D E S I G N E D AN D D E V E L O P E D U N D E R T H E AE G I S O F

NAHEP Component-2 Project “Investments In ICAR Leadership In Agricultural Higher Education”

Division of Computer Applications
ICAR-Indian Agricultural Statistics Research Institute
 Course Details

Course Name Diseases Of Fruit, Plantation And Medicinal And

Aromatic Crops

Lesson 2 Diseases of Banana

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judgement. Statement of fact and opinions expressed are those of the presenter individually and are not the opinion or
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completeness of the information presented.

1
Created by

Name Role University

CHIRAGKUMAR MANSUKHBHAI Junagadh Agricultural University,

Course Reviser
BHALIYA Junagadh

Acharya N.G. Ranga Agricultural

JYOSTHNA MK Course Reviewer
University, Guntur

2
Objectives of the Lecture
1. To study causes, etiology, symptoms, mode of spread and favorable condition of
various pre and post-harvest diseases of banana.
2. To be familiar with different management methods for banana diseases.
 Glossary of terms
1. Fungus: Fungus are eukaryotic or nucleated, spore bearing,
achlorophyllous, unicellular (yeast) or multicellular organism generally
reproduced by sexual or asexual method and whose filamentous,
branched somatic structure is typically covered by cell wall and cell wall
made up of either cellulose (oomycota) or chitin or some other complex
organic carbohydrate.

2. Symptoms: The external and internal reactions or alteration of a plant as

a result of disease.

3. Pathogen: An entity that can cause the disease.

4. Host: A living organism containing or invaded by a parasite, which obtains

its nutrients from the organism. or a plant that supports the growth and
development of the parasite that has infected it.
5. Obligate parasite: A parasite that can grow only on living organisms.
6. Primary inoculum: An inoculum that survives dormant in the winter or
summer and causes the original infections in the spring or in the autumn
is called a primary inoculum.

7. Primary infections: The infections causes by primary inoculum is called

primary infections.

8. Secondary inoculum: An inoculum produced from primary infections is

called a secondary inoculum.

9. Secondary infections: The infections causes by secondary inoculum is

called secondary infections.

10. Epidemiology: The study of the inter relationships between a given

pathogen, the environment and groups or populations of
the relevant hosts.
Introduction
• Banana (Musa sapientum) and plantain (Musa paradisiaca),both
commonly called banana fruit, are one of the most important
commercial fruit and vegetable crops grown all over the world in the
tropical and subtropical areas.

• Banana plantations suffer from many serious diseases such as Fusarium

wilt or Panama disease, Cercospora leaf spot or Sigatoka, Bacterial wilt
or Moko disease, burrowing nematode infestation, Bunchy top (a
nanavirus), anthracnose, and various other post-harvest fruit rots.

• Among this, some major diseases are given below.

 1. Fusarium wilt (Panama wilt)
• The disease was first reported from Australia in 1876 (ploetz,1992). Its
presence was noticed in Hawaii in 1904 and in India in 1911.

• In Jamaica the disease was first noticed in 1911. By 1932, the Fusarium wilt
had spread to almost all the countries that grow banana commercially. The
disease continues to be the most widespread and important problem in the
subtropics (Ploetz,1998).

• In India, the disease is in the southern states of Tamil Nadu, Kerala and
Karnataka but is becoming common in other areas also. Up to 100% incidence
has been reported on A susceptible variety in certain parts of Karnataka.

• The popular variety Gros Michel, mostly grown for export quality fruits, was
most susceptible and had to be replaced with Cavendish bananas which were
resistant, However, with the appearance of race 4 of the pathogen these
bananas are also becoming susceptible in many countries (Stover and
Melo,1972).
1.1 Symptoms (Singh, 2018)
 The conspicuous symptoms of Fusarium will appear on at least 5 months
old banana plants although 2-3 months old plants.
 The earliest signs, mostly inconspicuous, are faint yellow streaks on the
petiole of oldest, lowermost leaf.
 Two types of symptom development follow this stage. In the yellowing
type, there is progressive yellowing of the old leaves and eventual
collapse of the petiole. In the non-yellowing type (as in Gros Michel),the
leaf petioles collapse without chlorosis of the leaf (Stover,1962).
 The pseudostem often shows a more or less conspicuous longitudinal
splitting of the outer leaf sheath.
 The oldest plants in a mat are affected first. The young suckers rarely
develop external symptoms.
 In Fusarium wilt the pathogen does not infect the fruits and does not
cause discolouration of the fruits (Stover,1987). These symptoms
differentiate Fusarium wilt from bacterial wilt in which young suckers
are also affected and fruits are discoloured.
 Discoloured vascular strands varying from light yellow to dark brown are
the distinguishing internal symptoms of Fusarium wilt.
 It is pronounced in the rhizome but is not common in the roots.
However, roots of the diseased rhizomes are frequently blackened and
decayed. Longitudinal sections through the diseased root bases show
characteristic red strands passing into the stele of the rhizome.
Fig.1 Fusarium wilt on leaf and pseudostem

Figure courtesy:
https://images.app.goo.gl/xTSjyZhhK8XhKT5UA
https://images.app.goo.gl/97794D9Tu8VG2LveA
1.2 Etiology
 Fusarium wilt of banana is caused by Fusarium oxysporum f. sp. Cubense. It
comes in Kingdom: Fungi, Division: Ascomycota, Class: sordariomycetes,
Order: Hypocreales, Family: Nectriaceae.
 The mycelium is mainly intracellular, being typically found in
the xylem vesels. This mycelium produces microconidia in the host tissue.
 Conidia are borne at the apex of the main and lateral branches. The
macroconidia are pedicellate, sickle-shaped, 3-septate.

 Chlamydospores are abundantly formed by hyphal and conidial cells.

1.3 Mode of spread and survival
 Fusarium oxysporum f.sp. cubense is soil-borne through its thick walled
chlamydospores. These spores can remain dormant for several years
after the host dies.
 The primary spread of the disease is through infected rhizomes and
secondary spread is through micro and macro conidia through irrigation
water. Continuous cultivation results in build up of inoculum.
 The disease spreads mainly by contact of the root system of adjacent healthy
plants with spores released by the diseased plants.
 Nematodes also help in exposing the roots to infection (Newhall,1958).
1.4 Epidemiology
 Survival and growth of the fungus are generally greater in acidic or light
textured soils than in clayey or alkaline soils with high
calcium content (Stover,1962).
 Survival of the pathogen in field soil is best at 25% saturation.
 growth of the pathogen and disease development in the roots occurs at
temperatures of 21-27°C, but not at 34°C (Beckman and et al,1962).
 Saturated, poorly drained soils have been correlated with greater
disease incidence.

 The disease is favoured by relative humidity-85-90%, acidic soil pH (5.5 to

6.0), red loamy/sandy loam soil and presence of susceptible host.
1.5. Management (NIPHM, 2014)
• Use healthy planting materials and collect planting material from disease free
area.
• Avoid growing of susceptible cultivars viz., Rasthali, Monthan, Red banana and
Virupakshi.
• Grow resistant cultivar Poovan.
• Select tolerant varieties such as Dwarf Cavendish, Robusta, Fhia 1 (Gold fi
nger), Anai komban, Nivedya Kadali.
• It prevented by application of lime to soil.
• Select nematode free soil and follow drip irrigation.
• Dipping of suckers in carbendazim (0.1%) solution before planting.
• Soil drench of 0.1% carbendazim also found effective against wilt fungus.
2. Bacterial wilt (Moko wilt) of banana
• Disease was reported in Trinidad in the Moko plantain about the year 1890.
later it was recognized in countries like Malaysia and Sri Lanka, as well as Fiji,
Hawaii, Ethiopia, Libya and many other countries making it a disease of
worldwide occurrence.

• Although destructive in the Americas and spreading at other places, the disease
has the potential to cause severe losses in the future (Agrios,1988).

• In India the disease was first reported in West Bengal in 1968 and then in south
Indian states of Tamil Nadu and Kerala (Sevamani and Gnanamanickan,1987).

• However, except for reported losses of about 70% in south India during 1977-
78, there have been no reports of serious occurrence in India. probably because
of varietal resistance and crop cultural practice
2.1 Symptoms (Singh, 2018)
 Moko disease is a wilt disease which may be confused with Panama wilt of
banana. The symptoms start on rapidly growing young plants.
 The youngest three leaves turn pale green or yellow and collapse near the
junction of lamina and petiole. Most leaves collapse within 3-7 days.
 The characteristic symptoms occur on young suckers (unlike Fusarium wilt) that
have been cut back once and have begun regrowth. These are blackened,
stunted and may be twisted. If sucker leaves are present, these may turn yellow
or become necrotic.
 Vascular discolouration in plants that have not produced fruit bunches is
concentrated near the centre of the pseudostem, becoming less apparent on
the periphery.
 A firm brown dry rot is found within fruits of infected plants. This is a
distinguishing symptom of Moko disease. If the fruit symptoms are not present
the disease may be Fusarium wilt.
 Fig 2. Moko wilt on banana
Figure courtesy:
https://plantix.net/en/library/plant-diseases/300016/moko-disease//
https://apps.lucidcentral.org/pppw_v11/text/web_full/entities/banana_moko_disease_525.htm
2.2 Etiology
 Moko disease is caused by the bacterium Ralstonia solanacearum, earlier
known as Pseudomonas solanacearum.
 It comes under Domain: bacteria, Phylum: Pseudomonadota, Class:
Betaproteobacteria, Order: Burkholderiales, Family: Burkholderiaceae.
 Cells of the bacterium are rod-shaped, 0.5-0.7 x 1.5-2,5 µm in size and motile
by 1-4 polar flagella.

 They are Gram-negative. In culture all strains of the bacterium appear as small
butyrous colonies with a distinct dark red centre on tetrazolium chloride agar.
2.3 Mode of spread and survival
 The bacteria survive through infected rhizomes and also in soil for 6
months to 2 years.
 The spread is through use of infected rhizome, cutting machetes at the
time of planting, and through insects which carry the bacteria from
ooze on suckers and male flower bracts to healthy inflorescences and
other parts of the plant.
 Entry into the host is mostly through wounds such as those caused
during various cultural operations and during attack of insects and
nematodes.
2.4 Epidemiology (Thind,2001)
 The optimum temperature for growth is around 32°-35°C, maximum
41°C and minimum 10°C.
 The banana plant is often infected through the above ground parts.
Contaminated pruning tools and insects visiting flowers are common
sources of infection.
 Plants are particularly susceptible to insect transmitted infection when
the bracts fall off, leaving an open wound. Infection can also spread
through the roots of an infected banana mat or alternative weed host
to the roots of a healthy banana mat.

 A large number of weeds are the hosts to the disease.

 2.5 Management (NIPHM,2014) (Thind,2001)
 Providing good drainage.
 Disinfestation of tools with formaldehyde diluted with water in 1:3
ratio. Crop rotation (3 years rotation with sugarcane or rice) &
providing good drainage.
 Allow fallow period or flooding during off -season.
 Phytosanitary measures are necessary to prevent spread of the moko
disease. Fruits should not be transported from one country to another.
 Proper insecticide should be sprayed to kill the flower visiting insect
vectors. Proper weedicides should be used to kill the weed hosts and
also Heliconia spp. should not be planted near to the main fields.
 Keep the soil fallow or crop rotation should be done with non- host
crops for 12 months in case of strain B and 6 months in case of SFR
strain.
 Lastly, the soil fumigation with the chemicals like methyl bromide
should be done. The fumigation of planting material is also helpful.
3. Cercospora leaf spot or Sigatoka
• This leaf spot disease of banana was first detected in Java in 1902. The
name Sigatoka was given when it was found in epidemic form in the
plains of Sigatoka in Fiji Island in 1913.

• The disease is destructive in Central America, Africa, Eastern Australia,

Borneo, Java, Sumatra, Fiji, Malaysia, etc., but the economic importance
varies with the region.

• In India, the disease occurs in Tamil Nadu, Kerala, Bihar and Bengal and
mostly attacks the leaves.

• Although, Sigatoka is not considered a fatal disease (Ploetz,1998) in the

subtropics, mortality of plants is reported from Bihar.
3.1 Symptoms (Singh, 2018)
 The early symptoms of Sigatoka appear on the third or fourth leaves
from the top.
 The leaves that have opened about a month earlier show small,
indistinct, longitudinal, light yellow spots parallel to the side veins.
These early spots are 1-10 mm long and 0.5-1.0 mm wide.
 A few days later, the spots become 1-2cm long, turn brown with light
grey centres (eye spot appearance), and become readily visible. Upto
this stage there is not much damage.
 But when the spots further increase in size, the tissue around them
turns yellow and dies. Adjacent spots coalesce to form large dead areas
on the leaf. In severe infections, the entire leaves die within a few days.
  As a result of the loss of leaves the immature fruit bunches fail to fill out
and ripen and may fall. If the fruit is nearing maturity at the time of heavy
infection. the flesh ripens unevenly.
 Individual bananas appear undersized and angular in shape, their flesh
develops a buff pinkish colour, and they store poorly.

Fig 3. Sigatoka leaf spot on banana

Figure courtesy:
https://agritech.tnau.ac.in/crop_protection/banana_diseases/crop_prot_crop%20diseases_fruits_banana_8.html
3.2 Etiology
 The yellow Sigatoka is caused by the fungus Cercospora musae Zimm, but
mostly the causal organism is referred to by its perfect stage, Mycosphaerella
musicola Leach. There is another species, Mycosphaerella fijiensis, that causes
black Sigatoka.
 Mycosphaerella musicola comes in Kingdom: Fungi, Division: Ascomycota,
Class: Dothideomycetes, Order: Capnodiales, Family: Mycophaerellaceae.
 light yellow Conidia are produced on sporodochia on both sides of the leaf but
are usually more abundant on the upper surface. The conidia are slender, long,
septate, and hyaline. They measure 40-80 x 2.5-3.6 pm.
 Perithecia are formed during hot and humid weather. The perithecia measure
46.8-72.8 (av. 61.8) um in diameter. The asci in clusters are long, cylindrical,
and 28-36 x 8-11 um in size. Each ascus contains 8 hyaline, 2-celled ascospores
which measure 14-18 (12-15) x 3-4 μm.
3.3. Mode of spread and survival
 The pathogen can survive on dry infected leaves on the field soil. It is spread
through conidia and ascospores. Conidia are formed in humid weather
throughout the year and dispersed by raindrop splashes and by wind.
 Ascospores are shot out violently through the ostiole in response to wetting
of perithecia and are dispersed by air currents. They are responsible for long
distance spread of the pathogen while conidia are generally the most
important means of local spread.
3.4 Epidemiology
 Sigatoka spreads fast in a humid weather or periods of high rainfall at 23°-
25°C.
 Soils with poor drainage and low fertility favour the disease.
 Conditions which are conducive for increased humidity in the plantation are
favourable for the disease.
 Thick planting, presence of weeds and increased number of suckers promote
disease development Sprinkler irrigation also promotes the disease.
3.5 Management (NIPHM, 2014)
 Removal and destruction of the affected leaves.
 Prevent water accumulation around the plant and go for periodical weeding.
 Select tolerant varieties such as Ney Poovan, Pachanadan, Karpuravalli, Fhia 1
(Gold finger), Sannachenkadali
 Spraying of Mancozeb 75% WP @ 26 g in 10 liter of water or Propiconazole 25%
EC @ 0.1% (10 ml/10 l water) or Copper oxychloride 50% WP @ 40 gram in 10 l
of water along with sticker.
4. Bunchy top of banana
• It is also known as ‘strangles’ or ‘Curly top’ or ‘Cabbage top’. Bunchy
top is a destructive disease of banana in Asia, Australia, Egypt and
Pacific Islands. Among banana diseases other than the two wilts, bunchy
top is considered most destructive in the subtropics.

• In India it is particularly destructive in the state of Kerala which

contributes around 25% of total banana production in the country. It
was first reported from Bengal in 1925 and then in Bihar in 1940, Assam
in 1941 and Kerala in 1943.
4.1 Symptoms (Gupta and Sharma, 2005)
 Initial symptoms of the disease are exhibited on the leaves as irregular
green streaks along the secondary veins of the leaf sheaths.
 Bunching of leaves occur at the apex and such leaves show distinct rigidity.
 Bunched leaves form a rosette at the apex which is due to the failure of the
leaf stalks to elongate.
 The presence of interrupted dark green streaks along the secondary veins
of the lamina or along the midrib or petiole is considered to be the most
definite and reliable symptom of bunchy top (Singh, 1996).
 Fig 4. Bunchy top of banana
Figure courtesy:
https://en.wikipedia.org/wiki/Banana_bunchy_top_virus
https://www.agdia-emea.com/en/product/banana-bunchy-top-virus-2
4.2 Etiology

 The causal agent of bunchy top is a nanavirus known as Banana bunchy

top virus (BBTV). It was considered a luteovirus in which the particles
are isometric with ssRNA. However, in later studies it was reported as a
non-geminated ssDNA virus. The particles are 60 nm in diameter.
 It comes in Kingdom: Shotokuvirae, Phylum: Cressdnaviricota, Class:
Arfiviricetes, Order:Mulpavirales, Family: Nanoviridae, Genus:
Babuvirus.
4.3 Mode of spread and survival (Singh,2018)
 The virus is transmitted by the banana aphid, Pentalonia nigronervosa,
in a semi- persistent manner. It is not sap transmissible.
 All the suckers produced by a diseased plant carry the virus and they
constitute the most important source of spread of the disease from
plantation to plantation.
 The aphids cause the secondary spread during the growth of the plants.
4.4 Epidemiology
 The rate of multiplication of aphids is maximum when the minimum
temperature is about 18-20°C with relative humidity ranging between 41 and
84%.
 All stages of the aphid acquire and transmit the virus but the nymphs are most
efficient. To become infective, the aphid requires a minimum feeding period of
17 hours and transmits the virus to a susceptible plant by feeding on it for one
and a half h or more.
 These aphids occur around the base of pseudostem at soil level and for some
inches below the soil surface. They are also found between the outer leaf
sheaths and the pseudostems.
4.5 Management (NIPHM, 2014)
• Select suckers from disease free areas.
• Remove weeds, which help in attraction of aphids.
• Destruction of infected plant.
• Selection of healthy suckers for planting. Use of only certified banana
suckers for planting.
• Control the aphid by spraying phosphomidon (1 ml/l of water) or methyl o
demeton (2 ml/l of water).
• Follow strict quarantine measures during the introduction of new material
from one state to other state. The new crop should be regularly inspected
and the diseased plants destroyed as soon as noticed.
5. Anthracnose
• It is a serious disease in all the banana growing areas especially in Bihar
(Thakur and Mishra, 1966) and in Karnataka (Rawal and Ullasa, 1989).
5.1 Symptoms (Thind,2001)
 It attacks plants at all the stages of their development. Almost all the varieties
of banana have been reported to be susceptible to this disease.
 The table varieties like Harichal and Malbhog have been reported to be
severely attacked and in several cases banana cultivation had to be abandod.
 There are usually two types of infection. Latent infection usually originates in
the field on uninjured green fruits. The fungus penetrates the cuticle and
becomes latent as subcuticular hyphae.
 In contrast, non-latent infections usually begin during or after harvest. Young
latent infections appear as small black circular specks on the flowers, skin and
distal ends of banana hands.
 Fig. 5 Anthracnose on banana
Figure courtesy:
https://agritech.tnau.ac.in/crop_protection/banana_diseases/crop_prot_crop%20diseases_fruits_banana_8.html
5.2 Etiology
 Anthracnose rot is caused by Colletotrichum musae (Berk, and Curt.) von Arx
(syn. Gloeosporium musarum Cke. and Mass.).
 It comes in Kingdom: Fungi, Division: Ascomycota, Class: Sordariomycetes,
Order: Glomerellales, Family: Glomerellaceae.
 Acervuli on fruits, stalks, petioles and occasionally on leaves are usually
rounded or somewhat elongated and upto 400 m in diameter. Conidiophores
are cylindrical and tapering towards the apex, hyaline, septate, branched and
subhyaline at the base. They are upto 30 μm long and 3-5 um wide.
 Conidia are hyaline, aseptate, oval to elliptical or straight cylindrical with
obtuse apices or flattened at the base and obtuse at the apex. They appear
salmon pink in mass.
5.3 Mode of spread and survival
 These fungi survive on banana plants and diseased crop debris.
 conidia are disseminated by rains, wind and insects. In areas where banana
leaves are used for packing during transportation of fruit bunches chances of
infection from lesions on leaves and petioles are high.
 The infected bunch and finger stalks also provide inoculum for infection of
fruits during transit and storage.

5.4 Epidemiology
 Optimum germination of conidia has been obtained at 30°C.
 The optimum temperature for disease development on ripe bananas is 30-35°C.
The conidia germinate within a range of 85.7-100 per cent relative humidity.
 The disease seems to be restricted during the cold as well as
hot and dry months.
5.5 Management (NIPHM, 2014)
 Proper sanitation of handling and prompt cooling to 14° C are essential in
minimising the disease in cold storage.
 Avoid damage to fruits at harvest and transit
 Burn the infected materials
 Proper field sanitation
 Keep the field free of weeds and provide good drainage
 Fruit should be free from infection and as possible before it is transported,
stored and ripened
 Banana bunches should be harvested at correct stage of maturity.
 Proper fertilization prevents the infection.
6. Finger rot of banana
• This is the most severe disease among post-harvest diseases particularly
during transit in the boxes. The disease is also known as finger rot.

• In India, it has been reported to occur in Uttar Pradesh, Delhi, Maharashtra

and Andhra Pradesh.

• The fungi Botryodiplodia theobromae, Rhizopus oryzae, Aspergillus niger, A.

flavus and Fusarium equiseti have been associated with premature ripening
and storage rots reducing quantity of total soluble sugars, proteins, lipids,
ash, crude fibre, ascorbic acid and mineral elements.
6.1 Symptoms (Sharma and Gupta, 2005)
 Initially, the fruit rind is discoloured followed by appearance of water-
soaked spots.
 Infection starts from distal end and gradually the rotting progresses to
the stalk end. Finally, the fruits turn dark brown in colour.
 The fruit pulp is converted to black watery mass emitting sweetish
odour.
 In advance stages white or light grey cottony mycelial growth appear on
the rotten tissues followed by development of pycnidia. Raw infected
fruits also ripen prematurely and mature fruits are most susceptible.
 The pathogen is also responsible for causing stalk rot in which splitting
of stem occur. The fungus also extends through the cushions causing
finger stalk rot and finger dropping.
 Fig. 6 Finger rot on banana

Figure courtesy:
https://ucanr.edu/sites/Postharvest_Technology_Center_/files/222593.jpg
6.2 Etiology
 The disease is caused by Botryodiplodia theobromae Pat.
 It comes in Kingdom:Fungi, Division: Ascomycota, Class: Dothideomycetes,
Order: Botryosphaeriales, Family: Botryosphaeriaceae.
 The pycnidia are flask shaped, slightly sub-cuticular having small neck and
ostiole and black walls measuring 250-300 uum in size. The pycnidia may be
found in groups or singly. The conidia are produced on short conidiophores
which are bi-celled, straight and brown in colour measuring 25 x 15 um.
6.3 Mode of spread and survival
 The fungus B. theobromae is seed bome in seeded Musa spp. occurring in
the seed coat or micropylar plug.
 Conidia are responsible for secondary spread and are produced in the
decaying fruits in the pycnidia. These are disseminated by wind and water.
Wounds provide the avenues for the entry of the pathogen.

6.4 Epidemiology
 Disease spreads rapidly in tropical regions and is severe on fully ripened
fruits.
 Long transit periods are very favourable for infection to occur.
 High temperature ranging from 25-30°C favour the disease development.
6.5 Management (NIPHM, 2014)
 Wrap the banana fruit bunch in plastic bag prior to hot water dip.
 The fruits should be free from infection and as healthy as possible before
packing and transportation.
 Fruits should be harvested at proper stage of maturity and ripening during
transit should be avoided.
 Care must be taken to prevent bruising of fruits during picking and
subsequent handling.
 Heating up of stored fruits should also be avoided.
 Thiabendazole @ 300-500 ppm reduces the incidence of the disease and
control latent and apparent infections.
7. Banana mosaic (Infectious chlorosis)
• Infectious chlorosis, which has also invariably been described as banana
mosaic, is a serious disease of plantations. The disease was first recorded in
New South Wales, Australia in 1930 (Magee, 1930).

• In India, the disease was first reported from Maharashtra and presently it
occurs widely in all the banana growing areas of the country (Kamat and
Patel, 1951).

• Mali and Deshpande (1976) surveyed the Marathwada region and reported
the incidence upto 23 per cent in Parbhani district of Maharashtra. The
disease is prevalent in South and Central America, the Carribbean, India,
Australia and Philippines.
7.1 Symptoms (Gupta and Sharma, 2005)
 The leaves of severely infected plants exhibit large chlorotic or yellow patches.
 plants remain stunted and they seldom produce a fruit bunch.
 Early infection leads to sheath rot as well as heart rot phase.
 The fruits if developed on affected plants have no commercial value.
 Depending on prevailing weather conditions, the chlorotic stage may or may
not be accompanied by rotting of the heart leaf and central cylinder.
 Fig. 7 Banana mosaic (Infectious chlorosis)

Figure courtesy:
https://agritech.tnau.ac.in/crop_protection/banana_diseases/crop_prot_crop%20diseases_fruits_banana_6.html
7.2 Etiology
 The disease is caused by cucumber mosaic virus.
 It comes in Kingdom: Orthornavirae, Phylum: Kitrinoviricota, Class:
Alsuviricetes, Order: Martellivirales, Family: Bromoviridae.

7.3 Mode of spread and survival (Thind, 2001)

• The primary transmission is through infected daughter suckers from diseased
plants.
• The secondary spread of the disease is through Aphis gossypii.
• Cucumis sativus var khira serves as a reservoir of the virus.
7.4 Management (NIPHM, 2014)
• Destroy infected plants and weeds.
• Infected suckers should not be used for planting.
• Dry heat treatment of suckers at 40º C for 1 day.
• Weeds in the nearby areas should be removed as the virus survives in them in
off-season.
• Growing pumpkin, cucumber and other cucurbits between the rows of banana
crop should be avoided.
• Early detection by regular inspection of planting and eradication of diseased
plants from the field as soon as they are noticed.
• Control of insect vector by spraying Phosphomidon at 1 ml per liter or methyl
demeton at 2 ml per liter of water.
8. Tip over or Rhizome rot or Bacterial soft rot of
banana
The disease is wide spread in banana growing areas of the world (Edward et
al., 1979). In India, it is reported to be present in Tamil Nadu and Kerala.

8.1 Symptoms (Thind, 2001)

 The affected plants show discolouration and soft rotting of rhizomes and
suckers.
 They have scanty roots with dark brown lesions and necrotic tip. In many
cases, the pseudostem tips over breaking across the rotted stems
particularly at the ground level.
 The mature plants seldom show above ground symptoms until the disease
is well advanced. Such plants may produce small sized fruits which may fail
to emerge from the shoot tip Infected plants can be pushed over easily and
are very susceptible to wind damage.
 In severely infested soil newly planted rhizome may rot and fail to sprout.
When young plants are infected, a dark brown necrosis appears in the
lamina of the older leaves.
 Later, the plants become stunted and yellow. As the rhizome becomes
infected, pockets of dark water soaked areas develop.
 Infection may result in the production of cavities which resemble
root borer tunnels
 Fig. 8 Rhizome rot on banana

Figure courtesy:
https://agritech.tnau.ac.in/crop_protection/banana_diseases/crop_prot_crop%20diseases_fruits_banana_5.html
8.2 Etiology
 This disease is caused by Erwinia carotovora (Jones) Holland.
 It comes in Domain: Bacteria, Phylum: Pseudomonadota, Class:
Gammaproteobacteria, Order: Enterobacterales, Family: Erwiniaceae.

8.3 Mode of spread and survival (NIPHM, 2014)

 Bacteria survive in crop debris and infect by water splash through damaged
tissues.
 Worse in hot wet weather.
 The bacteria spread in contaminated water.

8.4 Epidemiology
 Higher temperatures favours the bacterial growth.
 high humidity are ideal growing conditions for the bacteria.
8.5 Management
 Remove infected plants and destroy.
 Drench with mancozeb 75% WP @ 600-800 g in 400 l of water/acre.
 Good drainage and soil conditioning can control the disease to some extent.
 Use disease free suckers.
 Remove plant residues after harvest.
 Dip suckers in copper oxychloride (40 g/10 l water) + streptocycline (2 g/10 l
water) for 30 minute before planting.
9. Banana burrowing nematode
• The nematode (Radopholus simils) is recorded from Asia, Africa, North
(Hawaii, Florida), South and Central America, the Caribbean, Europe, Oceania.

• The nematode is recorded from American Samoa, Australia, Cook Islands, Fiji,
Frecnh Polynesia, Guam, Federated States of Micronesia, New Caledonia,
Niue, Palau, Papua New Guinea, Samoa, Solomon Islands, and Tonga.

• In Fiji, the nematode is highly pathogenic on ginger, but less so on banana; in

other countries bananas are readily infected.
9.1 Symptoms
 The burrowing nematode destroys the roots of bananas and plantains, so that
the plants are starved of water, nutrients, and lack support.
 Consequently, (i) the mother plants and suckers grow slowly, the number and
size of leaves is smaller than normal, leaves are yellowish and fruit bunches
are small, or (ii) the plants fall down in heavy rain or winds before fruits are
mature, a symptom known as 'toppling'.
 The fine feeder roots are killed, whereas the larger anchoring roots develop
dark red streaks as far as the central parts, known as the stele.
 The lesions join together, and turn black as they are invaded by other
microorganisms. Rots occur.
 Finally, the rots form a ring around the root and kill it. The corms are also
infected, and black areas form, known as 'black heads'.
 As roots die, new ones grow from the corms and they also become
infected by nematodes and are killed.

Fig. 9 Burrowing nematode on banana

Figure courtesy :
https://apps.lucidcentral.org/ppp/
9.2 Etiology
 This disease is caused by Radopholus similis.
 It comes in Kingdom: Animalia, Phylum: Nematoda, Class: Secernentea,
Order: Tylenchida, Family: Pratylenchidae.
 The genus Radopholus constitutes an important group of endoparasitic,
migratory root nematodes inhabiting a wide variety of plants.
 The adult males and females of R. similis are vermiform and measure 0.5-0.8
mm in length. In females the lip region is rounded and marked by three striae
while in males the lip region is subspherical and striae may or may not be
present. There are two ovaries (posterior and anterior) in the females.
 Fertilization is not essential for egg production and the females lay both,
fertilized and unfertilized, eggs which measure 60-70 x 20-28 pm. The females
lay 2-4 eggs per day for about 7-8 days.
9.3 Mode of spread and survival (Singh,2018)
 The burrowing nematode can survive in sandy loam soil for 6 months in
the absence of the host roots.
 In India maximum number of the nematode are found in red loam soils
of south India. The highest population occurs during May-June.
 The nematode is generally not found in the top 15 cm soil. The most
common method of introduction of the nematode in new areas is the
use of infected suckers and rhizomes for planting.

9.4 Epidemiology
 Poor maintains of garden or neglected plantations are highly
susceptible.
9.5 Management (NIPHM, 2014)
 Deep ploughing during summer.
 Use of disease free planting material.
 Storage of large corms in the sun for two weeks prior to planting.
 Select healthy suckers.
 Avoid growing Robusta, Karpooruvally, Malbhog, Champa and Adukkar.
 Grow less susceptible varieties like Poovan, Kadali, Kunnan, Poomkalli.
 Intercropping of banana with Crotalaria juncea, marigold reduces burrowing
nematodes.
 Before planting, the suckers should be dipped in carbofuran 3% CG then shade
dry for 72 hrs then go for planting.
 Application of carbofuran @ 10 -15 gm/plant with FYM and the application of
neem cake @ 5kg/plant has also been found effective.
10. Banana bract mosaic (https://agritech.tnau.ac.in)
10.1 Symptoms
• The disease is characterized by the presence of spindle shaped pinkish to
reddish streaks on pseudostem, midrib and peduncle.

• Typical mosaic and spindle shaped mild mosaic streaks on bracts, peduncle
and fingers also observed

• Suckers exhibit unusual reddish brown streaks at emergence and separation of

leaf sheath from central axis.

• Clustering of leaves at crown with a travelers palm appearance, elongated

peduncle and half filled hands are its characteristic symptom.
 Fig.10 Bract mosaic on banana

Figure Courtesy:
https://agritech.tnau.ac.in/crop_protection/banana_diseases/crop_prot_crop%20diseases_fruits_banana_2.html
10.2 Etiology
 The causal organism is banana bract mosaic virus.
 It comes in Realm: Riboviria, Kingdom: Orthornavirae, Phylum: Pisuviricota,
Class: Stelpaviricetes, Order: Patatavirales, Family: Potyviridae, Genus:
Potyvirus.

10.3 Mode of spread and survival

 Banana bract mosaic virus transmitted by aphid.

 The virus is transmitted through aphid vectors. The virus is primarily spread
through infected suckers. In the field, aphids vectors such as Aphis
goosypii, and Rhopalosiphum maidis (Green corn aphid) transmits the
disease.
10.4 Management
• The diseased plants should be removed as and when noticed to avoid
the spread of the disease.

• Disease free planting materials should be used for new planting.

• The banana gardens should be kept free from weeds.

• Weeds in the nearby areas should be removed as the virus survives in

them in off-season.

• Early detection by regular inspection of planting and eradication of

diseased plants from the field as soon as they are noticed.
• Control of insect vector by spraying Phosphamidone at 1 ml per litre of
water or Methyl Demeton at 2 ml per litre or Monocrotophos at 1 ml
per litre of water.
11. Cigar-end rot
11.1Symptoms (https://www.midh.gov.in/technology/IPM-Banana-Revised-
Sept2011.pdf)
 The damage is caused on the young bunches in the form of necrosis at the end.
 The skin become folded and shrunken as the infection spread slowly along the
fingers, grey conidia are formed on the shrivelled stalk end of the fruit, like the
ash of cigar.
 The pulp tissue shows typical dry rot that is the characteristic feature of the
pathogen.
 Black pitting and spotting of fruit on account of drying of the finger gives an
appearance of a lighted cigar.
 The pulp undergoes a dry rot and becomes mummified.
 Fig. 11. Cigar end rot of banana
Figure courtesy:
http://tcbanana.blogspot.com/2012/01/fungal-disease-pre-post-harvest-cigar.html
11.2 Etiology
 The disease is caused by Verticillium theobromae (Turc.) Masonet Hughes.
 Conidiophores are solitary or in small groups.
 Conidia are hyaline, oblong to cylindrical. They are borne at the ends of
tapering phialides, aggregated into rounded, mucilaginous translucent heads.

11.3 Mode of spread and survival

 The disease is spread through wind and infected dying flower parts.

11.4 Epidemiology
 Warm and moist conditions favours the disease occurrence and the disease
spread is high in old and badly maintained plantations.
11.5. Management
(https://agritech.tnau.ac.in/crop_protection/banana_diseases
/crop_prot_crop%20diseases_fruits_banana_4.html)
 Removal pistils and perianth helps in reduction of the disease. Pistils should be
removed 8 to 11 days after bunch emergence.
 Bagging of developing fruits is also recommended.
 Young bunches should be opened up to the light and air and the bracts which
remain attached to the bunch should be removed especially during wet
weather
 The plantations should have enough aeration by avoiding overcrowding of
plants
 Improved sanitation helps in the reduction of the disease.
 The bunches may be sprayed with Copper oxychloride 0.25 per cent solution
along with a wetting agent @ 0.5 to 1.0 ml per liter of spray fluid
 Spraying of the peduncle with Carbendazim at 0.1% or Dithane M-45 at 0.1%
after shoot emergence.
12. Stem end rot or crown rot
Stem end rot disease, also known as crown rot or top rot, is a common fungal
disease that affects bananas and other tropical fruit crops. It primarily affects the
upper part of the fruit, near the stem end, hence the name "stem end rot” is
given.
12.1 Symptoms
 The infection occurs through the cut ends of the main stalk and spreads into
the crown and pedicel of fruits.
 Then the rot progresses to the fruits.
 The diseased portion turns black and dries.
 In main stalk rot (Ceratocystis paradoxa) the main stalk starts rotting. The
tissues become soft and black and emit a pleasant smell.
 Black mycelium of the fungus is seen in the rotting area.
 This spreads to hands and fruit stalks and then to the stem-end of the fruit.
Black spots are seen on the fruit surface.
 The flesh becomes soft and dark. The fruits show early premature ripening.
 Fig. 12 Crown rot of banana
Figure courtesy:
https://ucanr.edu/sites/Postharvest_Technology_Center_/files/222592.jpg
12.2 Etiology
 Many fungi are associated with these rots.
 In addition to the anthracnose fungus, others are Ceratocystis paradoxa,
Botryodiplodia theobromae, Ceratocystis paradoxa, Fusarium roseum,
Verticillium theobromae and Acremonium sp.
12.3 Mode of spread and survival
 Diseased plant debris and diseased standing plants are the major sources of
perennation of these fungi.
 Some of these fungi survive through chlamydospores and resistant conidia in
soil.
 In the rot caused by Ceratocystis paradoxa, the pathogen is introduced in
the plantation through infected rhizomes.
 The spores are dispersed by rain or wind.
 Usually it is the plantation soil adhering with fruit bunches that carries the
inoculum and when fruits are injured, they cause fruit rot.
 Infections in the plantations are through cut ends at the time of harvest.
12.4 Epidemiology
 Crown rot and stem end rot disease is more at 250 C temperature and 70-
100% relative humidity.
12.5 Management
 Proper crop management, including regular removal of dead leaves and
pruning of infected plant parts, can help reduce the risk of infection.
 Maintaining good air circulation and reducing humidity around the fruit
bunches can also be beneficial.
 Bananas should be harvested carefully to avoid causing injuries or wounds to
the fruit.
 Gentle handling during transportation and storage is crucial to prevent
damage that could facilitate infection.
 Pre-harvest spraying of Carbendazim at 0.1% or Dithane M-45 at 0.1% also
found effective.
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