Infectivity is influenced by parasite spore age and exposure to freezing: do shallow waters provide<i>Daphnia</i>a refuge from some parasites?

Duffy, Meghan A.; Hunsberger, Katherine K.

doi:10.1093/plankt/fby046

Cited by 21 publications

(27 citation statements)

References 17 publications

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“…Most important for this study, upon host death those spores are released into the water column where they can be consumed by a new host, completing the infection cycle (Metschnikoff 1884, Ebert 2005). In laboratory conditions, spores of both parasites are long‐lived relative to the length of an epidemic (Duffy and Hunsberger 2019), but in stratified lakes, they may sink out of the water column to lake sediments unless conditions are turbulent. It is while the parasite is in the water column during environmental dispersal that light could most strongly impinge on epidemics via direct effects on spores.…”

Section: Methodsmentioning

confidence: 99%

“…After the incubation period, incubated spore slurries as well as algal food (Ankistrodesmus falcatus ) were added to 150 mL filtered lake water, yielding spore concentrations of 2000 spores/mL of Pasteuria and 100 spores/mL of Metschnikowia in July and 250 spores/mL of Metschnikowia in August and November. Metschnikowia spore dose was increased in August and November because of low infection levels in the control treatment in July, with both 100 and 250 spores/mL being within the range typically used in lab experiments (Shocket et al 2018, Duffy and Hunsberger 2019). This water‐algae‐spore mixture was distributed among either 10 (July and August incubations) or 8 (November) 15mL centrifuge tubes.…”

Section: Methodsmentioning

confidence: 99%

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Shedding light on environmentally transmitted parasites: lighter conditions within lakes restrict epidemic size

Shaw

Hall

Overholt

et al. 2020

Ecology

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Parasite fitness depends on a successful journey from one host to another. For parasites that are transmitted environmentally, abiotic conditions might modulate the success of this journey. Here we evaluate how light, a key abiotic factor, influences spatiotemporal patterns of zooplankton disease where light varies seasonally, across lakes, and with depth in a lake. In an in situ experiment using those three sources of variation, we tested sensitivity of spores of two parasites to ambient light. Infectivity of both parasites was lower when exposed to ambient light in comparison to parasites exposed to otherwise similar conditions in the dark. The more sensitive parasite (the fungus, Metschnikowia) was damaged even under lower ambient light during late fall (November). With this differential sensitivity established, we evaluated links between light environment and natural outbreaks in lakes. Consistent with the incubations, epidemics of the less sensitive parasite (the bacterium, Pasteuria) started earlier in the fall (under higher ambient light), and both parasites had smaller outbreaks in more transparent lakes. Overall, light environment may impact the timing and size of disease outbreaks. Outbreaks could thus become exacerbated by human activities that darken waters, including lake browning associated with climate change and eutrophication.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Shedding light on environmentally transmitted parasites: lighter conditions within lakes restrict epidemic size

Shaw

Hall

Overholt

et al. 2020

Ecology

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“…All 1‐day incubations used stored (refrigerated) spores. They had lower infectivity than the 7‐day incubation at 20°C, likely because storage at 4°C also lowers spore infectivity (1‐ vs. 7‐day incubations at 20°C: p < .0001; Duffy & Hunsberger, ). The parameter φ (Figure d) shows the free‐living spore effect assuming that spores lose infectivity gradually over seven days as they are consumed by hosts (see Methods and Appendix S1) and normalized by transmission rate at 20°C (used for calculating transmission potential).…”

Section: Resultsmentioning

confidence: 99%

Can hot temperatures limit disease transmission? A test of mechanisms in a zooplankton–fungus system

et al. 2019

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Thermal ecology theory predicts that transmission of infectious diseases should respond unimodally to temperature, that is be maximized at intermediate temperatures and constrained at extreme low and high temperatures. However, empirical evidence linking hot temperatures to decreased transmission in nature remains limited. We tested the hypothesis that hot temperatures constrain transmission in a zooplankton–fungus (Daphnia dentifera–Metschnikowia bicuspidata) disease system where autumnal epidemics typically start after lakes cool from their peak summer temperatures. This pattern suggested that maximally hot summer temperatures could be inhibiting disease spread. Using a series of laboratory experiments, we examined the effects of high temperatures on five mechanistic components of transmission. We found that (a) high temperatures increased exposure to parasites by speeding up foraging rate but (b) did not alter infection success post‐exposure. (c) High temperatures lowered parasite production (due to faster host death and an inferred delay in parasite growth). (d) Parasites made in hot conditions were less infectious to the next host (instilling a parasite ‘rearing’ or 'trans‐host' effect of temperature during the prior infection). (e) High temperatures in the free‐living stage also reduce parasite infectivity, either by killing or harming parasites. We then assembled the five mechanisms into an index of disease spread. The resulting unimodal thermal response was most strongly driven by the rearing effect. Transmission peaked at intermediate hot temperatures (25–26°C) and then decreased at maximally hot temperatures (30–32°C). However, transmission at these maximally hot temperatures only trended slightly lower than the baseline control (20°C), which easily sustains epidemics in laboratory conditions and in nature. Overall, we conclude that while exposure to hot epilimnetic temperatures does somewhat constrain disease, we lack evidence that this effect fully explains the lack of summer epidemics in this natural system. This work demonstrates the importance of experimentally testing hypothesized mechanisms of thermal constraints on disease transmission. Furthermore, it cautions against drawing conclusions based on field patterns and theory alone. A free Plain Language Summary can be found within the Supporting Information of this article.

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“…All 1-day incubations used stored (refrigerated) spores. They had lower 329 infectivity than the 7-day incubation at 20°C, likely because storage at 4°C also lowers spore 330 infectivity (1 versus 7-day incubations at 20°C: p<0.0001) (Duffy & Hunsberger, 2019). The 331 parameter φ (Fig.…”

Section: Mechanisms 4 and 5: Rearing (ρ) And Free-living Spore (φ) Effementioning

confidence: 94%

Can hot temperatures limit disease transmission? A test of mechanisms in a zooplankton-fungus system

Shocket

Magnante

Duffy

et al. 2019

Preprint

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316 / 350 WORDS) 23 1. Thermal ecology theory predicts that transmission of infectious diseases should respond 24 unimodally to temperature, i.e., be maximized at intermediate temperatures and 25 constrained at extreme low and high temperatures. However, empirical evidence linking 26 hot temperatures to decreased transmission in nature remains limited. 272. We tested the hypothesis that hot temperatures constrain transmission in a zooplankton-28 fungus (Daphnia dentifera-Metschnikowia bicuspidata) disease system where autumnal 29 epidemics typically start after lakes cool from their peak summer temperatures. This 30 pattern suggested that maximally hot summer temperatures could be inhibiting disease 31 spread. 32 3. Using a series of lab experiments, we examined the effects of high temperatures on five 33 mechanistic components of transmission. We found that (1) high temperatures increased 34 exposure to parasites by speeding up foraging rate but (2) did not alter infection success 35 post-exposure. (3) High temperatures lowered parasite production (due to faster host 36 death and an inferred delay in parasite growth). (4) Parasites made in hot conditions were 37 less infectious to the next host (instilling a parasite 'rearing' or 'trans-host' effect of 38 temperature during the prior infection). (5) High temperatures in the free-living stage also 39 reduce parasite infectivity, either by killing or harming parasites. 40 4. We then assembled the five mechanisms into an index of disease spread. The resulting 41 unimodal thermal response was most strongly driven by the rearing effect. Transmission 42 peaked at intermediate-hot temperatures (25-26°C) and then decreased at maximally hot 43temperatures (30-32°C). However, transmission at these maximally hot temperatures only 44 trended slightly lower than the baseline control (20°C), which easily sustains epidemics 45 3 in laboratory conditions and in nature. Overall, we conclude that while exposure to hot 46 epilimnetic temperatures does somewhat constrain disease, we lack evidence that this 47 effect fully explains the lack of summer epidemics in this natural system. This work 48 demonstrates the importance of experimentally testing hypothesized mechanisms of 49 thermal constraints on disease transmission. Furthermore, it cautions against drawing 50 conclusions based on field patterns and theory alone. 51 4 INTRODUCTION 52

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Infectivity is influenced by parasite spore age and exposure to freezing: do shallow waters provideDaphniaa refuge from some parasites?

Cited by 21 publications

References 17 publications

Shedding light on environmentally transmitted parasites: lighter conditions within lakes restrict epidemic size

Shedding light on environmentally transmitted parasites: lighter conditions within lakes restrict epidemic size

Can hot temperatures limit disease transmission? A test of mechanisms in a zooplankton–fungus system

Can hot temperatures limit disease transmission? A test of mechanisms in a zooplankton-fungus system

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