Mycosphaerella fijiensis Morelet
1.- Taxonomy and phylogeny
Mycosphaerella fijiensis is a heterothallic fungi and its anamorph stage is Pseudocercospora fijiensis (M. Morelet) Deighton. It is a haploid, hemibiotrophic ascomycete within the class of the Dothideomycetes, order Capnodiales and family Mycosphaerellaceae. Its taxonomic placement is based on DNA phylogeny, morphological analyses and cultural characteristics.
Rhodes first described this fungus in the year of 1963 in samples collected from the Valley of Sigatoka, on Fiji. This report was in the same valley where fifty years early M. musicola was first recognized in banana cultivars. In February 1963, it was expected that by the end of 1964 the disease caused by M. fijiensis was affecting the whole island (Leach, 1964a), however some research assume that at the same time it was wide spread in the Southeast of Asia and South Pacific region (Jones, 2000). In 1972 this fungi was reported for the first time in the western hemisphere in Honduras, and in Africa in 1973. By 1991, the disease had been affecting banana crops in the Americas and sub-Saharan Africa (Ploetz, 2003). At the beginning the disease caused by M. fijiensis was called black leaf streak disease by Rhodes (1964). But years later it was called as black Sigatoka.
Morphologically, this fungus has been related to M. musicola and M. eumusae witch are able to attack musa species, but this pathogen has also been related genetically to Septoria tritici blotch pathogen of wheat, M. graminicola. These two together represent the Mycosphaerella branch of the fungal evolutionary tree, the largest genus of plant pathogenic fungi.
Recent studies accomplished by Crous in 2007 have demonstrated that the genus Mycosphaerella is polyphyletic, in this genus are included endophytes, mycoparasites and facultative saprobic plant pathogens (Crous, 2007). However, in case of bananas, different species of Mycosphaerella spp. can live on the same host (Arzanlou, 2008).
2.- Morphology
Conidia of M. fijiensis are produced in streaks early in their development, mainly on the lower leaf surface (Jones, 2000). Conidiophores are pale brown; single to six celled, straight to geniculate, occasionally branched, subcylindric, 16.5–62.5 x4–7um and in hypophyllous fascicles. Conidiogenous cells are up to 25 um long, 2–4um wide at the apex, and have 1–3 minutely thickened scars. Conidia are sub- hyaline, obclavate to cylindric obclavate, have an obclavate basal cell, usually six to eight-celled, 10–120um2.5–5um, with hila that are slightly thickened and darkened along the rim (Crous, 2002).
The pseudothecia are mainly globose, 47–85 um in diameter and immersed in the leaf tissue (Jones, 2000). They occur on both leaf surfaces although they are most common on the upper side. Their ostioles protrude above the leaf surface and are dark brown and conspicuous. Asci are bitunicate, obclavate and lack paraphyses, and the ascospores are colourless, 12.5–16 x2.5–3.8um, and two celled with a constricted septum. M. fijiensis grows very slowly on artificial media. At optimal temperatures, between 24 and 28°C, single conidia cultures reach 1cm in diameter after 38 days on potato dextrose agar (PDA). The color of the colonies can vary from white, grey, pink and black.
M. fijiensis produces bicellular ascospores while its anamorph Paracercospora fijiensis forms 1–10 septate conidia which are produced singly at the apex of conidiophores. M. musicola and M. fijiensis can only be distinguished by the morphology of their anamorph. More recently, a third Mycosphaerella (M. eumusae, anamorph Pseudocercospora eumusae) was reported in Southern and Southeast Asia (Carlier, 2000). Later, a broad study revealed that more than 20 Mycosphaerella species could be isolated from banana leaves (Arzanlou, 2010), but, except for M. musae causing a leaf freckle, the implication of these other Mycosphaerella species as leaf pathogens of bananas has not been determined.The host range of each pathogen is another important diference, M. musicola causes more severe damages in plantain species, as M. fijiensis is more common in banana plantations. The sizes of the ascospores vary in the M. musicola (36 - 72mm), M. fijiensis (47 – 85mm) and M. musae (42 – 51mm).
3. Life cycle and symptoms
In the case of M. fijiensis, conidia and ascospores, are infective, formed under high moisture conditions, and dispersed by rain and irrigation water. Because of its abundance and small size, ascospores are most important in terms of the dispersion of the disease in commercial plantation.
This fungi use an indirect way in order to infect the plant. The penetration of ascospores occurs via stomata on unfurlead leaf that provides and excellent microclimate for infection, besides the high number of stomata on this part of the leaf (Washington, 1998). The main factors for developing the infection are the moisture, and temperature the minimum, optimum, and maximum temperatures for this event are, respectively, 12 °C, 27 °C and 36 °C. Moreover the levels of humidity plays a determinate roll during the infection, has been demonstrated that conidia need a range of 92 to 100% of humidity, while ascospores needs 98 to 100% of humidity to germinate. This fact is related to the highest levels of infection in the rainy season driven by ascospores and the reduction of these levels on the dry season where temperature and humidity decrease (Jacome, 1993), that is the reason why in many production areas this disease occur year-round (Ploetz, 2000).
The symptoms caused by M. fijiensis in banana plants depends basically of the banana variety, the infection can be faster and more pathogenic. The complete process of infection can take between 10 to 14 days since the germ tube penetrate. The symptoms start with small reddish-brown streaks that runs in parallel to the leaf veins, which sum to form larger, dark- brown to black compound streaks. These streaks eventually form fusiform or elliptical lesions that coalesce, then, a water-soaked border with a yellow halo is formed which, eventually, merge to cause extensive leaf necrosis (Fig 3). The disease does not kill the plants immediately, but affect directly the photosynthetic capacity of leaves, decreasing the production and therefore the quantity and quality of fruit, moreover induce the premature ripening of fruit (Churchill, 2011).
As ascospores are disseminated by wind, the disease can be spread over long distances, BLSD has a strong potential progression in landscapes where Musa genotypes are quite frequent, which is the case in most tropical countries where bananas are grown. The control measurements of the disease should be maintained in the same terms for all growers in the region, using identical technical guidelines because disease and pathogen evolution in a specific geographic area has potential influence over a wider area (Laperyre, 2010).
4.- Importance and management
Bananas are one of the fourth most important crops in terms of economics and food security. India is the largest producer of bananas, meantime Ecuador is the largest banana exporter with approximately one-third of the market (Anonymous, 2009). Nonetheless all this industry is highly affected for this disease, the big and the small producers are affected for BLSD.
In the a banana-exporting country where BLSD has been introduced, the history of disease control always shows that control has becoming more difficult, this fact entails to increase the number of fungicide aplications. Costa Rica is one of the countries in Latin-America with highest numbers of fungicide applications per year (more than 30) (Gahul, 1994)
This increase is essentially due to the rapid adaptation of the fungus, becoming resistant to the systemic fungicides, which have a curative effect on the disease (Marin, 2003). The strong adaptation potential of this fungus is a consequence of its biological characteristics: importance of recombination, high population levels and high dispersion capacities. Two types of fungicides have been used for BLSD control: contact fungicides and systemic fungicides (Laperyre, 2010).
The cultural practices to decrease the infection level are not that common, because the bananas are a extensive crop is not suitable this type of management, but small-holders and organic producers of the fruit use the pruning to diminish the inoculum of the fungi in plantations.
Black sigatoka is a leaf-spot disease of banana plants caused by the ascomycete fungus Mycosphaerella fijiensis (Morelet), also known as black leaf streak. It was discovered in 1963 and named for its similarities with yellow Sigatoka, which is caused by Mycosphaerella musicola (Mulder), which was itself named after the Sigatoka Valley in Fiji. In the same valley an outbreak of this disease reached epidemic proportions from 1912 to 1923.[1]
According to new terminology, the Sigatoka disease complex is a cluster of three closely related fungi: Black Sigatoka and its congeners Yellow Sigatoka (Ps. musae) and eumusae leaf spot (Ps. eumusae).[2]
Plants with leaves damaged by the disease may have up to 50% lower yield of fruit, and control can take up to 50 sprays a year.[3]
M. fijiensis reproduces both sexually and asexually, and both conidia and ascospores are important in its dispersal. The conidia are mainly waterborne for short distances, while ascospores are carried by wind to more remote places (the distances being limited by their susceptibility to ultraviolet light). Over 60 distinct strains with different pathogenic potentials have been isolated. To better understand the mechanisms of its variability, projects to understand the genetic diversity of M. fijiensis have been initiated.[3]
When spores of M. fijiensis are deposited on a susceptible banana leaf, they germinate within three hours if the humidity is high or a film of water is present. The optimal temperature for germination of the conidia is 27 °C (81 °F). The germ tube grows epiphytically over the epidermis for two to three days before penetrating the leaf through a stoma.[4] Once inside the leaf, the invasive hypha forms a vesicle and fine hyphae grow through the mesophyll layers into an air chamber. More hyphae then grow into the palisade tissue and continue on into other air chambers, eventually emerging through stomata in the streak that has developed. Further epiphytic growth occurs before the re-entry of the hypha into the leaf through another stoma repeats the process.[5][6] The optimal conditions for M. fijiensis as compared with M. musicola are a higher temperatures and higher relative humidity, and the whole disease cycle is much faster in M. fijiensis.[5]
Black Sigatoka is also known as black leaf streak, causing streaks that run parallel to the leaves. It affects banana trees specifically in tropical climates; including Asia, West Africa, China, and South America.[7] Tropical weather is the preferred climate for banana cultivation, but it is also the environment where the pathogen thrives: hot and humid, with plenty of rainfall to aid in dispersal. The optimal environment of the pathogen is similar to that of the banana tree. The fungus infects mature banana leaves and will continue to cause infection without proper control.[8]
In the early stages of the infection of the plant, the lesions have a rusty brown appearance and appear to be faint, paint-like specks on the leaves. They become more visible on the undersides of the banana leaf as the lesions and leaves grow. The spots on the undersides of leaf are the fungus itself. The sign of the pathogen consists of the ascocarp which holds the ascospores used for dissemination to infect healthy new plants when the environment is conducive. The pathogen then survives on dead plant tissue as mycelium.[9] The dimensions of the lesions are characteristically 20 by 2 millimetres (25⁄32 in × 5⁄64 in) with a well defined wall surrounding it.[10] After further development, they become darker, sink into the leaf, and turn into depressions. The depressions themselves and the chlorosis surrounding them are the visible symptoms of the plant pathogen. They eventually will merge, causing the rapid decline of plant morphological and physiological function.[11] Leaves with large infectious lesions will start to degrade and collapse because the leaf spots interrupt the plant's ability to perform photosynthesis, leading to the ultimate death of the plant.[7]
The yellow leaf streak pathogen is in the same genus as that of black leaf streak. Yellow leaf streak shows smaller, yellow-green lesions that appear on top of the leaves.[7]
There are several ways to control black Sigatoka, either by cultural and chemical means or by genetic engineering. Cultural control includes the destruction of leaves that have been infected with M. fijiensis. This will help reduce the initial (ascospores) and secondary (conidia) spread of inoculum of new plant leaves and interrupt the pathogen's polycyclic disease cycle. Another way of reducing primary/secondary inoculums is via efficient drainage and irrigation. Keeping the environment around the plants at low humidity helps keep the ascospores/conidia produced by the pathogen from being dispersed in the water draining towards other healthy, susceptible hosts.[10] Other techniques include planting the banana trees more than 1,000 metres (3,300 ft) above sea level and practicing multi-cropping, mixing banana with other trees or vegetation.[8]
One form of chemical control is preemptive use of fungicides on banana trees in order to protect them from primary inoculum. The fungicide does not kill the pathogen itself, but works on the pre-necrotic spots on the leaves, stopping the secondary spores from inoculating new, healthy plant tissue. The best time to apply this protective fungicide is in the beginning of the season in order to stop any initial infection.[11] The class of fungicides widely used to control black leaf streak is the triazoles.[9] These are demethylation inhibitors and should be rotated with compounds having other modes of action to slow the development of resistance.[12] Leaves that have already been infected must be removed mechanically to save the rest of the tree.[11] Research has shown that there may be fungicide resistance developing for M. fijiensis. It has been observed that following the intensive application of chemicals, the fungus persisted and spread. The same observations were found in fields with no chemical interference; the belief now being that the untreated fields are “breeding grounds for (the) development of resistant strains”.[13] Methyl benzimidazole carbamates are also used and there is also resistance known to these.[14] Although fitness penalties are common in resistance evolution many MBC resistant pathogens do not suffer any penalty and a few have the opposite effect.[14] M. fijiensis is one such case: Romero et al., 1998 find MBC resistant isolates benefit from enhanced virulence (specifically tested with benomyl).[14]
Research today shows continuous action towards reinventing banana breeding programs. However, some cultivars of bananas are resistant to the disease. Research is done to improve productivity and fruit properties of these cultivars. A genetically modified banana variety made more resistant to the fungus was developed and was field tested in Uganda in the late 2000s.[15] Furthermore, the search for genetic resistance shows promise with the discovery of a protein that can produce a hypersensitive response to control M. fijiensis that is being introduced into banana trees. This may lead to the identification of a resistance gene that could be transferred to banana trees.[16]
The worldwide spread of the disease has been rapid, with its naming and first reported occurrence in 1963.[17][18] The disease was reported in 1972 in Honduras, from where it spread north to central Mexico and south to Brazil and into the Caribbean islands[18] in 1991.[19] The fungus arrived in Zambia in 1973 and spread to the banana-producing areas of Africa from that introduction.[18] The first occurrence of black Sigatoka in Florida was reported in 1999.[20] As it spread, Black Sigatoka replaced the yellow form and has become the dominant disease of bananas worldwide.[18][21]
The most likely route of infection is via the importation of infected plant material, and infection can spread rapidly in commercial areas where bananas are farmed in monoculture.[18] Removal of affected leaves, good drainage, and sufficient spacing also help to fight the disease. Although fungicides improved over the years, the pathogen developed resistance. Therefore, higher frequency of applications is required, increasing the impact on the environment and health of the banana workers. In regions where disease pressure is low and fungicide resistance has not been observed, it is possible to better time the application of systemic fungicides by using a biological forecasting system.[22]
Bananas are a principal crop for people with limited access to other resources, and the decrease in production of the fruit can limit their diet. There is also the possibility that the cost of bananas will rise with the substantial loss of bananas, leading to unaffordability.[10] M. fijiensis has been found in all regions of the world that are major producers of bananas and is a constraint for these countries; specifically, Africa, Asia, and South America. Black Sigatoka is a very destructive disease to the foliage of banana trees. The disruption of photosynthesis can reduce fruit yield by up to 50%.[8] Infection with black streak deaf can interrupt ripening, causing fruit to “ripen prematurely and unevenly, and as a result becoming unsuitable for export”.[11] A disruption in the maturation of the fruit can lead to a major shift in the economy of the international commerce. 10% of the bananas that are grown are sold to other countries while the other 90% is consumed by the farmers and local communities. Small farmers growing bananas for local markets cannot afford expensive measures to fight the disease. Black Sigatoka of Bananas threatens the fruit's economy and the lives of the people who depend on the fruit for subsistence.[23]
Black sigatoka is a leaf-spot disease of banana plants caused by the ascomycete fungus Mycosphaerella fijiensis (Morelet), also known as black leaf streak. It was discovered in 1963 and named for its similarities with yellow Sigatoka, which is caused by Mycosphaerella musicola (Mulder), which was itself named after the Sigatoka Valley in Fiji. In the same valley an outbreak of this disease reached epidemic proportions from 1912 to 1923.
According to new terminology, the Sigatoka disease complex is a cluster of three closely related fungi: Black Sigatoka and its congeners Yellow Sigatoka (Ps. musae) and eumusae leaf spot (Ps. eumusae).
Plants with leaves damaged by the disease may have up to 50% lower yield of fruit, and control can take up to 50 sprays a year.
Mycosphaerella fijiensis es un hongo ascomiceto patógeno.
Dentro de las enfermedades fúngicas que atacan al banano, la sigatoka negra es la más seria a nivel mundial, la cual es causada por el hongo Mycosphaerella fijiensis Morelet.
Este hongo ataca las hojas y provoca pérdidas de más de 50% en el rendimiento. A nivel mundial el costo para el control es estimado en aproximadamente US$ 2500 millones por año, lo que no incluye su costo sobre el ambiente (CICY, 2004). Cuando la producción de banano se realiza con fines de exportación, se hace indispensable mantener el follaje libre de la enfermedad, aspecto que se logra parcialmente con la aplicación de fungicidas protectantes y sistémicos (Patiño, 2003), lo que representa un costo anual de cerca de 350 millones de dólares para América Latina y 25 millones de dólares para Colombia (Peláez et al., 2006.). Su control trae consigo no solo problemas económicos, sino ambientales por el uso intensivo de estos compuestos, (Mourichon et al., 1997).
Esta enfermedad se identificó inicialmente en 1963, en la costa del sudoeste de Viti-Levu en las islas Fiyi, aunque hay evidencias de su presencia en Hawái y en algunas zonas del Pacífico desde mucho antes (Stover, 1972 citado por Aguirre, 2003), desde entonces se desplazó hacia las zonas bananeras del Pacífico y Asia. En América Latina la sigatoka negra se descubrió por primera vez en Honduras en 1972, distribuyéndose hacia el norte a Guatemala, Belice, el sur de México y hacia el sur como El Salvador, Nicaragua, Costa Rica, Panamá y Colombia (Mourichon, Carlier y Fouré, 1998; Ploetz, 1999 citado por Consuegra y Lorenzo, 2004).
La enfermedad llega a causar una reducción del 56,8 % en el peso del racimo cuando no se controla químicamente (Belalcázar, 1991), además, se presenta una maduración prematura de los racimos la cual es la principal causa de pérdidas económicas ocasionadas por la enfermedad (Marín y Romero, 1992 citado por Salazar et al., 2006). A lo antepuesto se le agrega el peligro de la pérdida de sensibilidad del patógeno hacia los fungicidas, dado el número limitado de químicos que existe para su control, hecho que viene afectando de forma negativa el sistema ecológico de la zona bananera, a través de la gran cantidad de agroquímicos que se arrojan al ambiente (Mourichon et al., 1997; Chica et al., 2004).
La sigatoka negra es causada por el hongo de la clase Ascomycetes Mycosphaerella fijiensis Morelet, cuyo estado imperfecto corresponde a Pseudocercospora fijiensis (Morelet) (Marín, 2003); por consiguiente, el agente causal puede propagarse mediante la producción de ascosporas y conidios (Aislant y Gámez, 2004).
El proceso infeccioso del hongo puede iniciarse a partir de ascosporas o conidios. El ciclo de vida del patógeno depende las condiciones atmosféricas, huésped y variabilidad del hongo (Sánchez y Cárdenas, 2002); después de la germinación de las ascosporas o conidios y la penetración de la hifa a través de los estomas inicia un proceso de infección caracterizado por la aparición de seis estados de desarrollo de los síntomas de la enfermedad. El ciclo se inicia con la germinación de las esporas, las cuales, después de su liberación y dispersión por acción del agua o el viento, se depositan sobre las hojas sanas o ya infectadas. Allí el inóculo germina para producir un tubo germinativo que se alarga y se ramifica rápidamente en busca de estomas, para luego penetrar en un tiempo que va de 2 a 6 horas. Para que este proceso ocurra es necesario la presencia de agua libre sobre las hojas (Merchán, 2000).
La temperatura óptima de germinación de estructuras oscila entre 26-28 ºC, aunque el efecto de la temperatura sobre la germinación se puede caracterizar mediante una función cuadrática de respuesta, con un óptimo estimado de 26,5 ºC. (Jácome y Stevenson, citados por Marín et al; 2003); las precipitaciones son consideradas un factor de especial relevancia en la dispersión del inóculo, de manera que se presenta una época de baja incidencia y otra de alta incidencia, según las épocas de sequía o de lluvia, respectivamente (Belalcázar y Merchán citado por Aislant y Gámez, 2004). Las ascosporas requieren ambientes saturados o agua libre para su germinación y elongación del tubo germinativo. Las conidias en contraste germinan a un amplio rango de humedades que va de 92 a 100%, en tanto que las ascosporas sólo germinan con humedades altas de 98 a 100%. Se presume, que teniendo en cuenta antecedentes de baja cantidad de agua requerida para germinación de conidias esta puede ser la fuente de inóculo responsable del desarrollo de la enfermedad en estaciones secas (Jácome y Stevenson, citados por Marín et al; 2003).
Las ascosporas o esporas de origen sexual se reproducen en las lesiones adultas, es decir, cuando se presenta en el haz manchas negras rodeadas de un halo amarillo y centro semihundido (Estadio 5), en el interior de los cuerpos fructíferos conocidos como ascocarpos o seudotecios.
Las conidias o esporas de origen asexual se producen sobre los conidióforos en las lesiones jóvenes, cuando se observan lesiones en las hojas de 3 mm de longitud de color café rojizo, visibles en el haz y el envés, denominadas pizcas (Estadio 2). Los conidios se desprenden de su tallo o conidióforo, por acción de agentes ambientales como el agua y el viento (AUGURA - Ceníbanano, 2007; Merchán, 2000 citado por Aislant y Gámez, 2004).
La sigatoka negra induce daños en los tejidos de la planta de banano desde antes de infectar la hoja, puesto que desde que hay contacto de las estructuras de dispersión del patógeno con la superficie de la hoja se observa desorganización de los tejidos (AUGURA – CENIBANANO, 2007). Las toxinas producidas por M. fijiensis afectan la fisiología de las células del mesófilo y éstas entran en un proceso de muerte celular que se expresa en los síntomas de manchas parduzcas hasta el color característico de necrosis entre las nervaduras secundarias de la hoja (Sánchez y Cárdenas, 2002). La presencia de las lesiones foliares se utiliza como método de diagnóstico y seguimiento de la enfermedad en las plantaciones comerciales.
Se le llama así a la práctica cultural del cultivo de las musáceas en el que se elimina mecánicamente con una herramienta filosa las partes de la hoja infectadas con sigatoka que están en esporulación activa.
Mycosphaerella fijiensis es un hongo ascomiceto patógeno.
Mycosphaerella fijiensis
La cercosporiose noire (ou sigatoka noir) est une maladie foliaire du bananier causée par le champignon ascomycète Mycosphaerella fijiensis (Morelet). Les plantes ayant leurs feuilles endommagées par la maladie peuvent avoir un rendement atteignant 50 % en moins de fruits. Le sigatoka noir, a été nommé ainsi pour sa ressemblance avec le sigatoka jaune (cercosporiose jaune) causé par Mycosphaerella musicola (Mulder), d'après le nom de la vallée de Sigatoka aux Fidji, où une éruption de cette maladie a atteint des proportions épidémiques de 1912 à 1923[1].
M. fijiensis se reproduit de façon sexuée et asexuée. Les conidies et les ascospores sont importantes toutes deux pour la dispersion. Les conidies sont principalement transportées par l'eau sur de courtes distances, tandis que les ascospores sont transportées par le vent vers des lieux plus éloignés (les distances étant limitée par leur sensibilité à la lumière ultraviolette). Plus de soixante souches distinctes avec des potentiels pathogènes différents ont été isolées. Afin de mieux comprendre les mécanismes de cette variabilité, un « Genetic diversity of Mycosphaerella fijiensis Project » a été lancé.
Lorsque des spores de M. fijiensis se déposent sur une feuille de bananier sensibles, elles germent dans les trois heures, si un film d'eau est présent ou si l’humidité est très élevée. La température optimale pour la germination des conidies est de 27 °C. Le tube germinatif croît comme un épiphyte sur l’épiderme pendant deux à trois jours avant de pénétrer dans la feuille par un stomate[2]. Une fois à l’intérieur de la feuille, l’hyphe invasif forme une vésicule et de fins hyphes grandissent à travers les couches du mésophylle dans une lacune. D'autres hyphes se développent ensuite dans le parenchyme palissadique et continuent dans d'autres lacunes, et finalement réémergent à travers les stomates de la tache qui s’est développée. Une croissance épiphytique se poursuit avant la rentrée de l’hyphe dans la feuille à travers un autre stomate, répétant ainsi le processus[3],[4]. Les conditions optimales de M. fijiensis, par comparaison avec M. musicola, sont des températures et une humidité relative plus élevées; par ailleurs, le cycle de la maladie est beaucoup plus rapide dans fijiensis[3].
Dans les plantations pour l’exportation, la cercosporiose noire est endiguée par de fréquentes applications de fongicides. L’enlèvement des feuilles atteintes, un bon drainage et un espacement suffisant aident aussi à lutter contre la maladie. Bien que les fongicides s’améliorent au fil des ans, l’agent pathogène développe une résistance. Par conséquent, une fréquence plus élevée d'application est nécessaire, ce qui augmente l’impact sur l'environnement et la santé des travailleurs des bananeraies. Dans un rapport du Conseil Départemental de l’Ordre des Médecins de Guadeloupe, le docteur Josiane Jospelage alerte sur la dangerosité de trois des principaux produits utilisés dans le cadre de la lutte contre la cercosporiose noire par épandage aérien[5].
Les petits fermiers cultivant des bananes pour le marché local ne peuvent pas se permettre des mesures coûteuses pour lutter contre la maladie. Cependant, certains cultivars de bananier sont résistants à la maladie. Des recherches sont effectuées pour améliorer la productivité et les propriétés des fruits de ces cultivars. Une variété de banane génétiquement modifiée mise au point en 2007, plus résistante au champignon, serait testée sur le terrain en Ouganda[6].
La maladie est présente dans presque toutes les régions du monde où sont cultivées les bananes[7]. L'Australie fait partie des rares exceptions[7]; celle-ci a cependant dû faire face à une introduction de la maladie en 2001, mais a réussi à l'éradiquer grâce à un programme strict de quarantaine[7].
Mycosphaerella fijiensis
La cercosporiose noire (ou sigatoka noir) est une maladie foliaire du bananier causée par le champignon ascomycète Mycosphaerella fijiensis (Morelet). Les plantes ayant leurs feuilles endommagées par la maladie peuvent avoir un rendement atteignant 50 % en moins de fruits. Le sigatoka noir, a été nommé ainsi pour sa ressemblance avec le sigatoka jaune (cercosporiose jaune) causé par Mycosphaerella musicola (Mulder), d'après le nom de la vallée de Sigatoka aux Fidji, où une éruption de cette maladie a atteint des proportions épidémiques de 1912 à 1923.
Mycosphaerella fijiensis, é un fungo ascomiceto patóxeno. Xera unha enfermidade chamada de sigatoka negra, principal doenza que afecta as bananeiras.
Dentro das enfermidades fúnxicas que atacan a bananeira, a sigatoka negra é a máis seria a nivel mundial, a cal é causada polo fungo Mycosphaerella fijiensis Morelet.
Este fungo ataca as follas e provoca perdas de máis de 50% no rendemento. A nivel mundial o custo para o control é estimado en aproximadamente 2.500 millóns de $ americanos por ano, o que non inclúe a pegada no medio ambiente (CICY, 2004). Cando a produción de banana se realiza con fins de exportación, faise indispensábel manter a follaxe libre da enfermidade, aspecto que se logra parcialmente coa aplicación de funxicidas protectantes e sistémicos (Patiño, 2003), o que representa un custo anual de preto de 350 millóns de dólares para América Latina e 25 millóns de dólares para Colombia.[2] O seu control trae consigo non só problemas económicos, senón ambientais polo uso intensivo destes compostos.[3]
Esta doenza identificouse inicialmente en 1963, na costa do Suroeste de Viti-Levu nas illas Fidxi, aínda que hai evidencias da súa presenza no Hawai e nalgunhas zonas do Pacífico desde moito antes,[4] desde entón desprazouse cara ás zonas bananeiras do Pacífico e Asia. En América Latina a sigatoka negra descubriuse por vez primeira en Honduras en 1972, distribuíndose cara ao norte a Guatemala, Belize, o sur de México e cara ao sur como O Salvador, Nicaragua, Costa Rica, Panamá e Colombia.[5]
A enfermidade chega a causar unha redución do 56,8 % no peso do acio cando non se controla quimicamente,[6] ademais, preséntase un madurecemento prematuro dos acios o cal é a principal causa de perdas económicas ocasionadas pola enfermidade.[7] Ao anteposto agrégaselle o perigo da perda de sensibilidade do patóxeno cara aos funxicidas, dado o número limitado de químicos que existe para o seu control, feito que vén afectando de forma negativa o sistema ecolóxico da zona bananeira, a través da gran cantidade de agroquímicos que se deitan no ambiente.[8]
A sigatoka negra é causada polo fungo da clase Ascomycetes Mycosphaerella fijiensis Morelet, cuxo estado imperfecto corresponde a Pseudocercospora fijiensis;[9] por conseguinte, o axente causal pode espallarse mediante a produción de ascosporas e conidios.[10]
O proceso infeccioso do fungo pode iniciarse a partir de ascosporas ou conidios. O ciclo de vida do patóxeno depende as condicións atmosféricas, hóspede e variabilidade do fungo;[11] despois da xerminación das ascosporas ou conidios e a penetración da hifa a través dos estomas inicia un proceso de infección caracterizado pola aparición de seis estados de desenvolvemento dos síntomas da enfermidade. O ciclo iníciase coa xerminación das esporas, as cales, despois da súa liberación e dispersión por acción da auga ou o vento, deposítanse sobre as follas sas ou xa infectadas. Alí o inóculo xermina para producir un tubo xerminativo que se alonga e se ramifica axiña na procura de estomas, para despois penetrar nun tempo que vai de 2 a 6 horas. Para que este proceso ocorra cómpre a presenza de auga libre sobre as follas.[12]
A temperatura óptima de xerminación de estruturas oscila entre 26-28 °C, aínda que o efecto da temperatura sobre a xerminación pódese caracterizar mediante unha función cuadrática de resposta, cun óptimo estimado de 26,5 °C.[13] as precipitacións son consideradas un factor de especial relevancia na dispersión do inóculo, de maneira que se presenta unha época de baixa incidencia e outra de alta incidencia, segundo as épocas de seca ou de choiva, respectivamente.[14] As ascosporas requiren ambientes saturados ou auga libre para a súa xerminación e elongación do tubo xerminativo. As conidias en contraste xerminan a un amplo rango de humidades que vai de 92 a 100%, en tanto que as ascosporas só xerminan con humidades altas de 98 a 100%. Presúmese, que tendo en conta antecedentes de baixa cantidade de auga requirida para xerminación de conidias esta pode ser a fonte de inóculo responsábel do desenvolvemento da enfermidade en estacións secas.[13]
As ascosporas ou esporas de orixe sexual reprodúcense nas lesións adultas, é dicir, cando se presenta no feixe manchas negras arrodeadas dun halo amarelo e centro semihundido (Estadio 5), no interior dos corpos frutíferos coñecidos como ascocarpos ou seudotecios.
As conidias ou esporas de orixe asexual prodúcense sobre os conidióforos nas lesións novas, cando se observan lesións nas follas de 3 mm de lonxitude de cor café avermellado, visíbeis no feixe e no envés, denominadas chiscos (Estadio 2). Os conidios despréndense do seu talo ou conidióforo, por acción de axentes ambientais como a auga e o vento.[15]
A sigatoka negra induce danos nos tecidos da planta da bananeira dende antes de infectar a folla, posto que desde que hai contacto das estruturas de dispersión do patóxeno coa superficie da folla obsérvase desorganización dos tecidos.[16] As toxinas producidas por M. fijiensis afectan a fisioloxía das células do mesófilo e estas entran nun proceso de morte celular que se expresa nos síntomas de tacas apardadas até a cor característica de necrose entre as nervaduras secundarias da folla.[11] A presenza das lesións foliares utilízase como método de diagnóstico e seguimento da enfermidade nas plantacións comerciais.
Chámaselle así á práctica cultural do cultivo das musáceas na que se elimina mecanicamente cunha ferramenta filosa as partes da folla infectadas con sigatoka que están en esporulación activa.
ka-negra (Mycosphaerella fijiensis)
Mycosphaerella fijiensis, é un fungo ascomiceto patóxeno. Xera unha enfermidade chamada de sigatoka negra, principal doenza que afecta as bananeiras.
De Zwarte Sigatokaziekte is een schimmelziekte die bananenplanten aantast en de bananenoogst tot de helft kan reduceren. De ziekte is vernoemd naar de Sigatokavallei op het eiland Viti Levu (Fiji), waar de ziekte tussen 1912 en 1923 epidemische vormen aannam.
De ziekte wordt veroorzaakt door de bladschimmel Mycosphaerella fijiensis (synoniem: Pseudocercospora fijiensis), een zeer agressieve schimmel die in hoog tempo resistentie tegen fungiciden ontwikkelt en hierdoor zeer moeilijk te bestrijden is. Samen met de Panamaziekte vormt deze ziekte een ernstige bedreiging voor de bananenteelt. Wetenschappelijk onderzoek richt zich op het opsporen van de natuurlijke resistentiegenen van de banaan, om middels genetische modificatie te komen tot een bananenvariant die niet kan worden aangetast door de schimmel.[1]
Zie de categorie Pseudocercospora fijiensis van Wikimedia Commons voor mediabestanden over dit onderwerp. De Zwarte Sigatokaziekte is een schimmelziekte die bananenplanten aantast en de bananenoogst tot de helft kan reduceren. De ziekte is vernoemd naar de Sigatokavallei op het eiland Viti Levu (Fiji), waar de ziekte tussen 1912 en 1923 epidemische vormen aannam.
De ziekte wordt veroorzaakt door de bladschimmel Mycosphaerella fijiensis (synoniem: Pseudocercospora fijiensis), een zeer agressieve schimmel die in hoog tempo resistentie tegen fungiciden ontwikkelt en hierdoor zeer moeilijk te bestrijden is. Samen met de Panamaziekte vormt deze ziekte een ernstige bedreiging voor de bananenteelt. Wetenschappelijk onderzoek richt zich op het opsporen van de natuurlijke resistentiegenen van de banaan, om middels genetische modificatie te komen tot een bananenvariant die niet kan worden aangetast door de schimmel.
A Sigatoka Negra é considerada a doença mais destrutiva da cultura da bananeira, tendo como agente causal o fungo Mycosphaerella fijiensís Var. difformis, cuja forma imperfeita é Paracercospora fijiensis.
As condições necessárias para o pleno desenvolvimento da doença são índices elevados de temperatura e umidade, porém a doença tem ocorrido em regiões de clima atípico e provocado perdas significativas.
Mycosphaerella fijiensis je grzib[5], co go ôpisoł M. Morelet 1969. Mycosphaerella fijiensis nŏleży do zorty Mycosphaerella i familije Mycosphaerellaceae.[6][7] Żŏdne podgatōnki niy sōm wymianowane we Catalogue of Life.[6]
Mycosphaerella fijiensis je grzib, co go ôpisoł M. Morelet 1969. Mycosphaerella fijiensis nŏleży do zorty Mycosphaerella i familije Mycosphaerellaceae. Żŏdne podgatōnki niy sōm wymianowane we Catalogue of Life.
