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Viruses and protists cause similar bacterial mortality in coastal seawater

476

Citations

22

References

1995

Year

TLDR

Coastal seawater from Santa Monica had bacterial abundances of ~6×10⁹ cells L⁻¹ in June and ~2×10⁹ cells L⁻¹ in November, with viral abundances of ~2×10¹⁰ particles L⁻¹ and ~1.5×10¹⁰ particles L⁻¹, respectively. Mesocosm experiments (80 L) in June and November used ³H‑thymidine and leucine incorporation to estimate bacterial production and mortality, enabling a comparison of viral lysis and protist grazing contributions. The results showed bacterial growth rates of 1–2 d⁻¹ in June and 1–3 d⁻¹ in November, and indicated that protist grazing and viral lysis contributed similarly to bacterial mortality, with loss estimates agreeing within ~30 % and highlighting significant energy dissipation by viruses.

Abstract

Mesocosms filled with 80 liters of coastal seawater from Santa Monica, California, were used twice (June and November) to budget bacterial production and loss, as well as to assess the relative significance of viral lysis and protist grazing in bacterial mortality. Bacterial abundance was ~6 × 10 9 cells liter ‒1 in June and 2 × 10 9 in November, with viral abundances ~2 × 10 10 particles liter ‒1 in June and 1.5 × 10 10 in November. Incorporation of [ 3 H]thymidine and leucine yielded essentially identical production estimates and allowed calculation of total bacterial mortality in these closed systems. Bacterial growth rates were 1–2 d ‒1 in June and 1–3 d ‒1 in November. Three independent lines of evidence indicated that bacterial mortality attributed to grazing by protists was about equal to that attributed to viruses: size fractionation of disappearance of labeled DNA, with a 50% reduction after protists were removed; comparison of protist grazing rates estimated with fluorescently labeled bacteria and virus production‐based bacterial lysis rates, with 40–50% of the total ascribed to viruses; and model‐based interpretation of the 3.3–4.6% of bacteria visibly infected with assembled intracellular viruses, suggesting that 24–66% of loss is due to infection. Redundant production and loss measurements as well as the independent loss process estimates agreed within ~30%, yielding a reasonably balanced budget. We believe the loss of bacteria to viruses reflects a significant dissipation of energy in this ecosystem and that viruses and protists contribute similarly to bacterial mortality.

References

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