Table 1.
Potential impact of hydric stress on female survival and infection prevalence during 7-day stress period
| Potential impact of hydric stress | Predicted measured effects | |||
|---|---|---|---|---|
| Hypothesis |
Direct negative effect on survival |
Increased parasite-induced mortality |
Female survival |
Infection prevalence |
| 1 | No | No | none | none |
| 2 | Yes | No | decreased | none |
| 3 | No | In early stages of infection (days 0-4) | decreased(days 0-4) | decreased |
| 4 | Yes | In early stages of infection (days 0-4) | decreased(days 0-7) | decreased |
| 5 | No | In late stages of infection (days 4-7) | decreased(days 4-7) | none |
| 6 | Yes | In late stages of infection (days 4-7) | decreased(days 4-7) | none |
Mortality incurred through the direct effect of hydric stress is distinguished from that due to increased parasite-induced mortality in females under stress. The occurrence of one or both of these sources of mortality and their timing leads to several possible hypotheses (1-6), each yielding distinct predicted patterns of measured female survival and overall oocyst prevalence. Because ookinetes and very young oocysts in early-dying females (days 0-4) are undetectable, an increase in parasite-induced female mortality in response to hydric stress at that stage translates in an apparent decrease in the prevalence of oocysts detected in females dying later in that experimental group (hypothesis 3 - in bold).