Exposure history determines pteropod vulnerability to ocean acidification along the US West Coast.

The pteropod Limacina helicina frequently experiences seasonal exposure to corrosive conditions (Ωar < 1) along the US West Coast and is recognized as one of the species most susceptible to ocean acidification (OA). Yet, little is known about their capacity to acclimatize to such conditions. We collected pteropods in the California Current Ecosystem (CCE) that differed in the severity of exposure to Ωar conditions in the natural environment. Combining field observations, high-CO2 perturbation experiment results, and retrospective ocean transport simulations, we investigated biological responses based on histories of magnitude and duration of exposure to Ωar < 1. Our results suggest that both exposure magnitude and duration affect pteropod responses in the natural environment. However, observed declines in calcification performance and survival probability under high CO2 experimental conditions do not show acclimatization capacity or physiological tolerance related to history of exposure to corrosive conditions. Pteropods from the coastal CCE appear to be at or near the limit of their physiological capacity, and consequently, are already at extinction risk under projected acceleration of OA over the next 30 years. Our results demonstrate that Ωar exposure history largely determines pteropod response to experimental conditions and is essential to the interpretation of biological observations and experimental results.

Transmission bottlenecks as determinants of virulence in rapidly evolving pathogens.

Transmission bottlenecks occur in pathogen populations when only a few individual pathogens are transmitted from one infected host to another in the initiation of a new infection. Transmission bottlenecks can dramatically affect the evolution of virulence in rapidly evolving pathogens such as RNA viruses. Characterizing pathogen diversity with the quasispecies concept, we use analytical and simulation methods to demonstrate that severe bottlenecks are likely to drive down the virulence of a pathogen because of stochastic loss of the most virulent pathotypes, through a process analogous to Muller's ratchet. We investigate in this process the roles of host population size, duration of within-host viral replication, and transmission bottleneck size. We argue that the patterns of accumulation of deleterious mutation may explain differing levels of virulence in vertically and horizontally transmitted diseases.