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Bacterial blight can affect the host plant throughout its life cycle and symptoms vary, to some extent, with plant age and organ affected.
The most common and conspicuous symptom is angular leaf spot which begins with dark-green, water-soaked spots, initially more clearly visible on the underside of the leaf lamina; the spots are angular in shape, being delimited by the smaller veins. Older spots become dark-brown or black and are visible on the upper surface of the leaves. The angular spots may be few in number in more resistant host material but, on susceptible cultivars, they can cover much of the leaf, causing chlorosis, followed by necrosis and distortion of the lamina. Similar spots may be found on the cotyledons of young seedlings where infection occurs from the soil or seed during germination and emergence. Under favourable conditions, infection may spread from the seedling cotyledon or the leaf onto the petiole and then to the main stem, leading to seedling mortality in susceptible cultivars.
In older plants, the lesions can girdle the main branches causing them to break, with the loss of leaves and fruiting branches. This phase of the bacterial blight syndrome is known as blackarm because of the blackened appearance of the affected petioles and branches.
Sometimes infection on the leaf occurs as water-soaked tissue, which later turns black, on either side of the main veins. This is referred to as vein blight and can occur together with, or occasionally in the absence of, angular leaf spot.
In older plants, water-soaked lesions can occur on the bracts of the epicalyx and more commonly on the developing boll. Bacterial boll rot begins as roughly spherical water-soaked spots on the boll surface which can expand to >1 cm in diameter on susceptible cultivars, becoming black as they age and penetrating the boll cortex to cause internal boll rot. The blight bacterium can also be introduced into the young boll during feeding on the seed by the cotton stainer (Dysdercus spp.). This causes the lint to become stained yellow or brown and sometimes leads to internal boll rot.
Control measures against bacterial blight are necessary in all the main cotton-growing areas of the world. Control is achieved mainly through the use of resistant varieties which have reduced the disease to a minor status on Upland cottons in many countries where it was once a serious problem. To ensure that it remains a minor disease, it is necessary to avoid the introduction of exotic races of the pathogen on imported seed and to continue screening for blight resistance in cotton breeding programmes.
There is considerable genetic variability for resistance to bacterial blight within the genus Gossypium. The full range of disease expression, from fully susceptible to highly resistant, is found in the Upland cottons (G. hirsutum). The highest degree of resistance is found in G. hirsutum var. punctatum. Little natural resistance occurs in G. barbadense. Knight (1945, 1946, 1954a) identified 10 major genes for blight resistance (B-genes) to which he ascribed the symbols B1 to B10. Eight of these genes were dominant or partially dominant in their expression. Most of these genes were transferred to the long-staple cotton cultivars and Knight's methods and genes continue to be exploited in the Sudan (Siddig, 1973) and elsewhere to produce cottons with a combination of B-genes which confers immunity to all known races of the blight pathogen (Hillocks, 1992). In the Sudan, most of the successful blight-resistant varieties contain the genes B2 and B6. A new race of the pathogen has appeared which is virulent to that gene combination, but a line (S2950) has been developed which is resistant to the new isolate (Wallace and El Zik, 1990). Varieties with resistance based on the genes B2 and B3 continue to provide protection against blight in many African countries (Hillocks and Chinodya, 1988) and also in South America (Ruano et al., 1988). However, B2B3 does not completely prevent disease occurrence and the disease can sometimes occur when conditions are highly favourable (Hillocks and Chinodya, 1988). In the USA, immunity to blight has been stable for over 20 years in some of the Tamcot varieties (Wallace and El Zik, 1990). Tamcot and other lines were immune when tested in India and most of the immune lines carried the genes B2, B3 and B7 (Meshram and Sheo, 1989). Screening for resistance can be based on naturally occurring leaf infection combined with inoculation with an appropriate mixture of virulent races of the pathogen, several different inoculation methods may be used (Brinkerhoff, 1970; Hillocks and Chinodya, 1988).
Cultural and Sanitary Methods
X. axonopodis pv. malvacearum cannot survive in the soil outside of crop residues and is therefore readily controlled with rotations. One crop season without cotton is usually sufficient to virtually eliminate crop residues as a source of primary inoculum. If this is combined with seed certification to ensure that crops used for seed production are free of bacterial blight, the disease can be controlled even where susceptible varieties are grown (Schnathorst, 1966). Cotton seed can also be treated with bactericides to reduce the risk of seed transmission (see Seed Treatment under Seedborne Aspects of Disease).
One of the earliest successful integrated control programmes for bacterial blight was carried out in the 1950s and 1960s in California, USA. This programme combined the use of acid-delinted seed obtained from blight-free areas with crop rotation, ploughing-in of crop residues, and the use of furrow irrigation in preference to sprinklers (Schnathorst, 1966). In Tanzania, recommendations for blight control include the use of seed dressing, rotation and the use of resistant varieties (Hillocks, 1981). In Zimbabwe, the combination of rotation and the use of blight-resistant Albar varieties keeps the disease at low levels (Hillocks and Chinodya, 1988).
Although bacterial blight is found in all the major cotton-producing areas of the world, it has declined in importance in the 1990s due to the wide availability of resistant varieties. However, it remains a potentially important disease because of the variability of the pathogen and the appearance of new races. Reports from Australia in 1980 indicated that bacterial blight was of increasing importance due to the proliferation of new races of X. axonopodis pv. malvacearum (Anon., 1980). The disease may also resurge as an important problem if screening for resistance is not maintained in variety improvement programmes, if seed treatment is discontinued, or if continuous cotton cultivation is practised.
Bacterial blight was one of the major constraints to cotton production when the crop was first introduced to Africa. The first programme to breed for resistance was initiated in the Sudan (Knight, 1946). The disease became prevalent in the USA during the 1950s (Schnathorst et al., 1960) and in India in the 1970s (Verma, 1986).
The main cause of yield loss is the blackarm symptom, which results from the loss of the fruiting branches (Arnold, 1965). X. axonopodis pv. malvacearum can also cause stand losses and loss of vigour at the seedling stage, when bacterial blight often begins. This pathogen is capable of damaging the boll, but only penetrates the carpel wall in the most susceptible cultivars. Boll rot can occur when the bacterium is introduced through the carpel wall on the stylet of insects such as species of Dysdercus (Hillocks, 1992). Lesions caused by bacterial blight can allow secondary invasion of fungal pathogens such as Aspergillus niger or Rhizopus stolonifer to take place (Ray, 1946). Raute and Ekbote (1985) report that yield/plant and its components (boll number/plant, average boll weight and halo length) were negatively correlated with disease intensity; ginning outturn was not affected by disease.
Disease severity can be influenced by many factors. There is a general tendency for stem infections to be closely associated with early leaf infection (Wickens and Logan, 1957). Increased rates of nitrogen have been associated with decreased severity of bacterial blight in Upland cotton (Rolfs, 1915; Presley and Bird, 1968). Planting regimes can also influence severity. Arnold and Arnold (1960) found that there was 8% infection when seeds were planted singly, the level of infection increasing to 62% when 6 seeds were planted/hole. In Uganda, Jameson (1950) reported that above average rainfall in the first quarter of the year reduced the incidence of blackarm. He also showed that the disease was least severe in areas with 8-9 cm of rain or more in February. Disease incidence was shown to increase when rainfall in the third quarter of the year was above average and was most severe in areas with 12 cm or more in August. This led to the suggestion that a wet close season favours rotting of infected debris from the previous crop. If the close season is dry, there may be an appreciable carry-over of infected material. If the carry-over is large, secondary spread can be of epidemic proportions and if small, the August rainfall could be the deciding factor in whether epidemics occur. Jameson and Thomas (1952) also consider the effect of rainfall distribution and time of planting as important factors in disease severity.
Disease severity in Kenya has been reported to be greatest at higher altitudes where rainfall is heaviest (Hastie, 1952). In Sudan, the relationship between amount and season of rainfall and disease incidence was also positively correlated. Blackarm incidence was correlated with September and October rainfall and there was an independent positive correlation with June rainfall. Dissemination of the disease was found to be largely dependent on the frequency of rainstorms in September-October. It was suggested that June rainfall serves to increase the amount of disease present before the September-October rains (Boughey, 1947).
In Africa, data on crop losses is available for only a few countries and in some cases dates back to 1948. In Sudan, complete crop failure was not unknown when highly susceptible varieties of G. barbadense were grown (El Nur, 1970). Losses of 20% were common and the yield loss from severe infection could be as high as 77%. Last (1960) also reported that yields were reduced by about 20%. Knight (1948) considered that the incorporation of blight resistance into Sudanese varieties was responsible for yield increases of up to 64%. From Uganda, Wickens and Logan (1957) reported that there was a significant depression of yield when seeds were inoculated with X. axonopodis pv. malvacearum. In 1950, Jameson reported that heavy yield losses occurred almost every year.
Uninfected crops were worth 49% more than crops where bacterial blight was present in Tanzania (Arnold and Arnold, 1960). Peat and Munro (1952) also reported that damage caused by the disease was appreciable. In 1949, Peat and Prentice concluded that crop losses might be about 20%. Arnold (1965) reported that the disease could reduce seed cotton yields by up to 350 kg/ha in a susceptible variety and that a gain of 340 kg/ha could be obtained by chemical disease control. In Kenya, Hastie (1952) stated that X. axonopodis pv. malvacearum was of paramount importance to the cotton crop. In East Africa generally, yield gains from seed dressings to control bacterial blight were around 60% (Wickens, 1961).
In India, losses of 5-20% were common in crops (Verma and Singh, 1971c). Late and very late sowing of crops resulted in yield reductions of 20.7-23.4 and 41.8-44.8%, respectively (Raj et al., 1989). Meshram and Raj (1992) reported that disease intensities of 56.4 and 53.2% resulted in losses of 25.08% and 23.68%, respectively. Meshram et al. (1988) reported losses of between 19 and 27% in different cultivars of cotton. An increase in yield from 1009 kg/ha of seed cotton in untreated plots to 2238 kg/ha in treated plots has been reported (Mathur et al., 1973). Bacterial blight continues to cause substantial losses in India where losses of 20-27% have been reported (Meshram et al., 1988; Meshram and Raj, 1992).
In Turkey the incidence of disease reached 100% in 1949, although the average rate of infection was 40% (Kaskaloglu, 1949).
In the USA, losses of between 34 and 59% were reported (Leyendecker, 1950; Bird, 1959). It is suggested that the percentage reduction in yield due to leaf infection appears to be about half the percentage of leaf drop caused by the disease (Bird, 1959). Leyendecker (1953, 1954) reports that 275,760 and 240,796 bales of cotton were lost to bacterial blight in 1952 and 1953, respectively. Reductions of cotton yield during 1955 and from 1952-1955 were 851 508 bales (Leyendecker, 1956). In Texas, three susceptible strains of cotton had an average loss of 18.6% which was equivalent to an average loss of ca $5 per acre (Bird, 1952). An epidemic in New Mexico in 1949 caused an estimated 35-59% reduction in yield (Leyendecker, 1950). It was estimated that in 1977, despite the use of resistant varieties, bacterial blight caused a total reduction of 3.6% in the North American crop. Negligible losses were recorded in the 1989-1990 season (Blasingame, 1990).