Impact of the COVID-19 Pandemic on the Welfare of Animals in Australia.

We report on the various responses in Australia during 2020 to minimize negative impacts of the COVID-19 pandemic on the welfare of animals. Most organizations and individuals with animals under their care had emergency preparedness plans in place for various scenarios; however, the restrictions on human movement to contain the spread of COVID-19, coupled with the economic impact and the health effects of COVID-19 on the skilled workforce, constituted a new threat to animal welfare for which there was no blueprint. The spontaneous formation of a national, multisectoral response group on animal welfare, consisting of more than 34 organizations with animals under their care, facilitated information flow during the crisis, which helped to mitigate some of the shocks to different organizations and to ensure continuity of care for animals during the pandemic. We conclude that animal welfare is a shared responsibility, and accordingly, a multisectoral approach to animal welfare during a crisis is required. Our experience demonstrates that to safeguard animal welfare during crises, nations should consider the following: a national risk assessment, clear communication channels, contingency plans for animal welfare, a crisis response group, and support systems for animal care providers. Our findings and recommendations from the Australian context may inform other countries to ensure that animal welfare is not compromised during the course of unpredictable events.

Antimicrobial nectar inhibits a florally transmitted pathogen of a wild Cucurbita pepo (Cucurbitaceae).

PREMISE OF THE STUDY: Floral nectars of many species contain antimicrobial chemicals, but their function in nectar is subject to debate. Previously, we have shown that Erwinia tracheiphila, the causative agent of bacterial wilt disease in cucurbits, can be transmitted via the floral nectaries. • METHODS: We used a disk diffusion assay (DDA) to determine the antimicrobial effects of nectar from a wild gourd on lawns of Escherichia coli and Erwinia tracheiphila. We also used E. tracheiphila to inoculate flowers of wild gourd plants, with and without nectar. • KEY RESULTS: The DDA showed that paper disks saturated with 10 µL of nectar inhibited the growth of E. coli on a larger area of the lawn than 40% glucose but a smaller area than 5% ampicillin for 12 h. On lawns of E. tracheiphila, nectar inhibited growth on a larger area than glucose for 24 h and there were no significant differences between ampicillin and nectar for12 h. A significantly larger proportion of the plants inoculated via flowers without nectar contracted wilt disease than plants with nectar. • CONCLUSIONS: These findings indicate that nectar reduces transmission of E. tracheiphila via the nectaries and reveal the potential for florally transmitted pathogens to influence the evolution of floral traits.

Behavioral effects of prenatal folate deficiency in mice.

BACKGROUND: Folate supplementation decreases the incidence of birth defects such as neural tube defects (NTDs). We and others have shown that gestational dietary folate deficiency that does not produce overt NTDs can alter fetal neural histology. Accordingly, murine offspring were examined for the possible functional consequences of prenatal folate deficiency. METHODS: CD-1 mice were fed a diet of chow containing 400, 600, or 1200 nmol of folic acid/kg of chow for eight weeks prior to breeding and until GD18, at which time all dams were placed on folate-replete chow. Behavioral tests of male and female offspring included righting reflex, negative geotaxis, forelimb hanging, motor coordination, open field activity, and elevated plus maze activity. RESULTS: Of greatest significance, the adult offspring that were prenatally folate-deficient exhibited more anxiety-related behavior in the elevated plus maze. Offspring of the 400 nmol of folic acid/kg of chow diet group exhibited significantly shorter durations in the open arms and longer durations in the closed arms. Further, these two behaviors were dose-related. There was also a trend for the prenatally folate-deficient adult mice to exhibit more thigmotaxis (wall-hugging) behavior in the open field, entering the central area less frequently than controls. There were few other differences in tested behaviors between folate-deficient and folate-replete mice. CONCLUSIONS: Prenatal folate deficiency that is repleted at birth can manifest later with increased anxiety 9-12 weeks after birth.

Atenolol developmental toxicity: animal-to-human comparisons.

BACKGROUND: Atenolol, 4-2'-hydroxy-3'-isopropyl-aminopropoxy) phenylacetamide, is a beta-adrenoreceptor blocker used for treatment of hypertension in pregnancy. Beta-blockers are reported to cause fetal harm (such as decreased birth weight) when administered to a pregnant woman. We evaluate published human and animal evidence of atenolol developmental toxicity and compare the manifestations in humans and in routinely-used animal models. METHODS: The comparison is based on the following criteria: comparability of pharmacokinetic/pharmacodynamic characteristics, type of adverse outcome, lowest adverse effect levels, and specificity and selectivity of effect. RESULTS: Manifestations of atenolol prenatal toxicity (placental changes, intrauterine growth retardation and changes in fetal weight in the absence of structural malformations) are similar in the tested animal species (rats and rabbits) and humans. The human seems to be more sensitive, however, because adverse embryo-fetal effects are reported at doses much lower than those in the tested species. In humans and rats, adverse embryo-fetal effects are induced by doses that are not maternally toxic. In the rabbit, however, such effects are seen only at maternally toxic doses, suggesting that in this species, developmental toxicity may be maternally mediated. CONCLUSIONS: The available data suggest animal-human concordance with regard to the nature and manifestations of atenolol prenatal toxicity. The animal models "predicted" developmental toxicity manifests as placental changes, intrauterine growth retardation and fetal weight decrease in the absence of structural malformations. Thus far, this is concordant with the data from humans, in whom intrauterine growth retardation has been observed but not structural abnormalities.