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The first symptom is a chlorosis of the youngest leaves usually on plants where the first fruit set is close to maturity. The chlorosis may intensify and affect the top half of the plant, which loses turgidity. The whole plant collapses. A dark brown to black lesion is seen on the surface of the stems of these plants where the first truss is attached, sometimes extending up to 30 cm in length. When the stem is split, the pith cavity is hollow in the region of the external lesion. Beyond the external lesion, the pith is dark brown and watersoaked but not soft. The leading edge of the pith discoloration is usually well defined. When the necrosis advances in the pith, the vascular system will be affected and turn brown. The pith necrosis and discoloration can extend throughout the stem from the soil level to just below the growing point, into the peduncles and into leaf rachides. Sometimes, and particularly in plants without external lesions, the pith is merely discoloured with or without cavities in the discoloured area. Plants collapse and die, or continue to grow very slowly. A copious, dirty-white, bacterial flux sometimes oozes from wounds, particularly from leaf scars where lower leaves have been removed, and dribbles down the stem. In older crops, plants that have been affected can be recognized by the prolific development of adventitious roots on the stem in the area where the pith is affected. After the initial symptoms, surviving plants may grow normally without any further external or internal symptom development. Where plants have recovered from attack, the stem diameter in the new growth is markedly decreased. In spite of the fact that the pith has completely disintegrated leaving a hollow cavity for much of the stem length, the plants appear to recover completely and produce a normal fruit crop (Scarlett et al., 1978). Older plants, where the first truss is fully grown although still green, are mostly attacked by this disease, but plantlets with pith necrosis were found in a nursery in Italy (Sesto et al., 1996).
Pepper (Capsicum annuum)
The pith of diseased plants is discoloured and/or necrotic and collapsed. Dark brown to black external stem lesions are sometimes present (Lopez et al., 1994; Rista et al., 1995; Scortichini et al., 1998). In Italy, field grown peppers showed chlorotic, wilting leaves and longitudinal sections of the stems revealed extensive pith necrosis; 15% of the plants were infected (Scortichini et al., 1998). The formation of adventitious roots has not been reported.
On pepper the disease has been observed only rarely in this host and appeared in areas where tomato pith necrosis was endemic in that year (Lopez et al., 1994).
Brownish lesions appear at the base of the stems with a dirty white mucous exudate. The lesions spread up the stems. The leaves, starting from the lower ones, turn yellow first at the tip and then on the whole leaf which finally dries up. Splits of the stem affected by the lesions show the pith first brown and watersoaked and then darker, soft and finally completely disintegrated. The vascular tissue in this area is also discoloured. In the end the affected part of the stem rots and the plant dies. The disease spreads more slowly in older plants. Adventitious roots grow out near the lesions. Infection probably arises from soil where tomatoes with severe pith necrosis have been grown in the previous year (Fiori, 1992).
Only pathogen-free seeds, treated and/or tested by a reliable method, should be used. Transplants should be disease-free.
Cultural Control and Sanitary Methods
As P. corrugata is a widespread opportunistic pathogen, cultural methods are most important for control.
Different preventive measures can be taken both in nursery and in the cultivation of tomato (Catara and Bella, 1996).
In nurseries it is important to use pathogen-free seeds according to certification schemes. Furthermore, due to the ability of the bacterium to survive in soil, virgin soil should be used, but if not, the soil should be sterilised. However, when plantlets were transplanted in fumigated soil, a higher disease incidence was observed; it was suggested that natural antagonists against P. corrugata were reduced by fumigation (Scortichini, 1989; Carroll et al., 1992). Thermal sensitivity of representative strains of the bacterium was assessed with the aim of developing control methods to reduce soil inoculum. Bacterial populations in soil were undetected only after a 30-min treatment at 60°C (Bella et al., 2003).
Chemical control (such as cupric compounds) at weekly intervals from emergence are suggested.
Excessive nitrogen should be avoided. Plants should be kept dry by rational irrigation and circulation and substitution of the air. Avoiding low night temperatures can prevent high humidity and free water on the plant surfaces.
Water used for irrigation should be checked for potential contamination with P. corrugata.
Sanitary methods such as disinfection of greenhouses and tools, regular disinfection of hands during cultural work, and avoiding wounding of plants are preventive measures against bacterial diseases in general (Naumann, 1980).
Although some authors recommend destroying plants as soon as they show symptoms in order to prevent dissemination of the disease (Naumann, 1980; Fiori, 1992), others advise growers not to remove them because spread among plants appears to be low (Lauber et al., 1992). Nevertheless, removal of infected plantlets is very important in nurseries.
All 12 tomato cultivars tested for resistance proved to be susceptible or highly susceptible. Some wild species were also resistant (Scortichini and Rossi, 1993).
In greenhouse tests three different strains of Agrobacterium radiobacter (K84, K1026 and K84 Agr-) reduced pith necrosis of tomato caused by P. corrugata (Lopez et al., 1991).
In many reports, the portion of plants attacked by P. corrugata is about 5-10% (Lai et al., 1983; Caroll et al., 1992; Scortichini, 1997), but in some cultivars in some crops, it may be up to 50% (Scarlett et al., 1978). Under conditions favourable for the disease, severe economic losses or total crop loss can occur in plantlets (Fiori et al., 1983a; Bayaa and Warrak, 1990; Alippi et al., 1993; Catara and Albanese, 1993; Rodriguez, 1995; Sesto et al., 1996; Moura et al., 1999), but this is rare. In addition, attacked plants can recover from the disease and crop normally (Scarlett et al., 1978). In tomato plants artificially inoculated with a strain of P. corrugata and P. mediterranea, a negative effect on total tomato yield and fruit size was observed (Moura et al., 2005).
This disease has been observed in pepper mainly in areas where tomato pith necrosis was reported (Lopez et al., 1994; Scortichini et al., 1998).
The virulence of different strains varies (Carroll et al., 1992; Sutra et al., 1997; Catara et al., 2002). In general, P. corrugata appears to be a weak, opportunistic pathogen. Due to its low-grade and opportunistic pathogenic character, plants with symptoms may recover from the disease (Scarlett et al., 1978).
Although it is a plant pathogen, P. corrugata has been successfully tested as a biological control agent in different pathosystems. More extensive studies were performed on Pythium root rot (Pythium aphanidermatum) of cucumber (Zhou and Paulitz, 1993; McCullagh et al., 1996) and for the take-all disease of wheat (Gaeumannomyces graminis; Ryder and Rovira, 1993; Schmidt et al., 1997). For the latter purpose a field release of a lacZ marked strain (strain 2140) was authorised in Australia and has been monitored over the years (Choi et al., 2003). Other applications included trials on disease control of: Fusarium dry rot of potatoes (Giberella pulicaris; Schisler et al., 1994; 1997); silver surf of potato (Helmintosporium solani; Chun and Shetty, 1994); bacterial ring rot of potato (Clavibacter michiganensis subsp. sepedonicus; Schroeder and Chun, 1995); crown gall on grapevine (Agrobacterium tumefaciens; Bell et al., 1995); Pythium damping off of maize (Pandey et al., 2001; Georgakoupoulus et al., 2002), cucumber (Georgakoupoulus et al., 2002) and sugarbeet (Schmidt et al., 2004); Citrus mal secco disease (Phoma tracheiphila; Coco et al., 2004); postharvest brown rot caused by Monilinia fructicola on nectarines and peaches (Smilanick et al., 1993); postharvest green mould in lemon (Penicillium digitatum; Smilanick and Denis Arrue, 1992; Cirvilleri et al., 2001) and postharvest grey mould on grape (Cirvilleri et al., 2001).