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Apple scab

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Not to be confused with Applecrab.
Apple scab
The main symptom of apple scab in infected trees is the development of brown lesions on the foliage and fruits.
Common namesAlso: sooty blotch
Causal agentsVenturia inaequalis
HostsApple
EPPO CodeVENTIN

owenApple scab is a common disease of plants in the rose family (Rosaceae) that is caused by the ascomycete fungus Venturia inaequalis.[1] While this disease impacts several plant genera, including Sorbus, Cotoneaster, and Pyrus, it is most widely associated with the infection of Malus trees, including species of flowering crabapple, as well as cultivated apple.[2][3] The first symptoms of this disease are found in the foliage, blossoms, and developing fruits of affected trees. Upon infection, these structures will develop dark, irregularly-shaped lesions.[4][5] Although apple scab rarely kills its host, infection typically leads to fruit deformation and premature leaf and fruit drop, which enhance the susceptibility of the host plant to abiotic stress and secondary infection.[6][7] The reduction of fruit quality and yield may result in crop losses of up to 70%, posing a significant threat to the economies of apple-producing regions.[6][7] To reduce yield losses caused by apple scab, growers often use a combination of preventative measures, such as sanitation and resistance breeding, and targeted fungicide treatments, which are supported through the use of predictive modelling systems.[8]

Apple scab on crabapple, lesions are visible on the leaves.

History and distribution

The earliest official reports of apple scab were made in 1819 by Swedish botanist, Elias Fries.[6] However, genetic studies have indicated that apple scab likely emerged in Central Asia.[9] As neither the spores nor conidia of this disease are capable of travelling great distances, it is likely that apple scab spread through the movement of domesticated apple trees by migrating humans.[9][8] By the end of the 19th century, the disease had spread to North America and Oceania alongside the importation of host plants. Today apple scab is present in nearly all regions where apples are cultivated, with the most significant infections occurring in temperate areas, where it is cool and moist in the spring.[8]

Disease cycle

The disease cycle begins in early spring, when cool temperatures and abundant moisture promote the release of sexual spores (ascospores) from overwintering structures (pseudothecia) found in the debris at the base of previously-infected trees.[5] Moisture is a critical factor in the development of the disease as rainfall not only triggers the release of ascospores in the spring, but also facilitates the infection of new hosts by helping the spores adhere to and germinate on the healthy tissue of new hosts.[6] It may also be noted that the release of ascospores is synchronized with budbreak and the unfurling of the host plant's first leaves.[8] Following their dissemination, ascospores are transported to the surfaces of newly-emerged leaves and blossoms by wind and splashing water.[1] The tissue is then penetrated either directly with a germ tube or using an appressorium, thus initiating a new infection.[8] Shortly after penetration, light green lesions develop on the infected tissue and gradually darken, expand, and pucker as the infection progresses.[5] Older foliar lesions are typically brown-green in colouration and irregularly shaped.[4] Older foliar lesions are typically brown-green in colouration and irregularly shaped.[4] Lesions on fruit are black or brown and irregularly shaped. Older fruit lesions cause the underlying tissue to become dry, corky, and eventually disfigured by splitting.[4] Within 10 days of infection, asexual conidia will develop on the darkened lesions and allow for the establishment of secondary infections in healthy leaf and fruit tissue. Under optimal conditions, this cycle may repeat every 1–2 weeks during the growing season.[4] At the end of the season, heavily-infected fruit and foliage will fall from the canopy, allowing for the development of pseuothecia, which serve as a source of primary inoculum for the next spring.

The reproductive conidia of Venturia inaequalis erupting through the cuticle of a crabapple leaf.

Predicting infection

First developed in 1944 by American plant pathologist, W.D. Mills, a Mills Table predicts the likelihood of an apple scab infection developing based on the average temperature and the number of hours of leaf wetness that the host plant is exposed to.[10] This prediction system has been rapidly adopted in both Europe and North America, where apple growers use it as an early warning system for new infections, allowing them to apply preventative fungicides when appropriate.[11] Several revisions have been made to the Mills Table since its creation. The most notable revision was made in 1989 by plant pathologists William MacHardy and David Gadoury, who determined that ascospores required 3 hours less than originally calculated in order to establish a new infection.[11] While other methods of prediction include ascospore maturation models and leaf orchard leaf canopy models, the Mills Table, combined with electronic weather monitoring, remains the most-widely used tool for predicting apple scab infection periods.[8]

Management of apple scab

Cultural controls

Cultural controls may be used as a first step when seeking to reduce the incidence of new infections. These practices include cleaning leaf litter from the base of previously-infected trees, as well as removing infected woody material from the canopy when performing annual pruning.[3] Doing so will reduce the amount of primary inoculum in the spring and subsequently delay the establishment the disease. Furthermore, regular pruning will improve air flow and light penetration in the canopy, which ultimately inhibits the development and spread of disease.[3]

Chemical controls

The management of apple scab using chemical controls is primarily concerned with the prevention primary infection cycle by reducing the efficacy of ascospores. As such, fungicides are typically applied early in the season, when ascospores are first released.[7] However, fungicide applications may also be made later in the season to prevent infection of old leaves, which can help reduce the amount of primary inoculum for the following season.[12] Benzimidazole fungicides are among the most commonly-used classes of fungicide for managing apple scab in conventional orchards; however, there is some evidence that the disease is developing resistance to this class of fungicides, along with several others, including demethylation inhibitors and quinone outside inhibitors.[13] To manage the development of fungicide resistance, growers can reduce the number of applications made throughout the season and alternate between different classes of fungicide.[8]

Resistance breeding programs

The first formal resistance breeding programs for apple scab began in the early 20th century with the development of the PRI Apple Breeding Program by Purdue University, Rutgers University, and the University of Illinois. Since its inception in 1945, the PRI Apple Breeding Program has used controlled crosses between cultivated apples and wild Malus species to develop 1500 resistant cultivars, 16 of which (including 'Prima,' 'Jonafree,' and 'Goldrush') have been named released into market.[14] Modern genetic work has found that a total of fifteen genes may confer resistance to apple scab.[6] Many of these genes have been isolated from wild Malus spp. populations in East Asia, where a high level of species diversity still remains.[8] Of these resistance genes, the Vf (Rvi6) gene is the most well-studied and is currently being used by researchers seeking to develop resistant cultivars using transgenic technology.[6] While the development of transgenic resistant cultivars may reduce management costs in orchards, limited market acceptance pose a barrier to adoption by commercial growers.[8] Moreover, researchers have observed a breakdown of resistance genes by Venturia populations, posing another significant barrier to the success of this technology.[15]

See also

References

  1. ^ a b "Apple Disease - Apple Scab". Penn State Extension. Retrieved 2020-02-18.
  2. ^ "Apple scab of apples and crabapples". extension.umn.edu. Retrieved 2020-03-09.
  3. ^ a b c admin (2015-03-06). "Apple Scab". Center for Agriculture, Food and the Environment. Retrieved 2020-03-09.
  4. ^ a b c d e Agriculture, Ministry of. "Apple Scab Management in British Columbia - Province of British Columbia". www2.gov.bc.ca. Retrieved 2020-02-02.
  5. ^ a b c Gauthier, Nicole (2018). "Apple scab". American Phytopathological Society. Retrieved 2020-02-02.{{cite web}}: CS1 maint: url-status (link)
  6. ^ a b c d e f Jha, G., Thakur, K., & Thakur, P. (2009). The Venturia Apple Pathosystem: Pathogenicity Mechanisms and Plant Defense Responses. Journal of Biomedicine and Biotechnology, 2009. doi:10.1155/2009/680160
  7. ^ a b c "Apple scab". Apple scab. Retrieved 2020-02-18.
  8. ^ a b c d e f g h i Bowen, Joanna K.; Mesarich, Carl H.; Bus, Vincent G. M.; Beresford, Robert M.; Plummer, Kim M.; Templeton, Matthew D. (2011). "Venturia inaequalis: the causal agent of apple scab". Molecular Plant Pathology. 12 (2): 105–122. doi:10.1111/j.1364-3703.2010.00656.x. ISSN 1364-3703. PMC 6640350. PMID 21199562.
  9. ^ a b Gladieux, Pierre (2008). "On the Origin and Spread of the Scab Disease of Apple: Out of Central Asia". PLoS One. 3 – via ProQuest.
  10. ^ Schumann, Gail (1991). Plant diseases: Their biology and social impact. St. Paul, Minnesota, USA: The American Phytopathological Society. pp. 173–177.
  11. ^ a b Singh, Krishna P. (September 2019). "Aerobiology, epidemiology and management strategies in apple scab: science and its applications". Indian Phytopathology. 72 (3): 381–408. doi:10.1007/s42360-019-00162-5. ISSN 0367-973X.
  12. ^ Li, B.; Xu, X. (2002). "Infection and Development of Apple Scab (Venturia inaequalis) on Old Leaves". Journal of Phytopathology. 150 (11–12): 687–691. doi:10.1046/j.1439-0434.2002.00824.x. ISSN 1439-0434.
  13. ^ Köller, Wolfram; Parker, D. M.; Turechek, W. W.; Avila-Adame, Cruz; Cronshaw, Keith (May 2004). "A Two-Phase Resistance Response of Venturia inaequalis Populations to the QoI Fungicides Kresoxim-Methyl and Trifloxystrobin". Plant Disease. 88 (5): 537–544. doi:10.1094/PDIS.2004.88.5.537. ISSN 0191-2917.
  14. ^ Janick, Jules (2006). "The PRI Apple Breeding Program" (PDF). HortScience. 41: 8–10.
  15. ^ Köhl, Jürgen; Scheer, Christian; Holb, Imre J.; Masny, Sylwester; Molhoek, Wilma (2014-10-15). "Toward an Integrated Use of Biological Control by Cladosporium cladosporioides H39 in Apple Scab (Venturia inaequalis) Management". Plant Disease. 99 (4): 535–543. doi:10.1094/PDIS-08-14-0836-RE. ISSN 0191-2917.
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