Compendium of Potato Diseases - (PDF, 101 mb) - USAID

the air temperature when tubers are in the soil within 2.5 cm of
the surface, remain on the ground after digging, or are held in
bags in the sun. (See also tuber greening.)
Selected References
NII'IS|-N. I.. WV. 1954. [he susceptibility of"seven potato varieties to
bruising and bacterial soft rot. Phytopathology 44:30-35.
(Prepared by W. .1.Hooker)
Internal Heat Necrosis
Considerable confusion exists both in symptom description
and in terminologv for the causal factors of internal necrosis of
tubers. The underlying cause of necrosis is believed to be
suboxidation of rapidly respiring internal tissues during active
tuber growth and high temperatures. (See also phosphorus
deficiency, vello\k d\\art. mop-top, and stem mottle.) In recent
literature, the name Eiserifleckigkeit refers specifically to
internal heat necrosis, whercas l'ropfenbildtung and Spraing are
used for stem mottle virus infections,
Symptoms
Syniplonis do not develop in vines. Affected tubers usually do
not sho%%external syniptoims. Necrosis may be severe toward the
center of larger tubers, appearing as light tal, dark yellowish to
reddish bro, n. or rust-colored Ifccks that become, in extreme
cases, dark brown or even black (Fig. II). 1n usually severe
s. mptonis may be identical to blacklicart. Necrotic flecks are
ustallyv clustered off-center in the pith towards the apical end.
Necrotic flecks are firtii, do niot break do%%n or predispose to rot,
and remain firm after cooking. Cortical tissues are seldom
aft ected. .\ relat ionship exists bctx\ en Iisenfleckigkeit atid acid
soils that ate Io\ iti calcium. (See also calciun deficiency.)
losses can be se\ere because of buyer discrimination against
internal discoloration.
.\ sonlew\hal similar disorder. present in Israel, produces
necrotic spots in the coritx near the vascular ring and maproduce
interior cavities. I)amage is visible from the tuber
sirft:ce. with h!:ckening of the eves at the apical end, sunken
surface spots. and a silvery sheen. No true rot develops, but
many affected tubers fail to sprout. Symptoms are believed to
develop intstorage following high field temperature before
har\est.
Ifistopathology
Suberin develops in walls of affected pith parenchyma cells.
Cell walls first become dark at the corners. Protoplasm becomes
granular and aggregates. Walls ofadjacent cells also darken and
finally collapse at the corners. l.ayers of peridermlike cells may
develop outside the necrotic tissue and may isolate it. Internal
pressure from periderm formation may cause the collapse of
necrotic cells, but cell lysogeny has not been observed. Starch
grains are generally absent in affected cells.
Epidemiology
Internal necrosis becomes progressively more severe during
the growing season and is most severe during hot, dry years in
light soils of sand. gravel, muck, or peat. Lack of adequate soil
moisture may be as influential as high temperature in
predisposing to internal necrosis. Disease is most severe in
tubers near the soil surface and progressively less frequent and
severe with increasing tuber depth. Straw mulch reduces soil
temperature and sexeritv of disease. Ini areas where the disease
was formerly severe, maintenance of good vine coverage of the
soil through adequate irrigation and good cultural practices has
almost eliminated the problem.
Discoloration does not increase and ma' decrease in storage
if affected tubers are not predisposed to storage rots.
Transmission through affected seed tubers has not been
observed, although spindly sprouts have been reported from
tubers exposed to 30-40°C.
Control
I) Cultivars differ in tolerance and sensitivity.
2) Maintain vine growth adequate to shade the ground
through the use of appropriate cultural practices (good fertility,
Fig. 12. Second growth: A, dumbbell; B, pointed end; C,
protruding eyes that later form knobs. Stoton end ineach case is
Fig. 11. Internal heat necro'sis, at left.
A
rr..
V,
11