Agriculture Reference
In-Depth Information
LATE SUMMER
LATE
SPRING
Progeny tubers
become contaminated
with Fusarium spores
as they develop, but
tubers are not infected.
Sprout rot and seed piece decay after planting
lead to uneven stands with weakened plants.
Wounds caused during
harvest and handling
allow spores on tuber
surface to enter tuber.
After planting, over
50% of
sprouts developing
on infected tubers
may become
diseased and killed.
Fusarium dry rot
disease cycle
Dry rot infection in
storage often leads
to secondary
bacterial soft rot.
In storage, dry rot develops rapidly at
temperatures above
60
ºF and relative
humidity above 95%.
Seed pieces start to
decay during seed
storage proir to planting.
FALL
EARLY
SPRING
Seed pieces are infected
during cutting in spring.
Pathogen overwinters on infected tubers and in soil.
WINTER
Fig. 11.3.
The disease cycle of
Fusarium sambucinum
, causal agent of Fusarium dry rot.
the conditions favorable for potato growth, such
as soil temperature between
10
and 25°C,
6-7
pH,
and soil O
2
content of about
15-
20%. Cultural
practices that favor inoculum survival include
rotations shorter than
4
years, inadequate water
management, rotation with alternative suscep-
tible hosts, shortening of intervals between
haulm/vine killing and harvest, and harvesting
when soil and tuber pulp temperatures are out-
side the optimal range (variety dependent but
generally from
10
to 25°C; Fiers
et al
., 2012).
Several pathogens have resting spores that
can survive in the soil for extensive periods in the
absence of known hosts. Examples of such
pathogens that cause potato diseases include
Colletotrichum
coccodes
(black dot),
Fusarium
spp.
(dry rot),
Rhizoctonia solani
(black scurf),
H. sola-
ni
(silver scurf),
Spongospora subterranea
(powdery
scab),
Streptomyces
spp. (common scab),
P. eryth-
roseptica
and
Phytophthora nicotianae
(pink rot),
Pythium ultimum
(Pythium leak),
Sclerotinia scle-
rotiorum
(white mold and stem rot) and
S. endobi-
oticum
(potato wart). In the following paragraphs,
some major diseases with soil survival phases will
be addressed.
C. coccodes
(Wallr.) S. Hughes is the causal
agent of black dot. The disease is named for the
minute, pinprick-sized sclerotia that develop and
appear as small, black dots on host tissues, in-
cluding roots, tubers, and stems. Up to 30% yield
reductions have been reported due to infection
of roots by the pathogen (Tsror
et al
., 1999). In-
fected tubers exhibit silver to brown lesions with
sclerotia. These blemishes reduce tuber quality,
particularly in cultivars destined for the fresh
market (Read and Hide, 1995).
C. coccodes
is an
effective saprophyte and is common in soils of all
potato growing regions (Read and Hide, 1995).
Both seed- and soilborne inoculum of
C. coccodes
can cause disease (Read and Hide, 1988; Lees
et al
., 2010; Pasche
et al
., 2010). In several stud-
ies, soilborne inoculum resulted in a greater host
plant colonization than seedborne inoculum
(Dashwood
et al
., 1992; Denner
et al
., 1998).
Furthermore, soilborne inoculum has been cor-
related highly to black dot severity on daughter
