Sintomi forma apoplettica di Mal dell'Esca (Trichoderma e Mal dell'Esca)
Schema diffusione Mal dell'Esca e Eutipiosi (Trichoderma e Mal dell'Esca)
Phaeocremonium aleophilum agente del Mal dell'Esca (Trichoderma e Mal dell'Esca)
Phoemoniella chlamydospora agente del Mal dell'Esca (Trichoderma e Mal dell'Esca)
Schema del processo di diffusione di Mal dell'Esca (Trichoderma e Mal dell'Esca)
Schema diffusione eutipiosi (Trichoderma e Mal dell'Esca)

Trichoderma and Esca Disease                                                                                                  Download the PDF file

Dott. Agr. Paolo Turconi


Esca Disease Complex

The Esca Disease is a degenerative pathology of the woody tissues of the vine, identified as a syndrome or perhaps better as "Esca Disease Complex".

This identification is due to its complex (and still not completely clear) etiology with a probable primary colonization of Phaeomoniella chlamydospora and Phaeoacremonium aleophilum tracheomycotic agents in particular of xylematic vessels, to which follows a cariogen agent Fomitiporia mediterranea. To these pathogens that we could define basic agents can be added numerous other mushrooms such as Eutypa lata, Phomopsis viticola, Botryosphaeria obtusa and numerous others (some studies suggest about 60).




Phaeoacremonium aleophilum                                          Phaeomoniella chlamydospora


The infection occurs initially through pruning cuts and other wounds and spreads more or less quickly until the infected plant is brought to death.

It is a pathology that can have a long latency before manifesting obvious symptoms, for this reason the risk of diffusion within the vineyard over the years is very high (use of infected equipment for pruning).


Slow Form Evolution

The first process leads to the formation of a clear and soft necrosis in a central position and involves three fungi: Phaeomoniella chlamydospora (PCH), Phaeoacremonium aleophilum (Pal) and Fomitiporia Mediterranea (Fm). At first, small black dots will be displayed, in which Phaeomoniella chlamydospora is located. Then there is the formation of a small necrosis from the pink marrow, due to Phaeoacremonium aleophilum. This necrosis develops and mixes with the black dots to form the brown necrosis which takes center position. This wood is then colonized by Fomitiporia Mediterranea, to form a clear and tender necrosis, which will gradually expand. In this case, we observe the symptoms of the slow form of the Esca Disease, whatever the stage of necrosis in the vine (Larignon 2004, Larignon 2009).



The second process leads to the formation of a clear and tender necrosis in a sectoral position and involves Eutypa lata (El), the cause of brown necrosis, and Fomitiporia Mediterranea which degrades brown into a white and soft caries. This necrosis can evolve to occupy almost all the wood.



Note that the two processes can be observed on the same plant (Larignon and Dubos, 1997; Larignon, 2009).

Evolution of the Apoplectic Form

According to Letousey et al. (2010), the study of the fulminating form of the Esca Disease shows that the photosynthetic mechanisms are highly disturbed seven days before the leaves undergo the stroke (drying). Visually there is no sign to suggest that the plant will soon express leaf symptoms. This alteration is detectable at a physiological level with a sharp decline in assimilation of CO2, stomatal closure, decreased activity of photosystem II and a decrease in the transcription of some genes associated with photosynthesis. In contrast, some defense genes are overexpressed in the leaves 7 days before and during the expression of visible symptoms on the plant. Therefore, the plant perceives stress, even before the visible expression of the disease, is a type of active defense response. This perception is at most one day before the leaf is totally burned.


The apoplectic form is often associated with an excess of water in the soil with high temperatures (Surico et al., 2006), the alteration of water transport in the plant has also been studied due to malfunctions of the xylem. Thus, Edwards et al. (2006) observed a decrease in stomatal conductance following the water deficit in infected plants.



The four types of CODIT subdivision barriers described by Shigo and Marx in 1977

(1) development of cellular growths and secretion of gummy substances in the xylem vessels;

(2) morphological changes of cells at the end of each growth ring;

(3) plant defense reactions involving parenchymal rays;

(4) formation of a barrier zone in the cambio.


Occlusions of xylematic vessels



Symptoms on leaves

Beginning of irregular chlorotic areas in the inner area until the area is completely dry.

The damage is caused both by water stress resulting from xylem occlusion, and by toxic metabolites (polysaccharides and others) released by pathogenic fungi or by wood degradation reaction products translocated to the leaves.



Evolution of foliar symptoms on red grape vines (left) and on white grape vines (right)


Symptoms on trunk

As seen previously they may have different evolutions but they are always accompanied by tissue browning.



Symptoms on whole plant



Symptoms of the apoplectic form

The expression of symptoms in the leaves and in the berries is not linked to the presence of fungal mycelium: the assumption is that produce molecules that act at a distance (toxins) from the point of release (Mugnai et al. 1999). Some of these molecules have been identified. Many molecules of Phaeomoniella chlamydospora (PCH) including isosclérone and scytalone, cis-4-hydroxy-scytalone, 1,3,8-trihydroxynaphtalene (1,3,8-THN), 2,4,8-trihydroxytetralone (2,4 , 8-THT), 3,4,8-trihydroxytetralone (3,4,8-THT), flavioline, 2-hydroxyjuglone (2-HJ, traces), and 4-Hydroxybenzaldehyde have been identified. Isosclérone and scytalone are also produced by Phaeoacremonium aleophilum (PAL). The fact that they are produced by both Pch and Pal is the reason why they have been extensively studied for their involvement in the event of foliar symptoms (Brown et al., 2007). In comparison,  Fomitiporia mediterranea produces fewer molecules, the two main 6-methoxymelleine and 2,2-dimethyl-4-6-carbaldehyde oxochoman (Fkyera et al., 2000). The function of these molecules is not clearly determined.



Relationship with the vines

In the graph below the average susceptibility to the Esca Disease (France) of the different vines. It can be observed how different clones of the same vine have different susceptibility.




Trichoderma and Esca Disease

The Esca Disease is a pathologic complex that can hardly be cured; it is therefore necessary to set up preventive strategies.

Numerous studies have shown the effectiveness of Trichoderma in preventing the occurrence of infections. However, the mechanism of action has not yet been fully clarified.

The detection of the ability of Trichoderma to remain on plant tissues (especially on pruning wounds) for a long time has been detected, but not quantified. In South Africa (Mutawila et al., 2011), they have actually shown that Trichoderma, applied on pruning wounds, is able to grow in the tissues (xylem and marrow) of vine shoots and to reduce, but not to cancel, the ability to develop Phaeomoniella chlamydospora in the same tissues.

Some highlight the formations of barriers to entry of pathogens as the main (if not exclusive) way of action of the Trichoderma.

This interpretation, in our opinion, is not completely correct. Already in the past some research had shown how the effectiveness of Trichoderma increased when the application was already in the nursery, even better if applied in the rooting of cuttings (Di Marco and Osti, 2007) almost had a sort of effect of immunization and accumulation.

In a recent study (Morin M. et al., 2012) the positive effect of Trichoderma was highlighted; but the peculiarity is that an artificial infection was made 1 month after the application of Trichoderma, on an artificially caused wound, effectively eliminating any Trichoderma fragments present. This procedure used would exclude the barrier effect as a mode of action of the Trichoderma against the infection of the agents of the Esca Disease.

Usually not much considered when talking about the action of Trichoderma, the induction of resistance is probably the mechanism that most influences the successful outcome of the application against the Esca Disease.

During the Plant-Trichoderma interaction, numerous elicitors are released by Trichoderma's hyphae that can induce different types of signals transmitted inside the plant, for example from salicylic acid (SA), jasmonic acid (JA), Abscisic Acid (ABA) or from reactive oxygen species (ROS), triggering defense protein expression. As a result of the activation of the related genes, the plant produces enzymes involved in the direct suppression of pathogens, that is to improve the biochemical and structural barriers of the plant. Depending on the strain of Trichoderma, plant species as well as biotic and abiotic conditions, Trichoderma-activated defense reactions may oscillate between the two types of systemic resistance: systemic induced resistance (ISR) and acquired systemic resistance (SAR).

Recent studies have identified a secondary metabolite of Trichoderma harzianum called harzianolide that influences the expression of 6 defense-related genes involved in signal transmission (eg salicylic acid (PR1 and GLU) and jasmonate/ethylene (JERF3)).

Other studies have identified the marked induction of the activity of phenylalanine ammonia-lyase (PAL), polyphenol oxidase (PPO), peroxidase (PO) and cinnamyl alcohol dehydrogenase (CAD) enzymes and in the ferulic, r-coumaric and gallic acid accumulation , all involved in the natural defense mechanisms implemented by plants.

Often there is an increase in the concentration of polyphenolic compounds (including lignin) which increase the mechanical strength of the fabrics.

The induction of resistance as an effective mechanism would explain both the highlighted accumulation effect of the early use of Trichoderma, and its action even when the barrier effect is overcome by the pathogenic inoculum.


Trichoderma and efficacy







Trichoderma strategy of application

We reaffirm the need for a preventive use of Trichoderma, better if starting from the nursery.

Nursery: localized application along the row 1 kg / ha *.

Transplantation: localized application with the first irrigation at a dose of 0.25/1 g * per plant depending on the density of the plant).

Current cultivation: application at the beginning of spring, located along the row (fertigation or in conjunction with weeding) at a dose of 1-2.5 kg/ha depending on the situation of the plant and the varietal susceptibility. In particularly difficult situations it may be appropriate to repeat the application in September.


Read related articles:

- Prevenzione integrata dal Mal dell’esca - TERRA E VITA

Impiego di Trichoderma contro il mal dell’esca della vite - INFORMATORE AGRARIO

Il Mal dell’Esca della vite, alcuni aspetti relativi alla difesa - NOTIZIARIO ERSAL

Presenza del Mal dell’Esca nell’area viticola della provincia di Teramo - UNIVERSITÀ DI BOLOGNA - FACOLTÀ DI AGRARIA

Il Mal dell’Esca della Vite - ARSIA REGIONE TOSCANA

La lotta contro il Mal dell'Esca - INFORMATORE FITOPATOLOGICO

Risposta varietale della vite al Mal dell'Esca - TESI Guerretta_Patrick

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Sezione al microscopio elettronico di fasi occlusi da Mal dell'Esca (Trichoderma e Mal dell'Esca)
Sintomi su foglia di Mal dell'Esca (Trichoderma e Mal dell'Esca)
Sintomi su tronco di Mal dell'Esca (Trichoderma e Mal dell'Esca)
Suscettibilità dei vitigni a Mal dell'Esca (Trichoderma e Mal dell'Esca)
Efficacia di Trichoderma nel controllo di Mal dell'Esca