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Sigatoka disease of banana

Mycosphaerella musicola
This information is part of a full datasheet available in the Crop Protection Compendium (CPC). Find out more information on how to access the CPC.
©CAB International. Published under a CC-BY-NC-SA 4.0 licence.

Distribution

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Host plants / species affected

Main hosts

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Musa acuminata (wild banana)

List of symptoms / signs

Leaves - abnormal colours
Leaves - necrotic areas

Symptoms

Many descriptions of the development of symptoms have been published (Meredith, 1970). The earliest symptom is a light-green, narrow speck about 1 mm in length on the upper surface of the leaf. The speck develops into a streak several millimetres long and 1 mm or less in width running parallel to the leaf veins. The streak elongates and expands laterally to become elliptical in shape and turns rusty red. A water-soaked halo forms around the lesion when the leaf is turgid. This is best seen in the early morning when dew is present on the leaf. This infiltrated tissue quickly turns brown and a young spot is formed. The dark-brown centre of the spot later shrinks and appears sunken and the halo turns a darker brown. The sunken area becomes grey and the halo darker brown forming a well-defined ring around the mature spot, which remains distinct even after the leaf tissue has died. On leaves of young plants, individual spots tend to be larger and more spherical. Mature spots are normally 4-12 mm in length. Symptom development from specks through streaks to spots has been divided into various stages by different authors (Leach, 1946; Klein, 1960, Brun, 1963). Stover (1972) and Stover and Simmonds (1987) have compared these stages.

Leaf tissue surrounding spots turns yellow. This is initially more pronounced on the leaf margin side of the spot. If the infection density is high, large areas of leaf tissue around the spots yellow and eventually become necrotic with dark-brown borders. Where mass infection occurs, areas of necrotic leaf become whitish-grey within a dark border and the outlines of individual lesions are not well defined.

Counting down from the first fully opened leaf, earliest symptoms are first seen on the third or fourth leaf of susceptible plants in an active state of growth, but sometimes appear on the second leaf if conditions are very favourable for infection. Mature spot symptoms are found on older leaves. The overall effect is that the severity of the disease increases in a descending order down the plant. On resistant plants, symptoms may appear only on the very oldest leaves or not at all. Plants with bunches appear more diseased because clean, new leaves are not being produced to displace old leaves with symptoms.

Symptoms of Sigatoka disease are described by Jones (2000b).

Prevention and control

Cultural Methods

The removal and destruction of badly spotted leaves ('trash') from banana plantations is used to reduce inoculum levels. Heavily diseased leaves can also be buried within the plantation or piled on top of one another to prevent the effective discharge of ascospores from most leaves.

Host-Plant Resistance

The major cultivars in the Cavendish subgroup (AAA genome) producing export dessert bananas are highly susceptible to Sigatoka disease. However, many banana cultivars grown by smallholders, such as 'Mysore' (AAB), 'Bluggoe' (ABB), 'Pisang Awak' (ABB) and 'Saba' (ABB), are highly resistant. Cultivars in the Plantain subgroup (AAB) also have resistance at low altitudes, but this is lost at high altitudes in Central and South America, and Cameroon. The wild banana Musa balbisiana (BB) is highly resistant to Sigatoka disease and, as a general rule, the greater the 'B' component in the genome of a cultivar, the greater the resistance of that cultivar to Sigatoka. However, some diploid cultivars derived from M. acuminata, such as 'Pisang Lilin' (AA) and 'Paka' (AA), are also highly resistant and have been used as pollen sources in breeding for resistance to Sigatoka (Jones, 2000b). A full summary of current information on the reaction of banana cultivars to Sigatoka is given in 'Host Range'.

Although Sigatoka (Mycosphaerella musicola) is still important in countries such as Australia, Brazil and India, black leaf streak/black Sigatoka (M. fijiensis) is now attracting more attention in breeding programmes because it has replaced Sigatoka in many banana-growing areas as the major leaf spot problem. Although Sigatoka is hard to find in locations invaded by black leaf streak/black Sigatoka, it is believed to survive at a low level in the leaf spot population.

Black leaf streak/black Sigatoka attacks many cultivars resistant to Sigatoka. Although most cultivars that are resistant to black leaf streak/black Sigatoka are also resistant to Sigatoka, some hybrids bred at the Fundacion Hondureña de Investigación Agricola (FHIA), Honduras are more susceptible to Sigatoka than black leaf streak/black Sigatoka. This indicates that there may be different resistance mechanisms acting against the two pathogens.

Chemical Control

Due to the variable regulations around (de-)registration of pesticides, we are for the moment not including any specific chemical control recommendations. For further information, we recommend you visit the following resources:

Impact

Until the discovery and spread of black leaf streak disease, Sigatoka or yellow Sigatoka, as it is now often called, was the most important foliar disease of banana. It was first recorded in Java (Zimmermann, 1902) and later in the Sigatoka valley on the island of Viti Levu, Fiji (Philpott and Knowles, 1913; Massee, 1914), the location giving its name to the disease. Herbarium specimens indicated that Sigatoka was present in Sri Lanka in 1919 and the Philippines in 1921. The disease was first found in Australia in 1924. In the 1930s, Sigatoka was reported throughout the Central American-Caribbean region. It was also recorded in Surinam Guyana and Colombia in South America, Tanzania and Uganda in East Africa, China and West Malaysia. Reports from West Africa, India and Brazil began in the 1940s and the disease was recorded in most other banana-growing countries for the first time in the 1950s and 1960s (Stover, 1962).

Sigatoka's rapid global dissemination in the 1930s from original areas of distribution in the 1920s led to speculation that spores of the causal fungus were carried by air currents between continents (Stover, 1962). However, long-distance spread was more likely to have occurred by the uncontrolled movement of propagating material and/or diseased banana leaves used to wrap produce. It is highly likely that the disease may have been present at a low level in many countries for some time before it came to the attention of local plant pathologists. Today, Sigatoka is regarded as having a worldwide distribution, although it has not been recorded in the Canary Islands, Egypt or Israel (Meredith, 1970; CABI/EPPO, 1997).

On a vegetatively growing banana plant, the most efficient leaves for photosynthesis are the second to fifth counting down the profile (Robinson, 1996). Lower leaves are progressively less efficient as they are ageing and later senescing. Leaves are not static and on a vigorous plant of a cultivar in the Cavendish subgroup (AAA) growing under optimal environmental conditions with one new leaf appearing every 7 to 8 days, the most efficient leaf area is renewed monthly. On a less vigorous plant growing under suboptimal environmental conditions, this renewal time can be extended to several months. Although a banana plant has the internal ability to partially compensate for lost photosynthetic assimilation due to leaf area destruction, it is important that leaves two to five remain as free of excessive shade, severe leaf tearing and disease as possible otherwise assimilation potential is greatly reduced (Robinson, 1996).

Sigatoka disease is very destructive if left uncontrolled. Leaf spots caused by the disease can coalesce which leads to the premature death of large areas of leaf tissue thus reducing the photosynthetic capabilities of the plant. However, Sigatoka appears to have little effect on vegetative growth in the tropics as measured by the rate of leaf emergence, rate of increase in plant height and height of the plant at the time of shooting (Leach, 1946). This is because the effects of the disease are not sufficiently great on leaves two to five to cause a severe deficit of the assimilates used to power plant growth. Unfortunately, the effect of Sigatoka on fruit development is considerable. After shooting, leaf production ceases and the plant is unable to replace those leaves damaged by Sigatoka. Plants of 'Williams' (AAA, Cavendish subgroup) with fewer than five viable leaves at harvest, a viable leaf being defined as one with more than 30% healthy tissue, produce lighter bunches (Ramsey et al., 1990). The greater the damage and the earlier it occurs after shooting, the greater the effects on yield. On 'Williams' plants with between zero and two viable leaves at harvest, yields are reduced on average by around 25-29% (Ramsey et al., 1990). If Sigatoka is left uncontrolled, it is not uncommon for plants to have four or fewer leaves at shooting and none shortly afterwards (Meredith, 1970). Yield losses would be expected to be highest in these cases.

Sigatoka also disturbs the physiology of fruit resulting in premature ripening (Meredith, 1970; Stover, 1972; Wardlaw, 1972). Premature ripening can occur in the field if plants are severely diseased or in transit to markets if moderately affected. Some field ripening of bunches occurs on 'Williams' plants with fewer than 11 viable leaves at harvest, which reduces marketable yields, and on all bunches on plants with fewer than four viable leaves at harvest, which results in total marketable yield loss (Ramsey et al., 1990). When fruit ripens in transit, consignments are devalued because of uneven ripening and increased risk of post-harvest problems. In Australia, badly affected shipments are often condemned because of the risk of infection by fruit fly, which is an interstate quarantine concern.

Sigatoka caused widespread disruption to the export trades when first introduced to the Latin American-Caribbean region. In Mexico, production fell from 525,000 t in 1937, the year after Sigatoka was first recorded, to 240,000 t in 1941. Exports from the State of Tabasco ceased entirely. In Honduras, production declined to less than one-third of the level prior to the introduction of the disease. Sigatoka caused crop losses of 25-50% in Guadeloupe in 1937. In Ecuador, out of 62 million bunches produced in 1954, only 19 million were fit for export because of uncontrolled Sigatoka on small farms. In subsequent years, the damage was reduced by the timely application of chemicals. However, 15-17 fungicide applications were required every year to control Sigatoka, which considerably increased the cost of production (Meredith, 1970). The cost of Sigatoka control in the north Queensland growing area of Australia has been estimated to be 14% of total production costs (Jones, 1991).

Because of its seriousness, developing a commercial cultivar with Sigatoka resistance became a priority in banana breeding programme (Jones, 2000d). However, this endeavour was not successful. Although Sigatoka is still important in certain locations, such as Australia, Brazil and the Windward Islands, black leaf streak is now attracting more of the banana breeder's attention because it has replaced Sigatoka in many banana-growing areas as the major leaf spot problem. Sigatoka is hard to find in most areas invaded by black leaf streak, but M. musicola is believed to survive at a low level in the leaf spot pathogen population. Indeed, it has been identified in coastal Nigeria on 'SH3362' (AA) a hybrid that is susceptible to Sigatoka, but has resistance to black leaf streak (C Pasberg-Gauhl and F Gauhl, Nigeria, personal communication, 1994). Sigatoka is also still present in the Philippines many years after the introduction of black leaf streak. Sigatoka is more adapted to cooler temperatures than black leaf streak and is dominant at altitudes over 1200-1500 m in tropical countries where both diseases occur.