The epidemiology and control of crucifer chocolate spot.
In the 1991/92 season, a leaf spotting disease of crucifer seedlings appeared at a number of nurseries in Kwazulu-Natal (KZN) Province. Towards the end of 1996, the disease had also been detected in Western and Northern Provinces, and even in Zambia. The disease appeared in nurseries during warm humid conditions. It initially started as small, water-soaked spots on leaves, which later expanded and coalesced, forming halo regions surrounded by a dark brown to black ring. Due to the typical dark brown spots, the disease was named crucifer chocolate spot (CCS). From the studies conducted by Qhobela & Laing (1994), the causal agent of CCS was found to be a Xanthomonas campestris pathovar that was in symbiotic association with a unique bacteriophage. Koch's postulates were conducted. The causal agent of CCS was inoculated on cabbage seedlings (6-8 weeks old), and the seedlings subjected to post-inoculation periods of approximately 48 hours at 28-30°C, and relative humidity (RH) of ≥70%. The best method of inoculation was achieved when the leaves were pricked with pins prior to application of the inoculum (≥10(7)cfu/ml). The latent period of CCS varied from 2-6 days, depending on RH, temperature, nutritional status of the host and other factors within the crop pathosystem. Artificial inoculation studies showed the host range of CCS X. campestris to be similar to X. campestris pv. armoraciae and X. campestris pv. campestris. All the pathogens were able to infect cabbage, cauliflower, broccoli and lettuce plants during artificial inoculation. A hypersensitive response was elicited on pepper, tomato, and tobacco plants. Electron microscopic studies showed epiphytic colonization by CCS X. campestris, and also the colonization of xylem, phloem and parenchyma tissues. Although xylem tissues were also colonized, the V-shaped lesions and vein blackening characteristics typical of X. campestris pv. campestris were not observed. Profuse multiplication of the pathogen resulted in rupturing of cell organelles and cell membranes. Different crucifer cultivars from two seed companies were found to have varying levels of susceptibility to CCS disease during artificial inoculation, with levels of leaf area infected ranging from 0% to 34%. Disease severity was also affected by seasonal variations. None of the seed-lots tested in this research were found to be infected by CCS X. campestris, although some were infected by other xanthomonads. Chemical seed treatment (soaking in bactericide solutions at 30°C for two hours) with biocides; e.g., Kocide 101, copper oxychloride, and copper ammonium carbonate was more effective than hot water treatment (50°C for 30 min). All seed treatments lowered pathogen levels, however, none resulted in complete control of seedborne inoculum. Percentage germination of seed was low for chemical treatment compared to the hot water treatment. Disease levels were reduced with increased rates of Ocean 3.1.3 (38) fertilizer applied, with significant differences in the percentage leaf area infected at obtained at application levels of 400 ppm. Increased levels of N, P, K, Zn and Cu in leaf tissues were associated with low levels of disease severity. Copper bactericides; e.g., Kocide 101, Copper Count N, Copper Ammonium Carbonate B and Copper oxychloride were more effective than quaternary ammonium compounds in reducing disease levels (≤30%). The combination of copper bactericides and mancozeb improved the performance of the copper compounds. Application of copper bactericides up to four times the recommended dosage did not result in increased efficacy. CCS was found in 80% of KZN nurseries surveyed between December 1995 and December 1996. During this period, it was not detected from Mpumalanga and Northern Provinces. Factors that contributed to CCS disease outbreaks include favourable climatic conditions (≥ 40% RH, ≥24°C), wounding of seedlings by pests, and nutrient stress.