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

necrosis extending into the tuber to various depths (Fig.
67B-G). Firm, brown circular lesions (up to 2.5 cm in diameter)
may be present elsewhere on the tuber surface. In transverse
section at the stem end, slight to severe vascular browning is
evident, and the vascular ring may have a few thick, black
strands (up to I mm in diameter) or more numerous, smaller
brown to tan, netlike strands in the vascular ring. Highly
diagnostic, but not present in every tuber, is a water-soaked,
firm, light brown to tan discoloration extending 3-5 mm on
either side of the vascular ring. This discolored area isfirm, does
not produce exudate as in bacterial ring rot or brown rot, and
usually shows little tendency to break down with secondary rots.
Vascular necrosis extending into the eyes may cause eyes to be
brown and necrotic,
Oxvsporum Wi/. Usually milder than eumartii wilt, this
disease is a typical vascular wilt in contrast to the other
Fusarium wilts described here, which are more nearly cortical
rots. Symptoms appear during the middle of the growing
season, wilt is rapid, giving the impression that the lower stem
has been cut off- and the plant is prematurely killed. Yellowing
begins at the lower leaves and progresses up the plant. Vascular
discoloration of the stem is confined to portions below or
slightly above the soil line. Tubers generally show discoloration
of the vascular strands and usually no stem end rot.
Tuber infection through wounds or possibly lenticels causes
circular lesions and a di y rot in storage. This condition has been
associated with high humidity and temperature.
Av'enacutn Wilt. This disease is comparable in severity to
oxysporum wilt and generally less severe than eumartii wilt. It
develops from mid to late season. Symptoms may be more
severe on one side of the plant. Wilting and rapid collapse of the
plant are common in hot, dry weather. A different response,
possibly when growing conditions are more favorable, consists
of chlorosis at bases of apical leaves, followed by general
bunching of leaflets, chlorosis of the plant beginning at the base,
shortening of internodes, carbohydrate accumulation in
aboveground portions of the plant, red or purple pigmentation,
and aerial tubers in leafaxils. The plant resembles those affected
by mycoplasma or psyllid yellows. However, vascular
discoloration may be seen in the lower portion of the stem up to
six inches above the soil. Tip burn and loss of lower leaves is
common. Early season infection produces severely dwarfed
plants similar to those with yellow dwarf disease.
Tubers show dry stem end rot and vascular tissue that is
discolored brown, lacks the water-soaked border of eumartii
but is characteristically dry, and may be gray to pink.
/-. solani Wilt. This wilt is distinct from eumartii wilt. It is
characterized by rotting of the root system, the stem pith, and
the lower and underuround stem, with dry shredding of the
strands ofwoody tissue, and wilting and yellowing of foliage. In
moist conditions rosetting of tops and aerial tubers appear.
Tuber infection follows wound infection and differs from
other wilts in lacking typical vascular discoloration. Neither
stolons nor tubers are directly infected from the parent plant.
Causal Organisms
Taxonomy of genus Fusarium is complex. Species designations
used here are those used in disease discriptions. Designation
of species by the system of Sryder and Hansen is given in
synonyms.
The four pathogens associated with the Fusarium wilts are: F.
eumnartii Carp. (syn. F. solani f. sp. eumartii (Carp.) Snyd. &
Hans.): F. oxisporuw Schl. (syn. F. o.ry'sporum Schl. f. sp.
tuherosi (Wr.) Snyd. & Hans.); F avenaceun (Fr.) Sacc. (syn.
F. roseum (Lk.) Snyd. & Hans.); and F.solani (Mart.) App. &
Wr. (syn. F. solani f. sp. eumartii (Carp.) Snyd. & Hans.).
Descriptions on the basis of spore characteristics will not be
attempted because of the well known variability of Fusariumas
influenced by environmental factors.
Isolations of F.eumartiiare readily obtained from roots and
less readily from stems. Discolored tissue from upper stems and
tuber apices is sterile. Isolation from stored tubers is difficult,
Tissue discoloration develops in advance of the fungus and is
apparently associated with toxic substances.
F. o.x.spforun is easily isolated from roots and lower stems
and, with difficulty, from stored tubers. Wilting is, in part, due
to toxins.
F. avenaceum is successfully isolated from vascular
discolored stem tissue below or close to the soil line and from
discolored vascular tuber tissue.
F. solani is readily isolated from discolored stem tissue.
Histopathology
Diseases caused by the four wilt fungi are essentially similar.
Root tips, following infection from the soil, become watersoaked.
Epidermal cells of young roots are invaded. Cell walls
become sc lened and swollen, and cortical necrosis follows.
Xylem of roots and stems is invaded; vessels become plugged
with granular material; and surrounding cells of outer phloem
and cortex break down in ways varying with the particular
pathogen involved.
Disease Cycle
Fusarium wilts are typically soilborne, and the disease is
transmitted with varying degrees of effectiveness from inoculum
within and on seed tubers.
F. eumaruii survives in field soil for long periods without
noticeable reduction in pathogenicity when potatoes are again
planted in the field. Because of this disease, many fields have
been abandoned for potato production. The other wilt
organisms may be shorter-lived in the absence of potatoes, but
evidence is lacking.
Planting potatoes in artificially infested soil or placing
inoculum on freshly cut seed efficiently establishes the disease.
Infection isthrough roots into the stem and, except for F.solani,
from the stem through the stolon into the developing tubers.
Infected seed pieces with stem end rot transmit disease to the
new plant, more efficiently with eumartii than with oxysporum.
Inoculum is introduced into new fields primarily through the
planting of infected seed tubers. Contintal potato production,
particularly replanting infected tubers, accelerates inoculum
buildup. Inoculum is dispersed from infested fields by surface
drainage water, windblown soil, soil carried on implements, etc.
Epidemiology
Wilts are most severe at high temperatures and particularly
when plants are under stress in dry, hot growing conditions.
Although evidence is lacking, the rosette symptom with aerial
tubers probably follows increased availability of water and
somewhat cooler temperatures.
F.eumartii is capable of infection at lower soil temperatures
(20 and 24 C), whereas F. oxy'sporum and F. avenaceum are
more pathogenic at 280 C. F.solani in culture can grow at 350 C
but grows most rapidly at 300 C.
Other Hosts
The cultivated potato is the only known natural host for the
several Fusarium spp. causing wilt of the crop. Morphologically
similar pathogens attack plants of widely divergent types.
Species differentiation has been based on pathogenicity specific
to a particular plant species. Several Solanum spp. related to
potato have been experimentally infected with F. eumartii.
Resistance
Minor differences in resistance within S. tuberosum are
known, but identified resistance is not sufficiently high to be of
general use. S. spegazzinii, S. acaule, and S. kurizianum seedlings
carry considerable resistance to root infection by F.
eumarhii in infested soil.
Control
I) Grow potatoes in land free from wilt fungi.
2) Tubers infected with Fusarium wilt should not be used for
seed.
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