Diseases of Sweetpotato

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Diseases of Sweetpotato
Kwame Ogero and Rene van der Vlugt
Contents
1 Introduction . . . . . . . ............................................................................ 3
2 Fungal Diseases ............................................................................... 4
2.1 Alternaria Leaf Spot and Leaf Petiole and Stem Blight (Alternaria bataticola,
A. tenuissima, A. alternata) .................................... ....................... 4
2.2 Chlorotic Leaf Distortion (Fusarium denticulatum) ................................. 5
2.3 Leaf and Stem Scab (Sphaceloma batatas Sawada) ................................. 7
2.4 Cercospora (Passalora bataticola) and Pseudocercospora Leaf Spots
(Pseudocercospora timorensis (Cooke)) .............................................. 8
2.5 Fusarium Wilt (Fusarium oxysporum) ................................................ 9
2.6 Phomopsis Leaf Spot (Phyllosticta Leaf Blight) (Phomopsis ipomoea-batatas
Punith) ................................................................................. 11
2.7 Black Rot (Ceratocystis fimbriata) ................................................... 12
2.8 Java Black Rot (Lasiodiplodia theobromae) ......................................... 14
2.9 Rhizopus Soft Rot (Rhizopus stolonifer) ............................................. 17
2.10 Fusarium Surface Rot (Fusarium oxysporum) and Fusarium Root Rot (Fusarium
solani) ............................. ................................. ................... 19
2.11 Foot Rot (Plenodomus destruens) .................................................... 21
2.12 Circular Spot (Sclerotium rolfsii)..................................................... 23
2.13 Sclerotial Blight (Sclerotium rolfsii)............ ...................................... 25
2.14 Charcoal Rot (Macrophomina phaseolina) ........................................... 27
2.15 Geotrichum Sour Rot (Geotrichum candidum) ....................................... 28
2.16 Dry Rot (Diaporthe phaseolorum) ................................................... 30
2.17 Mottle Necrosis (Pythium spp.) ....................................................... 31
2.18 Scurf (Monilochaetes infuscans) ...................................................... 34
K. Ogero (*)
Crop and Systems Sciences Division, International Potato Center (CIP), C/o Tanzania Agricultural
Research Institute (TARI) –Ukiriguru, Mwanza, Tanzania
e-mail: K.Ogero@cgiar.org
R. van der Vlugt
Laboratory of Virology, Plant Sciences, Wageningen University and Research (WUR),
Wageningen, The Netherlands
e-mail: rene.vandervlugt@wur.nl
© Springer Nature Switzerland AG 2023
W. H. Elmer et al. (eds.), Handbook of Vegetable and Herb Diseases, Handbook of Plant
Disease Management, https://doi.org/10.1007/978-3-030-35512-8_29-1
1

2.19 Violet Root Rot (Helicobasidium mompa)........................................... 37
2.20 Other Minor Fungal Diseases ......................................................... 38
3 Bacterial and Phytoplasma Diseases ......................................................... 38
3.1 Bacterial Wilt (Ralstonia solanacearum) .............................................. 38
3.2 Bacterial Stem and Root Rot (Dickeya dadantii) ........................... ........... 41
3.3 Streptomyces Soil Rot (Pox) (Streptomyces ipomoeae)............................... 42
3.4 Sweetpotato Little Leaf (Candidatus Phytoplasma aurantifolia) ..................... 43
4 Viral Diseases ................................................................................. 44
4.1 Sweet Potato Chlorotic Stunt Virus (SPCSV) . . . ...................................... 44
4.2 Sweet Potato Feathery Mottle Virus (SPFMV) ........................................ 46
4.3 Sweet Potato Virus Disease (SPVD) . . . . . . . . . . . . . . . . . . . . . . ............................. 47
4.4 Sweet Potato Mild Mottle Virus (SPMMV) ........................................... 48
4.5 Sweepoviruses .......................................................................... 49
5 Nematode Diseases ........................................................................... 50
5.1 Root-Knot Nematode (Meloidogyne spp.) ............................................. 50
5.2 Lesion Nematode (Pratylenchus spp.) ................................................. 52
5.3 Reniform Nematode (Rotylenchulus spp.) ............................................. 53
5.4 Stem Nematode/Brown Ring (Ditylenchus dipsaci,D. destructor) ................... 55
References ........................................................................................ 56
Abstract
Sweetpotato is the sixth most important food crop globally. Whereas in developed
countries like Canada, Europe, and the United States, it is considered a vegetable,
it is a major staple food crop in sub-Saharan Africa. Cropping systems and
varietal preferences vary between temperate and tropical countries. This influ-
ences the type of diseases encountered in temperate and tropical countries. Some
diseases occur globally, but severity may differ between different regions. Viruses
pose the greatest challenge to sweetpotato production globally. Sweet potato virus
disease (SPVD) caused by synergistic interaction between sweet potato chlorotic
stunt virus (SPCSV) and sweet potato feathery mottle virus (SPFMV) can cause
between 56% and 98% yield losses. The crop is also affected by bacterial diseases
such as bacterial wilt caused by Ralstonia solanacearum and Streptomyces soil
rot caused by Streptomyces ipomoeae among others. Over 32 fungal diseases
have been reported in sweetpotato, infecting the crop both in the field and in
storage. Field fungal diseases include leaf spot and leaf petiole and stem blight
caused by several species of Alternaria. Economically important storage fungal
diseases include black rot, java black rot, and Rhizopus soft rot. The crop is also
affected by various nematodes. The importance of sweetpotato diseases varies
geographically. For instance, whereas SPVD and other viruses are economically
important in sub-Saharan Africa, nematodes do not cause significant loss and do
not warrant control. This chapter discusses the geographic distribution of the
different diseases, their importance, and management practices.
Keywords
Sweetpotato · Cropping systems · Sweet potato virus disease · Ralstonia
solanacearum ·Alternaria · Black rot · Nematodes
2 K. Ogero and R. van der Vlugt

1 Introduction
Sweetpotato is a dicotyledonous root crop belonging to the family Convolvulaceae.
It has an extended storage root, which accumulates more edible component than the
Irish potato (Solanum tuberosum). The color of the stem and leaves varies from
green to totally purple due to the accumulation of anthocyanins (Laurie and
Niederwieser 2004). The general leaf outline varies from round to almost divided
with some varieties having deeply lobed margins. The shape and size of the storage
root can be between round and long, irregular, or curved depending on the variety
and environmental factors (Woolfe 1992). The color of the storage root skin ranges
from white to dark purple, and the color of the fleshy roots in the field may be purple
or vary from white to orange in various distributions.
The exact origin of sweetpotato is still not well documented. However, historical
evidence suggests that it originated from Central or South American lowlands. South
American indigenous communities have probably cultivated the crop since 3000 B.
C. Therefore, it is believed to have originated from the region between Yucatan
Peninsula of Mexico and Orinoco river in Venezuela and spread to the rest of the
world by explorers (Clark et al. 2013; Zhang et al. 2004) and introduced to Europe
and Asia and spread to Africa by the sixteenth century (Allemann et al. 2004).
The wild progenitors of sweetpotato have not been documented. It is believed that
the cultivated varieties of sweetpotato, which are hexaploid, resulted from the
hybridization between tetraploid primitive and diploid weedy sweetpotato (Sauer
1993). It is possible that wild hexaploids are available, but according to history,
cultivars were independently domesticated in different regions.
Sweetpotato is the only economically important food crop of the family
Convolvulaceae and ranks sixth in production globally after wheat, rice, maize,
Irish potato, barley, and cassava (International Potato Center 2020). Among root and
tuber crops, it ranks third in acreage, behind Irish potato and cassava. In Eastern and
Southern Africa, it is third to cassava and Irish potato among the major root and tuber
crops, both in cultivation and consumption, and thus plays an important role in food
security and nutrition in Africa (Ewell and Mutuura 1994). In sub-Saharan Africa, it
is considered a food security crop, which provides a reliable source of food before
maturity of other crops. It is largely grown by small-scale farmers for household
consumption and income generation (Mutegi 2005). The region accounts for about
5% of global production, whereas China accounts for 75%.
Sweetpotato is easily propagated and cultivated and has good productivity in both
high- and low-input agricultural systems. Due to its ease of cultivation, low fertilizer
requirements, and high adaptability, it is considered a major staple food crop in
subsistence and rural economies. It has a significant potential to contribute to the
alleviation of widespread food shortages in many developing countries and can be
cultivated by farmers with limited resources because it requires few inputs and early
maturing varieties take 3 months to mature (Mwanga et al. 2002). Besides its direct
use as table and feedstock, sweetpotato is also a candidate for the production of
renewable plant products such as ethanol, high-grade starches, stable natural dyes,
and vitamin precursors (beta-carotene for vitamin A) (Woolfe 1992). About 80% of
Diseases of Sweetpotato 3

the dry matter in sweetpotato storage roots consist of carbohydrates, which are
principally type C starches that are quite susceptible to α-amylase digestion (Shin
et al. 2005). The high percent of fermentable biomass in the sweetpotato roots makes
it a potential energy crop for ethanol production. The orange-fleshed varieties have
high levels of beta-carotene, a forerunner of vitamin A, whereas the purple-fleshed
varieties are rich in antioxidants.
2 Fungal Diseases
2.1 Alternaria Leaf Spot and Leaf Petiole and Stem Blight
(Alternaria bataticola, A. tenuissima, A. alternata)
2.1.1 Geographic Occurrence and Impact
Alternaria leaf spots are widely distributed but less destructive. However, leaf petiole
and stem blight are more severe causing significant yield losses. It is a major problem
in Eastern Africa. It has also been reported in Asia, Cuba, and South America.
2.1.2 Symptoms
Symptoms include brown lesions on older leaves (Fig. 1). The lesions have target-
like concentric rings with well-defined margins.
Wide yellow haloes may sometimes surround the lesions. Stem and petiole blight
are associated with small, gray-to-black oval lesions. The lesions are mostly found
on stems and petioles but can sometimes appear on leaves (Fig. 2). They have light-
colored centers and may appear bleached during dry periods. Humid conditions lead
Fig. 1 Dark-brown lesions
with concentric rings. (Photo
credit: S. Nelson)
4 K. Ogero and R. van der Vlugt

to enlarged black lesions, which eventually coalesce and girdle killing the stems and
petioles. In addition, defoliation may occur on older leaves.
2.1.3 Biology and Epidemiology
Leaf spot and leaf petiole and stem blight has been reported to be caused by several
species of Alternaria. These include Alternaria bataticola, A. tenuissima, and
A. alternata. These are opportunistic pathogens that attack a wide range of plants.
They can survive on sweetpotato plants, alternative hosts, and in soil. Dispersion of
conidia is by wind and splashing water. The conidia are produced within the lesions.
Disease development is best under high humidity and during rainfall. Moderate to
heavy dew may also favor disease development. Symptoms take 3–6 days to
develop.
2.1.4 Management
Control of this disease is by use of disease-free planting material, use of resistant
varieties, and good on-farm practices such as sanitation by destroying debris from
previous crop and crop rotation.
2.2 Chlorotic Leaf Distortion (Fusarium denticulatum)
2.2.1 Geographic Occurrence and Impact
Chlorotic leaf distortion has been reported in Brazil, Kenya, Peru, and the United
States of America. Mostly, its effects are not economically significant.
2.2.2 Symptoms
Youngest leaves become chlorotic especially on vine terminals and sometimes turn
bright yellow, almost bleached in appearance (Fig. 3). Severity of the chlorosis
increases as the disease progresses and may affect the entire leaf. The disease results
in pink coloration on cultivars with purple leaves. The leaves regain most of their
Fig. 2 Necrotic lesions on
sweetpotato petioles caused
by Alternaria bataticola.
(Photo credit: C. A. Lopes)
Diseases of Sweetpotato 5

normal color with maturity. Sometimes the disease leads to leaf distortion and
stunting.
Infected plants also have a white deposit resembling salt on partially enlarged
open leaves (Fig. 4). The deposits have been reported to be clumps of fungal mycelia
and conidia.
2.2.3 Biology and Epidemiology
Chlorotic leaf distortion is caused by the fungus Fusarium denticulatum, which was
initially known as Fusarium lateritium. It infests the outside of the shoot tip without
invading the plant. Older leaves are also not affected. The mycelia colonize a
substance that is secreted onto the surfaces of meristems, leaf primoridia, and
young developing leaves that are yet to open. The fungal mycelia tend to stop
growing once the leaves open and expose the fungal structures, leading to recovery
of individual leaves (as they mature). Warm, sunny, and humid weather conditions
Fig. 3 Chlorosis on youngest
leaves of a sweetpotato plant
infected with chlorotic leaf
distortion. (Photo credit: C. A.
Clark)
Fig. 4 White salt-like deposit
of fungal mycelia and conidia
on young leaves. (Photo
credit: International Potato
Center)
6 K. Ogero and R. van der Vlugt

favor symptom development. It takes 3–6 weeks for symptoms to appear once a
plant is infected. The fungus can therefore be easily transmitted through use of
infected planting material. It can also be transmitted to healthy plants during
transplanting because conidia occur on affected plants. Spread of the pathogen is
also possible through splashing of rainwater, wind, and true seed, which are inter-
nally contaminated.
2.2.4 Management
In controlling the disease, it is important to use disease-free planting material and to
avoid harvesting botanical seeds from infected plants. There is no chemical control
for the fungus, and the insignificant yield losses do not provide an economic
incentive to control the disease.
2.3 Leaf and Stem Scab (Sphaceloma batatas Sawada)
2.3.1 Geographic Occurrence and Impact
Leaf and stem scab has been reported in Australia, Asia, South Pacific islands, and
Hawaii where it is most common. Brazil and Puerto Rico have also reported the
disease, but it is not very common. The disease has been associated with more than
50% yield losses. Yield reduction is more severe when the plants are infected early in
the season because it leads to poor formation of storage roots. Infected plants
produce fewer edible roots.
2.3.2 Symptoms
Symptom expression starts with small brown lesions on leaf veins. The veins
become corky resulting in vein shrinkage and leaf curling (Fig. 5). On stems, the
lesions appear slightly raised, with purple to brown centers and lighter-brown
margins. The lesions eventually join forming scab-like structures.
Fig. 5 Scab lesions on
sweetpotato leaves and
petioles. (Photo credit:
J. O’Sullivan)
Diseases of Sweetpotato 7

2.3.3 Biology and Epidemiology
The disease is caused by the fungus Sphaceloma batatas Sawada. The fungus grows
slowly, and hyphae are sparsely spread on affected tissue. Primary infection has been
associated with the ascigerous stage of this fungus, Elsinoe batatas, also observed in
infected tissue. The disease is prevalent in regions with frequent fog, rain, or dew
accumulation.
2.3.4 Management
Varieties with good resistance to the disease are available. Chemical control can be
achieved with benomyl and chlorothalonil. It is also important to ensure proper field
sanitation. Only disease-free planting material should be used. Overhead irrigation
should be avoided because it might lead to wet, humid conditions which favor the
disease. Rotation with other crops can also help reduce inoculum.
2.4 Cercospora (Passalora bataticola) and Pseudocercospora Leaf
Spots (Pseudocercospora timorensis (Cooke))
2.4.1 Geographic Occurrence and Impact
Pseudocercospora leaf spot was first reported in Africa. It is mainly found in Africa,
Asia, and Australia. It has also been reported in South America and the Caribbean,
but it is not common there. Cercospora was first described in the USA and is
primarily found in South America and the Caribbean. Although widespread, the
two diseases have been major issues only in isolated instances.
2.4.2 Symptoms
The two diseases produce similar lesions on infected plants. However, those of
Cercospora are a bit smaller. The color of the lesions can vary from uniformly dark
brown to black or pale gray, with light centers and dark borders. They can be circular
or irregular when demarcated by veins (Fig. 6).
2.4.3 Biology and Epidemiology
The two diseases were originally thought to be one –cercospora leaf spot. However,
it was later discovered that in sweetpotato they were two very similar but distinct
diseases. Pseudocercospora leaf spot is caused by Pseudocercospora timorensis
(Cooke) previously known as Cercospora timorensis Cooke and is synonymous
with C. batatas (C. batatae). Cercospora leaf spot is caused by the fungus Passalora
bataticola (Cif. & Bruner) synonymous with C. bataticola (Cif. & Bruner) and
Phaeoisariopsis bataticola (Cif. & Bruner). Development of both diseases is favored
by hot and wet weather. They produce conidia on long conidiophores protruding
from leaf stomata mainly on the abaxial side. The conidia are spread by wind and
rainwater. The fungi can survive on weed hosts in addition to debris of sweetpotato
plants.
8 K. Ogero and R. van der Vlugt

2.4.4 Management
There are no specific control measures given the rare cases of yield losses. However,
on-farm management strategies such as crop rotation and removal of debris from
previous crop can help reduce disease incidences.
2.5 Fusarium Wilt (Fusarium oxysporum)
2.5.1 Geographic Occurrence and Impact
Fusarium wilt has been reported in most areas where sweetpotato is grown, but it is
prevalent in cooler temperate regions. Where there are no resistant varieties, the
disease can cause more than 50% yield losses.
2.5.2 Symptoms
Symptom expression starts when the crop begins rapid growth. Older leaves start to
turn yellow followed by wilting and eventually falling off (Fig. 7). Yellowing of
leaves is usually one sided. The vine may become stunted and in severe cases turn
tan to light yellow.
The pith within the stem may decay, leading to plant death (Fig. 8). The vascular
tissues of the stem become discolored. This is usually used as an early diagnostic
symptom.
The lower stem may appear purplish and the cortex can rupture exposing brown
to black affected tissue. The surface of a dead vine has a pinkish extramatrical
growth with numerous macroconidia and microconidia of the pathogen (Clark et al.
2013).
2.5.3 Biology and Epidemiology
Fusarium wilt can be caused by three phylogenetic clusters of the fungus Fusarium
oxysporum. Fusarium oxysporum f. sp. batatas has two races: race 0 and
Fig. 6 Circular spots on a
leaf infected with Cercospora
leaf spot. (Photo credit:
T. Ames)
Diseases of Sweetpotato 9

race 1. Race 0 is predominant in the USA Southeast, whereas race 1 occurs in
California. The other cluster is F. oxysporum f. sp. nicotianae, which can also
infect tobacco. Fusarium oxysporum is soilborne and can survive in the soil and
plant debris for many years. The pathogen enters vascular wounds at fresh scars
shortly after planting. Symptoms appear 2–3 weeks after infection. However, new
infections can appear throughout the growing season. The optimum temperature
for disease development is 28–30 C, but the disease can develop at lower
temperature and across a wide range of soil moisture from 28% to 75%. Severity
is highest when soil moisture is low. The pathogen can be disseminated through
movement of infested soil, infected planting material, and storage roots. The type
of soil also influences disease incidence. This is mostly dependent on availability
of soil microorganisms that reduce the rate of germination of chlamydospores and
germ tube growth. Plants infected with chlorotic leaf distortion are less susceptible
to Fusarium wilt.
Fig. 7 Yellowing of leaves
on a sweetpotato plant
infected with Fusarium wilt.
(Photo credit: W. J. Martin)
Fig. 8 Internal decaying of a
sweetpotato stem infected
with Fusarium wilt. (Photo
credit: M. Truter and
R. Sutherland)
10 K. Ogero and R. van der Vlugt

2.5.4 Management
Fusarium wilt is best managed with resistant varieties. On-farm management strat-
egies such as crop rotation can reduce pathogen populations. However, rotation
alone cannot eliminate the pathogen. Use of clean planting material is also important.
Vines should be cut about 2–5 cm above the soil surface. Dipping planting material
in fungicides such as benzimidazole and thiabendazole can help reduce transmission
through the vegetative propagation cycle.
2.6 Phomopsis Leaf Spot (Phyllosticta Leaf Blight) (Phomopsis
ipomoea-batatas Punith)
2.6.1 Geographic Occurrence and Impact
Phomopsis leaf spot is found worldwide, in the humid tropical and subtropical
regions where sweetpotato is grown. It is not a major problem in terms of yield
loss but can reduce the quality of vines for use as planting material or fodder. The
disease is inconsequential to storage root production because it is usually present
only in mature leaves and toward the end of the growing season.
2.6.2 Symptoms
The leaves of infected plants have irregularly shaped lesions that are whitish or tan to
brown in color. The lesions form on both the upper and lower sides of the leaf and are
usually surrounded by dark-brown or purple border (Fig. 9). The lesions are more
prominent on the upper surface and measure 5–10 mm in diameter.
The lesions contain black pycnidia at the center. These serve as diagnostic signs
of the pathogen.
Fig. 9 Leaf blight lesions
caused by Phomopsis
ipomoea-batatas Punith.
(Photo credit: T. Ames)
Diseases of Sweetpotato 11

2.6.3 Biology and Epidemiology
The disease is caused by Phomopsis ipomoea-batatas Punith. This fungus is spread
by hyphae and unicellular conidia borne in pycnidia. The pycnidia occur alone and
are 100–125 μm. They have septate conidiophores that may be occasionally
branched. The pathogen overwinters in decaying leaves and is not known to have
other hosts. Spores are spread mainly through splashing water. Spread also occurs
through wind and use of infected planting material. Disease development is favored
by wet weather.
2.6.4 Management
Control measures are not warranted because the disease is of little economic
importance. However, field sanitation can help reduce or eliminate the disease.
2.7 Black Rot (Ceratocystis fimbriata)
2.7.1 Geographic Occurrence and Impact
The disease is of great economic importance in Southeast Asia and Oceania where it
reduces yield and quality of storage roots. It was a major disease in south-eastern
USA before 1970 but was successfully controlled through an integrated program
comprised of field sanitation and application of fungicides. However, it re-emerged
along the East Coast around 2012 and several other states in 2015. Black rot can
cause significant losses in storage, plant bed, and in the field.
2.7.2 Symptoms
Afirm, dry, and dark-colored rot develops on infected storage roots (Fig. 10a). The
rot does not usually extend into the cortex except when it has invaded through a deep
wound (Fig. 10b). The periderm is usually intact over the decayed cortex.
The lesions begin at wounds, lateral roots, or lenticels. The pathogen produces a
fruity ester-like smell. The odor is from amyl-acetate, a volatile compound produced
after infection. The roots also develop a bitter taste due to the phytoalexin,
ipomeamarone, produced as a response to the infection. White mycelia and black
Fig. 10 Storage roots with external (a) and internal (b) black rot lesions. (Photo credit: A. Scruggs
and L. Quesada)
12 K. Ogero and R. van der Vlugt

perithecia of C. fimbriata can be observed on the lesion surface using a hand lens
(Fig. 11). This is a key diagnostic feature for the pathogen.
Using infected roots as planting material leads to perpetuation of the fungus on
new plants in the bed and after transplanting. Infected plants may rot below ground
developing dark, sunken cankers. Severe infections may lead to yellowing, wilting,
and plant death (Fig. 12).
2.7.3 Biology and Epidemiology
Black rot is caused by the ascomycete Ceratocystis fimbriata. The fungus has a wide
host range, but isolates are host specific; hence, sweetpotato isolates can only cause
disease on the crop or other morning glories (Ipomoea spp.). Transmission of
C. fimbriata can occur throughout the growing cycle of the crop. Spread is through
use of infected planting material, contaminated tools, infested soil, and insects such
as the sweetpotato weevil (Cylas formicarius). The pathogen produces thick-walled
Fig. 11 White mycelia and black perithecia of C. fimbriata on the surface of infected storage root.
(Photo credit: A. Scruggs and L. Quesada)
Fig. 12 Sunken cankers on
the below-ground part of
sweetpotato stems infected
with black rot. (Photo credit:
W. J. Martin)
Diseases of Sweetpotato 13

chlamydospores, which enables it to persist in crop debris in soil for several years.
Disease development in the field is optimal at temperatures of 23–27 C. However,
infection can occur at 10–34 C. Favorable soil moisture is 0.1 to 0.2 bars.
Presprouting roots at warm temperatures also increases the infection rate.
2.7.4 Management
Black rot can be managed effectively through sanitation and chemical control.
Farmers should use disease-free planting material. Transplants should be cut at
least 2 cm above the soil surface. Other cultural methods include:
a) Avoiding fields with a history of C. fimbriata.
b) Field rotation for 3–4 years.
c) Avoid washing and packing storage roots from infected crops.
d) Curing storage roots at 30–35 C and 85–90% relative humidity for 5–10 days
after harvesting.
e) Fumigation of equipment and storage facilities. This can be done using chemicals
such as methyl bromide or chloropicrin.
f) Removing plant debris and alternate hosts from the field.
In addition to cultural control, the fungus can be managed using fungicides such
as thiabendazole and difenoconazole. However, this is only effective in treating
planting material to kill fungal spores on the surface. Fungicide treatment is not
effective once the crop has been infected. Host resistance is used in China and Japan.
2.8 Java Black Rot (Lasiodiplodia theobromae)
2.8.1 Geographic Occurrence and Impact
Java black rot is one of the most devastating storage diseases of sweetpotato and
occurs worldwide with high severity in warm regions compared to temperate
regions. Extent of damage on stored roots is dependent on length of exposure with
long storage periods, leading to infection of many roots.
2.8.2 Symptoms
Infected roots develop brown to reddish brown lesions (Fig. 13). These turn solid
black as disease development progresses. The center of the lesions is solid black and
surrounded by brown margins. Rotting may begin from one or both ends of the root
(Fig. 14). Later, mature mycelium and stromatic tissue lead to hardening and
complete blackening of the lesions (Fig. 15). Black stromatic masses protrude
through the periderm of infected roots at later stages forming the key diagnostic
feature of java black rot (Fig. 16).
Roots completely decay 2 weeks after infection, dry out, and become mummified
(Fig. 16). Decay in storage is restricted to the terminal 1–2 cm of the root.
At initial stages of disease development, java black rot may be confused with
black rot and charcoal rot. Fusarium rots may also resemble the disease to a lesser
14 K. Ogero and R. van der Vlugt

Fig. 13 Brown lesions of
java black rot on one end of
Okinawan purple-fleshed
sweetpotato. (Photo credit:
S. Nelson)
Fig. 14 External views of
sweetpotato roots infected
with java black rot. (Photo
credit: S. Nelson)
Fig. 15 Black stromatic
masses of Lasiodiplodia
theobromae protruding
through the periderm. The
stromatic domes contain
pycnidia which shed black
powdery spores. (Photo
credit: S. Nelson)
Diseases of Sweetpotato 15

extent. Java black rot, charcoal rot, and black rot (C. fimbriata) can be distinguished
as follows:
•Java black rot: The fungus produces pycnidia containing dematiaceous two-celled
conidia.
•Charcoal rot: Microsclerotia of the fungus are scattered through the storage root.
•Black rot: Perithecia of the fungus are formed on the surface of the lesion.
2.8.3 Biology and Epidemiology
Java black rot is caused by the fungus Lasiodiplodia theobromae, which can survive
in soil, on decaying plant debris, or free for many years. Soilborne inoculum initiates
primary infections. The fungus enters storage roots through wounds. The pathogen
does not infect properly cured roots. However, secondary infections may occur
during storage mostly through wounds formed during handling. The secondary
infections can be more destructive than primary infection especially if roots previ-
ously stored in cold temperatures are exposed to warm temperatures. Poor aeration
exacerbates secondary infections because of the elevated level of carbon dioxide.
The disease develops best at 20–30 C and can do well over a wide range of relative
humidity. However, very high humidity levels limit disease development. Suscepti-
bility of storage roots to L. theobromae increases with storage time. Roots stored for
5–8 months are more susceptible compared to freshly harvested roots. Lasiodiplodia
theobromae can be transmitted through use of infected planting material, contami-
nated equipment, insects such as the sweetpotato weevil (Cylas formicarius) and
cockroaches, run off water, and infested wash water.
2.8.4 Management
Java black rot can be controlled through the following means:
•Use of disease-free planting material.
•Washing and disinfecting previously used storage containers and harvesting tools.
Fig. 16 Sweetpotato roots
mummified following severe
infection with java black rot
pathogen, Lasiodiplodia
theobromae. (Photo credit:
S. Nelson)
16 K. Ogero and R. van der Vlugt

•Harvest and handle roots carefully to minimize wounding. Roots should be
properly cured and stored at approximately 16 C after harvesting. Maintain the
temperature until consumption. Curing should be done at 30–34 C and 90%
relative humidity for 4–7 days. Recurring of roots should be avoided.
•Crop rotation for 2–3 years.
•Timely harvesting to avoid flooding or cold temperatures.
•Growing sweetpotato on raised ridges may help improve aeration.
•Application of fungicides after handling minimizes infections. However, few
effective fungicide treatments are available for roots meant for human
consumption.
2.9 Rhizopus Soft Rot (Rhizopus stolonifer)
2.9.1 Geographic Occurrence and Impact
Rhizopus soft rot caused by Rhizopus stolonifer is prevalent in temperate and
subtropical regions but can also be found in tropical areas. It can cause significant
economic losses if the roots are not harvested and handled with care.
2.9.2 Symptoms
Symptoms begin at the wounded area where the pathogen enters the sweetpotato
root. Infected sweetpotatoes are soft and moist and have a stringy flesh (Nelson
2009) (Fig. 17).
The periderm remains intact but for a few cracks from where white to grey fungal
mycelium protrude and can be seen on the surface resembling whiskers (Fig. 18).
The mycelia produce black sporangia.
Fig. 17 Watery and stringy
flesh of orange-fleshed
sweetpotato root infected with
Rhizopus soft rot. (Photo
credit: A. Scruggs and
L. Quesada)
Diseases of Sweetpotato 17

The infection progresses from one or both ends and produces an alcohol-like
smell which attracts fruit flies. In addition, Rhizopus soft rot produces unique white
to grey mycelia “whiskers”on the surface unlike bacterial soft rot.
2.9.3 Biology and Epidemiology
Rhizopus soft rot is mainly a postharvest disease whose causative agent, Rhizopus
stolonifer, is omnipresent making it difficult to eliminate (Scruggs and Quesada-
Ocampo 2016a). Rhizopus Stolonifer is saprophytic and can survive on dead or
decaying sweetpotato debris. A second Rhizopus species, R. oryzae, can also cause
the disease at temperatures above 30 C. Several Mucor spp. also cause soft rot of
sweetpotato. These include Mucor racemosus, M. circinelloides, and M. piriformis.
The Mucor spp. are active at lower temperatures, 2–5C, and are also saprophytic
initially producing pectic enzymes that degrade root tissue before infection. Rhizo-
pus soft rot may be restricted sometimes and in such case, it is known as collar or
ring rot.
Rhizopus stolonifer sporangiospores can be air- or soilborne and enter
sweetpotato roots through wounds. Transmission is aided by contaminated
harvesting equipment, wash lines, packing equipment, and transportation containers.
Spores germinate and grow on wounds producing thick mycelia. The fungus pro-
duces pectolytic enzymes (amylase, pectinase, and cellulase) that kill the tissue in
advance, leading to infection since the fungal hyphae can only invade dead tissue.
Optimum temperature for R. stolonifer in culture is 28 C, but sweetpotato infection
is best at 20 C because of increased production of pectolytic enzymes. Optimum
relative humidity for disease development is 75–84% (at 23 C). Higher relative
humidity does not favor spore germination with few infections occurring at 93–99%
relative humidity. However, once an infection is established, it continues to enlarge
at 50–100% RH.
Proper curing reduces chances of infection. Extended exposure of harvested roots
to sunlight and high temperatures before curing may lead to heat damage making the
roots more susceptible. Chilling also predisposes the storage roots to the disease.
Heavy rainfall, flooding, and low temperatures during harvesting increase the risk of
Fig. 18 White to grey mycelia with black sporangia developing on a sliced root (a) and an intact
root (b). These are the key diagnostic features of Rhizopus soft rot. (Photo credits: (a) S. Nelson and
(b) Gerald Holmes, Strawberry Center, Cal Poly San Luis Obispo, Bugwood.org)
18 K. Ogero and R. van der Vlugt

infection. Susceptibility of roots during storage changes with time. The roots are
most resistant at harvest. Resistance reduces rapidly during storage reaching the peak
at 100–175 days. Resistance gradually increases afterwards.
2.9.4 Management
Rhizopus soft rot is best managed by reducing the number of available sites for
infection. This is because it is not practically possible to avoid contact between
sweetpotato roots and Rhizopus spp.
•Proper harvesting and postharvest handling to reduce wounding.
•Curing immediately after harvesting to encourage formation of wound periderm.
•Field sanitation to get rid of sweetpotato debris.
•Avoid harvesting during rainy conditions.
•Store roots at 85% humidity and 13 C with proper ventilation.
•Use disinfected equipment and containers during harvesting, storage, and
transportation.
•Fungicides such as dicloran and fludioxonil have been shown to protect the roots
from infection.
2.10 Fusarium Surface Rot (Fusarium oxysporum) and Fusarium
Root Rot (Fusarium solani)
2.10.1 Geographic Occurrence and Impact
Fusarium surface rot is common in areas where sweetpotato roots are stored for long
periods after harvest. It has been reported in the USA but is likely to be globally
distributed because Fusaria species that cause this disease are commonly found in
soils of most sweetpotato growing areas. Fusarium root rot has been reported in
southeastern USA where it is considered a serious disease, in China, and in South
Korea (Yang et al. 2018).
2.10.2 Symptoms
Fusarium surface rot causes circular lesions on storage roots. The lesions are light to
dark brown, firm, and dry and do not extend into the root beyond the vascular ring
(Fig. 19). Long storage of roots leads to drying of the tissue within and around the
lesions. The tissue shrinks and the roots eventually harden and mummify.
Fusarium root rot also forms lesions that are circular and with light and dark
brown concentric rings (Fig. 20). It is difficult to differentiate it from surface rot
during the initial stages. However, it later extends past the periderm entering the
central parenchyma of the root while forming open cavities in the tissue (Fig. 21).
With disease progression, infected tissue shrinks and dries, leading to mummifica-
tion of the root. In most cases, Fusarium root rot begins at either the distal or
proximal end of the storage root. This phase of the disease is known as Fusarium
end rot. In advanced stages, lesions become dry and sunken with white mycelia on
the outside or in the inner cavities. Fusarium root rot also has a stem canker phase
Diseases of Sweetpotato 19

whereby sprouts from infected seed roots develop a dark brown to black necrosis at
the base. This progresses slowly up the stem and may be restricted to the nodes.
Sometimes the stem splits above the decayed tissue. Using infected planting material
transfers the canker to the field where it continues to develop, leading to stunting and
yield reduction. The infection can be transmitted from the vine to the storage roots.
2.10.3 Biology and Epidemiology
Surface rot is caused by Fusarium oxysporum, whereas root rot is caused by
Fusarium solani. Both fungi are soilborne and can persist in the soil for many
years. The fungi enter storage roots through wounds. Disease development occurs
during storage but do not spread to other roots unless they develop new wounds.
Fusarium oxysporum does not spread to sprouts, only infecting mother roots. On the
Fig. 19 Cross section of a
storage root infected with
Fusarium surface rot. Note
that the lesion is limited to the
cortex. (Photo credit:
T. Ames)
Fig. 20 Sweetpotato root
infected with Fusarium root
rot showing necrotic lesions
that have extended beyond the
vascular ring and dry, open
cavities with white mycelia of
F. solani. (Photo credit:
A. Scruggs and L. Quesada)
20 K. Ogero and R. van der Vlugt

other hand, F. solani can be transmitted from storage roots to sprouts when infected
roots are used as seed (da Silva and Clark 2013). This leads to formation of the stem
canker. Fusarium solani causes maximum disease development at 29 C (Scruggs
and Quesada-Ocampo 2016b). Additionally, high relative humidity (100%) and high
levels of initial inoculum (7 mm) significantly increase disease development. Fusar-
ium root rot only occurs during long-term storage but not during transit.
2.10.4 Management
•Field sanitation and proper handling of roots after harvesting
•Reducing wounding during harvesting and curing roots immediately after
harvesting
•Controlling the presence of the root-knot nematodes (Meloidogyne spp.) and
other insects that injure the periderm
•Using pathogen-free planting material reduces transmission of F. solani
•Avoid fields known to be infested with F. solani
•Rotation with nonhost plants for 5 years
•Use clean harvesting and packing equipment
•Cut transplants at least 2 cm above the soil surface to avoid spreading stem canker
•Treat seed roots with an effective fungicide, for example, thiabendazole, before
bedding to prevent new infections
2.11 Foot Rot (Plenodomus destruens)
2.11.1 Geographic Occurrence and Impact
Foot rot (die-off) is not of great economic significance but can cause considerable
damages in the field and storage if proper sanitation is not done. In the past, losses of
25–80% have been reported in Argentina and Brazil following use of infected but
symptomless planting material (Lopes and Silva 1993). Implementation of clean
seed programs significantly reduced the disease incidence in USA. The disease has
been reported in Argentina, Brazil, Caribbean, Peru, and USA.
Fig. 21 Concentric
overlapping rings on a storage
root infected with Fusarium
root rot. (Photo credit: Gerald
Holmes, Strawberry Center,
Cal Poly San Luis Obispo,
Bugwood.org)
Diseases of Sweetpotato 21

2.11.2 Symptoms
Severely infected plants turn yellow on lower leaves then wilt and die. Minimal
infection leads to brown necrotic lesions at or below the soil surface (Fig. 22). This
may also originate from infected seed root and extend up the stem. Lower portion of
the stem rots and the root system disintegrates. Infected parts develop black
pycnidia. Decay of storage roots begins at the proximal end leading to firm, dry,
dark brown necrosis that covers a large portion of the root. Peeling the periderm
reveals pycnidia of the pathogen (Fig. 23).
Fig. 22 Brown to black
necrotic lesions at the base of
sweetpotato plants infected
with Foot rot. (Photo credit:
C. Lopes)
Fig. 23 Black pycnidia on a
storage root infected with the
foot rot fungus, Plenodomus
destruens. (Photo credit: W. J.
Martin)
22 K. Ogero and R. van der Vlugt

2.11.3 Biology and Epidemiology
Foot rot of sweetpotato is caused by the fungus Plenodomus destruens. The fungus is
closely related to and can be easily confused with Phomopsis phaseoli. Plenodomus
destruens survives on plant debris but does not persist for very long in the soil. The
infection is simultaneous with the vegetative cycle of sweetpotato. Healthy but
wounded roots in storage can pick up the infection from conidia surviving on the
surfaces of infected roots. The conidia can also survive on sprouts of bedded infected
roots. Use of infected planting material is one of the major modes of transmission. In
Brazil, foot rot has been reported to be caused by the fungus Diaporthe kongii
(Almeida et al. 2020).
2.11.4 Management
•Use of healthy planting material
•Two-year crop rotation
•Treating seed roots with a fungicide, for example, Thiabendazole
•Some genotypes in Brazil, for example, Princesa have been shown to be resistant
2.12 Circular Spot (Sclerotium rolfsii)
2.12.1 Geographic Occurrence and Impact
Circular spot is present worldwide and has a wide host range. It does not cause
serious losses but can sometimes cause significant losses in the USA.
2.12.2 Symptoms
Infected roots develop round lesions that have clearly defined margins (Fig. 24). The
diameter of the lesions varies with varieties. Common commercial varieties in the
USA develop lesions measuring 1–2 cm in diameter. The lesions are mostly shallow
(1–5 mm) and are restricted to the vascular cambium. However, highly susceptible
varieties may develop extensive rots. Serious decaying can also be caused by
Fig. 24 Circular spot lesions
on a storage root infected with
Sclerotium rolfsii. (Photo
credit: W. J. Martin, APS)
Diseases of Sweetpotato 23

flooding late in the season. The lesions are brown with slightly darker margins. The
tissue within the lesion is yellowish brown to brown, soft, and wet at harvest. It
changes to dark brown, sunken, and leathery as it dries out in storage. Cracks may
develop at the center. Infected roots develop a bitter taste.
The lesion dries out after a few days in storage making isolation of the pathogen
difficult. Peeling off the dried lesion exposes a healed wound surface. Exposing
storage roots to moist and warm conditions at harvest makes the fungus to spread,
leading to enlargement of the lesions and formation of large fans of coarse, white
mycelia. The mycelia may cover the surfaces of surrounding roots.
The circular spot lesions can be confused with lesions caused by Streptomyces
ipomoeae, which causes Streptomyces soil rot (pox). However, in circular spot:
•Roots are rarely indented or constricted where the lesions form.
•Necrotic lesion is at first soft, moist, and yellowish brown. On the other hand,
Streptomyces soil rot lesions are black and corky.
•Lesions do not form the healed appearance associated with soil rot lesions.
•Affected tissue is bitter in taste, whereas that affected by soil rot has an earthy
flavor.
2.12.3 Biology and Epidemiology
Circular spot is caused by Sclerotium rolfsii. The fungus also causes Sclerotial blight
(also known as southern blight, southern stem rot, and bed rot). However, in circular
spot, signs of S. rolfsii are rarely seen in association with the lesions. In Sclerotial
blight, hyphae and sclerotia of the fungus are usually prominent. The two diseases
have not been shown to occur simultaneously in the field.
The fungus can survive in the soil for many years. Infection is aided by moisture
and organic matter in the soil. Sclerotium rolfsii is a saprophytic fungus that kills the
plant tissue in advance. It produces pectolytic enzymes and cellulase, which
degrades the tissue. The cell walls and middle lamellae are destroyed to facilitate
infection. The fungus also produces high amounts of oxalic acid. Disease develop-
ment is optimum at 28–30 C and high humidity. Spread is through mycelia growing
on the soil surface, mycelial fragments, and sclerotia, in surface water, or mechan-
ically. Incidence and severity vary from field to field and year to year. Infection
occurs at later stages of crop development.
2.12.4 Management
•Avoid fields with a known history of S. rolfsii
•Early harvesting since the disease occurs late in the season
•Crop rotation
•Use of soil amendments to stimulate growth of antagonistic microorganisms
24 K. Ogero and R. van der Vlugt

2.13 Sclerotial Blight (Sclerotium rolfsii)
2.13.1 Geographic Occurrence and Impact
Sclerotial blight (also known as southern blight, southern stem rot, and bed rot)
occurs exclusively in seed beds and is therefore a problem only in temperate and
subtropical regions where it can cause serious damage. It is not common in cooler
latitudes of temperate regions. In the field, the disease is present at any stage of
growth affecting several plants that girdle and die, leading to 5–20% losses.
2.13.2 Symptoms
The disease develops mostly after sprouts from seed roots have emerged from the
soil. Infected plants start to wilt and eventually die (Fig. 25). Infected plants have
necrotic bases and break off easily if pulled from the soil. At the onset of symptoms,
white mycelia grow on the soil surface and sometimes on the plants if the canopy is
dense. Numerous sclerotia are formed on the mycelia. These are initially white
masses of hyphae which later turn brown taking an appearance of a mustard seed
(Fig. 26).
Fig. 25 Symptoms of sclerotial blight on infected sweetpotato plants. Wilting and death of
seedlings (a), mycelia on the collar region of plants (b), aerial mycelia, mycelial mat along with
sclerotia observed on rootzone soil (cand d) (Paul et al. 2017)
Diseases of Sweetpotato 25

2.13.3 Biology and Epidemiology
The fungus infects plants near the soil surface and spreads over the whole plant. It
produces sclerotia, which survive on plant debris and overwinters for a long time
infecting the next crop or those nearby (Paul et al. 2017). Sclerotium rolfsii has a
wide host range including many monocots and dicots and can survive in the soil
without a host as sclerotia for many years. The fungus can be spread by mycelia
growing on soil surfaces, movement of infested soil, and mechanically.
Disease development is best at high relative humidity and temperature
(28–30 C). The saprophytic fungus kills plant tissue in advance before infection
by producing pectolytic enzymes and cellulase. It also produces high amounts of
oxalic acid. Transplanting plants with sclerotial blight to the field stops disease
development.
2.13.4 Management
•Deep plowing. The sclerotia do not survive when buried 8 inches or deeper.
•Crop rotation with nonhost crops. Use bed sites that have not been planted with
sweetpotato for at least 3 years.
•Use of soil amendments to stimulate multiplication of antagonistic
microorganisms.
•Treating seed roots with a fungicide such as dicloran before bedding.
•Use pathogen-free planting material.
•Less susceptible varieties are available in the USA, for example, Beauregard.
Fig. 26 Sclerotia of S. rolfsii
on the soil surface and bases
of infected plants. (Photo
credit: M. Stahr and
L. Quesada)
26 K. Ogero and R. van der Vlugt

•Bed covers should be removed as soon as sprouts emerge from seed roots buried
in the soil. This avoids injuries caused by excess heat. Damaged foliage can serve
as a source of nutrients and stimulatory volatiles for growth of S. rolfsii.
2.14 Charcoal Rot (Macrophomina phaseolina)
2.14.1 Geographic Occurrence and Impact
Charcoal rot is widespread in tropical and subtropical regions. It causes minimal
losses on stored sweetpotato roots.
2.14.2 Symptoms
Charcoal rot symptoms develop during storage beginning as firm, moist rot that is
reddish brown to brown. This is initially restricted to the cortex. Eventually the
fungus crosses the vascular cambium causing rotting of the pith. Infected tissue has
two distinct zones:
a) Outer zone that is black due to the presence of mature sclerotia (Fig. 27)
b) Inner decaying zone with reddish brown tissue
Fig. 27 Proximal end of a
sweetpotato root infected with
charcoal rot. (Photo credit:
Alan Henn, Mississippi State
University, Bugwood.org)
Diseases of Sweetpotato 27

The disease affects the whole root that dries, hardens, and eventually mummifies.
The periderm remains intact over the decayed root. Lesions that develop from the
ends may become restricted (Fig. 28).
2.14.3 Biology and Epidemiology
Charcoal rot is caused by the fungus Macrophomina phaseolina. This is a sapro-
phytic fungus that survives in the soil for many years as free sclerotia. It also survives
on plant debris. It has a wide host range including crops grown in rotation with
sweetpotato such as soybean, sorghum, cotton, and corn. It may occur as an
endophyte in crops such as soybean. Disease development is optimum at
29–31 C. It is more common in very warm storage facilities and crates located
next to heaters. Scalding of harvested roots by sunlight also increases infection.
2.14.4 Management
•Avoiding heat stress during storage
•Store roots at 15–16 C
•Use clean storage facilities and packing equipment
2.15 Geotrichum Sour Rot (Geotrichum candidum)
2.15.1 Geographic Occurrence and Impact
This is a common disease worldwide and can lead to significant postharvest losses
when the root temperature is high, and air-exchange is low. Flooding of fields close
to harvesting can also lead to significant losses.
Fig. 28 Restricted rot on one
end of a sweetpotato root
infected with charcoal rot.
(Photo credit: Alan Henn,
Mississippi State University,
Bugwood.org)
28 K. Ogero and R. van der Vlugt

2.15.2 Symptoms
Geotrichum sour rot is associated with various symptoms that are highly dependent
on availability of favorable conditions. The most common symptom is a wet, soft rot
of the storage root that has a distinct fruity, alcohol, or sour odor (Fig. 29).
Removal of favorable conditions leads to collapse of the affected areas (Fig. 30).
The collapsed tissue becomes firm overtime. Collapsed tissue usually has irregular
margins and the lesions vary in size and shape. Sunken, circular lesions measuring
15–20 mm in diameter have been reported in the USA (Holmes and Clark 2002).
Removal of favorable conditions also stops the decay and leads to formation of
abscission zones around the lesions.
Tufts of white mycelia may develop on the surface of the root (Fig. 31).
Fig. 29 A wet, soft rot on a
sweetpotato root infected with
Geotrichum candidum. (Photo
credit: L. Quesada)
Fig. 30 Shallow collapse of
the cortical tissue of a root
infected with Geotrichum sour
rot. (Photo credit: Gerald
Holmes, Strawberry Center,
Cal Poly San Luis Obispo,
Bugwood.org)
Diseases of Sweetpotato 29

2.15.3 Biology and Epidemiology
Geotrichum sour rot is caused by Geotrichum candidum. The fungus is soilborne
and is spread by wind and water. Geotrichum candidum is restricted to places with
high water availability and can grow at very low oxygen levels but not anaerobically.
Sweetpotato is exposed to the fungus at all stages (from the field to the market), but
the disease rarely develops. Disease development is favored by high moisture, high
temperature, and low oxygen. Decay is rapid above 20 C and limited below 5 C.
2.15.4 Management
•Plant sweetpotato on fields that have good drainage
•Ensure there is adequate ventilation in storage facilities
•Minimize injuries
•Cure roots soon after harvest
•Avoid harvesting during wet conditions
•Store roots when they are dry
2.16 Dry Rot (Diaporthe phaseolorum)
2.16.1 Geographic Occurrence and Impact
Dry rot is a minor storage disease and has been reported in the USA and Republic of
Korea.
2.16.2 Symptoms
The decay is usually limited to one end of the root (Fig. 32). It advances from the end
causing the root to shrink and wrinkle (Lee et al. 2016). Decayed tissue is firm and
dry and eventually becomes mummified. The disease causes a lesion that is light to
dark brown on the outside and dark brown to black on the inside. As the diseases
progresses, pycnidia break through the periderm and can be seen as minute, black,
raised bodies on the surface.
Fig. 31 White mycelia on the
surface of a sweetpotato root
infected with Geotrichum
candidum. (Photo credit:
Gerald Holmes, Strawberry
Center, Cal Poly San Luis
Obispo, Bugwood.org)
30 K. Ogero and R. van der Vlugt

2.16.3 Biology and Epidemiology
Dry rot is caused by Diaporthe phaseolorum. The pathogen is found in seed beds, in
the field, and to a lesser extent in storage. It requires a wound for infection. Infection
of plants in seed beds is optimum at 30 C. Several weeds including Ipomoea spp.
serve as alternate hosts. Use of infected roots as planting material transfers the
infection to the sprouts. These form a reddish-brown to black decay (like that of
Ceratocystis fimbriata) at the base.
2.16.4 Management
The disease does not cause sufficient losses to warrant control. However, where
needed, control measures include:
•Avoid injuring roots during harvesting and postharvest handling
•Cure roots immediately after harvesting
•Treating seed roots with fungicides
2.17 Mottle Necrosis (Pythium spp.)
2.17.1 Geographic Occurrence and Impact
The disease has been reported to be more important in cooler regions. It has been
reported in the USA and Japan (Tojo et al. 2007). It only causes significant losses in
isolated situations when moisture is excessive.
2.17.2 Symptoms
A marbled decay develops on infected roots when soil temperature is 18–20 C
(Fig. 33).
Skins of infected roots have finger-shaped slightly sunken brown spots (Fig. 34).
These may vary in size from small and circular to large spots that coalesce into an
irregular outline. The size of the surface lesions is often not related to the extent of
internal decay. Small lesions may be associated with extensive internal decay and
vice versa.
At temperatures below 18 C, infected roots develop a cheesy type of mottle
necrosis that may be confused with bacterial soft rot or Rhizopus soft rot. The roots
have large, continuous lesions unlike the labyrinthine lesions common with the
Fig. 32 A sweetpotato root
infected with dry rot decayed
on one end. (Photo credit:
C. Averre, K. Sorensen, L. G.
Wilson, and N. Leidy)
Diseases of Sweetpotato 31

marbled type of the disease. Infected root has the same or slightly grayer flesh color
as healthy roots. In addition, affected root has the consistency of soft cheese.
Mottle necrosis has a third type, the band type, which is indistinguishable from
the ring rot caused by Rhizopus spp. Lesions of the band type are not sunken like
those of the marbled and cheesy types but are shallow and restricted to the cortex by
the vascular ring. The lesions are more lateral than longitudinal from their point of
origin forming band/ring-like appearance. Tissue of affected root is firm and choc-
olate brown.
Infected tissue contains abundant and distinctive mycelia of the pathogen. How-
ever, the infected tissue does not often have sporangia and oogonia. The disease may
also affect the adventitious root system, leading to a rot that cannot be differentiated
from other root rots such as those caused by Rhizoctonia solani and Streptomyces
ipomoeae. The decay on adventitious roots advances several centimeters from the
ends. Infected roots are light brown to dark black with sloughed cortex.
Fig. 33 Marbled decay on
storage roots infected with
mottle necrosis. (Photo credit:
Gerald Holmes, Strawberry
Center, Cal Poly San Luis
Obispo, Bugwood.org)
Fig. 34 Finger-shaped
sunken spot on a storage root
infected with mottle necrosis,
caused by Pythium spp.
(Photo credit: F. Francesco)
32 K. Ogero and R. van der Vlugt

2.17.3 Biology and Epidemiology
Mottle necrosis is caused by various species of Pythium. Pythium ultimum and
P. scleroteichum are the main ones. Pythium spinosum has been reported to cause
the disease in Japan; P. aphanidermatum from other plants has caused the disease in
artificially inoculated sweetpotato. Pythium ultimum is the most frequently associ-
ated with adventitious root rot. It is the most isolated pathogen and causes damping-
off, root rot, and soft rot on several plant species. Pythium scleroteichum is only
found in nature in sweetpotato with mottle necrosis and in adventitious roots
associated with infected storage roots.
Pythium spp. are omnipresent in the soil and associated adventitious root rot often
begins in seed beds and continues in the field. It is assumed that the pathogen spreads
from adventitious roots into storage roots. This is because lesions of the disease are
usually centered at points where adventitious roots originate from storage roots.
Hyphae rapidly ramify, both inter- and intracellularly, within the tissue of infected
storage roots. Cells become filled with hyphae and cell walls are penetrated at right
angles following the formation of appressoria and narrowly constricted
penetration pegs.
Mottle necrosis is prevalent in fields with intermediate soil texture than those with
fine or coarse soils. Adventitious root rot is more common in plant beds with sandy
and wet soil on which sweetpotato has been grown frequently. The disease is most
destructive late in the season especially after a cool, rainy period. Optimal temper-
ature for growth of the pathogens in culture is 25–32 C. However, successful
inoculation of storage roots is often at 12–15 C. In Japan, the disease has been
reported to develop on most cultivars at 15 C and only some at 25 C. The marbled
type of the disease occurs at 18–22 C, whereas the cheesy type occurs below
18–22 C. Disease development does not happen at the common curing tempera-
tures. In addition, it does not develop after harvest. Storage roots contract the disease
while in the field, but damage does not continue in storage.
2.17.4 Management
The disease is not common in commercial production of sweetpotato and manage-
ment is rare. The disease is however best managed by avoiding infection, for
example, through:
•Avoiding harvesting storage roots during cool, wet conditions
•Crop rotation
Use of less susceptible varieties can also reduce disease incidence. The extent of
development of mottle necrosis and adventitious root rot in the field differ by
cultivar. Cultivars with high dry matter and white flesh appear particularly suscep-
tible. It can therefore be a disease of interest in Africa where white-fleshed varieties
dominate.
Diseases of Sweetpotato 33

2.18 Scurf (Monilochaetes infuscans)
2.18.1 Geographic Occurrence and Impact
Scurf (previously known as soil stain) has been reported in the USA, Italy, and many
Pacific islands including Papua New Guinea and Japan. Damage is mostly cosmetic.
However, when severe, it can make storage roots shrink due to increased water loss
during prolonged storage.
2.18.2 Symptoms
Scurf symptoms are restricted to the surface of storage roots (Fig. 35). Storage roots
develop dark brown to black spots on the surface. In most cases, only a few scattered
lesions are formed on the root (Fig. 36). However, in severe cases, the spots enlarge
and coalesce covering almost the entire root (Fig. 37). Severely infected roots may
also form small cracks while shrinking in storage. The color of the lesion depends on
Fig. 35 Scurf lesions are
restricted to the root surface
and do not extend into the
flesh. (Photo credit:
S. Meyers)
Fig. 36 Scattered lesions
commonly formed on storage
roots infected with scurf.
(Photo credit: Gerald Holmes,
Strawberry Center, Cal Poly
San Luis Obispo, Bugwood.
org)
34 K. Ogero and R. van der Vlugt

the skin color with copper-skinned cultivars having brown lesions and red ones
having almost black lesions.
The disease is difficult to distinguish from boron deficiency, which usually has
raised lesions and develops in storage. Use of infected seed roots spreads scurf to
sprouts causing superficial discoloration on the stems. Transplanting infected slips
(vines) spreads the pathogen to daughter roots (Fig. 38). Lesions are therefore more
common on proximal ends of storage roots. Conidial chains of the fungus can be
observed on the surface with the aid of a hand lens or microscope (Fig. 39). This is
the main diagnostic feature of the pathogen.
2.18.3 Biology and Epidemiology
Scurf is caused by the fungus Monilochaetes infuscans, which only attacks under-
ground portions of the crop in the field. Depending on soil type, the pathogen can
Fig. 37 A storage root with a
severe case of scurf. The
lesions have coalesced to
cover a half of the root
surface. (Photo credit:
S. Butler)
Fig. 38 A hill of sweetpotato
storage roots showing spread
of scurf infection from
infected vine to the proximal
end of daughter roots. (Photo
credit: F. Francesco)
Diseases of Sweetpotato 35

survive in the soil for 1–3 years. Survival is higher in fine-textured soils and is
favored by higher organic matter content. Use of animal manure as is common in
sub-Saharan Africa may increase the disease incidence. The fungus has a narrow
host range, which is restricted to Ipomoea spp.
The disease is favored by high humidity and optimum temperature of 24 C.
Additionally, disease development is best when soil moisture is neither excessive nor
limiting for plant growth. The disease is often worse during rainy seasons. Scurf only
invades the skin (periderm) of storage roots and lesions continue to enlarge in
storage. Moisture during storage may lead to new lesions and root-to-root spread.
Primary transmission of M. infuscans occurs when infested soil comes into direct
contact with storage roots. Spread can also occur when infected planting material is
used, healthy roots and infected roots mixed, and contaminated equipment and storage
facilities are used. Spores dislodged from roots during postharvest handling can be
distributed by air leading to contamination of equipment and packing containers.
2.18.4 Management
•Use disease-free planting material. If using storage roots as seed, carefully select
those without scurf symptoms. Treat the seed roots with a fungicide before
bedding. Thiabendazole and dicloran have been shown to be effective. However,
the pathogen has been reported to be resistant to benomyl. If using vine cuttings
or cut sprouts, make sure to source from healthy plants and cut at least 2 cm above
the soil surface. Do not pull sprouts from the soil.
•Locate seed beds in areas that have been free from sweetpotato for at least 3 years.
•Crop rotation (2–3 years in light soil e.g., sandy loam; 3–4 years in heavier soils
or those rich in organic matter).
•Use clean equipment and storage facilities.
•Disinfect equipment and storage facilities before use.
•Avoid mixing diseased roots with healthy ones during storage.
Fig. 39 Microscopic view of
the surface of infected root
showing conidial chains of the
scurf causing fungus,
Monilochaetes infuscans.
(Photo credit: S. Butler)
36 K. Ogero and R. van der Vlugt

2.19 Violet Root Rot (Helicobasidium mompa)
2.19.1 Geographic Occurrence and Impact
The disease has been reported in Southeast Asia countries including China, India,
Japan, Korea, and Taiwan (Uetake et al. 2003). Serious losses can occur under
conditions favorable for disease development.
2.19.2 Symptoms
Decay of fibrous roots beginning at the tips eventually destroys the entire root
system. Storage roots decay from the distal to the proximal end (Figs. 40 and 41).
Foliage becomes chlorotic and older leaves may senesce and fall off prematurely.
Infected roots are covered by purplish brown to violet mycelial mat, hence the name
“violet root rot.”Sclerotia are formed on the base of the stem near the soil surface.
Fig. 40 Sweetpotato root that
has rotten following infection
with violet root rot. (Drawing
credit: Hua and Zhou)
Fig. 41 Distal to proximal
end decay of a carrot infected
with violet root rot. (Photo
credit: L. du Toit)
Diseases of Sweetpotato 37

Purplish-brown mycelial mats may develop on the soil surface surrounding the
infected plant. Decaying roots emit an alcohol odor.
2.19.3 Biology and Epidemiology
Violet root rot is caused by the fungus Helicobasidium mompa (Nakamura et al.
2004).It is soilborne and can survive there for at least 4 years. Spread is mainly
through movement of infested soil but also by infested manure and infested irriga-
tion water. The fungus is found outside the sweetpotato in the early part of the season
and forms infection cushions in the middle lamella of the periderm. Later, hyphae
penetrate from the infection cushions into the parenchyma causing root decay. The
fungus also produces pectolytic enzymes. Disease development is best during wet
seasons when there is high moisture late in the season. The fungal basidiospores
grow at 17–35 C and mycelia at 8–35 C. Both processes occur optimally at 27 C.
Poor soil drainage, nutrient deficiencies, low soil pH, and continuous cultivation of
sweetpotato also favors the disease.
2.19.4 Management
•Rotation with cereals for more than 3 years.
•Soil fertility management to increase soil fertility and improve soil structure.
Lime amendments may be used to reduce soil acidity.
•Use early maturing cultivars.
•Field sanitation.
•Early harvesting.
2.20 Other Minor Fungal Diseases
The following fungal diseases have also been reported on sweetpotato but are not
economically important (Table 1).
3 Bacterial and Phytoplasma Diseases
3.1 Bacterial Wilt (Ralstonia solanacearum)
3.1.1 Geographic Occurrence and Impact
Bacterial wilt has been reported in China and can cause 30–80% yield decline (Chen
et al. 2012). Sometimes infected plants fail to develop roots and die soon after
transplanting.
3.1.2 Symptoms
Symptoms include wilting, stunting, root and stem rot, defoliation, and vascular
discoloration (Fig. 42). Infection starts at the base of the plant. The base of the stem
becomes water soaked then turns yellow and finally turns dark brown. Vascular
discoloration also appears in storage roots. Internally, longitudinal yellowish-brown
38 K. Ogero and R. van der Vlugt

Table 1 Minor fungal diseases of sweetpotato
Disease Causal fungus
Part of plant
affected Symptoms
Punky rot Trichoderma koningii Storage root Circular, light brown, and
wrinkled lesions. Flesh is
firm, moist, and brown at
the center of the lesion.
White mycelia and masses
of green spores on the
surface
Blue mold rot Penicillium spp. Storage root Firm, dry to slightly moist,
and brown tissue. White
mycelia on root surface that
eventually get covered with
masses of blue to bluish-
green spores
Alternaria rot Alternaria spp. Storage root Moist, firm rot. Infected
tissue turns light brown
then darker brown
Gray mold rot Botrytis cinerea Storage root Infected tissue turns gray
and is soft with a watery
consistency and a starchy
odor
Sclerotinia rot Sclerotinia sclerotiorum Stems, crowns,
and storage
roots in the
field
Water-soaked pink to
brown lesions. White
cottony mycelia on the
surface. Black sclerotia are
produced later. Wilting of
leaves and rotting of stems
Phymatotrichum
root rot
Phymatotrichopsis
omnivora
Storage root Firm and dry decay that is
initially restricted to the
surface. The surface is dark
brown to black initially,
later mycelia appear as
white protuberances and
brown- to buff-colored
strands
Fusarium
adventitious root
rot
Fusarium solani and
Fusarium javanicum
Mostly
adventitious
roots;
sometimes
storage roots
Storage roots are small and
cracked with long brown to
black lesions. Extensive
damage of adventitious
roots leads to stunting, leaf
abscission, premature
flowering, yield reduction,
and plant death
Septoria leaf spot Septoria bataticola Leaves Small, chalky white lesions
with dark brown borders
White rust (leaf
mold or blister rust
Albugo ipomoeae-
panduratae
Leaves,
petioles and
stems
Chlorotic lesions on upper
leaf surfaces (may become
necrotic in some
sweetpotato varieties).
(continued)
Diseases of Sweetpotato 39

streaks occur, whereas the root surface may develop grayish-brown water-soaked
lesions depending on severity.
3.1.3 Biology and Epidemiology
Bacterial wilt of sweetpotato is caused by Ralstonia solanacearum (formerly Pseu-
domonas solanacearum). The pathogen is soilborne and can be carried in planting
Table 1 (continued)
Disease Causal fungus
Part of plant
affected Symptoms
Galls on petioles and stems
leading to distortion. Lower
leaf surface contains
pustules which turn white
as they break open
releasing sporangia
Rhizoctonia stem
canker
(Rhizoctonia rot or
Rhizoctonia sprout
rot)
Rhizoctonia solani Stems and
leaves
Foliar yellowing, stunting,
and death of sprouts due to
rotting of underground
parts. Sunken cankers on
the stem, near the soil
surface
Slime molds Common species
include Fuligo
violacea, Physarum
plumbeum and
Stemonitis spp.
Surfaces of
stems, leaves,
and sometimes
storage roots
Large masses of brown
spores. Jellylike, slimy
coating on plant surfaces
which can vary from white
to yellow to purple
depending on the species
involved
Fig. 42 Wilting of leaves and
stem and vascular
discoloration in sweetpotato
plants infected with bacterial
wilt. (Photo credit: T. Ames)
40 K. Ogero and R. van der Vlugt

material. The bacterium can persist in the soil for up to 3 years and can be spread
through irrigation water or rain run-off. It can enter healthy plants through wounds
especially during transplanting or weeding. The disease develops best at a relative
humidity greater than 85% and temperatures of 20–40 C. Optimum temperature is
27–35 C. High soil acidity also favors disease development. Year-round cultivation
of sweetpotato and poorly drained clay loam soils favor disease development.
3.1.4 Management
Control of the disease is through the use of resistant cultivars, field sanitation, use of
disease-free planting material, rotating with a flooded crop (e.g., rice) or a nonhost
crop, and avoidance by planting the crop during cooler months.
3.2 Bacterial Stem and Root Rot (Dickeya dadantii)
3.2.1 Geographic Occurrence and Impact
The disease has been reported in China and the USA but may have a wider
geographic distribution. Losses associated with this disease can be economically
important.
3.2.2 Symptoms
Leaves of infected plants start to turn yellow and a black, water-soaked rot occurs on
the bottom of the stems gradually extending to the top (Fig. 43a). Eventually, the
entire plant collapses and dies. Storage roots develop a soft rot which progresses
during storage (Fig. 43b). It can also be important when storage roots are bedded for
vine production. The rot causes a rapid softening of the tissue without affecting its
color. The rotting is mostly inside the root with little evidence of decaying on the
outside.
3.2.3 Biology and Epidemiology
Bacterial stem and root rot is caused by the bacterium Dickeya dadantii formerly
known as Pectobacterium chrysanthemi and Erwinia chrysanthemi. It is widespread
in warm and humid regions. It infects the host through wounds and is not known to
survive in soil unless with crop debris or weed hosts. It is spread mainly through
infected planting material. It can also be transmitted through contaminated irrigation
water and harvesting equipment. Disease development occurs best at temperatures
above 30 
.
C. Low levels of oxygen also favor disease development. The disease is
dormant in well-aerated soils or at temperatures below 27 
.
C.
3.2.4 Management
Less susceptible varieties should be used and wounding at all stages of crop
production should be avoided. In addition, vine cuttings to be used as planting
material should be cut above the soil surface. These should only come from
disease-free plants.
Diseases of Sweetpotato 41

3.3 Streptomyces Soil Rot (Pox) (Streptomyces ipomoeae)
3.3.1 Geographic Occurrence and Impact
Streptomyces soil rot has been reported in the United States of America and Japan
but may also occur elsewhere. It reduces both yield and quality of storage roots
produced.
3.3.2 Symptoms
Symptoms include necrotic lesions on storage roots (Fig. 44a). These can be circular
or irregular, less than 5 mm deep, and with a diameter of less than 3 cm. Constriction
near the point of infection may give the root a dumbbell shape (Fig. 44b). The
disease can also cause black, necrotic decay on adventitious roots. Severe rotting of
the adventitious roots may lead to stunting of vines, chlorosis, and bronzing of
foliage, wilting, and premature flowering.
3.3.3 Biology and Epidemiology
Streptomyces soil rot is caused by Streptomyces ipomoeae which is soilborne and
can persist in the soil as spores for many years even without a sweetpotato crop.
Disease development is favored by dry alkaline soils (pH above 5.2). The pathogen
also infects other members of the morning glory family. Transmission of
S. ipomoeae is through movement of soil, infected/infested planting material, and
Fig. 43 Black stems (a) and rotting of storage root from the inside (b) following infection with
Dickeya dadantii. (Photo credit: (a) V. Duarte and (b) C. A. Clark)
42 K. Ogero and R. van der Vlugt

digestive tracts of livestock when fed with infected storage roots. Infection of fibrous
roots is through direct penetration without the formation of any specialized penetra-
tion structures. Primary overwintering structure is thought to be spiral chains of
spores.
3.3.4 Management
The best way of controlling the disease is through use of resistant varieties and
several of them have been released in the USA and Japan. Other control measures
include: maintaining a low soil pH, for example, by applying sulfur, fumigation of
soil, timely irrigation to ensure the soil is always moist, and rotation with other crops
to reduce severity. In addition, planting material should be sourced from areas where
the disease is absent.
3.4 Sweetpotato Little Leaf (Candidatus Phytoplasma
aurantifolia)
3.4.1 Geographic Occurrence and Impact
Sweetpotato little leaf disease also referred to as witches’-broom has been reported in
China, Japan, Korea, Papua New Guinea, Taiwan, the Solomon Islands, Niue, Palau,
Malaysia, Indonesia, New Caledonia, and Vanuatu. No report of the disease has been
made outside the Pacific islands and Southeast Asia; 50% yield losses have been
reported.
3.4.2 Symptoms
Disease manifestation starts with vein clearing. This is followed by distinctly smaller
and chlorotic leaves. There is a proliferation of axillary shoots, leading to a bushy
appearance (Fig. 45). Leaves may roll upwards near the margins. Roots and stems
lack latex. Stunting and branching of the root system may also occur.
Fig. 44 Necrotic lesions (a) and a dumbbell-shaped constriction (b) on sweetpotato storage roots
infected with Streptomyces ipomoeae. (Photo credit: (a) G. Holmes and (b) C. Averre)
Diseases of Sweetpotato 43

3.4.3 Biology and Epidemiology
Sweetpotato little leaf disease is caused by the phytoplasma “Candidatus Phyto-
plasma aurantifolia”in the peanut witches’-broom group. The pathogen has a wide
host range including other Ipomoea species. Spread is by leafhoppers including
Orosius lotophagorum (Kirkaldy) and Nesophrosyne ryukyuensis Ishihara. Disease
incidence and spread is directly related to vector abundance and movement. Dry
areas that favor leafhopper multiplication are the most affected. The phytoplasma
can also be transmitted through infected planting material. A long incubation period
of 50–186 days increases the chances of spreading the disease through exchange of
planting material.
3.4.4 Management
The disease can be controlled by using disease-free planting material selected from
healthy plants and ensuring proper field sanitation. Infected plants should always be
uprooted from the field. In addition, other morning glories should be removed
whenever spotted.
4 Viral Diseases
4.1 Sweet Potato Chlorotic Stunt Virus (SPCSV)
4.1.1 Geographic Occurrence and Impact
Sweet potato chlorotic stunt virus (SPCSV) is the main yield-limiting virus in
sweetpotato and has been reported in all producing areas except the Pacific (Clark
et al. 2012). Though reported, the virus is very rare in the USA. When occurring
alone, SPCSV can cause 50% or more yield reduction (Ogero et al. 2019). Up to
98% yield losses have been reported when it co-infects with sweet potato feathery
Fig. 45 Bushy appearance
and small leaves on vines of a
sweetpotato crop infected
with little leaf disease. (Photo
credit: H. Tsatsia and
G. Jackson)
44 K. Ogero and R. van der Vlugt

mottle virus, leading to a disease complex known as sweet potato virus disease
(SPVD) (Ndunguru et al. 2009).
4.1.2 Symptoms
Infection of sweetpotato by SPCSV may lead to interveinal chlorosis and interveinal
purpling of older leaves (Fig. 46) (Clark et al. 2013; Loebenstein 2015).
Other symptoms include mild vein yellowing, swollen veins on the lower leaf
surfaces, and some sunken secondary veins on upper leaf surfaces. The symptoms
vary geographically, and severity and type of symptoms depends on the variety.
Some varieties show no symptoms.
4.1.3 Biology and Epidemiology
SPCSV is transmitted in a semipersistent manner by whiteflies of which Bemisia
tabaci (Gennadius) is the most common vector. The whitefly needs several hours of
feeding to acquire or transmit the virus efficiently. Use of infected planting material
leads to perpetuation of the virus within farm systems. SPCSV has a synergistic
effect when it occurs with other viruses. It suppresses host resistance enabling other
viruses to cause more severe symptoms compared to when they occur alone. The
incidence of SPCSV is greatest in tropical countries where sweetpotato is grown
year-round. There are two distantly related strains of SPCSV. The first strain is
known as West African (WA) and occurs worldwide except East Africa. The second
strain is called East African (EA), which is the only strain found in East Africa, and it
is also found in China and Peru (Tairo et al. 2005).
4.1.4 Management
SPCSV and other sweetpotato viruses are mainly controlled by using clean planting
material (tested as virus-free), use of resistant varieties, and employing on-farm
management strategies such as field isolation.
Fig. 46 Interveinal purpling
of older leaves caused by
SPCSV. (Photo credit:
K. Ogero)
Diseases of Sweetpotato 45

4.2 Sweet Potato Feathery Mottle Virus (SPFMV)
4.2.1 Geographic Occurrence and Impact
Sweet potato feathery mottle virus (SPFMV) occurs worldwide. Individually,
SPFMV can cause from negligible to 40% yield loss (Adikini et al. 2016).
4.2.2 Symptoms
SPFMV is mostly asymptomatic. Appearance of symptoms is usually influenced by
cultivar susceptibility, growth stage, level of stress, and strain virulence. If present,
common symptoms include irregular chlorotic spots sometimes bordered by purplish
pigment (Fig. 47).
Some varieties may show chlorosis along midribs and faint to distinct chlorotic
spots with or without purple margins (Ames et al. 1997).
4.2.3 Biology and Epidemiology
SPFMV is a potyvirus transmitted nonpersistently by a wide range of aphids
including Aphis gossypii, Myzus persicae, A. craccivora, and Lipaphis erysimi.
The cotton aphid (A. gossypii Glover) and the green peach aphid (M. persicae
Sulzer) have been reported as the key transmitters (Wosula et al. 2012,2013).
Probing of about 20–30 s is enough to transmit the virus. Extensive sequence
comparisons have shown four key strains of SPFMV: (a) East African (EA) strain,
(b) common (C) strain, (c) russet crack (RC) strain, and (d) ordinary (O) strain. Both
the RC and EA strains cause sweet potato virus disease (SPVD) complex when they
co-infect with SPCSV. Replanting of infected planting material leads to perpetuation
of SPFMV from season to season.
Fig. 47 Chlorotic spots
surrounded by purplish
pigment on a sweetpotato
plant infected with SPFMV.
(Photo credit: K. Ogero)
46 K. Ogero and R. van der Vlugt

4.2.4 Management
Control of SPFMV is through use of clean planting material and good field sanitation
through on-farm management strategies such as rogueing.
4.3 Sweet Potato Virus Disease (SPVD)
4.3.1 Geographic Occurrence and Impact
Sweet potato virus disease (SPVD) has been reported mainly in sub-Saharan Africa
where sweetpotato is grown year-round. It is the most devastating disease of
sweetpotato and can cause up to 98% yield losses. It can also lead to a reduction
of up to 40% of carotenoid content in orange-fleshed varieties.
4.3.2 Symptoms
SPVD leads to severe stunting of infected crops (Fig. 48a). Leaves become distorted
(small, narrow, and/or fan-shaped) (Fig. 48b). Initial symptoms may include vein-
clearing and severe chlorotic spotting.
4.3.3 Biology and Epidemiology
SPVD is caused by a synergistic interaction between SPCSV and SPFMV described
in Sects. 2.1 and 2.2. SPCSV makes sweetpotato more susceptible to SPFMV
through suppression of natural virus-silencing mechanism. SPFMV replication is
often rapid in plants infected with SPCSV. Since SPFMV occurs worldwide and
SPCSV is less widespread, the occurrence and spread of SPCSV is the limiting factor
in SPVD development. Greatest losses from SPVD are usually in tropical countries
where whitefly abundance is high and sweetpotato is cultivated throughout the year.
This ensures persistence of the disease inoculum from one cropping cycle to another.
4.3.4 Management
Three major alternatives exist in managing viruses in sweetpotato: (1) deploying
resistant cultivars, (2) using clean virus-tested planting material, and (3) employing
Fig. 48 Stunting (a) and fan-shaped leaves (b) on sweetpotato plants infected with SPVD. (Photo
credit: K. Ogero)
Diseases of Sweetpotato 47

good on-farm management practices. Whereas landraces and cultivars with high
levels of resistance to SPVD do exist, no immunity to the disease exists, and
depending on the pressure of the different viruses in the environment, all genotypes
can become infected in the field (Gibson and Kreuze 2015). Complementary to the
use of genetic resistance could be the production and use of clean virus-tested
planting material. Although this may work well in countries where sweetpotato is
grown as a cash crop and large-scale farmers can make the investments necessary to
obtain such planting material, it is economically unfeasible for smallholder farmers
producing mostly for subsistence. On-farm management strategies such as rogueing,
proper isolation, and positive selection for clean seed are therefore important
(Thomas-Sharma et al. 2016). In addition, farmers specializing in seed production
can use net protected structures to protect clean seed from virus re-infection (Ogero
et al. 2019).
4.4 Sweet Potato Mild Mottle Virus (SPMMV)
4.4.1 Geographic Occurrence and Impact
Sweet potato mild mottle virus (SPMMV) has been reported in Eastern Africa,
Southern Africa, China, India, Indonesia, New Zealand, Peru, Philippines, and
Papua New Guinea. Effect of SPMMV on yields is unknown.
4.4.2 Symptoms
Sweetpotato plants infected with SPMMV exhibit mottling, leaf distortion, and
systemic vein chlorosis (Fig. 49). Stunting may also occur. The symptoms are not
easily detected in the field.
Fig. 49 Systemic vein chlorosis (a) and mottling (b) on sweetpotato plants infected with SPMMV.
(Photo credit: K. Ogero)
48 K. Ogero and R. van der Vlugt

4.4.3 Biology and Epidemiology
SPMMV is transmitted in a nonpersistent manner by the whiteflyBemisia tabaci
(Gennadius). It belongs to Ipomovirus genus. The virus is also spread through
recycling of infected planting material from one cropping cycle to the next.
4.4.4 Management
Control of SPMMV is the same as that of SPFMV, SPCSV, and SPVD already
described earlier.
4.5 Sweepoviruses
4.5.1 Geographic Occurrence and Impact
Sweepoviruses are sweetpotato-infecting begomoviruses. They are called so because
they are phylogenetically distinct from the new and old world begomoviruses. They
have been reported in the United States of America, Brazil, Kenya, Peru, Italy,
Taiwan, Korea, Argentina, and Japan. Sweepoviruses have been reported to cause
between 10% and 80% yield loss depending on cultivar susceptibility (Kim et al.
2015; Wanjala et al. 2020). This happens even without clear symptom appearance in
the infected plants.
4.5.2 Symptoms
Symptoms include upward curling and vein swelling of young plants. Leaves may
also develop vein chlorosis (Fig. 50). Different Ipomoea species and sweetpotato
genotypes tend to develop either leaf curl or yellow vein, but generally they do not
develop both. Mature plants show few or no symptoms.
Fig. 50 Yellow veins on a
sweetpotato plant infected
with a sweepovirus. (Photo
credit: K. Ogero)
Diseases of Sweetpotato 49

4.5.3 Biology and Epidemiology
Sweepoviruses belong to the family Geminiviridae (genus Begomovirus). Plant to
plant transmission occurs semipersistently via whiteflies (Bemisia tabaci cryptic
species complex). Transmission rates depend on whitefly populations and exposure
time. Just like other sweetpotato viruses, sweepoviruses can be perpetuated from
season to season through recycling of infected planting material.
4.5.4 Management
Control of sweepoviruses is the same as that of the other viruses described earlier.
5 Nematode Diseases
5.1 Root-Knot Nematode (Meloidogyne spp.)
5.1.1 Geographic Occurrence and Impact
The root-knot nematode is the most important nematode affecting sweetpotato and
occurs worldwide where the crop is grown (Karuri et al. 2017). Damage can be
serious, affecting both yield and quality.
5.1.2 Symptoms
The root-knot nematode leads to stunting and yellowing of affected plants. Galls are
formed on the fibrous and storage roots of affected plants (Fig. 51). Egg masses of
the nematode can be seen on the surfaces of the galls. The eggs are initially white but
turn dark brown as they mature. Storage roots of some varieties may crack longitu-
dinally (Fig. 52). Other symptoms include root necrosis and blister-like protuber-
ances from the surface of storage roots.
Fig. 51 Galls on storage roots (left) and fibrous roots (right). (Photo credit: (left) C. Parada and
L. Quesada, (right) H. Collins and L. Quesada, NCSU)
50 K. Ogero and R. van der Vlugt

5.1.3 Biology and Epidemiology
Several species of nematodes of the genus Meloidogyne cause root knot in
sweetpotato. These include Meloidogyne incognita (southern root-knot nematode),
Meloidogyne enterolobii (guava root-knot nematode, synonym Meloidogyne
mayaguensis), Meloidogyne javanica (javanese root-knot nematode), Meloidogyne
hapla (northern root-knot nematode), and Meloidogyne arenaria (peanut root-knot
nematode). However, M. incognita,M. enterolobii, and M. javanica are the main
species causing serious damage to sweetpotato. Meloidogyne enterolobii can break
host resistance to M. incognita. Root-knot nematodes are obligate parasites with
some species having a limited host range, whereas others infect almost all plants.
Meloidogyne incognita reproduces parthenogenetically but can produce males under
stress conditions. It is globally distributed and has a very extensive host range,
making it difficult to control by crop rotation. Meloidogyne javanica does not
complete its life cycle on sweetpotato but can cause serious injury. It also has a
wide range of host plants. It is mainly found in tropical and subtropical regions.
Meloidogyne spp. are soilborne, beginning their life cycle as eggs and juveniles
surviving in the soil. Transmission can occur through infected tissue or infested soil
moved via planting material or equipment. They can also be spread through irrigation
water and flooding. Most juveniles die during winter or in the absence of a host crop.
The egg is therefore the primary survival stage. The parasites also lay their eggs beneath
the surfaces of storage roots therefore enhancing their survival and transmission.
Meloidogyne spp. molt four times as they develop into adults. Eggs develop into
first-stage juveniles which undergo molting within the egg to form second-stage
juveniles. The second-stage juvenile is the only infective stage of the nematode. It
emerges out of the egg and moves through the soil onto the plant roots where it enters
the host through either young fibrous roots, ruptures from fibrous roots emerging from
storage roots, or via cracks along the storage root. The life cycle is between 28 and
35 days depending on temperature. Reproduction is favored by higher temperatures
Fig. 52 Cracking of storage
roots caused by Meloidogyne
incognita. (Photo credit:
H. Collins and L. Quesada)
Diseases of Sweetpotato 51

with temperatures below 18 C limiting growth. The nematodes are best adapted to the
coarse-textured sandy loam soils commonly used for sweetpotato production, and
damage is exacerbated by moderately dry conditions. Damage by the nematodes on
roots reduces uptake of water; hence, providing adequate water can reduce damage.
Fluctuations in soil moisture can also cause cracking on storage roots. To distinguish
the cause of cracking, look for presence or absence of egg masses or sedentary females
embedded in root tissue. Damage caused by root-knot nematodes can increase sus-
ceptibility of the affected crop to fungal and bacterial diseases.
5.1.4 Management
Meloidogyne spp. can be controlled through host resistance, cultural, and chemical
control. Varieties that are resistant to Meloidogyne spp. have been developed in most
countries. High temperatures can however breakdown the resistance. Cultural methods
such as field sanitation reduce the nematode populations. Rotation with maize and
sorghum has been reported as successful. Avoid cutting vines very close to the soil.
Nematicides are widely used in countries where the nematodes can cause a serious
problem. Fumigants such as metam sodium and 1,3-dichloropropene can be applied
by broadcasting or as subsurface treatment prior to planting. Control measures are not
necessary in countries where nematodes are not a big problem to sweetpotato.
5.2 Lesion Nematode (Pratylenchus spp.)
5.2.1 Geographic Occurrence and Impact
The lesion nematode is widespread globally, but serious losses of up to 30% have
only been reported in Japan.
5.2.2 Symptoms
Affected plants become stunted due to extensive damage on the root system. Being a
migratory endoparasite, the nematode moves through the plant’s roots causing small
necrotic lesions while and feeds. Storage roots develop blackish brown lesions,
which are often invaded by saprophytic fungi and bacteria leading to further decay
(Fig. 53).
5.2.3 Biology and Epidemiology
Pratylenchus brachyurus Godfrey is the most common species of the lesion nema-
tode in the USA where it causes minor losses. Pratylenchus coffeae is the principal
species in Japan and has been associated with significant losses. Lesion nematodes
are migratory endoparasites that move through the roots leaving once the lesion they
form is parasitized by secondary organisms, for example, fungi and bacteria. Juve-
niles and adults enter the roots and move intercellularly and intracellularly through
the cortex. Eggs are deposited either singly or in groups within the root. Reproduc-
tion in Pratylenchus is temperature dependent and the average life cycle is about
35–42 days. However, this varies with species. Pratylenchus penetrans takes
52 K. Ogero and R. van der Vlugt

30–86 days, while P. coffeae in sweetpotato takes 30–40 days at 25–30 Cto
50–60 days at 20 C.
5.2.4 Management
Use of organic amendments such as manure leads to an increase in the nematode’s
natural enemies, therefore reducing its population. A wide host range limits effec-
tiveness of crop rotation. The nematode can infest maize, wheat, soybean, and
potato. Suitable rotation crops include French marigold, showy rattlebox, sun
hemp, and peanut. Several cultivars with some levels of resistance to P. coffeae
have been developed in Japan. Chemical control via nematicides can also work.
Shoot-tip culture has been shown to restore infected plants to original quality and
yield in China.
5.3 Reniform Nematode (Rotylenchulus spp.)
5.3.1 Geographic Occurrence and Impact
The reniform nematode is common in tropical and subtropical regions. It has been
reported in Africa, Caribbean islands, China, India, Japan, Philippines, USA, and in
many islands in the Pacific. The nematode infection reduces quality and yield of
storage roots. Yield reduction ranges from 44% to 60% depending on the initial
population.
5.3.2 Symptoms
The symptoms are not very clear and can be confused with those caused by other
nematodes. Common symptoms may include stunting of infected plants because of
damage on fibrous roots (Fig. 54). The foliage may become yellow and wilt
eventually.
Fig. 53 Necrotic lesions on
storage roots. (Photo credit:
H. Kawagoe and
H. Nakasono)
Diseases of Sweetpotato 53

Storage roots may be distorted in shape, cracked, reduced in size, and delayed in
development. The cracks are usually caused by early infection and they enlarge as
the roots grow. The cracks, however, appear healed at maturity, because the juveniles
and adult females do not inhabit them (Fig. 55).
5.3.3 Biology and Epidemiology
The most important reniform nematode to sweetpotato is Rotylenchulus reniformis.
It is an obligate sedentary endoparasite with a wide host range. Another species,
R. borealis, is found only in Africa and Europe and has a limited host range.
Rotylenchulus variabilis has been reported in Kenya.
Rotylenchulus reniformis is a well-adapted soilborne pathogen and can survive in
air-dried soil kept at 20–25 C for up to 7 months. It can survive in soil as eggs,
Fig. 54 Death of fibrous
roots following infection with
the reniform nematode. (Photo
credit: C. de la Cruz)
Fig. 55 Cracks on storage
roots infected with the
reniform nematode. (Photo
credit: C. A. Clark)
54 K. Ogero and R. van der Vlugt

juveniles, young females, and males. Juveniles are differentiated within the egg and
undergo one molt to develop into the second-stage. The second-stage juvenile
undergoes three additional molts to develop into a young female or male. Adult
stage and egg production occur 16 days after inoculation, whereas life cycle from
egg to eggs takes 18–29 days but may be faster with higher temperatures. Young
females establish feeding sites in the endodermis of the plant. Penetration into the
root is perpendicular to the root’s longitudinal axis with most of the nematode
protruding outside. The posterior of the nematode enlarges as it begins feeding,
developing into a kidney-shaped mature female.
The nematode can inhabit a wide range of soils but prefers fine-textured soils.
Dissemination occurs with soil movement. It quickly spreads once introduced in a
field. Spread can also occur through infested planting material. Optimum tempera-
ture for disease development is 29.5 C. The reniform nematode can withstand
dehydration and undergoes anhydrobiosis to survive for longer periods. It is not
found inside storage roots but can inhabit the soil adhering to them.
5.3.4 Management
Rotation with nonhost crops (maize, sorghum, sugarcane, rice, oat, peanut, and some
varieties of soybean) can help minimize the populations of the nematode. Nemati-
cides can also reduce the populations of the nematode and reduce damage
occasioned on both fibrous and storage roots. Fumigants used to control the nema-
tode include metam sodium, 1,3-dichloropropene, and metam potassium. Non-
fumigant nematicides include ethroprop and oxamyl. Ethoprop is applied on soil
before planting, whereas oxamyl is used to treat planting material. No resistant
cultivar exists, but level of damage can vary.
5.4 Stem Nematode/Brown Ring (Ditylenchus dipsaci,
D. destructor)
5.4.1 Geographic Occurrence and Impact
The stem nematode is mostly problematic in China, but it is distributed worldwide.
Losses of 20–50% have been reported in China (Fan et al. 2015).
5.4.2 Symptoms
Infected storage roots contain brown or black tissue within the flesh (Fig. 56).
Decaying may continue due to secondary infections by opportunistic organisms
such as fungi and bacteria. Minor infections lead to cell shrinkage on storage
roots, and large air gaps (aerenchyma) occur in the tissue due to loss of water. Starch
grains are small and distorted. Severe infections lead to great cell shrinkage and large
air gaps, and starch grains are greatly reduced or absent. The roots are mostly
affected during storage. No symptoms have been observed in the field.
Diseases of Sweetpotato 55

5.4.3 Biology and Epidemiology
Brown ring (stem nematode) disease of sweetpotato is caused by two species of the
stem nematode: Ditylenchus dipsaci and D. destructor. Disease development is best
at temperatures between 22 C and 27 C. Storage of roots at the recommended
temperature of 13–19 C reduces disease progress.
5.4.4 Management
The disease can be minimized by maintaining proper storage temperature, using less
susceptible varieties, and uninfected planting material. There are ongoing efforts to
develop resistant cultivars in China (Fan et al. 2015).
Acknowledgments The authors acknowledge funding provided by the CGIAR Research Program
on Roots, Tubers and Bananas (RTB) and the Bill and Melinda Gates Foundation (BMGF) through
a grant to SweetGAINS project (ID: OPP121332). RTB was financially supported by CGIAR Fund
Donors, including the NWO (www.nwo.nl) Prof. Christopher Clark provided useful review on the
initial draft.
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