The intensity of a pathogen infection plays a key role in determining how the host responds to infection. Hosts with high infections are more likely to transmit infection to others, and are may be more likely to experience progression from infection to disease symptoms, to being physiologically compromised by disease. Understanding how and why hosts exhibit variation in infection intensity therefore plays a major part in developing and implementing measures aimed at controlling infection spread, its effects, and its chance of persisting and circulating within a population of hosts. To track the relative importance of a number of variables in determining the level of infection intensity, we ran field-surveys at two breeding sites over a 12 month period using marked larvae of the common midwife toad (Alyes obstetricans) and their levels of infection with the amphibian pathogen Batrachochytrium dendrobatidis (Bd). At each sampling occasion we measured the density of larvae, the temperature of the water in the 48 h prior to sampling, the period of time the sampled individual had been in the water body, the developmental (Gosner) stage and the intensity of Bd infection of the individual. Overall our data suggest that the temperature and the duration of time spent in the water play a major role in determining the intensity of Bd infection within an individual host. However, although the duration of time spent in the water was clearly associated with infection intensity, the relationship was negative: larvae that had spent less than 3–6 months in the water had significantly higher infection intensities than those that had spent over 12 months, although this infection intensity peaked between 9 and 12 months. This could be due to animals with heavier infections developing more quickly, suffering increased mortality or, more likely, losing their mouthparts (the only part of anuran larvae that can be infected with Bd). Overall, our results identify drivers of infection intensity, and potentially transmissibility and spread, and we attribute these differences to both host and pathogen biology.

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