Sorghum Diseases in India

S. hermonthica predominates in Sahelian and
sub-Sahelian Africa and S. asiatica predominates
in northwestern India, southern Africa, and
parts of eastern Africa.
Yield losses in pearl millet due to specific diseases
have been estimated, but this information
is scanty and usually very localized, generally
applying only to specific years or experiments.
The relative importance, on a global basis, of the
major pearl millet diseases is not known. Therefore,
ICRISAT's pearl millet pathologists (S.B.
King, S.D. Singh, R.P. Thakur, and J.Werder)
have attempted to estimate global yield losses to
diseases based on a general understanding of
yield losses in the major pearl millet production
areas. Our estimate of the relative importance of
pearl millet diseases (excluding nematodes) are
as follows: downy mildew 45%, Striga spp 32%,
smut 9%, ergot 7%, rust 3%, viruses, >1%, and
other diseases 3%. Downy mildew is especially
important in India and to a somewhat lesser degree
in western Africa, and Striga is especially
important in western Africa.
This review presents information in some detail
on only the more important diseases of pearl
millet, worldwide. I have attempted to identify
important gaps in knowledge that should receive
research attention in the future, and I have
reported very little on what I consider to be the
less important diseases, although some of these
may be important in some locations in some
years.
Downy Mildew
Sclerospora graminicola was first reported on
pearl millet in India by Butler (1907), but downy
mildew (DM) did not become a serious problem
on a national level until after the widespread
cultivation in India of hybrids in the late 1960s.
The first of several major epidemics occurred in
1971 (Safeeulla 1976; Singh et al. 1987a). These
hybrids were evidently bred under little downy
mildew pressure and were based mainly on the
male-sterile line from Georgia, Tift 23A, that was
bred in the absence of downy mildew and was
highly susceptible to it. In 1970, India recorded a
record grain production in the pearl millet crop
exceeding 8 million t, attributed largely to the
widespread cultivation of hybrids. However, in
the following year a drop in grain production of
more than 40% was attributed mostly to downy
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mildew and to the increased vulnerability of the
crop resulting from the greater genetic uniformity
introduced by hybrids (Pokhriyal et al.
1976; Safeeulla 1977).
There is little question about the taxonomy of
the downy mildew pathogen; Sclerospora graminicola
(Sacc.) Schroet. is the accepted name. It
was first described as Protomyces graminicola on
Setaria verticillata by Saccardo in 1876 but a few
years later was renamed 5. graminicola by Schroeter.
There appear to be two distinct pathotypes
of S. graminicola, one that attacks Setaria spp and
another that attacks pearl millet, although they
are morphologically the same (Williams 1984a).
Considerable information is available on the
biology, epidemiology, and control of S. graminicola
and pearl millet downy mildew (Safeeulla
1976; Nene and Singh 1976; Williams 1984a;
Shetty 1987; Singh et al. 1987b). The fungus produces
both sexual spores (oospores) and asexual
spores (sporangia, zoospores). It is heterothallic,
requiring the presence of two mating types for
production of oospores, though such combinations
are not required for infection and subsequent
asexual spore production (Michelmore et
al. 1982). Only two mating types have been
found, and there is compatibility between those
from western Africa and those from the Indian
subcontinent (Idris and Ball 1984). The nuclear
condition of S. graminicola, particularly of sporangia
and their production, has been described
(Safeeulla 1976; Shetty and Ahmed 1981), but
further clarification is desirable.
There is little doubt that S. graminicola can be
transmitted as oospores on the seed surface or as
mycelium in embryonic tissues of seed. However,
there seems to be no agreement on whether
mycelia-infected seed is capable of giving rise to
downy mildew infection on pearl millet plants
(Sundaram et al. 1973; Shetty et al. 1977; Williams
1979; Williams et al. 1980). There is ample
evidence of virulence differences in the pathogen
in India and Africa (Girard 1975; Shetty and
Ahmed 1981; Ball 1983; Singh and Singh 1987),
with isolates from Nigeria and Niger being the
most aggressive (Ball et al. 1986).
Field-screening techniques involving a sick
plot, infector rows, or a combination of both
have been developed and are being used with
varying degrees of success at a number of locations
in India and in several countries in western
Africa. The success of the infector row system
depends heavily on sporangial production, dis-