Tomato diseases: diagnosis, causes and control

Savvas Pastopoulos, Agronomist MSc — Pastopoulos Agronomics, Neos Mylotopos, Pella, Greece

Tomato is attacked by more pathogens than any other vegetable crop in the Mediterranean, and most of them produce a similar picture on the foliage. What follows organises the diseases not alphabetically but by the way they are diagnosed: where the symptom starts, how it spreads within the plant, and what a cut through the stem reveals. It covers fungi, oomycetes, bacteria, phytoplasmas, viruses and viroids, with an explicit distinction between the open field and the greenhouse, where the same diseases behave differently.

1. The method: three questions before any diagnosis

The commonest mistake in tomato diagnosis is trying to identify the pathogen from the shape of the lesion. Dozens of different causes produce a brown spot on a leaf. The distinction comes from three questions, in this order.

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2. Differential diagnosis table

The table groups by where the symptom starts. The markers OUTDOOR GREENHOUSE show where each disease matters most.

The table directs the suspicion. It does not replace laboratory identification, which is essential for the bacteria, the viruses and the viroids.

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3. Blossom-end rot — a disorder, not a disease

Before looking for any pathogen, this picture has to be ruled out. It is the commonest misdiagnosis in tomato, and it leads to sprays that have no chance whatever of working.

3.1 The mechanism — why the fruit loses the contest

Calcium moves through the plant almost exclusively via the xylem, and its movement depends on transpiration. It is therefore driven towards the organs with the highest transpiration rate — that is, the leaves [8]. The fruit transpires very little and so loses the contest for the same xylem stream.

The essence of the disorder is therefore a transport failure, not a shortage of supply: factors such as erratic irrigation, high humidity and root stress prevent calcium from reaching the fruit [8].

3.2 How it is told apart from a pathogen rot

3.3 What actually reduces it

The same transport mechanisms explain other physiological fruit disorders as well, such as cracking from an abrupt change in water status, and sunscald on fruit left exposed after de-leafing.

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4. Leaf spot diseases

3.1 Early blight — Alternaria solani

It is among the most important foliar diseases throughout the Mediterranean basin [1]. It produces dark spots with concentric rings, often surrounded by a chlorotic halo. As it develops it causes defoliation starting from the older leaves and moving towards the younger ones, while necrotic lesions also appear on flowers, stems and fruit, where they expand from the point of peduncle insertion [1].

Resistance management matters particularly here: resistant strains have been recorded, especially against the respiration inhibitors, and the literature stresses the need for rotation of modes of action with an emphasis on multi-site products [1].

3.2 Septoria leaf spot — Septoria lycopersici

It produces circular to oval necrotic lesions with a light grey centre and dark margins. On older leaves the lesions are surrounded by a chlorotic halo, and pycnidia form in their centre — the feature that separates it from early blight [1].

The lesions coalesce, the leaf becomes chlorotic and falls, and the fruit is left exposed to the sun. Losses reach around 50% once defoliation touches 75% of the plant [1]. The pathogen overwinters on wild solanaceous hosts — black nightshade and related species act as an inoculum reservoir, so clearing the field margins is part of control [1].

3.3 Late blight — Phytophthora infestans

It is not covered by the Mediterranean review, but it is the disease that can destroy an open-field crop within a few days. It is an oomycete, not a fungus, a fact with direct practical consequences for the choice of active substances.

The picture is characteristic: large, water-soaked, brown areas on the leaf, often with white downy growth on the underside under humid conditions. On the fruit it produces a firm, brown, irregular rot. Nights with heavy dew and fog are as dangerous as rain.

3.4 Powdery mildew — Leveillula taurica and Oidium neolycopersici

Two different pathogens with a different picture, and telling them apart is simple:

For L. taurica, conidial germination occurs over a range of 10 to 37 °C with an optimum at 20 °C, while leaf colonisation is optimal at 15 to 25 °C [7]. Symptom severity is high where prolonged periods of 10 to 15 °C coincide with daytime relative humidity of 85 to 95% [7].

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5. Grey mould and the rots

Botrytis cinerea attacks more than 200 plant species and occurs both in the field and under protection, with the damage inside greenhouses distinctly more serious [1].

The typical symptoms are soft rots, water-soaking of the parenchyma and grey masses of conidia. Stem lesions can lead to complete collapse of the plant [1]. On ripe fruit the soft rots occur mainly postharvest, while on unripe fruit it produces the «ghost spots» — a host defence response that makes the fruit hard to market [1].

Transmission is mainly by air-borne conidia from infected plants or plant debris. No seed transmission has been reported. The fungus overwinters as sclerotia in the soil and in decayed residues, lasting until the following growing season [1].

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6. The soil-borne wilts

Three pathogens, one picture to the eye — wilting with yellowing from the bottom — and three different decisions. The distinction is made by where the discolouration stops.

5.1 Fusarium wilt — Fusarium oxysporum f. sp. lycopersici

It is among the most widespread soil-borne diseases of tomato across the Mediterranean and attacks both transplants and established plants, in the greenhouse and in the open field [1].

The first symptoms are yellowing of the lower leaves, often confined to one part of the plant only because of the sectorial spread of the pathogen within the vessels [1]. After penetrating the root, the fungus colonises the cortex and enters the xylem, producing the characteristic dark brown discolouration that extends high up the stem and leads to wilting and death [1].

Losses reach 45 to 55% and can extend to 70% under favourable conditions, that is at 27 to 30 °C [1]. In the Mediterranean, races 1 and 2 predominate; race 3 has a more limited distribution, mainly in Turkey, Egypt and Algeria [1]. This has direct practical value, because cultivar resistance is race-specific.

5.2 Crown and root rot — F. oxysporum f. sp. radicis-lycopersici

It is one of the most destructive soil-borne diseases and is today present in most Mediterranean countries, infecting plants at transplanting or during cultivation [1].

Losses range from 20 to 60% and can reach 90% under conditions optimal for the pathogen [1].

5.3 Verticillium wilt — Verticillium dahliae

The fungus moves acropetally through the water-conducting vessels and causes a vascular wilt, with brown discolouration visible when the plant is cut. Symptoms start on the older leaves and progress to the younger, with desiccation extending from the leaf tip towards the petiole [1]. The plant reacts by forming barriers within the vessels, but it is precisely these occlusions that lead to withering [1].

Losses reach 20 to 50%, with the greatest impact in the 21 to 30 °C range, which is optimal for the pathogen [1].

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7. Bacterial diseases

6.1 Bacterial canker — Clavibacter michiganensis subsp. michiganensis

It is the most important bacterial disease of tomato worldwide and is classified as an EPPO A2 quarantine organism [1].

Because the bacterium colonises the vascular tissue, symptoms appear over the whole plant: the leaf margins roll upward, wilt and dry, with the wilting affecting either parts or the whole plant. On the stem, yellowish or brown longitudinal streaks appear, at which tumour-like structures may form. On the fruit, tiny dark lesions surrounded by bright halos develop — the characteristic «bird's-eye» spots [1].

6.2 Bacterial speck — Pseudomonas syringae pv. tomato

It attacks tomato in the greenhouse and in the open field. Two races, 0 and 1, have been identified, based on the response of cultivars carrying or lacking the Pto resistance gene; the more virulent race 1 has been reported in Italy, Portugal and Tunisia [1].

On the leaves, water-soaked angular spots appear first, converging, darkening and becoming surrounded by a chlorotic halo. On the stems it produces elongated necrotic lesions, while on the fruit it produces tiny rounded dots a few millimetres across with a green halo, which immediately reduce marketable value [1].

Seedling losses reach 20 to 25%, while with early infection yield losses can reach 75% [1].

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8. Phytoplasmas — stolbur

Stolbur is caused by Candidatus Phytoplasma solani and during outbreaks can cause yield reductions of up to 80% [1].

The leaves are reduced in size, distorted and curled, showing yellowing and in some cases reddening [1]. The flowers are distorted and remain sterile.

The measures are healthy propagating material, constant monitoring of the vectors and of symptom onset, timely detection and removal of infected plants and of the spontaneous reservoirs of inoculum [1].

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9. The viruses

Here the logic changes. For viruses there is no curative treatment. Management means healthy material, vector control, hygiene and roguing. The table summarises the mode of transmission, because that determines what has to be done.

8.1 TSWV — tomato spotted wilt virus

The first leaf symptoms are confused with cold injury, as the young leaves take on a purple colouration on the lower laminas. Chlorotic spots then appear, become necrotic and merge, giving the leaf a brown-violet colour — the characteristic «bronzing» [1]. The necrosis extends onto petioles, stems and flowers. On the fruit, light green spots of around one centimetre form and later become necrotic, sunken and brownish, with a corky texture and deep longitudinal cracks near the peduncle, leading to early fruit drop [1].

Where positive plants are found, all symptomatic plants and their neighbours, weeds included, are removed and destroyed [1]. There are many strains and they recombine frequently, generating new variants that overcome the genetic resistance bred into commercial cultivars [1] — which explains why a resistant cultivar can fail.

8.2 CMV — cucumber mosaic virus

A virus of enormous adaptability: it infects more than 1,200 plant species and is transmitted by more than 80 aphid species in a non-persistent manner [1]. The most efficient vectors are Myzus persicae and Macrosiphum euphorbiae. It is also transmitted by seed and through ten species of dodder [1].

With early infections, within 15 to 20 days of transplanting, leaf malformations, stunted growth and apical dwarfing occur, giving the plant a bushy appearance [1]. The most destructive symptom is the lethal necrosis caused by the necrogenic strain, which leads to decay and death within 2 to 3 weeks of infection [1]. Losses reach 100% [1].

8.3 TYLCV and TYLCSV — yellow leaf curl

At least two viruses are responsible for the disease, and genetic recombination between them occurs frequently, giving rise to new hybrid genomes [1].

The leaflets have their margins visibly yellowed and turned upward, resembling a small cup, with reduced surface and distortion [1]. The plant takes on a bushy appearance with upright axillary and apical shoots. Flower abscission, failure to set fruit and the production of unmarketable fruit follow, because of small size or pale colour [1]. In colder periods the yellow takes on purple shades resembling cold damage [1].

That last point is the good news: because transmission runs exclusively through the whitefly, vector control and netting are genuinely effective. Bemisia tabaci is a complex of almost 40 cryptic species and transmits over 40 different viruses [1]. Commercial cultivars with varying degrees of resistance are today the main tool for containing the damage [1].

8.4 ToBRFV — the newest and most serious threat

It was first identified in Israel and Jordan in 2014–2015, spread rapidly, and was soon assigned as an EPPO A2 quarantine pathogen [1].

Symptoms vary widely with cultivar and conditions, and the variation is associated with the photoperiod, the temperature and the age of the plant at infection [1]. The commonest are leaf deformation, mosaic and blistering, interveinal yellowing especially in young leaves, longitudinal stem necrosis, suberification and necrosis of the sepals, necrosis on pedicels and petioles, fruit abscission and marbling of the fruit [1].

Transmission is basically mechanical, but it also occurs through contaminated seed or fruit [1]. Spread within the crop occurs by direct contact, through infected sap from operators, clothing, pots, working tools and nutrient solutions, through propagating material, and through bumblebees (Bombus terrestris) [1].

8.5 ToMV — tomato mosaic virus

It attacks mainly solanaceous hosts, with losses of 25 to 70% [1]. It is easily transmitted by seed, as external contamination, and in smaller quantities in the endosperm — but never in the embryo. It remains active in the infected seed for at least ten years [1].

It is also transmitted very easily from plant to plant during cultural operations. No insect vector has been demonstrated [1]. Before sowing, thermotherapy at 70 °C for 24 hours or seed dressing can be applied to eliminate the virus [1].

8.6 PepMV — pepino mosaic virus

Losses range from 30 to 80% [1]. Symptoms appear 2 to 3 weeks after infection and spread within the row — a picture that in itself indicates mechanical transmission [1].

For seed, dry heating at 72 to 74 °C for 2 to 3 days or disinfection are effective [1].

8.7 PMoV — parietaria mottle virus

Its incidence ranges from 3 to 30%, but is considered underestimated because of confusion with the symptoms of TSWV, ToMV and CMV [1]. Parietaria officinalis plays a key role in the epidemiology, because it transmits the virus by its own seed; eliminating the weed from the margins of tomato fields is essential [1].

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10. Viroids

Potato spindle tuber viroid (PSTVd) causes losses in tomato of 50 to 90%, depending on the cultivar [1].

Management rests on certified propagating material, removal of infected or suspect plants, control of aphid vectors and of spontaneous hosts, and disinfection of tools and machinery between operations [1].

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11. The vectors: thrips, whiteflies, aphids

In tomato, insect control is not a separate chapter from the plant protection of the virus diseases — it is the same chapter. The table shows how much vector control delivers in each case.

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12. Hygiene and prevention in the greenhouse

The three pathogens that today decide the fate of a greenhouse unit — ToBRFV, PepMV and ToMV — share one characteristic: they are transmitted by contact. No treatment addresses them. What follows is not a set of good-practice recommendations; it is the plant protection programme itself.

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13. What climate change changes

The review devotes a separate chapter to the subject, and its conclusions are not generalities.

High temperatures stimulate the development of fungal, viral and viroid diseases, while increased CO₂ levels have been shown to exacerbate disease caused by grey mould [1]. Overall, for a series of pathogens — among them grey mould, F. o. f. sp. radicis-lycopersici, Verticillium, TSWV, ToMV, PepMV and PSTVd — increased pathogenicity or enhanced transmission rates have been reported [1].

For ToBRFV and PMoV no such reports are yet available [1]. The review notes that their spread is probably linked to other trends, chiefly the globalisation of the seed industry [1] — a distinction worth holding on to, because it shows the problem is not solved by climate measures but by checks on the material.

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14. The key points

15. Sources

The numbers in the text refer to the list below.

• [1] Panno, S., Davino, S., Caruso, A.G., Bertacca, S., Crnogorac, A., Mandić, A., Noris, E. & Matić, S. (2021). A Review of the Most Common and Economically Important Diseases That Undermine the Cultivation of Tomato Crop in the Mediterranean Basin. Agronomy 11(11):2188. The principal source of this article, specific to the Mediterranean: all the loss percentages, the temperatures, the vector transmission times, the symptoms of each pathogen, the seed thermotherapy requirements and the chapter on climate change.
• [2] EPPO Global Database — Clavibacter michiganensis subsp. michiganensis. Source for the A2 quarantine status and the distribution.
• [3] EPPO Global Database — Tomato brown rugose fruit virus (ToBRFV). Source for the quarantine status and the spread of ToBRFV in the EPPO region.
• [4] Greek Ministry of Rural Development and Food — Plant Protection Products Database. The only valid source for which products are permitted on tomato in Greece, at what rate and with what pre-harvest interval. In every other country the national authorisations apply.
• [5] Late Blight — Tomato, UC IPM Pest Management Guidelines, University of California Statewide IPM Program; and Late blight of tomato and potato, University of Minnesota Extension. Sources for the 10 to 22 °C range, for infection in about 10 hours at relative humidity above 90%, and for the ~12 hours of wetness at 20 to 25 °C.
• [6] Effects of Temperature on Events in the Infection Cycle of Two Clonal Lineages of Phytophthora infestans Causing Late Blight on Tomato and Potato in Brazil. Plant Disease 93(5):459. Source for lesions appearing in 3 to 5 days and for the shortest incubation period at 22 °C.
• [7] Powdery mildew on tomatoes, Cornell University, Long Island Horticultural Research and Extension Center; and Powdery mildew, University of Florida IFAS. Sources for the distinction between Leveillula taurica and Oidium neolycopersici as to the sporulating surface, for conidial germination at 10 to 37 °C with an optimum at 20 °C, for colonisation at 15 to 25 °C, and for infection even at 50% relative humidity.
• [8] Managing Blossom End Rot in Tomatoes and Peppers, Iowa State University Extension and Outreach; and Blossom-end rot: a century-old problem in tomato (Solanum lycopersicum L.) and other vegetables. Sources for its characterisation as a physiological disorder rather than a disease, for calcium transport through the xylem under the control of transpiration, for the fact that raising soil calcium does not necessarily reduce the disorder, and for the role of erratic irrigation, humidity and root stress.
• Photographs: archive of Pastopoulos Agronomics.