Agriculture Reference
In-Depth Information
7.7 AFFECTED HOST TISSUE AND PATHOGEN MULTIPLY AT
COMPARABLE RATES
This is the common situation with foliar and root diseases in arable agricultural and
annual horticultural crops. After harvest, the pathogen population usually decreases
over the off-season. Then the crop starts to grow again, typically producing leaves
and roots in a roughly exponential pattern until competition slows growth to a steady
rate, before ceasing at maturity or flowering. This 'expolinear' pattern (Goudriaan,
1973) has been shown to apply to many crops, from
Vicia
beans to wheat, although
the rate of growth will vary, particularly because of temperature variations.
Nonetheless many crops, such as cereals, produce new leaves at the same time as
older leaves are dying off. Net crop growth arises because the new leaves appearing
are more numerous or bigger than the old ones dying. Typical crop doubling times at
the start of the growing season are a week or less, corresponding to leaf area index
increasing by around 10% per day.
The pathogen population dynamics in this case are determined by the relative
rates of multiplication of host and pathogen and by the fate of the pathogen on dead
host tissue. Because both host and pathogen are continually being born and dying,
disease severity may be a very poor measure of the pathogen population.
Furthermore, the deductions of the previous section no longer apply and many more
patterns of growth or decline are possible. If the pathogen can exist and sporulate on
dead tissue, it may be necessary only to allow for host growth (Johnson and Teng,
1990; Lalancette and Hickey, 1986). If the pathogen is multiplying faster than the
host tissue, disease severity and the pathogen population will increase; if the reverse
occurs, the population will decline.
Host tissue born recently, within one latent period of the present, cannot be
visibly diseased. If the pathogen did not affect the death rate of host tissue, the
pathogen population would tend to increase so that all host tissue becomes infected,
even if invisibly. However, most pathogens tend to accelerate the death of host
tissue on which they are growing and more heavily infected tissue will tend to die
faster than lightly infected tissue. If the pathogen also dies when the host dies, then
an equilibrium may exist, with a steady but dynamic population density substantially
less than the maximum possible (Shaw and Peters, 1994). Furthermore, the effect of
the host tissue dying is to reduce the standing population of pathogen substantially
more
than the population of the host. In effect, therefore, the host is regulating the
pathogen population; this can actually be an evolutionary force leading to more
rapid death of infected tissue (van den Berg and van den Bosch, 2004).
There is evidence for temporary equilibria like this existing in some UK
grasslands, where disease levels in perennial plants, principally the grass
Holcus
lanatus
, were steady at about 6% of green tissue infected throughout the summer in
several years (Peters, 1994). This may also be an informative way to look at cereal
disease levels during the vegetative growth phase, although it is unlikely that an
equilibrium would be reached because there is rapid net growth of the crop
throughout the season.
Once the crop reaches maturity and tissue turnover ceases, disease will tend to
increase according to the patterns discussed in the previous section. However, the
