Plant Disease Models and Forecasting: Changes in Principles and Applications over the Last 50 Years.

This review gives a perspective of selected advances made since the middle of the 20th century in plant disease modeling, and the associated increase in the number of models published during that time frame. This progress can be mainly attributed to advances in (i) sensors and automatic environmental data collection technology, (ii) instrumentation and methods for studying botanical epidemiology, and (iii) data analytics and computer science. We review the evolution of techniques for developing data-based (empirical) models and process-based (mechanistic) models using the wheat rusts as a case study. We also describe the increased importance of knowledge about biological processes for plant disease modeling by using apple scab as a second case study. For both wheat rusts and apple scab, we describe how the models have evolved over the last 50 years by considering certain milestones that have been achieved in disease modeling. Finally, we describe how plant disease models are used as part of a multi-modeling approach to develop decision-making tools in the application of integrated pest management.

Dynamics of Diaporthe ampelina Conidia Released from Grape Canes that Overwintered in the Vineyard.

Phomopsis cane and leaf spot (PCLS) is an important disease of grapevines that is mainly caused by Diaporthe ampelina. Dispersal dynamics of D. ampelina spores were investigated in two vineyards, one in northern Italy and one in Montenegro, by using spore samplers that collected α- and ß-conidia from rain water running off from PCLS-affected canes. The canes were collected from each vineyard, deployed, and overwintered in the corresponding vineyards. In each of three years (2016, 2017, and 2018), conidial dispersal was investigated during one (Montenegro) or two (Italy) growing seasons following the deployment of the PCLS-affected canes. In the first growing season following cane deployment in both vineyards, α-conidia were mostly found in runoff water after grapevine bud break, especially in April and May, and ß-conidia were regularly found in numbers comparable to those of α-conidia, most frequently from June to September. In Italy, high numbers of α- and ß-conidia were also collected during the second growing season following cane deployment. The dispersal dynamics of α-conidia over time were described by a Gompertz equation using hydrothermal time (i.e., the accumulated effect of temperature on the maturation rate of pycnidia on days in which the number of hours of wetness was ≥6 or 9 h), with R2 and concordance correlation coefficient >0.9. Rain (≥0.2 mm) was a good predictor of conidial dispersal, with an overall accuracy of 0.97. These results increase our understanding of D. ampelina spore dispersal and should be integrated into warning systems for PCLS management.

Temporal Dispersal Patterns of Phaeomoniella chlamydospora, Causal Agent of Petri Disease and Esca, in Vineyards.

Although the fungus Phaeomoniella chlamydospora is the most commonly detected causal agent of Petri disease and esca, two important fungal grapevine trunk diseases, little is known about the dispersal patterns of P. chlamydospora inoculum. In this work, we studied the dispersal of P. chlamydospora airborne inoculum from 2016 to 2018 in two viticultural areas of eastern (Ontinyent) and northern (Logroño) Spain. The vineyards were monitored weekly from November to April using microscope slide traps, and P. chlamydospora was detected and quantified by a specific real-time quantitative (qPCR) method set up in this work. The method was found to be sensitive, and a good correlation was observed between numbers of P. chlamydospora conidia (counted by microscope) and DNA copy numbers (quantified by qPCR). We consistently detected DNA of P. chlamydospora at both locations and in all seasons but in different quantities. In most cases, DNA was first detected in the last half of November, and most of the DNA was detected from December to early April. When rain was used as a predictor of P. chlamydospora DNA detection in traps, false-negative detections were observed, but these involved only 4% of the total. The dispersal pattern of P. chlamydospora DNA over time was best described (R2 = 0.765 and concordance correlation coefficient = 0.870) by a Gompertz equation, with time expressed as hydrothermal time (a physiological time accounting for the effects of temperature and rain). This equation could be used to predict periods with a high risk of dispersal of P. chlamydospora.

Reduction of Botrytis cinerea Colonization of and Sporulation on Bunch Trash.

Botrytis bunch rot (BBR) of grapevine, caused by Botrytis cinerea, is commonly managed by fungicide (FUN) sprays at flowering (A), at prebunch closure (B), at veraison (C), and before harvest. Applications at A, B, and C are recommended to reduce B. cinerea colonization of bunch trash and the production of conidia during berry ripening. The effects of these applications were previously evaluated as reductions in BBR severity at harvest rather than as reductions in bunch trash colonization and sporulation by B. cinerea. This study investigated the effects of FUNs (a commercial mixture of fludioxonil and cyprodonil), biological control agents (BCAs; Aureobasium pullulans and Trichoderma atroviride), and botanicals (BOTs; a commercial mixture of eugenol, geraniol, and thymol) applied at different timings (A, B, C, or ABC) compared with a nontreated control (NT) on B. cinerea bunch trash colonization and sporulation in vineyards. The ability of B. cinerea to colonize the bunch trash (as indicated by B. cinerea DNA content) and sporulate (as indicated by the number of conidia produced under optimal laboratory conditions) was highly variable, and this variability was higher between years (2015 to 2018) than among the three vineyards and three sampling times (i.e., 1 week after applications at A, B, and C). B. cinerea sporulation on bunch trash was significantly lower in plots treated with FUN than in NT in only 3 of 18 cases (3 vineyards × 2 years × 3 sampling times). FUN applications, however, significantly reduced B. cinerea colonization of bunch trash compared with NT; for colonization, BCA efficacy was similar to that of FUN, but BOT efficacy was variable. For all products, colonization reduction was the same with application at A versus ABC, meaning that the effect of an early season application lasted from flowering to 1 week after veraison. These results indicate that the early season control of B. cinerea is important to reduce the saprophytic colonization of bunch trash, especially when the risk of BBR is high.

Consideration of Latent Infections Improves the Prediction of Botrytis Bunch Rot Severity in Vineyards.

The current study validated a mechanistic model for Botrytis cinerea on grapevine with data from 23 independent Botrytis bunch rot (BBR) epidemics (combinations of vineyards × year) that occurred between 1997 and 2018 in Italy, France, and Spain. The model was operated for each vineyard by using weather data and vine growth stages to anticipate, at any day of the vine-growing season, the disease severity (DS) at harvest (severe, DS ≥ 15%; intermediate, 5 < DS < 15%; and mild, DS ≤ 5%). To determine the ability of the model to account for latent infections, postharvest incubation assays were also conducted using mature berries without symptoms or signs of BBR. The model correctly classified the severity of 15 of 23 epidemics (65% of epidemics) when the classification was based on field assessments of BBR severity; when the model was operated to include BBR severity after incubation assays, its ability to correctly predict BBR severity increased from 65% to >87%. This result showed that the model correctly accounts for latent infections, which is important because latent infections can substantially increase DS. The model was sensitive and specific, with the false-positive and false-negative proportion of model predictions equal to 0.24 and 0, respectively. Therefore, the model may be considered a reliable tool for decision-making for BBR control in vineyards.

Mo-derived perivascular macrophage recruitment protects against endothelial cell death in retinal vein occlusion.

BACKGROUND: To decipher the role of monocyte-derived macrophages (Mφs) in vascular remodeling of the occluded vein following experimental branch retinal vein occlusion (BRVO). METHODS: The inflammation induced by laser-induced BRVO on mice retina was evaluated at different time points by RT-PCR looking at inflammatory markers mRNA level expression, Icam-1, Cd11b, F4/80, Ccl2, and Ccr2 and by quantification of Iba1-positive macrophage (Mφ) density on Iba1-stained retinal flatmount. Repeated intraperitoneal EdU injection combined with liposome clodronate-induced monocyte (Mo) depletion in wildtype mice was used to differentiate Mo-derived Mφs from resident Mφs. Liposome clodronate Mo-depleted wildtype mice and Ccr2-deficient mice were used to evaluate the role of all CCR2+ and CCR2neg Mo-derived Mφs on EC apoptosis in the occluded vein. RESULTS: cd11b, ICAM-1, F4/80, Ccl2, and Ccr2 mRNA expression were increased 1, 3, and 7 days after vein occlusion. The number of parenchymal (parMφs) and perivascular (vasMφs) macrophages was increased 3 and 7 days after BRVO. The systemic depletion of all circulating Mos decreased significantly the BRVO-induced parMφs and vasMφs macrophage accumulation, while the deletion of CCR2+-inflammatory Mo only diminished the accumulation of parMφs, but not vasMφs. Finally, apoptotic ECs of the vein were more numerous in fully depleted, liposome clodronate-treated mice, than in Ccr2-/- mice that only lack the recruitment of CCR2+ inflammatory Mos. CONCLUSIONS: BRVO triggers the recruitment of blood-derived parMφs and vasMφs. Interestingly, vasMφs accumulation was independent of CCR2. The observation that the inhibition of the recruitment of all infiltrating Mφs increases the vein EC apoptosis, while CCR2 deficiency does not, demonstrates that CCR2neg Mo-derived vasMφs protect the ECs against apoptosis in the occluded vein.

Thinning of the RPE and choroid associated with T lymphocyte recruitment in aged and light-challenged mice.

PURPOSE: Thinning of the RPE and the underlying vascular layer, the choroid, is observed with age in many human eye disorders. The reasons for this thinning are ill-defined. Here, we highlight the possible role of T lymphocyte recruitment in choroidoretinal thinning in aged and light-challenged mice. METHODS: In age and light challenge models, we measured chemokine concentrations using enzyme-linked immunosorbent assay and used flow cytometry to characterize lymphocyte populations. We quantified thinning in eye immunosections and RPE65 expression using quantitative PCR. RESULTS: Age and light challenge led to increased levels of the lymphotactic protein CXCL10 alone (aging) or in conjunction with CXCL9 (light challenge). Increased numbers of CD3+ T lymphocytes, most of them CD8+ cytotoxic T lymphocytes, were also observed in the choroid and retina of old mice and following light challenge. Influx of T lymphocytes was associated with RPE and choroidal thinning and diminished expression of RPE65 mRNA, an essential enzyme of the visual cycle. CONCLUSIONS: The observations from this study suggest that cytotoxic CD8(+) T lymphocytes might participate in choroidal and RPE degeneration and that modulation of T lymphocyte recruitment might be a novel strategy to reduce choroidoretinal dysfunctions observed with age and following photo-oxidative stress.

Thermodynamic characterization of amyloid polymorphism by microfluidic transient incomplete separation.

Amyloid fibrils of proteins such as α-synuclein are a hallmark of neurodegenerative diseases and much research has focused on their kinetics and mechanisms of formation. The question as to the thermodynamic stability of such structures has received much less attention. Here, we newly utilize the principle of transient incomplete separation of species in laminar flow in combination with chemical depolymerization for the quantification of amyloid fibril stability. The relative concentrations of fibrils and monomer at equilibrium are determined through an in situ separation of these species based on their different diffusivity inside a microfluidic capillary. The method is highly sample economical, using much less than a microliter of sample per data point and its only requirement is the presence of aromatic residues (W, Y) because of its label-free nature, which makes it widely applicable. Using this method, we investigate the differences in thermodynamic stability between different fibril polymorphs of α-synuclein and quantify these differences for the first time. Importantly, we show that fibril formation can be under kinetic or thermodynamic control and that a change in solution conditions can both stabilise and destabilise amyloid fibrils. Taken together, our results establish the thermodynamic stability as a well-defined and key parameter that can contribute towards a better understanding of the physiological roles of amyloid fibril polymorphism.

Intravenous scAAV9 delivery of a codon-optimized SMN1 sequence rescues SMA mice.

Spinal muscular atrophy (SMA) is the most common genetic disease leading to infant mortality. This neuromuscular disorder is caused by the loss or mutation of the telomeric copy of the 'survival of motor neuron' (Smn) gene, termed SMN1. Loss of SMN1 leads to reduced SMN protein levels, inducing degeneration of motor neurons (MN) and progressive muscle weakness and atrophy. To date, SMA remains incurable due to the lack of a method to deliver therapeutically active molecules to the spinal cord. Gene therapy, consisting of reintroducing SMN1 in MNs, is an attractive approach for SMA. Here we used postnatal day 1 systemic injection of self-complementary adeno-associated virus (scAAV9) vectors carrying a codon-optimized SMN1 sequence and a chimeric intron placed downstream of the strong phosphoglycerate kinase (PGK) promoter (SMNopti) to overexpress the human SMN protein in a mouse model of severe SMA. Survival analysis showed that this treatment rescued 100% of the mice, increasing life expectancy from 27 to over 340 days (median survival of 199 days) in mice that normally survive about 13 days. The systemic scAAV9 therapy mediated complete correction of motor function, prevented MN death and rescued the weight loss phenotype close to normal. This study reports the most efficient rescue of SMA mice to date after a single intravenous injection of an optimized SMN-encoding scAAV9, highlighting the considerable potential of this method for the treatment of human SMA.

A Systematic Map of the Research on Disease Modelling for Agricultural Crops Worldwide.

In this work, we developed a systematic map to identify and catalogue the literature pertaining to disease modelling for agricultural crops worldwide. Searches were performed in 2021 in the Web of Science and Scopus for papers reporting any type of disease model for 103 crops. In total, 768 papers were retrieved, and their descriptive metadata were extracted. The number of papers found increased from the mid-1900s to 2020, and most of the studies were from North America and Europe. More disease models were retrieved for wheat, potatoes, grapes, and apples than for other crops; the number of papers was more affected by the crop's economic value than by its cultivated area. The systematic map revealed an underrepresentation of disease models for maize and rice, which is not justified by either the crop economic value or by disease impact. Most of the models were developed to understand the pathosystem, and fewer were developed for tactical disease management, strategic planning, or scenario analysis. The systematic map highlights a variety of knowledge gaps and suggests questions that warrant further research.

Modulation of DRG neurons response to semaphorin 3A via substrate stiffness.

Semaphorin 3A (Sema3a) is a chemotropic protein that acts as a neuronal guidance cue and plays a major role in dorsal root ganglion (DRG) sensory neurons projection during embryo development. The present study evaluated the impact of stiffness in the repulsive response of DRG neurons to Sema3a when cultured over substrates of variable stiffness. Stiffness modified DRG neurons morphology and regulated their response to Sema3a, reducing the collapse of growth cones when they were cultured on softer substrates. Sema3a receptors expression was also regulated by stiffness, neuropilin-1 was overexpressed and plexin A4 mRNA was downregulated in stiffer substrates. Cytoskeleton distribution was also modified by stiffness. In softer substrates, ßIII-tubulin and actin co-localized up to the leading edge of the growth cones, and as the substrate became stiffer, ßIII-tubulin was confined to the transition and peripheral domains of the growth cone. Moreover, a decrease in the α-actinin adaptor protein was also observed in softer substrates. Our results show that substrate stiffness plays an important role in regulating the collapse response to Sema3a and that the modulation of cytoskeleton distribution and Sema3a receptors expression are related to the differential collapse responses of the growth cones.

Development and Validation of a Mechanistic Model That Predicts Infection by Diaporthe ampelina, the Causal Agent of Phomopsis Cane and Leaf Spot of Grapevines.

Phomopsis cane and leaf spot (PCLS), known in Europe as "excoriose," is an important fungal disease of grapevines caused by Diaporthe spp., and most often by Diaporthe ampelina (synonym Phomopsis viticola). PCLS is re-emerging worldwide, likely due to climate change, changes in the management of downy mildew from calendar- to risk-based criteria that eliminate early-season (unnecessary) sprays, and the progressive reduction in the application of broad-spectrum fungicides. In this study, a mechanistic model for D. ampelina infection was developed based on published information. The model accounts for the following processes: (i) overwintering and maturation of pycnidia on affected canes; (ii) dispersal of alpha conidia to shoots and leaves; (iii) infection; and (iv) onset of disease symptoms. The model uses weather and host phenology to predict infection periods and disease progress during the season. Model output was validated against 11 independent PCLS epidemics that occurred in Italy (4 vineyards in 2019 and 2020) and Montenegro (3 vineyards in 2020). The model accurately predicted PCLS disease progress, with a concordance correlation coefficient (CCC) = 0.925 between observed and predicted data. A ROC analysis (AUROC>0.7) confirmed the ability of the model to predict the infection periods leading to an increase in PCLS severity in the field, indicating that growers could use the model to perform risk-based fungicide applications.

SOCS3-mediated blockade of JAK/STAT3 signaling pathway reveals its major contribution to spinal cord neuroinflammation and mechanical allodynia after peripheral nerve injury.

Neuropathic pain after peripheral nerve injury, associated with local neuroinflammation in the spinal cord, is a severe incapacitating condition with which clinical treatment remains challenging. Inflammatory molecules signal through various intracellular transduction pathways, activation of which may amplify and cause spreading of the inflammatory response. We showed recently that spinal nerve lesion leads to rapid activation of Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) signal transduction pathway in dorsal spinal cord microglia in relation with enhanced levels of spinal interleukin-6 (IL-6) protein. Here, we selectively inactivated JAK/STAT3 signaling in rat dorsal spinal cord glia through local, lentiviral-mediated production of the suppressor of cytokine signaling SOCS3, a physiologic inhibitory protein of JAK/STAT3, and analyzed its consequences in a preclinical model of neuropathic pain. The targeted blockade of JAK/STAT3 activity prevented the abnormal expression of IL-6, CC chemokine ligand CCL2, and activating transcription factor ATF3 induced in the spinal cord by chronic constriction injury of the sciatic nerve (CCI) and substantially attenuated mechanical hypersensitivity (allodynia) in rats. In naive rats, intrathecal administration of a proalgesic cytokine IL-6 rapidly activated microglial JAK/STAT3 and induced downstream changes closely resembling CCI-evoked alterations. We identified downstream mechanisms through which JAK/STAT3 pathway activation leads to the spreading of neuroinflammation. Our findings reveal that JAK/STAT3 signaling plays a major role in spinal cord plasticity and mechanical allodynia associated with peripheral nerve injury.

A network meta-analysis provides new insight into fungicide scheduling for the control of Botrytis cinerea in vineyards.

BACKGROUND: Control of Botrytis bunch rot (BBR) is currently based on the application of fungicides at four timings corresponding to specific growth stages of vines: end of flowering (A), pre-bunch closure (B), veraison (C) and before harvest (D). The current research provides a network meta-analysis of 116 studies conducted between 1963 and 2016 in nine countries, in which 14 strategies (based on combinations of 1, 2, 3, or 4 sprays applied in A, B, C, and/or D) were compared. RESULTS: When a one-spray strategy was applied, BBR control was more effective with sprays applied in A, C, or D than B. With a two-spray strategy, strategy AC provided similar control as strategy BC; strategy CD also provided good control. For a 3-spray strategy, the best disease control was consistently obtained with strategy ACD. Four-spray strategy ABCD provided the best control but often involved needless sprays so that the routine application of four sprays is not justified. CONCLUSIONS: Spraying at timing A seems to be very important for achieving efficient and flexible disease control. Flexibility is reduced by spraying at timing B rather than A. © 2018 Society of Chemical Industry.

JAK/STAT3 pathway is activated in spinal cord microglia after peripheral nerve injury and contributes to neuropathic pain development in rat.

Peripheral nerve lesion leads to the production of interleukin 6 (IL-6)-related neuropoietic cytokines involved in nerve protection and regeneration. This family of cytokines mainly signal through the signal transducer and activator of transcription (STAT) pathway that is locally activated in injured nerves. IL-6 is also involved in pain that frequently arises from peripheral nerve lesion. We investigated the possible activation of this major IL-6 signaling system in the spinal cord after peripheral nerve injury and its role in neuropathic pain. Ligation of L5-L6 spinal nerves (SNL) evoked an accumulation of active, phosphorylated form of STAT3 in microglial cells of dorsal spinal cord mostly in projection areas of injured nerves. SNL resulted also in a massive induction of IL-6 mRNA expression in dorsal root ganglia and increased concentration of IL-6 in dorsal spinal cord. Intrathecal injection of anti-rat IL-6 antibodies prevented the SNL-induced accumulation of phospho-STAT3 in the spinal cord. STAT3 pathway blockade with Janus kinase 2 inhibitor AG490 attenuated both mechanical allodynia and thermal hyperalgesia in SNL rats. These data show that in response to SNL injury Janus kinase/STAT3 system is activated mainly through IL-6 signaling in spinal microglia and that this transduction pathway participates in development of pain associated with nerve alteration.

Lentiviral-mediated Targeted NF-κB Blockade in Dorsal Spinal Cord Glia Attenuates Sciatic Nerve Injury-induced Neuropathic Pain in the Rat.

Neuropathic pain developing after peripheral nerve injury is associated with altered neuronal and glial cell functions in the spinal cord. Activated glia produces algogenic mediators, exacerbating pain. Among the different intracellular pathways possibly involved in the modified glial function, the nuclear factor κB (NF-κB) system is of particular interest, as numerous genes encoding inflammation- and pain-related molecules are controlled by this transcription factor. NF-κB is a pleiotropic factor also involved in central nervous system homeostasy. To study its role in chronic pain, it is thus essential to inhibit the NF-κB pathway selectively in activated spinal glial cells. Here, we show that when restricted to spinal cord and targeted to glial cells, lentiviral vector-mediated delivery of NF-κB super- repressor IκBα resulted in an inhibition of the NF-κB pathway activated in the rat spinal cord after sciatic nerve injury (chronic constriction injury, CCI). Concomitantly, IκBα overproduction prevented the enhanced expression of interleukin-6 and of inducible nitric oxide synthase associated with chronic constriction injury and resulted in prolonged antihyperalgesic and antiallodynic effects. These data show that targeted blockade of NF-κB activity in spinal glia efficiently alleviates pain behavior in CCI rats, demonstrating the active participation of the glial NF-κB pathway in the development of neuropathic pain after peripheral nerve injury.

Pest categorisation of Apiosporina morbosa.

The Panel on Plant Health performed a pest categorisation of the fungus Apiosporina morbosa, the causal agent of black knot, for the EU. The identity of the pest is well established and reliable methods exist for its detection/identification. The pest is listed in Annex IIAI of Directive 2000/29/EC and is not known to occur in the EU. Apiosporina morbosa is present in Alaska, Canada, Mexico and the continental states of the USA. The major hosts of A. morbosa are Prunus domestica and Prunus cerasus; the host status of other Prunus species and hybrids is uncertain because of contradictory reports or lack of information. The pest could potentially enter the EU on host plants for planting and plant parts originating in infested third countries. Wood of Prunus spp. is also a pathway of entry, but of minor importance. The current pest distribution and climate matching suggest that the pest could establish and spread in the EU wherever the hosts are grown. In the infested areas, the pest causes girdling of twigs and occasionally of larger branches, whereas trees with multiple infections loose vigour, bloom poorly, and become unproductive, stunted and susceptible to winter injury and infection by other pathogens. The presence of black knots makes trees unsuitable for timber production. It is expected that the pest introduction and spread in the EU would impact host production. Uncertainty exists on whether the agricultural practices and chemical control methods applied in the EU could prevent the establishment and spread of A. morbosa. A. morbosa meets all the criteria assessed by EFSA for consideration as potential Union quarantine pest. As the pest is not known to occur in the EU, this criterion to consider it as Union regulated non-quarantine pest is not met.

Biology and Epidemiology of Venturia Species Affecting Fruit Crops: A Review.

The fungal genus Venturia Sacc. (anamorph Fusicladium Bonord.) includes plant pathogens that cause substantial economic damage to fruit crops worldwide. Although Venturia inaequalis is considered a model species in plant pathology, other Venturia spp. also cause scab on other fruit trees. Relative to the substantial research that has been conducted on V. inaequalis and apple scab, little research has been conducted on Venturia spp. affecting other fruit trees. In this review, the main characteristics of plant-pathogenic species of Venturia are discussed with special attention to V. inaequalis affecting apple, V. pyrina affecting European pear, V. nashicola affecting Asian pear, V. carpophila affecting peach and almond, Fusicladium oleagineum affecting olive, F. effusum affecting pecan, and F. eriobotryae affecting loquat. This review has two main objectives: (i) to identify the main gaps in our knowledge regarding the biology and epidemiology of Venturia spp. affecting fruit trees; and (ii) to identify similarities and differences among these Venturia spp. in order to improve disease management. A thorough review has been conducted of studies regarding the phylogenetic relationships, host ranges, biologies, and epidemiologies of Venturia spp. A multiple correspondence analysis (CA) has also been performed on the main epidemiological components of these Venturia spp. CA separated the Venturia spp. into two main groups, according to their epidemiological behavior: the first group included V. inaequalis, V. pyrina, V. nashicola, and V. carpophila, the second F. oleagineum and F. eriobotryae, with F. effusum having an intermediate position. This review shows that Venturia spp. affecting fruit trees are highly host-specific, and that important gaps in understanding the life cycle exist for some species, including V. pyrina; gaps include pseudothecia formation, ascospore and conidia germination, and mycelial growth. Considering the epidemiological information reviewed, this paper shows that the use of Mills tables to predict infection periods should be avoided for Venturia spp. other than V. inaequalis.

Pest categorisation of Venturia nashicola.

The Panel on Plant Health performed a pest categorisation of Venturia nashicola, the causal agent of Asian pear scab, for the European Union (EU). The pathogen is a well-defined, distinguishable fungal species affecting Pyrus pyrifolia var. culta, P. ussuriensis and P. bretschneideri in Asian countries. P. communis (European pear) is not a host of V. nashicola, but the host status of other Pyrus species is unclear. V. nashicola is not known to occur in the EU. It is listed in Annex IIAI of Directive 2000/29/EC. The pathogen could potentially enter the EU on host plants for planting and fruit originated in infested countries. There are no climatic factors limiting the potential establishment and spread of the pathogen in the EU, as its epidemiology is similar to those of Venturia inaequalis (apple scab) and Venturia pyrina (European pear scab), which are well-established in the EU. The hosts are present in the EU, but no data were found on their abundance and distribution. In the infested areas, V. nashicola causes premature leaf and fruit drop and fruit distortion resulting in considerable yield/quality losses. The introduction of the pathogen into the EU could cause yield/quality losses and environmental consequences because of the additional fungicide sprays for disease control. Cultural practices and chemical measures applied in the infested areas reduce the inoculum sources but they cannot eliminate the pathogen. Phytosanitary measures are available to mitigate the risk of introduction and spread of the pathogen in the EU. All criteria assessed by EFSA for consideration as a potential Union quarantine pest are met. As V. nashicola is not known to occur in the EU, this criterion assessed by EFSA to consider it as a Union regulated non-quarantine pest is not met.

Pest categorisation of Pseudocercospora angolensis.

The Panel on Plant Health performed a pest categorisation of Cercospora angolensis, the fungus responsible for Pseudocercospora fruit and leaf spot of citrus, for all territories except of the Union territories defined in Article 1 point 3 of Regulation (EU) 2016/2031. C. angolensis is listed in Annex IIAI of Directive 2000/29/EC and is not known to be present in the EU. The pathogen, which has recently been reclassified as Pseudocercospora angolensis, is a well-defined, distinguishable fungal species affecting all cultivated Citrus spp. and Fortunella japonica plants. It is currently distributed in sub-Saharan Africa (altitudes 80-1,800 m) and Yemen. Although the epidemiology of P. angolensis is not well understood, infection is favoured by warm temperatures and humidity. The current distribution of the pathogen and climate matching suggests that it might not be well adapted to Mediterranean climates. However, the pathogen is also present in arid areas of Yemen and can infect young fruit with short wetness durations. Uncertainty exists on whether and at which extent the irrigation applied to EU citrus orchards can make the microclimate favourable for P. angolensis. There are no eco-climatic factors limiting the potential spread of the pathogen in the EU. Long-distance spread occurs by wind-disseminated conidia and movement of infected plants for planting and fruit. Short-distance spread occurs via water splash and/or wind-driven rain. In the infested areas, the disease causes premature abscission of young leaves and fruit resulting in yield losses up to 50-100%. Cultural practices and chemical measures applied in the infested areas reduce inoculum but they cannot eliminate the pathogen. All criteria assessed by EFSA for consideration as a potential Union quarantine pest are met. As P. angolensis is not known to occur in the EU, this criterion assessed by EFSA to consider it as a Union regulated non-quarantine pest is not met.