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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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Within- and between-treatment relationships between mean reproductive parasite loads, latency time and virulence. Each circle represents the mean for a single parasite selection line, averaged over three replicate assay tubes. Black circles denote selection lines from early-killing, open circles selection lines from late-killing treatments. Regression lines illustrate correlations within treatments. Squares indicate the treatment means, averaged over selection line means. Error bars represent standard error. Parasite load = number of reproductive forms per infected individual on day 7; latency time = time until 50% of infected hosts produce infectious forms; virulence = Log-transformed host density uninfected minus log-transformed host density infected in the individual assay (i.e., larger positive values indicate higher virulence).
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Figure 5: Within- and between-treatment relationships between mean reproductive parasite loads, latency time and virulence. Each circle represents the mean for a single parasite selection line, averaged over three replicate assay tubes. Black circles denote selection lines from early-killing, open circles selection lines from late-killing treatments. Regression lines illustrate correlations within treatments. Squares indicate the treatment means, averaged over selection line means. Error bars represent standard error. Parasite load = number of reproductive forms per infected individual on day 7; latency time = time until 50% of infected hosts produce infectious forms; virulence = Log-transformed host density uninfected minus log-transformed host density infected in the individual assay (i.e., larger positive values indicate higher virulence).

Mentions: Correlations between five characters were analyzed (Table 1). When pooling the means of selection lines from the two treatments, we obtained statistically significant overall correlations between latency time and reproductive or infectious parasite loads, with relatively large effect sizes (note that we did not correct p-values for multiple testing [30]). Selection lines with a higher reproductive load (indicating higher within-host replication during the first week) had a shorter latency time (Figure 5a) and larger infectious parasite loads. Shorter latency was also associated with higher final loads. In contrast with the positive association between treatments means, reproductive load was negatively correlated with virulence: selection lines with a faster accumulation of reproductive loads during the first week after infection tended to be less virulent later on (Figure 5b). These correlations also held across selection lines within treatments (Table 1). The remaining overall correlations had small effect sizes (/r/ < 0.3), and in several cases, the within-treatment correlations differed in sign and magnitude (illustrated for latency time and virulence in Figure 5c).


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)

Within- and between-treatment relationships between mean reproductive parasite loads, latency time and virulence. Each circle represents the mean for a single parasite selection line, averaged over three replicate assay tubes. Black circles denote selection lines from early-killing, open circles selection lines from late-killing treatments. Regression lines illustrate correlations within treatments. Squares indicate the treatment means, averaged over selection line means. Error bars represent standard error. Parasite load = number of reproductive forms per infected individual on day 7; latency time = time until 50% of infected hosts produce infectious forms; virulence = Log-transformed host density uninfected minus log-transformed host density infected in the individual assay (i.e., larger positive values indicate higher virulence).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Within- and between-treatment relationships between mean reproductive parasite loads, latency time and virulence. Each circle represents the mean for a single parasite selection line, averaged over three replicate assay tubes. Black circles denote selection lines from early-killing, open circles selection lines from late-killing treatments. Regression lines illustrate correlations within treatments. Squares indicate the treatment means, averaged over selection line means. Error bars represent standard error. Parasite load = number of reproductive forms per infected individual on day 7; latency time = time until 50% of infected hosts produce infectious forms; virulence = Log-transformed host density uninfected minus log-transformed host density infected in the individual assay (i.e., larger positive values indicate higher virulence).
Mentions: Correlations between five characters were analyzed (Table 1). When pooling the means of selection lines from the two treatments, we obtained statistically significant overall correlations between latency time and reproductive or infectious parasite loads, with relatively large effect sizes (note that we did not correct p-values for multiple testing [30]). Selection lines with a higher reproductive load (indicating higher within-host replication during the first week) had a shorter latency time (Figure 5a) and larger infectious parasite loads. Shorter latency was also associated with higher final loads. In contrast with the positive association between treatments means, reproductive load was negatively correlated with virulence: selection lines with a faster accumulation of reproductive loads during the first week after infection tended to be less virulent later on (Figure 5b). These correlations also held across selection lines within treatments (Table 1). The remaining overall correlations had small effect sizes (/r/ < 0.3), and in several cases, the within-treatment correlations differed in sign and magnitude (illustrated for latency time and virulence in Figure 5c).

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