The COVID-19 pandemic is intricately linked to biodiversity loss and ecosystem health.

The ongoing COVID-19 pandemic, caused by zoonotic SARS-CoV-2, has important links to biodiversity loss and ecosystem health. These links range from anthropogenic activities driving zoonotic disease emergence and extend to the pandemic affecting biodiversity conservation, environmental policy, ecosystem services, and multiple conservation facets. Crucially, such effects can exacerbate the initial drivers, resulting in feedback loops that are likely to promote future zoonotic disease outbreaks. We explore these feedback loops and relationships, highlighting known and potential zoonotic disease emergence drivers (eg, land-use change, intensive livestock production, wildlife trade, and climate change), and discuss direct and indirect effects of the ongoing pandemic on biodiversity loss and ecosystem health. We stress that responses to COVID-19 must include actions aimed at safeguarding biodiversity and ecosystems, in order to avoid future emergence of zoonoses and prevent their wide-ranging effects on human health, economies, and society. Such responses would benefit from adopting a One Health approach, enhancing cross-sector, transboundary communication, as well as from collaboration among multiple actors, promoting planetary and human health.

Uptake and transmission of Toxoplasma gondii oocysts by migratory, filter-feeding fish.

From bottlenose dolphins, to walruses, to sea otters, the parasitic protozoan Toxoplasma gondii is infecting marine mammals around the world. Whereas the terrestrial transmission pathways of T. gondii are well-described, the transmission pathway by which marine mammals are being infected is unknown. We hypothesize that migratory filter feeders, specifically northern anchovies (Engraulis mordax) and Pacific sardines (Sardinops sagax), are serving as biotic vectors for T. gondii within the marine environment. By filtering oocysts from seawater, these fishes could be transporting the oocysts from nearshore to pelagic environments. In this study, we experimentally exposed northern anchovies and Pacific sardines to T. gondii oocysts under laboratory conditions. Following exposure, the fishes' alimentary canals were harvested and assayed for the presence of T. gondii by PCR. Fish exposed to as few as 1197 oocysts/L seawater tested positive for T. gondii by PCR. In total, the PCR assay detected T. gondii DNA in 66% (40/61) of the exposed fishes. Oocyst infectivity was confirmed by mouse bioassay: 30% (7/23) of mice developed toxoplasmosis when fed fish exposed to 100,000 oocysts/L. This study demonstrates that both northern anchovies and Pacific sardines can filter T. gondii oocysts out of seawater under experimental conditions. Our experiments with anchovies demonstrated that the oocysts persisted in the fish for at least 8h post-exposure and our experiments with sardines demonstrated that the oocysts remained infectious inside the fish's alimentary canals.