Agriculture Reference
In-Depth Information
released into the soil when plants die or are harvested (Entwistle and Munasinghe,
1978).
There is a considerable literature on the epidemiology of the disease (Coley-
Smith, 1988; Entwistle, 1990; Metcalfe and Wilson, 1999; Clarkson
et al.,
2004).
(b) Epidemiology
Host and soil effects are important in the epidemiology of white rot. Firstly, for plant
infection to occur, the sclerotia held in check by soil fungistasis have to receive a
stimulus from specific factors released as exudates by the roots of onions (Esler and
Coley-Smith, 1983). When this occurs sclerotia germinate producing hyphae that
may grow 1 to 2 cm through the soil to infect the roots of onions. They penetrate the
root epidermis producing appressoria and infection cushions and the hyphae enter
between cell wall junctions (Metcalfe and Wilson, 1999). Then they invade the
hypodermis and grow into the cortex of the roots. During the early stages of
infection, cell death is limited to the cells penetrated by the hyphae of
S. cepivorum
;
however, onion cell walls in the path of the leading infection hyphae often dissolve
before the hyphal tips reach them. This was shown to be indicative of enzymic
action by certain pectinases (Metcalfe and Wilson, 1999).
Plant-to-plant spread of
infection may occur in densely-sown or closely-spaced crops.
Secondly, soil temperature is a critical factor affecting germination of sclerotia,
mycelial growth and root infection of onions. Sclerotial germination is favoured by
temperatures between 10 and 20
o
C (Fig. 19.5); outside this range, germination is
slow but returns to normal when temperature is restored to 15
o
C. Thus, in the UK,
sclerotial germination is poor during the winter but improves in spring and early
summer (Fig. 19.5); later in the summer, germination may be inhibited by high soil
temperatures - sclerotia cannot survive temperatures of 35
o
C and above (Entwistle
and Munasinghe, 1978). As a result, disease losses are high in overwintered crops in
the autumn and spring, when temperatures are suitable for infection, (the optimum is
between 15 to 18
o
C
- Crowe and Hall, 1980), but
white rot may be of minor
importance in hot summers (Entwistle and Munasinghe, 1978). In countries with hot
climates, white rot may be confined to the cooler summer months (Coley-Smith,
1988).
Sclerotial germination is little affected by pH values varying from 4.8 to 8.5
(Entwistle and Granger, 1977); there was a decrease in germination of sclerotia as
soils became drier or wetter than field capacity (-300 millibars) (Crowe and Hall,
1980). Recent studies (Clarkson
et al.,
2004) showed that over 90% of sclerotia were
degraded at high water potentials where the soil was nearly saturated. This
confirmed the findings of previous workers (Crowe and Hall, 1980) and those of
Leggett and Rahe (1985) and Crowe and Carlson, (1994) who used flooding to
degrade sclerotia as a means of controlling the disease.
Sclerotia may persist in the soil from at least four to 20 years (Entwistle and
Munasinghe, 1978; Entwistle, 1990). Attempts to forecast white rot based on
assessments of the numbers of sclerotia per given weight of soil have met with
variable results within and between countries (Entwistle, 1990). Newer models
