We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure no-reply@cambridge.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
A large class of diseases is dependent on juvenile hosts for transmission because younger hosts are typically more susceptible to disease. Studies have investigated the epidemiological consequences of juvenile susceptibility, but why species retain such high susceptibility in the juvenile stage remains a puzzle. Life-history theory predicts that hosts should evolve to be more resistant as juveniles than as adults because early infection is costlier. Studies of anther-smut on wild carnations show that disease persistence is strongly dependent on the presence of a highly susceptible juvenile class. While there is evidence of genetic variation in juvenile resistance, the majority of plant families are highly susceptible at this stage, so juvenile resistance may be less beneficial than assumed. To understand how the costs and benefits of resistance and life-history traits affect the evolution of age-specific resistance, we developed a general analytical model of age-specific resistance, which shows that if there is genetic variation for the onset of resistance, selection and numerical feedbacks often drive the evolution of adult resistance but maintain juvenile susceptibility. The implications of these results are discussed.