translated into seasonal timing.

High pathogenicity avian influenza viruses (HPAIVs) cause high morbidity and mortality in poultry species. HPAIV prevalence means high numbers of infected wild birds could lead to spill over events for farmed poultry. How these pathogens survive in the environment is important for disease maintenance and potential dissemination. We evaluated the temperature-associated survival kinetics for five clade 2.3.4.4 H5Nx HPAIVs (UK field strains between 2014 and 2021) incubated at up to three temperatures for up to ten weeks. The selected temperatures represented northern European winter (4 °C) and summer (20 °C); and a southern European summer temperature (30 °C). For each clade 2.3.4.4 HPAIV, the time in days to reduce the viral infectivity by 90% at temperature T was established (DT), showing that a lower incubation temperature prolonged virus survival (stability), where DT ranged from days to weeks. The fastest loss of viral infectivity was observed at 30 °C. Extrapolation of the graphical DT plots to the x-axis intercept provided the corresponding time to extinction for viral decay. Statistical tests of the difference between the DT values and extinction times of each clade 2.3.4.4 strain at each temperature indicated that the majority displayed different survival kinetics from the other strains at 4 °C and 20 °C.

OBJECTIVE: To establish normative data for selected ocular diagnostic tests and commensal conjunctival microflora and describe the incidence of ocular pathology in Chilean flamingos.
METHODS: A total of 41 Chilean flamingos were examined at the Blank Park Zoo in Des Moines, Iowa.
METHODS: In 20 flamingos, blink rate was assessed undisturbed in their exhibit, then gentle manual restraint was used to assess palpebral fissure length (PFL), aqueous tear production (phenol red thread test [PRTT] in one eye, endodontic absorbent paper point tear test [EAPPTT] in the other), intraocular pressure (IOP; rebound tonometry), and fluorescein staining. Twenty-one other flamingos were brought to a darkened area for neuro-ophthalmic examination, slit lamp biomicroscopy, and indirect ophthalmoscopy. Swabs from seven flamingos were used for ocular microbiome evaluation.
RESULTS: Results are presented as mean ± standard deviation (range). Flamingos comprised 23 females/18 males, aged 11 ± 9.1 (0.7-40) years. Test results: blink rate, 3.7 ± 2 (1-9) blinks/min; PFL, 11.2 ± 1.2 (9-14) mm; IOP, 14 ± 3.2 (10-22) mmHg; EAPPT, 10.2 ± 2.8 (9-14) mm/min; PRTT, 6.8 ± 2.5 (3-13) mm/15 s. Dazzle reflex was positive in four birds examined. Pathologies included cataracts (n = 7 birds), corneal fibrosis (n = 3), endothelial pigment (n = 2), uveal cysts (n = 1), lens luxation (n = 1), and uveitis (n = 1). Ocular microbiome showed high diversity of taxa.
CONCLUSIONS: Baseline ocular parameters and incidence of ophthalmic pathology assist veterinarians with disease screening for Chilean flamingos, while the ocular microbiome showed high diversity.

We report 16S rRNA gene amplicon data on the succession of intestinal microbiomes in migratory bird, Eurasian Wigeon (Mareca Penelope) wintering around Osaka, Japan. This study could serve as baseline data for comparison with microbiomes in migratory birds.

Organisms regularly adjust their physiology and energy balance in response to predictable seasonal environmental changes. Stressors and contaminants have the potential to disrupt these critical seasonal transitions. No studies have investigated how simultaneous exposure to the ubiquitous toxin methylmercury (MeHg) and food stress affects birds\' physiological performance across seasons. We quantified several aspects of energetic performance in song sparrows, Melospiza melodia, exposed or not to unpredictable food stress and MeHg in a 2×2 experimental design, over 3 months during the breeding season, followed by 3 months post-exposure. Birds exposed to food stress had reduced basal metabolic rate and non-significant higher factorial metabolic scope during the exposure period, and had a greater increase in lean mass throughout most of the experimental period. Birds exposed to MeHg had increased molt duration, and increased mass:length ratio of some of their primary feathers. Birds exposed to the combined food stress and MeHg treatment often had responses similar to the stress-only or MeHg-only exposure groups, suggesting these treatments affected physiological performance through different mechanisms and resulted in compensatory or independent effects. Because the MeHg and stress variables were selected in candidate models with a ΔAICc lower than 2 but the 95% confidence interval of these variables overlapped zero, we found weak support for MeHg effects on all measures except basal metabolic rate, and for food stress effects on maximum metabolic rate, factorial metabolic scope and feather mass:length ratio. This suggests that MeHg and food stress effects on these measures are statistically identified but not simple and/or were too weak to be detected via linear regression. Overall, combined exposure to ecologically relevant MeHg and unpredictable food stress during the breeding season does not appear to induce extra energetic costs for songbirds in the post-exposure period. However, MeHg effects on molt duration could carry over across multiple annual cycle stages.

OBJECTIVE: To determine normal ocular parameters of the MacQueen\'s bustard (Chlamydotis macqueenii) and describe ophthalmic lesions in a captive bred population.
METHODS: Captive breeding population of 257 Macqueen\'s bustards.
METHODS: All birds were screened for ocular abnormalities using direct ophthalmoscopy. Abnormalities were photographed. Normative values for Schirmer tear test-1 (STT-1), applanation tonometry, aerobic and anaerobic bacterial culture, fungal culture, and transcorneal ocular ultrasonography were derived from multiple cohorts of clinically normal adult birds. Five birds with ocular pathology also underwent transcorneal ultrasonography. Statistical comparisons for normative values between OD and OS, and males and females were made using a paired t-test or Mann-Whitney U-test, with a significance level of p < .05.
RESULTS: Mean tear production based on Schirmer tear test 1 (STT-1) was 10.16 ± 4.61 mm/min (3-21 mm/min). Mean intraocular pressure (IOP) was 12.42 ± 4.94 mm Hg (5-26 mm Hg). Staphylococcus species were the most isolated bacteria from the conjunctival surfaces of normal birds (85%). Significant differences were found in transcorneal ultrasonographic measurements between males and females for axial globe length (p = .032), vitreous body depth (p = .049) and lens thickness (p = .0428). Corneal fibrosis was the most observed ocular abnormality amongst eyes with pathological changes (39%).
CONCLUSIONS: Schirmer tear testing, tonometry and transcorneal ultrasound can easily be utilized in MacQueen\'s bustards and provide reproducible results. Normal parameters for these tests were determined, and common pathological ocular changes were described in this species.

Somatosensation is essential for animals to perceive the external world through touch, allowing them to detect physical contact, temperature, pain, and body position. Studies on rodent vibrissae have highlighted the organization and processing in mammalian somatosensory pathways.1,2 Comparative research across vertebrates is vital for understanding evolutionary influences and ecological specialization on somatosensory systems. Birds, with their diverse morphologies, sensory abilities, and behaviors, serve as ideal models for investigating the evolution of somatosensation. Prior studies have uncovered tactile-responsive areas within the avian telencephalon, particularly in pigeons,3,4,5,6 parrots,7 and finches,8 but variations in somatosensory maps and responses across avian species are not fully understood. This study aims to explore somatotopic organization and neural coding in the telencephalon of Anna\'s hummingbirds (Calypte anna) and zebra finches (Taeniopygia guttata) by using in vivo extracellular electrophysiology to record activity in response to controlled tactile stimuli on various body regions. These findings reveal unique representations of body regions across distinct forebrain somatosensory nuclei, indicating significant differences in the extent of areas dedicated to certain body surfaces, which may correlate with their behavioral importance.

Meat and eggs from chicken are the major source of animal protein for the human population. The cryopreservation of poultry species is needed to guarantee sustainable production. Here, we describe the existing cryopreservation technologies for avian reproductive cells using embryonic germ cells, spermatozoa and ovarian tissues. We outline strategies to reconstitute chicken breeds from their cryopreserved embryonic germ cells using surrogate hosts and discuss the perspectives for genetic conservation and reconstitution of chicken and wild avian species using surrogate host animals.

Anthropogenic changes to the environment expose wildlife to many pollutants. Among these, tropospheric ozone is of global concern and a highly potent pro-oxidant. In addition, human activities include several other implications for wildlife, e.g., changed food availability and changed distribution of pathogens in cities. These co-occurring habitat changes may interact, thereby modulating the physiological responses and costs related to anthropogenic change. For instance, many food items associated with humans (e.g., food waste and feeders for wild birds) contain relatively more ω6-than ω3-polyunsaturated fatty acids (PUFAs). Metabolites derived from ω6-PUFAs can enhance inflammation and oxidative stress towards a stimulus, whereas the opposite response is linked to ω3-derived metabolites. Hence, we hypothesized that differential intake of ω6-and ω3-PUFAs modulates the oxidative stress state of birds and thereby affects the responses towards pro-oxidants. To test this, we manipulated dietary ω6:ω3 ratios and ozone levels in a full-factorial experiment using captive zebra finches (Taeniopygia guttata). Additionally, we simulated an infection, thereby also triggering the immune system\'s adaptive pro-oxidant release (i.e., oxidative burst), by injecting lipopolysaccharide. Under normal air conditions, the ω3-diet birds had a lower antioxidant ratio (GSH/GSSG ratio) compared to the ω6-diet birds. When exposed to ozone, however, the diet effect disappeared. Instead, ozone exposure overall reduced the total concentration of the key antioxidant glutathione (tGSH). Moreover, the birds on the ω6-rich diet had an overall higher antioxidant capacity (OXY) compared to birds fed a ω3-rich diet. Interestingly, only the immune challenge increased oxidative damage, suggesting the oxidative burst of the immune system overrides the other pro-oxidative processes, including diet. Taken together, our results show that ozone, dietary PUFAs, and infection all affect the redox-system, but in different ways, suggesting that the underlying responses are decoupled despite that they all increase pro-oxidant exposure or generation. Despite lack of apparent cumulative effect in the independent biomarkers, the combined single effects could together reduce overall cellular functioning and efficiency over time in wild birds exposed to pathogens, ozone, and anthropogenic food sources.