I - --ii

36
Results
Epiphytotic Spread of the Disease
In both years three different cultivars were used but this report includes only
results of the susceptible local landrace ILC 1929 and the resistant selection ILC
482. They were studied at four different planting dates, but in the 1979-80 season
the seedlings from the two later planting dates were destroyed by birds. Figure 1
shows the epiphytot'.; curves for disease incidence percentage and disease intensity
for 1979-80. It is worth noting that at the date of the first reading in early
March the disease incidence of the early planted susceptible crop was already
30%, which indicates that disease development must have started by mid-February.
Both cultivars developed a very high percentage of diseased plants but
differed significantly in their disease intensity ratings. Though nothing is known
on the type of resistance in ILC 482, it may be partly associated with the fungus
growth rate and sporulation after infection.
The data obtained up to April 28 in the 1980-81 growing season are presented
in Figure 2. They confirm all findings from the previous season and also indicate
the effect of late planting on the epiphytotics. Only the latest planting date
brought the disease intensity of the susceptible cultivar down to acceptable
levels. Again, the disease did not occur before mid-February, even with the
earliest planting date. A striking feature in both years was the extremely fast
disease development that began during mid-March.
Infection Conditions
The results presented above raise the question about the environmental factors
that control infection. As spores are only released from pycnidia if they are wet,
wetness of the plant surface must be a pre-condition for surface contamination
and effective short or long distance spread by wind. A study of the wetness
duration and temperature requirements for successful infection was therefore
carried out to determine the climatic conditions necessary for disease development.
It was found that the disease intensity increased with increased wetness
duration over a wide range of temperatures (Fig. 3). However, a steep increase at
shorter wetness durations of up to 10 hours was only apparent between 9 and
21'C. The irregularities occurring at 15'C were not significant and probably
stemmed from insufficient environmental control in the growth chambers used.
If one excludes all infection data below 1%as insignificant, the limiting
conditions for infection can be defined. Figure 4 shows that no infection occurred
below 6C irrespective of the wetness duration and under wetness periods shorter
than 6 hours irrespective of the prevailing temperature. The maximum temperature
allowing infection must be close to 30'C.