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Infected seedlings may be killed before or after emergence, often producing damping-off symptoms: brown, moist rot of the root, hypocotyls and leaves, which are sometimes enveloped more or less by the olive-grey mycelium of the fungus (Neergaard, 1945; Maude, 1966; Årsvol, 1969; Netzer and Kenneth, 1969; Strandberg, 1984, 1987; Nowicki, 1995a). Incidence of damping-off was more expressed at high (25°C) temperature (Maude, 1966; Tahvonen, 1978). It may be generally true that, following seedling infection, secondary inoculum is spread to infect leaves or additional, healthy plants under conditions which are favourable for the disease from plants which are infected, but not killed (Neergaard, 1977). It was experimentally demonstrated by Maude (1966) that dense sowing resulted in intensified foliage blight.
Lesions produced on leaf and petiole tissues are generally dark-brown to black, and chlorosis of surrounding tissues is observed. Gradually, the spots increase in size and become confluent. Finally, the whole leaf becomes greyish-black, while the leaflets become curly and convolute. When infection is severe, the whole top may be killed (Meier et al., 1922; Hooker, 1944; Neergaard, 1945; Maude, 1966; Årsvol, 1969; Ellis, 1971; David, 1988). The older leaves are more heavily infected than the young ones (Hooker 1944; Maude, 1966; Hentschel and Glits, 1976; Soteros, 1979b). It has been suggested that resistance of young carrot leaves to A. dauci is due to their higher content of reducing sugars and tannin, and low nitrogen content (Ali and Roy, 1981).
Attack of roots by A. dauci was first observed in the USA by Chupp and Sherf (1960). Then, Schneider (1961) proved the fungus to be the cause of a serious root disease in Germany. Contrary to these reports, Soteros (1979b) did not detect any effect of the pathogen on carrot roots in the field. Schneider (1961), Årsvol (1969) and Bedlan (1991) found that A. dauci was also a pathogen responsible for root decay during storage. According to Årsvol (1969), attack on the roots usually starts in mechanical injuries. The lesions are irregular in shape, dark-brown to black. The decay is dark-brown to black, firm and shallow. Schneider (1961) observed the attack of roots at temperatures higher than 15°C and in an experiment carried out by Årsvol (1969), no infection occurred below 12°C. Likewise, no attack of the pathogen on stored roots was observed by Soteros (1979b).
The fungus also attacks flower-stalks and umbels, producing dark longitudinal spots, and finally attacks flowers and immature seeds (Meier et al., 1922; Neergaard, 1945; Strandberg, 1983). Strandberg (1983) observed symptoms of the disease caused by A. dauci on all parts of inflorescences and seed-stalks. All flower parts were susceptible to infection. Fruits (mericarps), which in practice are called seeds, were infected and colonized from very early developmental stages to maturity. The fungus was normally confined to the pericarp tissues of viable seeds. At the earlier stages of seed development, the infection led to the extensive colonization of embryo and endosperm by the pathogen and such seeds lost their viability, being also shrivelled and discoloured. Lesions are not noticeable on seeds, but infected seeds are smaller and their quality is affected (Neergaard, 1977).
In order to avoid introducing A. dauci with sowing material, Scott and Wenham (1972) advocated that infected seeds should be identified by routine health tests and treated before being released to growers.
The growing of host cultivars which are resistant or tolerant to the pathogen minimizes the need for fungicidal control. There are several examples of lines or cultivars showing some resistance to leaf blight caused by A. dauci. Although out of 90 breeding lines and 241 plant introduction lines of carrot which were screened by Strandberg et al. (1972) in Florida, USA, none were immune, nine showed high resistance to A. dauci and maintained their foliage throughout the growing period without any fungicidal protection. Reports on resistance or tolerance to this pathogen originate from the USA (Baker, 1978; Bruemmer and White, 1986; Peterson et al., 1988; Pike et al., 1991), from Brazil (Ikuta et al., 1983; Reifschneider and Della Vecchia, 1985; Aguilar et al., 1986; Brenner et al., 1987; de Muniz and da Ponte, 1988; Fancelli and Kimati, 1991a; Boiteux et al., 1993; Ribeiro et al., 1993; Corbaz and Perko, 1995), Cuba (Castellanos-Linares et al., 1984), India (Sandhu and Dhiman, 1985) and Russia (Ivanyuk et al., 1989).
A heritability estimate for resistance to A. dauci was described by Vieira et al. (1991) and Boiteux et al. (1993). In response to infection by A. dauci, carrot leaves regenerated from tissue cultures showed chloroplasts with loss of stroma and membrane damage (Dugdale et al., 1993). Iprodione tolerant strains of A. dauci have been detected (Fancelli and Kimati, 1991b). No differences in the pathogenicity of the fungal strains were observed on resistant cultivars, whereas iprodione-sensitive strains were more pathogenic than iprodione-tolerant strains on sensitive cultivars (Fancelli and Kimati 1991a).
The possibility of using phytoalexin production in carrot cell cultures to evaluate leaf blight susceptibility was investigated by Bruemmer and White (1986). Cultivars which were most tolerant of A. dauci produced more elicitors of 6-methoxymellein (6MM) than the susceptible ones. However, analysis of the data revealed that only 61% of the variation in 6MM production was explained by differences in susceptibility.
In the USA, hybrid carrot seeds are produced in dry areas partly because better seed yields and quality are obtained. Some, but not all, of these regions are not very conducive to the development of diseases caused by Alternaria spp. If primary inoculum is greatly reduced or is not introduced with stock seeds, seeds produced in these areas are usually free from pathogens. In leading seed companies, breeders' seed and especially stock seeds are tested for pathogens and, in many cases, routinely treated regardless of test results. Moreover, spatial isolation of seed fields required for hybrid seed production is ascertained by seed producers who are growing hybrid crops in the area. Spatial isolation along with equipment sanitation eliminates opportunities for the spread of secondary inoculum between fields. These practices have resulted in a very low incidence of pathogenic Alternaria spp. on hybrid carrot seed produced in the northwestern USA (Strandberg, 1992).
Although Maude (1966) indicated that it seemed unlikely that infected plant residues might play a commercially important role as a source of disease, it was shown by Schmidt (1965) that crop rotation was necessary to avoid plant infection. Chupp and Sherf (1960) indicated 3-year or even longer rotations as important. Potassium deficiency increased the susceptibility of the plant to attack by A. dauci (Neergaard, 1945).
The number of infested seeds in commercial seed lots may be significantly reduced in seed processing by the removal of undersized seeds as well as parts of plant debris which are often carrying the pathogen. This has been clearly demonstrated by Strandberg (1983).
In the greenhouse, a UV-absorbing vinyl film inhibited sporulation of A. dauci on carrot (Sasaki et al., 1985).
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Reduction of leaf surface caused by the disease prevents full root development (Ellis, 1971). There are reports of fields which were completely destroyed by the fungus (Neergaard, 1945). In North Carolina, epidemics of A. dauci on carrots caused up to 90% defoliation and reduced yield by up to 82% (Strider, 1963). In the estimates for annual losses in the USA in 1951-1960, Alternaria blight together with Cercospora blight accounted for 2% (Neergaard, 1977). Severe loss of leaves and petioles from disease damage prohibits efficient mechanized harvesting (Strandberg, 1992). The development of A. dauci in the second year of carrot seed production often leads to a decrease in seed yield (Neergard, 1977).