Sorghum Diseases in India

Sclerotia in the soil germinate to produce ascospores
that become airborne and infect individual
florets through fresh stigmas. The ovary
becomes infected, and within 5 to 7 days a sticky
viscous liquid (honeydew) containing microand
macroconidia exudes from diseased florets.
Secondary spread is believed to occur by splashing
rain and by physical contact among panicles.
Insects can carry inoculum from diseased to
healthy panicles (Sharma et al. 1983; Verma and
Pathak 1984), but evidence suggesting that insects
are important in disease epidemiology
seems circumstantial.
Infected florets produce sclerotia that reach
maturity at about the same time as grain. Several
alternative grass hosts have been reported, including
Panicum antidotale (Thakur and Kanwar
1978) and Cenchrus ciliaris (Singh et al. 1983), but
the importance of these inoculum sources in disease
epidemiology is not clearly understood.
There is no confirmation of virulence differences
among isolates of C. fusiforrnis. It is believed that
moderate temperature and high humidity favor
disease development (Ramaswamy 1968; Siddiqui
and Khan 1973b), but precise information is
not available. In India, epidemics have been associated
with rainy weather; in western Africa
ergot generally occurs more frequently in the
higher rainfall areas. Factors influencing sclerotial
germination are not well understood.
Cultural control methods, including intercropping,
early sowing, adjusting soil fertility,
and deep plowing to bury sclerotia have been
suggested (Thakur 1984), but the practicality
of these methods at the farmer's level is not
known. Fungicidal control, demonstrated experimentally
by Thakur (1984), is not economical
for farmer use. Avoiding sowing of sclerotiacontaminated
seed is likely to have some merit.
Considerable evidence indicates that high availability
of pollen during protogyny helps to control
the disease (Thakur et al. 1983c). Control of
ergot through pollen management might be possible
in farmers' fields, but the technique has not
been tested fully.
Disease resistance may hold some promise as
a means of ergot control, but there are definitely
some problems, especially for hybrids. Resistance
could not be assessed adequately until the
development of a reliable field screening technique
that restricted pollen-based escape to a
low level (Thakur et al. 1982). Resistance was not
found in accessions of germplasm, but crosses
100
between less susceptible plants followed by
pedigree breeding and selection under high disease
pressure produced numerous lines and sibbulks
with very high levels of resistance (