Windows of vulnerability: Seasonal mismatches in exposure and resource identity determine ocean acidification's effect on a primary consumer at high latitude.

It is well understood that differences in the cues used by consumers and their resources in fluctuating environments can give rise to trophic mismatches governing the emergent effects of global change. Trophic mismatches caused by changes in consumer energetics during periods of low resource availability have received far less attention, although this may be common for consumers during winter when primary producers are limited by light. Even less is understood about these dynamics in marine ecosystems, where consumers must cope with energetically costly changes in CO2 -driven carbonate chemistry that will be most pronounced in cold temperatures. This may be especially important for calcified marine herbivores, such as the pinto abalone (Haliotis kamschatkana). H. kamschatkana are of high management concern in the North Pacific due to the active recreational fishery and their importance among traditional cultures, and research suggests they may require more energy to maintain their calcified shells and acid/base balance with ocean acidification. Here we use field surveys to demonstrate seasonal mismatches in the exposure of marine consumers to low pH and algal resource identity during winter in a subpolar, marine ecosystem. We then use these data to test how the effects of exposure to seasonally relevant pH conditions on H. kamschatkana are mediated by seasonal resource identity. We find that exposure to projected future winter pH conditions decreases metabolism and growth, and this effect on growth is pronounced when their diet is limited to the algal species available during winter. Our results suggest that increases in the energetic demands of pinto abalone caused by ocean acidification during winter will be exacerbated by seasonal shifts in their resources. These findings have profound implications for other marine consumers and highlight the importance of considering fluctuations in exposure and resources when inferring the emergent effects of global change.

Type III hypersensitivity reaction with immune complex deposition in 2 critically ill dogs administered human serum albumin.

OBJECTIVE: To describe 2 cases of vasculitis that were attributed to a type III hypersensitivity reaction in critically ill dogs occurring 8-16 days postadministration of human serum albumin (HSA). CASE OR SERIES SUMMARY: Skin biopsies were obtained from 3 different sites in 2 critically ill dogs that developed vasculitis 8-16 days following treatment with HSA. Histopathological findings from both dogs indicated epidermal pallor, widespread edema and hemorrhage, degenerative neutrophilic perivascular infiltrates, and multifocal areas of neutrophilic or leukocytoclastic vasculitis. Immunohistochemical staining using an anti-human serum albumin rabbit antibody suggested that the antigen-antibody complexes seen in the dermis were associated with the administration of HSA. NEW OR UNIQUE INFORMATION PROVIDED: In this case series, we documented a leukocytoclastic vasculitis and probable antigen-antibody complexes to human albumin in the dermis of 2 critically ill dogs after administration of HSA. Previously, type III hypersensitivity reactions had only been reported in healthy dogs that had received HSA. This report also describes the potential use of immunohistochemical staining to detect the HSA antigen in tissue sections through the use of specifically labeled antibodies.