Banana diseases and pests

  • Published on 11/05/2016 - Published by Cirad
  • FruiTrop n°240 , Page From 109 to 117
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Panama disease

Panama disease or Fusarium Wilt was first identified in 1874 in Australia. It is now observed in almost all tropical and subtropical banana production zones. It is caused by the soil fungus Fusarium oxysporum sp. cubense (FOC).

panama disease
panama disease

Different races have been identified. Under certain conditions (soil type, climate, crop intensification, drainage, etc.) each can cause serious vascular damage to the different banana varietal groups, making them practically non-productive.

Race 1 originated in Asia and spread widely via movement of plant material in the form of suckers when the major export banana cultivation areas were established in the early Twentieth Century. It caused by the progressive disappearance of production of the Gros Michel variety in the Caribbean and Latin America in the 1940s and 1950s, when the variety formed the basis of international trade. Gros Michel was replaced in the industrial plantations by the resistant Cavendish varieties discovered in South-East Asia and that are now the fruits traded internationally. It should be noted that Gros Michel is still the reference for dessert banana consumption in most African and Latin American countries; production is still substantial at approximately 6 million tonnes per year. It appears that race 1 is not active in the areas in which it is cultivated extensively and combined with other varieties and other crops (hence at low density). Experiments conducted in Colombia have shown that Panama disease gains importance when the growing of Gros Michel is intensified (density greater than 1 000 plants per ha).

gros michel
gros michel
panama disease on petite naine
panama disease on petite naine

Race 2 affects the Bluggoe subgroup (ABB, cooking bananas).

Race 3 affects Heliconia spp. and sometimes Gros Michel.

Race 4, identified in the Canary Islands in 1931, affects the Cavendish group sporadically and under certain environmental conditions but only in subtropical zones (Canary Islands, South Africa, Taiwan, Australia) where it is relatively well controlled by the appropriate cultural techniques (buffer zones, fallow, etc.).

Race T4 has just appeared in Mozambique (though also in Jordan). It is a relatively recent form, described in 1990. It afflicts Cavendish group varieties, but hitherto had only been found in the wet tropical zones of Asia, especially Taiwan, Indonesia, Malaysia, South China, Australia and the Philippines. In 2011, FruiTrop published a full set of recommendations (see FruiTrop no.191, July-August 2011, pages 20 and 21), to be followed very closely in order to apply effective preventive measures. An ad-hoc committee of scientists specialising in this disease was formed in order to investigate the origin of its introduction and analyse the risks of extension. This alarming news has reactivated the world phytosanitary monitoring networks, particularly in Latin America.

All the specialists agree that the main cause of the spread of the disease is the movement of plant material (suckers and corms) from susceptible, infected plantations. Contamination via the soil from an infected area is very slow.

Prevention and control

As for numerous soil pathogens, control methods are limited and consist essentially of keeping areas containing the outbreaks in quarantine. Not much international work is being performed on this disease, study of which is complicated. Control methods are not specific to bananas and are and will remain very limited. Conventional genetic improvement remains an important and as yet little-explored pathway.

International awareness of the importance of respecting rules for the movement of germplasm and the wide adoption of tissue culture plants by the banana industry should limit the present risks. The dispersion of race T4 is under surveillance. However, with strict control of germplasm movement and the surveillance and eradication of infected plants, the prospect of rapid spread of the disease is very improbable.

Sigatoka leaf streak diseases

Banana production is confronted with two main types of leaf streak disease: Yellow Sigatoka and Black Sigatoka. They are caused by parasitic leaf fungi. The pathogen of Yellow Sigatoka is Mycosphaerella musicola and that of Black Sigatoka is Mycosphaerella fijiensis.

black sigatoka
black sigatoka
yellow sigatoka
yellow sigatoka

A new fungal species, Mycosphaerella eumusa, that may be responsible for a new, even more aggressive form of Black Sigatoka, seems to be spreading in Asia and the Indian Ocean, but this remains to be confirmed (it has also been detected in Nigeria in West Africa).

Propagation is from banana plant to banana plant in continental zones. Maritime zones form a natural obstacle. Although the risk of natural spread of spores by wind does exist, the spread of the disease from one zone to another is usually the result of uncontrolled transfers of germplasm. Black Sigatoka is present in all the producer countries in Latin America, Africa and Asia. The countries of the Caribbean arc were long protected by their island status. The presence of the diseases in St Vincent and Guiana was confirmed in 2009. It was reported officially in St Lucia in early 2010, in Martinique in September 2010 and in Guadeloupe in early 2012.

distribution of black sigatoka in the caribbean arc
distribution of black sigatoka in the caribbean arc

Although Black Sigatoka has not yet been detected in Dominica it is certain to reach the island, probably fairly soon.

The fungus that causes the disease destroys the foliage. The disease takes the form of small elongated black streaks that soon become necrotic. Necrosis spreads and may destroy all the leaves of the plant before the bunch is cut. This results in smaller yields and very ripe fruits that are unsellable.

The sequence is precisely the same as that caused by Yellow Sigatoka, a fungal disease present on all the continents for about 60 years. With support from CIRAD, rational chemical control of the disease was established by professionals in Martinique and Guadeloupe. Warning methods (biological and meteorological) based on the weekly observation of biological and meteorological descriptors in plantations make it possible to monitor the dynamics of the disease and to apply appropriate treatments. Yellow Sigatoka has been controlled in recent years with a small number of sprayings: an average of five to seven a year in West Indian plantations. These rational control methods can now be applied in the management of Black Sigatoka.

There are fundamental differences between the two leaf streak diseases. Unlike Yellow Sigatoka, Black Sigatoka can develop on export bananas and also on plantains and other cultivated varieties that are also very susceptible to the disease. It spreads rapidly and is very difficult to control. Depending on the country, the strategies used and production conditions (climate, crop management sequences, etc.), the management required ranges from just a few interventions to more than 50 sprayings per year.

Different control strategies

In the main Latin American producer countries, export banana plantations form vast agroindustrial units in alluvial plains. Given the areas of the estates (several hundred or even several thousand hectares), there is little outside contamination. There are no outbreaks of the disease in the immediate neighbourhood of agroindustrial plantations. Agroclimatic homogeneity makes it possible to organise and rationalise the spraying of large units. Low labour costs facilitate the cleansing work required in the form of regular deleafing. In this context, the impact of spraying in terms of nuisance is not always taken into account by the large companies, who do not hesitate to use systematic control strategies leading to more than 50 sprayings per year. In this case, spraying is often performed at less than weekly intervals, and generally involves contact fungicides (chlorothalonil, dithiocarbamates, etc.) that by definition are not very effective, and so have a small curative effect. Systemic fungicides are sometimes used but usually in ‘cocktails’ that are mixes of systemic, penetrating and contact substances prepared as emulsions in oil. 

CIRAD has developed rational control strategies that, for the control of Yellow and Black Sigatoka, are based on warning systems involving either scouting in the plantation or the observation of meteorological descriptors (precipitation, evaporation, temperature, etc.). This strategy has been applied in different countries to control Yellow Sigatoka and also Black Sigatoka. This is the case in particular in Guadeloupe, Martinique, Cameroon and Côte d’Ivoire. The main objectives are as follows:

-          improving the effectiveness of control while reducing the number of sprayings per year;

-          limiting the risks of the selection of fungal strains that are resistant to the systemic fungicides used;

-          reducing pollution and thus achieving greater respect for human health and the environment (urban centres, rivers, water bodies, reservoirs, etc.).

The strategy is also based on the rational, alternate use of systemic fungicides (benzimidazoles, triazoles, strobilurins) and penetrating fungicides (morpholines, etc.) which are mixed with refinery oils that are also fungistatic and applied at low volume (13 to 15 litres per hectare), prolonging the effectiveness of each spraying and hence reducing the number of sprayings required each year.

The systemic fungicides on the market have a single-site mode of action on the pathogen and the risk of the appearance of resistant strains is high if they are used irrationally or abused. In Central America, benzimidazoles were used massively when they came on to the market and resistance was observed only two years after they began to be used to control Black Sigatoka. This made it necessary to use more contact fungicides (15 to 40 kg active substance per hectare per year). The same phenomenon was then observed in these production zones with Black Sigatoka when triazoles and then strobilurins were used.

Thanks to the warning methods and hence the reduced number of sprayings, the phenomenon did not appear in Cameroon and Côte d’Ivoire for 10 or even 15 years of use of the fungicides to control Black Sigatoka.

In Guadeloupe and Martinique, the problems started to appear with control of Yellow Sigatoka after 20 or even 30 years of rational use of these fungicides using warning methods.

black sigatoka 1
black sigatoka 1
black sigatoka
black sigatoka

New essential control methods

Present control strategies cannot be used indefinitely. The European legislation in force in the French West Indies makes it technically impossible to use rational control strategies based on the alternation of several active substances with different modes of action. Only two fungicides in the triazole family can currently be used for aerial spraying.

A strobilurin fungicide and another in the morpholin group received marketing authorisations at the end of 2008, but they are not used to control Sigatoka diseases as the authorisation is accompanied by a 100-metre unsprayed buffer zone and this is incompatible with aerial spraying.

Actions can be envisaged to address this problem of regulations, such as reducing the buffer zone to 50 metres, using land-based sprayers and technical developments to reduce the drift of fungicide sprays, the registration of new systemic fungicides, requests for derogations, etc. — but the legislation may well become increasingly restrictive in the future.

The feasibility of the implementation of rational control is based on the status of the fungal strains with regard to curative fungicides. If the strains are (see status of invasive strains) or become resistant to these fungicides (see risks of the rapid mutation of M. fijiensis), this will irremediably compromise the implementation of such strategies.

Other methods must therefore be sought to control or regulate Black Sigatoka. Breeding new hybrid varieties with lasting resistance and good agricultural and organoleptic potential is a component of integrated management to be favoured for the control of Black Sigatoka.

These varieties must be incorporated in innovative, sustainable cropping systems that also include cultural control methods (optimum plant management, rational inoculum management using mechanical cleansing techniques, etc.) that will thus make it possible to reduce the negative environmental impacts of commercial plantations and in particular reduce the application of pesticides.

Think of adopting an overall approach combining new hybrids resistant to Black Sigatoka and cropping systems that enable sustainable conservation of resistance.

Bacterial diseases

Bacterial diseases are an increasing concern for growers because of the way in which they spread and the lack of resistant varieties. 

Moko disease

caused by Ralstonia solanacearum (biovar 1 race 2)
formerly  Pseudomonas solanecearum

moko disease
moko disease

Two types of symptoms are observed depending on whether the bacterium is spread via the soil or by the planting tools used (machetes, etc.) or by insects that visit male flowers or their scars after abscission. Upward bacterial colonisation results first in chlorosis and the wilting of the three youngest leaves and then the death of the plant. A cross-section of the pseudostem (or corm) reveals reddish-brown colouring of the vascular vessels. The presence of abundant bacterial exudate is a further sign of bacterial infection. If the contaminated plant bears a fruit bunch, the bacterium colonises all the vascular bundles of the fruits via the rachis. Accumulation of ethylene may cause the premature yellowing of the fruits and cross sections display serious browning. When the bacterium is spread by a machete for example after the cutting of the pseudostem, the contaminated suckers blacken and become stunted in 2 to 4 weeks. The disease was described for the first time in Trinidad in 1910 and is still absent from the Lesser Antilles, except in Trinidad and Grenada. In contrast, it spread rapidly in the Amazon basin in Brazil and in eastern Peru, going as far as northern Guatemala and southern Mexico. It covers a large geographic area. Moko disease spread to the Philippines in 1968 via plant material. There are no resistant varieties or chemical control methods. Only eradication and quarantine give results.

Bacterial wilt

Banana Xanthomonas Wilt (BXW),
Banana Bacterial Wilt Disease (BBW),
caused by Xanthomonas campestris pv. musacearum

xanthomonas wilt
xanthomonas wilt

The symptoms are observed above all on the emergence of spear leaves, especially at flowering. Flower bracts become discoloured and the male bud blackens and shrivels. The leaves yellow, wilt, blacken, dry and crumble (including the pseudostem). Yellow or brown vascular streaks are observed throughout the plant together with pale bacterial secretion on a section at the base of the pseudostem or at the corm. This causes bunches to wilt, with premature maturation and a reddish brown colour inside the fruit. The plant dies within a month of the appearance of any of these symptoms (one month after infection). The disease is spread by foraging insects, infected plant material (suckers, bunches and leaves), tools and man, and also by animals, run-off, rainwater splashes and wind. There are no resistant varieties. Control is by a quarantine period lasting for several months and the destruction of infected plants and those nearby. Free movement of animals is forbidden. This wilt was observed and described in Enset in Ethiopia in about 1968 (this affected the staple foodstuff of 12 million people), and then in Uganda where it has spread since 2001 (75 km per year). Uganda is the second largest banana producer with 10.5 million tonnes (250 to 450 kg per person) and this had decreased by nearly 40% in 2006. The spread has been rapid, with the disease reaching the Democratic Republic of Congo in 2004, Rwanda in 2005 and Burundi, Tanzania and Kenya in 2006.

Viral diseases

Viral diseases of the banana (dessert and cooking fruits) have spread increasingly in recent years as a result mainly of the ease of plant movement and demand for diversification. They consist of banana bunchy top disease and mosaic diseases including banana mosaic, banana streak disease and bract mosaic. The economic damage varies, affecting all cultivated bananas and both large estates and village plantations. Banana bunchy top disease (caused by the banana bunchy top babuvirus, BBTV) can cause losses of 90 or even 100 percent of production. Banana streak disease (caused by the banana streak badnavirus, BSV) causes losses of 40 to 60 percent, and banana bract mosaic (caused by the banana bract mosaic potyvirus, BBrMV) results in losses of more than 40%. Spread is either by vector from outbreaks or by the use of infected germplasm—suckers or tissue culture plants—or, in the special case of BSV, from so-called ‘silent’ bananas with a virus sequence incorporated in the genome of the species Musa balbisiana and capable of producing viral particles in particular as a result of stress (abiotic phenomena, weather conditions, intensive in vitro or in vivo propagation of plant material, etc.). 

Banana bunchy top disease (BBTV)

The plants are markedly stunted and rosetted at the top. The narrow, erect, brittle leaves display strongly chlorotic borders. The characteristic symptom is the appearance of discontinuous dark green streaks along the pseudostem, the main leaf vein and the secondary veins. When the mother plant is infected, so are all the suckers. The most effective vector is the banana aphid Pentalonia nigronervosa.

bunchy top
bunchy top

Mosaic diseases

Banana mosaic caused by the Cucumber mosaic cucumovirus
(CMV)

Infected plants display leaf chlorosis and mottling of the main vein and the pseudostem. Secondary infections may appear in the form of bacterial rots in the sheaths forming the pseudostem. The virus can be spread by a broad range of aphids. The disease can also be spread by pruning tools.

Banana streak disease
(BSV)

The leaf lamina displays discontinuous yellow streaks that rapidly become necrotic. The main vein is unaffected. In severe forms of the disease, the cigar tip becomes necrotic and the plant dies. If the mother-plant is infected so are all the suckers.

banana streak disease
banana streak disease

The disease is transmitted by various mealybug species— Planococcus citri, Saccharicoccus sacchari and  Dysmicoccus brevipes. In recent years, BSV infections unrelated to external contamination have been described in various parts of the world. There are two different causes: 1) tissue culture plants derived from micropropagated healthy interspecific hybrid varieties of banana and 2) the hybrid progeny of crosses between healthy Musa acuminata (genome A) and Musa balbisiana (genome B) parents. Various abiotic stresses cause the appearance of the disease in these hybrids, correlated with the presence in the genome of the M. balbisiana parent of endogenous viral sequences of BSV (e-BSV) containing all the information required to synthesise the infectious virus.

Banana bract mosaic
(BBrMV)

The first stages of infection consist of greenish yellow streaks turning into brownish red necrosis on the leaf lamina and veins. Yellow mottling or whitish streaks are seen on the pseudostem according to the variety infected. Bract mosaic is the final symptom. The disease is transmitted to all the suckers by aphids ( Ropalosiphum madiis, Myzus persicae).

Prevention and control

The only control method available today to fight these banana virus diseases is control of the vector and the use of healthy plant material. Indeed, there are no bananas with natural resistance to these diseases and no cure other than eradication after a virus attack.

The procedure to be followed is based mainly on the use of disease-free germplasm—suckers or tissue culture material screened for viruses—and the cutting back of weed growth where aphids multiply.

Banana borers

Originating in South-East Asia, the banana borer has spread to all subtropical and tropical banana and plantain production regions. The insect ( Cosmopolites sordidus) is 9 to 16 mm long and 4 mm wide. It moves freely in the soil at the feet of banana plants or in plant debris. It is nocturnal and very sensitive to drying. The pest is spread mainly via infested plant material. The adults do no damage. The females lay eggs in the banana rhizome and the larvae feed on this, digging tunnels. These tunnels disturb water and mineral supply of plants, lengthen the production cycle, cause serious decreases in yield and weaken the anchorage of the plants, making them more sensitive to wind. Strong attacks can lead to the death of the plant. In addition to classic chemical treatment, the use of healthy planting material (tissue culture plants) used in clean soil (after fallows) is a method of borer control. New borer trapping methods using pheromones (sordidin) are available. A control system combining entomophagous nematodes and sordidin traps is being developed.

borer
borer
banana borer on a corm
banana borer on a corm

However, the banana borer remains a major pest constraint for banana crops—whether on industrial plantations or smallholdings (plantains are very susceptible to the banana borer). It seems fairly unlikely that improved varieties can be bred rapidly. Control on a farm scale based on the use of traps and maintaining low levels of infestation are being studied, and may in time form an alternative to chemical control.

Nematodes

Numerous nematode species parasitise banana roots and corms. Root knot nematodes ( Meloidogyne spp.) and spiral nematodes ( Helicotylenchus spp.) are found all over the world in all kinds of crop. However, the most damage is caused by the migrating nematodes Pratylenchus spp. and Radopholus similis. The latter species is found everywhere in the hottest banana growing zones and especially in intensive plantations where it arrived via germplasm movements during the spread of the crop during the past two centuries. Pratylenchus coffeae is also present in the hottest zones but is generally indigenous and found mainly on plantain crops. Pratylenchus goodeyi prefers cooler areas and originated on the Africa plateaux. It is observed in certain subtropical zones such as the Canary Islands, for example.

nematode
nematode

Underground enemies

Pratylenchus spp and Radopholus similis are migratory endoparasites whose full biological cycle lasts for 20-25 days in root and corm tissues. Juvenile forms and females are always mobile and can leave the roots when conditions are no longer favourable. These migratory forms can then colonise other roots. As they move within and between cells, these nematodes feed on parenchyma cell cortical cytoplasm, destroying cell walls and creating tunnels that become necrotic and can extend to the whole of the cortex. Root and corm necrosis may be aggravated by other pathogens (fungi and bacteria). In particular, fungi of the genus Cylindrocladium are pathogenic and can cause lesions similar to those made by nematodes. The combination of the two pests may cause very serious damage under certain conditions. The destruction of underground tissue leads to a decrease in water and mineral nutrition resulting in slowed plant growth and development. This can lead to severe decrease in bunch weight and lengthen the period between harvests. Furthermore, destruction of the roots weakens the anchorage of the plants in the ground and increases the risk of toppling, especially during hurricane periods, with a strong economic impact.

Prevention and control

Control methods involving the application of chemicals (mainly organophosphorus compounds and carbamates) that carry substantial sanitary and environmental risks are still used in intensive plantations. For this reason, in spite of their efficacy and very easy application, their use will be increasingly limited in favour of alternative control measures. These include cultural practices improving soil fertility (tillage, irrigation, organic ameliorators, etc.) that indirectly improve plant tolerance to pest pressure. More direct methods such as the use of fallow and the planting of micropropagated bananas are now in common use and lead to a strong decrease in nematode populations (cf. Phytoma No. 584, July-August 2005).

Post-harvest diseases

Storage diseases (wound anthracnose, ripe-fruit (quiescent) anthracnose and crown rots) strongly limit the sale of exported bananas. Colletotrichum musae causes both forms of anthracnose, while crown rots result from a larger parasite complex consisting of C. musae but also other organisms: Fusarium, Verticillium, Botryodiplodia, etc.

Distinction is made between two forms of anthracnose:

-          Ripe-fruit (quiescent) anthracnose:brown lesions develop on fruits after ripening and subsequently in the sales channel. This disease rarely has serious commercial consequences.

-          Wound (non-quiescent) anthracnose: broad brown lesions occur on fingers wounded during harvesting or packing. The symptoms are observed when fruits are unpacked after sea transport and have serious commercial consequences.

wound anthracnose
wound anthracnose

Crown rotsare fungi that spread from cut surfaces when fruits are prepared at the packing stage. This damage is also visible after sea transport and has serious commercial consequences.

The fungi that cause post-harvest diseases are widespread in banana plantations and hence on bunches if these are not protected. In other words, control of infection begins when the inflorescence shoots at the top of the leaf cluster. Anthracnose results mainly from contamination by Colletotrichum musae in the field. It is not possible to detect infected fruit with the naked eye at harvesting but a test can be performed more than three weeks before cutting. Fruits are infected mainly during the first month of flowering. Spores are spread by water and develop on the organs when they start to decompose (old leaves, bracts and above all flowers). Control of the disease must begin in the field and then continue in the packing shed.

Hands can be contaminated by crown rot at various stages in the chain. This greatly complicates the implementation of control measures, but hand contamination by washing water is probably the main cause.

Chemical control of these diseases does not always yield satisfactory results. Indeed, it is sometimes ineffective according to the production zone, and the time of the year and resistance to fungicide has developed in the various fungal species involved. Finally, interest in developing methods other than chemical control is increasing. Indeed, these post-harvest treatments raise two crucial problems—the risks of residues in fruits and the processing of fungicide discharges near packing stations.

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