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Effects of shortened host life span on the evolution of parasite life history and virulence in a microbial host-parasite system.

Nidelet T, Koella JC, Kaltz O - BMC Evol. Biol. (2009)

Bottom Line: Overall, shorter latency time was associated with higher parasite loads and thus presumably with more rapid within-host replication.In contrast, we found little evidence for such trade-offs across parasite selection lines within treatments; thus, to some extent, these traits may evolve independently.This study illustrates how environmental variation (experienced by the host) can lead to the evolution of distinct parasite strategies.

View Article: PubMed Central - HTML - PubMed

Affiliation: UPMC University Paris 06, Laboratoire de Parasitologie Evolutive - UMR 7103, 7 quai St-Bernard, 75252 Paris, France. tnidelet@gmail.com

ABSTRACT

Background: Ecological factors play an important role in the evolution of parasite exploitation strategies. A common prediction is that, as shorter host life span reduces future opportunities of transmission, parasites compensate with an evolutionary shift towards earlier transmission. They may grow more rapidly within the host, have a shorter latency time and, consequently, be more virulent. Thus, increased extrinsic (i.e., not caused by the parasite) host mortality leads to the evolution of more virulent parasites. To test these predictions, we performed a serial transfer experiment, using the protozoan Paramecium caudatum and its bacterial parasite Holospora undulata. We simulated variation in host life span by killing hosts after 11 (early killing) or 14 (late killing) days post inoculation; after killing, parasite transmission stages were collected and used for a new infection cycle.

Results: After 13 cycles (approximately 300 generations), parasites from the early-killing treatment were less infectious, but had shorter latency time and higher virulence than those from the late-killing treatment. Overall, shorter latency time was associated with higher parasite loads and thus presumably with more rapid within-host replication.

Conclusion: The analysis of the means of the two treatments is thus consistent with theory, and suggests that evolution is constrained by trade-offs between virulence, transmission and within-host growth. In contrast, we found little evidence for such trade-offs across parasite selection lines within treatments; thus, to some extent, these traits may evolve independently. This study illustrates how environmental variation (experienced by the host) can lead to the evolution of distinct parasite strategies.

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Proportion of infected hosts producing infectious forms over the course of 13 days after inoculation. A higher proportion of infectious hosts indicates a shorter latency time. Values for parasites from early- and late-killing treatments were averaged over selection line means. Error bars represent standard error.
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Figure 2: Proportion of infected hosts producing infectious forms over the course of 13 days after inoculation. A higher proportion of infectious hosts indicates a shorter latency time. Values for parasites from early- and late-killing treatments were averaged over selection line means. Error bars represent standard error.

Mentions: To follow the subsequent development of infection, we sampled infected assay populations at different time points over the course of two weeks. The first hosts producing infectious forms were observed on day 7 after inoculation (1.6% of all infected individuals; all other infections were still at the reproductive stage). The proportion of such infectious hosts was significantly higher in populations infected with parasites from the early-killing treatment than in populations infected with parasites from the late-killing treatment (MANOVA on the proportion of infectious forms bearing individuals, day 7–13: F1,19 = 6.38, p = 0.0212). This effect was most pronounced on day 7 (ANOVA: F1,18 = 5.41, p = 0.0320) and on day 9 (F1,18 = 5.48, p = 0.0249), when there was a 20% difference in the proportion of infectious hosts (Figure 2). From logistic curve fits, we estimated the time until 50% of the hosts in a population were producing infectious forms. On average, parasites from the early-killing treatment had reached this point more than half a day earlier (8.81 ± 0.15 d) than parasites from the late-killing treatment (9.35 ± 0.19 d; treatment effect: F1,18 = 5.35, p = 0.0328). Thus, early parasites had a shorter latency time.


Effects of shortened host life span on the evolution of parasite life history and virulence in a microbial host-parasite system.

Nidelet T, Koella JC, Kaltz O - BMC Evol. Biol. (2009)

Proportion of infected hosts producing infectious forms over the course of 13 days after inoculation. A higher proportion of infectious hosts indicates a shorter latency time. Values for parasites from early- and late-killing treatments were averaged over selection line means. Error bars represent standard error.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2666652&req=5

Figure 2: Proportion of infected hosts producing infectious forms over the course of 13 days after inoculation. A higher proportion of infectious hosts indicates a shorter latency time. Values for parasites from early- and late-killing treatments were averaged over selection line means. Error bars represent standard error.
Mentions: To follow the subsequent development of infection, we sampled infected assay populations at different time points over the course of two weeks. The first hosts producing infectious forms were observed on day 7 after inoculation (1.6% of all infected individuals; all other infections were still at the reproductive stage). The proportion of such infectious hosts was significantly higher in populations infected with parasites from the early-killing treatment than in populations infected with parasites from the late-killing treatment (MANOVA on the proportion of infectious forms bearing individuals, day 7–13: F1,19 = 6.38, p = 0.0212). This effect was most pronounced on day 7 (ANOVA: F1,18 = 5.41, p = 0.0320) and on day 9 (F1,18 = 5.48, p = 0.0249), when there was a 20% difference in the proportion of infectious hosts (Figure 2). From logistic curve fits, we estimated the time until 50% of the hosts in a population were producing infectious forms. On average, parasites from the early-killing treatment had reached this point more than half a day earlier (8.81 ± 0.15 d) than parasites from the late-killing treatment (9.35 ± 0.19 d; treatment effect: F1,18 = 5.35, p = 0.0328). Thus, early parasites had a shorter latency time.

Bottom Line: Overall, shorter latency time was associated with higher parasite loads and thus presumably with more rapid within-host replication.In contrast, we found little evidence for such trade-offs across parasite selection lines within treatments; thus, to some extent, these traits may evolve independently.This study illustrates how environmental variation (experienced by the host) can lead to the evolution of distinct parasite strategies.

View Article: PubMed Central - HTML - PubMed

Affiliation: UPMC University Paris 06, Laboratoire de Parasitologie Evolutive - UMR 7103, 7 quai St-Bernard, 75252 Paris, France. tnidelet@gmail.com

ABSTRACT

Background: Ecological factors play an important role in the evolution of parasite exploitation strategies. A common prediction is that, as shorter host life span reduces future opportunities of transmission, parasites compensate with an evolutionary shift towards earlier transmission. They may grow more rapidly within the host, have a shorter latency time and, consequently, be more virulent. Thus, increased extrinsic (i.e., not caused by the parasite) host mortality leads to the evolution of more virulent parasites. To test these predictions, we performed a serial transfer experiment, using the protozoan Paramecium caudatum and its bacterial parasite Holospora undulata. We simulated variation in host life span by killing hosts after 11 (early killing) or 14 (late killing) days post inoculation; after killing, parasite transmission stages were collected and used for a new infection cycle.

Results: After 13 cycles (approximately 300 generations), parasites from the early-killing treatment were less infectious, but had shorter latency time and higher virulence than those from the late-killing treatment. Overall, shorter latency time was associated with higher parasite loads and thus presumably with more rapid within-host replication.

Conclusion: The analysis of the means of the two treatments is thus consistent with theory, and suggests that evolution is constrained by trade-offs between virulence, transmission and within-host growth. In contrast, we found little evidence for such trade-offs across parasite selection lines within treatments; thus, to some extent, these traits may evolve independently. This study illustrates how environmental variation (experienced by the host) can lead to the evolution of distinct parasite strategies.

Show MeSH
Related in: MedlinePlus