Alternaria solani

Alternaria solani infects stems, leaves and fruits of tomato (Solanum lycopersicum L.), potato (S. tuberosum), eggplant (S. melongena L.), bell pepper and hot pepper (Capsicum spp.), and other members of the family Solanaceae.[8] Distinguishing symptoms of A. solani include leaf spot and defoliation, which are most pronounced in the lower canopy. In some cases, A. solani may also cause damping off.[9][10]

On tomatoes

On tomato, foliar symptoms of A. solani generally occur on the oldest leaves and start as small lesions that are brown to black in color. These leaf spots resemble concentric rings – a distinguishing characteristic of the pathogen – and measure up to 1.3 cm (0.51 inches) in diameter.[11] Both the area around the leaf spot and the entire leaf may become yellow or chlorotic. Under favorable conditions (e.g., warm weather with short or abundant dews), significant defoliation of lower leaves may occur, leading to sunscald of the fruit.[11] As the disease progresses, symptoms may migrate to the plant stem and fruit. Stem lesions are dark, slightly sunken and concentric in shape. Seedlings can develop small, dark, partially sunken lesions which grow and elongate into circular or oblong lesions.[7] Basal girdling and death of seedlings may occur, a symptom known as collar rot.[11] In fruit, A. solani invades at the point of attachment to the stem as well as through growth cracks and wounds made by insects, infecting large areas of the fruit[11] Fruit spots are similar in appearance to those on leaves – brown with dark concentric circles. Mature lesions are typically covered by a black, velvety mass of fungal spores that may be visible under proper light conditions.[8][11]

Stem lesion of Alternaria solani

Alternaria solani is a deuteromycete[13] with a polycyclic life cycle. Alternaria solani reproduces asexually by means of conidia. A.solani is generally considered to be a necrotrophic pathogen, i.e. it kills the host tissue using cell wall degrading enzymes and toxins and feeds on the dead plant cell material [14]

The life cycle starts with the fungus overwintering in crop residues or wild members of the family Solanaceae, such as black nightshade.[11] In the spring, conidia are produced. Multicellular conidia are splashed by water or by wind onto an uninfected plant. The conidia infect the plant by entering through small wounds, stomata, or direct penetration. Infections usually start on older leaves close to the ground. The fungus takes time to grow and eventually forms a lesion. From this lesion, more conidia are created and released. These conidia infect other plants or other parts of the same plant within the same growing season. Every part of the plant can be infected and form lesions. This is especially important when fruit or tubers are infected as they can be used to spread the disease.[15]

In general, development of the pathogen can be aggravated by an increase in inoculum from alternative hosts such as weeds or other solanaceous species.[4] Disease severity and prevalence are highest when plants are mature.[11]

Alternaria solani spores are universally present in fields where host plants have been grown.[3]

Free water is required for Alternaria spores to germinate; spores will be unable to infect a perfectly dry leaf.[5] Alternaria spores germinate within 2 hours over a wide range of temperatures but at 26.6–29.4 °C (80–85 °F) may only take 1/2 hour. Another 3 to 12 hours are required for the fungus to penetrate the plant depending on temperature. After penetration, lesions may form within 2–3 days or the infection can remain dormant awaiting proper conditions [15.5 °C (60 °F) and extended periods of wetness]. Alternaria sporulates best at about 26.6 °C (80 °F) when abundant moisture (as provided by rain, mist, fog, dew, irrigation) is present. Infections are most prevalent on poorly nourished or otherwise stressed plants.[16]

Early blight caused by A. solani is the most destructive disease of tomatoes in the tropical and subtropical regions. Each 1% increase in intensity can reduce yield by 1.36%, and complete crop failure can occur when the disease is most severe.[19] Yield losses of up to 79% have been reported in the U.S., of which 20–40% is due to seedling losses (i.e., collar rot) in the field.[20]

A. solani is also one of the most important foliar pathogens of potato. In the U.S., yield loss estimates attributed to foliar damage, which results in decreased tuber quality and yield reduction, can reach 20-30%.[4] In storage, A. solani can cause dry rot of tubers and may also reduce storage length, both of which diminish the quantity and quality of marketable tubers.[4]

Because A. solani is one of numerous tomato/potato pathogens that are typically controlled with the same products, accurately estimating both the total economic loss and the total expenditure on fungicides for control of early blight is difficult. Best estimates suggest that total annual global expenditures on fungicide control of A. solani is approximately $77 million: $32 million for tomatoes and $45 million for potatoes.[6]

Though the causal pathogen is distributed worldwide and can cause crop yield reductions, early blight has never caused widespread famine or other sudden and major detrimental effects on humanity. The disease is not to be confused with late blight, which is caused by the oomycete Phytophthora infestans. Late blight disease together with the socio-economic situation at the time was responsible for the Great Famine of Ireland in the 1840s.

• Index Fungorum
• USDA ARS Fungal Database
• Japanese Fungi on Plants: Alternaria solani
• Resistance to Alternaria solani in Hybrids Between a Solanum tuberosum Haploid and S. raphanifolium. B. Weber and S. H. Jansky. Phytopathology doi:10.1094/PHYTO-05-11-0146.