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or genetic units of pathogen in an area will vary for almost every pathosystem. It
will usually be neither simple nor independent of the environment and host.
Finally, it should be noted that the study of pathogen population dynamics will
rarely be possible in isolation from the host population dynamics, since most
pathogens affect growth and reproduction of their hosts.
7.3 TIME-SCALES
A natural time-scale for changes in a pathogen population is set by the generation
time of the pathogen, the time taken for one propagule to infect and give rise to
another. However, for pathogens with complex life-cycles, there may be more than
one natural time-scale, depending on which life stage is being considered. For
example, in a heterocyclic rust, the generation time of asexually produced,
physiologically independent, individuals in a uredinial cycle may be much shorter
than the generation time of sexually produced genetically distinct individuals, say
from telium to telium.
Often, this notion of generation time will broadly correspond to the latent period
for a typical fungal pathogen. It differs in that it refers to the time when, on average,
new infections are actually formed under the prevailing conditions, rather than to
when infectious pathogen stages are produced. A detailed discussion of definitions
of generation time is quite complicated (Charlesworth, 1994) but the average age of
an individual when its offspring infect is adequate for the purposes of this chapter.
As an example, Lovell et al. (2004) measured the latent period of Mycosphaerella
graminicola on the flag leaf of wheat cv. Riband as about 300°C days above a base
temperature of 2.4°C: this is, for example, 30 days at an average temperature of
8.6°C. If rainfall were rare, the generation time might be substantially longer than
this. However, in a rainy period, the generation time would correspond closely to the
latent period. For systemic virus diseases, the generation time may also be related to
vector biology since, with a slow-moving vector, it may on average take a
considerable extra time after a plant becomes infectious before it actually causes
further infections.
'Short-term' may be used to refer to a few pathogen generations. For a rapidly
reproducing pathogen such as Phytophthora infestans (cause of late blight of
potato) , this may mean a few weeks; for a forest pathogen like Cocoa swollen shoot
badnavirus (CSSV), it may mean a few years. However, patterns of short-term
change may differ greatly depending on whether the host population is also
changing. Beresford and Royle (1988) introduced the term 'pathocron' defined as
the ratio of the latent period to the 'phyllocron' or leaf emergence interval. They
stressed its usefulness in clarifying how host growth affected the expression of
disease. The case of an annually reproducing pathogen like Sclerotinia sclerotiorum
(cause of pink rot of celery and other diseases of vegetables, and stem rot of
sunflower) suggests that, in general, it will be useful to consider the relative time-
scales over which pathogen and host populations change. For example, although
CSSV has a long 'generation' time, its host the cocoa tree ( Theobroma cacao) has
an even longer generation time and the host population will normally change little
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