Conidiomata pycnidial, subepidermal, erumpent, dark, thick-walled, flattened to globose, varying in size, often 100-300 µm diameter, with or without a beak;beak to 76 µm. Phialides hyaline, simple or branched, sometimes septate, 10-16 µm long, arising from the innermost layer of cells lining the cavity. Alpha conidia hyaline, aseptate, sub-cylindrical, 5-8 x 2-3 µm. Beta conidia filiform, curved, hyaline, septate, 18-32 x 0.5-2.0 µm, non-germinating. Hyphae hyaline, septate, 2.5-4.0 µm diameter (see Edgerton and Moreland, 1921;Sherf and MacNab, 1986;Singh, 1987).
Infection is easily visible in the field on close examination of leaves, stems and fruits;characteristic conidiomata appear as black pinhead-sized structures, which are often concentrically arranged on fruits. Infected fruits are soft and mushy or mummified and black. Infection of seed may be confirmed using the methods described for Seed Health Tests in 'Seedborne Aspects'.
Related invasive species
- Phomopsis vexans
Related Farm Practice
- Soil
P. vexans is a pynicidial anamorph with a teleomorph in the genus Diaporthe. Easily seedborne and producing large numbers of conidia, it causes disease in Solanum melongena [aubergine/brinjal/eggplant], its only significant host. This ranges from poor seed germination and damping-off of seedlings, to leaf and stem lesions and to fruit rot, both in the field and after harvest. The fungus has been reported from widely distributed areas of most continents, but only a few of those are in Europe and Africa, even though the climates are favourable. Seed transmission may explain its broad historical distribution, but limitation of its host range to a non-staple vegetable crop can allow for its avoidance and eradication by cultural methods. As a result, perhaps, it does not appear often on lists of restricted pathogens, even though it may cause yield losses of more than 50%.
The symptoms range from poor germination and seedling blight to fruit rot. Post-emergence damping-off of seedlings results from infection of the stem just above the soil surface. The symptoms on leaves are more prominent during the early stages of plant growth. At first the lesions are small, more or less circular, and buff to olive, later becoming cinnamon buff, with an irregular blackish margin (Pawar and Patel, 1957). Irregular spots result from coalescence. After transplanting, leaves coming into contact with the soil may become infected directly or develop leaf spot due to infection by conidia. Lesions on the petiole or the lower part of the midrib can result in death of the entire leaf. Affected leaves may drop prematurely, and the blighted areas become covered with numerous black pycnidia.
On stems and branches, elongated, blackish-brown lesions are formed, eventually containing pycnidia. The diseased plant bears smaller leaves and the axillary buds are often killed. When stem girdling occurs, the shoot above the infected area wilts and dries up and the plant may be toppled by the wind (Edgerton and Moreland, 1921;Pawar and Patel, 1957;Sherf and MacNab, 1986). Pycnidia develop readily in lesions on young stems, but rarely on older ones (Harter, 1914).
On the fruits the symptoms appear first as minute sunken greyish spots with a brownish halo, which later enlarge and coalesce, producing concentric rings of yellow and brown zones. These spots increase in size and form large rotten areas on which conidiomata often develop concentrically, covering most of the rotten fruit surface. Pycnidia on fruit are larger than those on stems and leaves (Harter, 1914). If the infection enters the fruits through the calyx, the whole fruit may become mummified due to dry rot (Pawar and Patel, 1957).
Rot may appear in fruit, in transit after harvest (Sherf and MacNab, 1986).
P. vexans has been considered to be restricted to Solanum melongena [eggplant/aubergine] (Edgerton and Moreland, 1921;Pawar and Patel, 1957;Sherf and McNab, 1986), but there are reports of pathogenicity to Capsicum annuum (pepper) and Lycopersicon esculentum [ Solanum lycopersicum ] (tomato) (Sawada, 1959;Tai, 1979) as well as of isolation from Acacia arcuaefolia (Mathur, 1979), Prunus armeniaca (apricot) (Dal Bello and Sisterna, 2000;Cho and Shin, 2004), and seeds of Sorghum bicolor (Mathur, 1979) and interception on imported Capsicum frutescens (BPI, 2009 [1945]). In India, it has been reported to infect some wild Solanum species in inoculation trials (Datar and Ashtaputre, 1988), and Solanum incanum (Dubey et al., 1987). Edgerton and Moreland (1921), nevertheless, were unable to obtain infection of tomato, pepper, potato [ Solanum tuberosum ] or wild Solanum species, and Pawar and Patel (1957) report identical results for tomato, pepper and potato, as well as finding no infection of Solanum nigrum. Those reports did not specify the plant parts inoculated, but uninjured tomato and pepper fruits were found to be unaffected by the fungus in parallel trials with brinjal [ S. melongena ] in India (Chaudhary and Hasija, 1979). Both young and fruiting pepper and tomato plants sprayed with suspensions of conidia were not infected (Harter, 1914).