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== Disease cycle ==
== Disease cycle ==
The disease cycle begins in early spring, when cool temperatures and abundant moisture promote the release of sexual spores ([[ascospore]]s) from overwintering structures ([[pseudothecia]]) found in the debris at the base of previously-infected trees.<ref name=":0" /> [[Ascospore|Ascospores]] may be disseminated over long distances by wind or within a short range by splashing water.<ref name=":2" /> Following their dissemination, [[ascospores]] land on the surface of newly-emerged leaves and blossoms and penetrate the underlying tissue using a [[germ tube]]. Shortly after penetration, light green [[lesions]] develop on the infected tissue and gradually darken, expand, and pucker as the infection progresses.<ref name=":0" /> Older foliar lesions are typically brown-green in colouration and irregularly shaped<ref name=":1" />. 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.<ref name=":1" /> Within 10 days of infection, asexual [[Conidium|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<ref name=":1" />. At the end of the season, heavily-infected fruit and foliage will fall from the canopy, allowing for the development of [[Pseudothecia|pseuothecia]], which serve as a source of primary inocula for the next spring.
The disease cycle begins in early spring, when cool temperatures and abundant moisture promote the release of sexual spores ([[ascospore]]s) from overwintering structures ([[pseudothecia]]) found in the debris at the base of previously-infected trees.<ref name=":0" /> 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.<ref name=":33">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</ref> It may also be noted that the release of ascospores is synchronized with [[budbreak]] and the unfurling of the host plant's first leaves.<ref name=":83">{{Cite journal|last=Bowen|first=Joanna K.|last2=Mesarich|first2=Carl H.|last3=Bus|first3=Vincent G. M.|last4=Beresford|first4=Robert M.|last5=Plummer|first5=Kim M.|last6=Templeton|first6=Matthew D.|date=2011|title=Venturia inaequalis: the causal agent of apple scab|url=https://bsppjournals.onlinelibrary.wiley.com/doi/abs/10.1111/j.1364-3703.2010.00656.x|journal=Molecular Plant Pathology|language=en|volume=12|issue=2|pages=105–122|doi=10.1111/j.1364-3703.2010.00656.x|issn=1364-3703|pmc=PMC6640350|pmid=21199562}}</ref> Following their dissemination, [[ascospores]] are transported to the surfaces of newly-emerged leaves and blossoms by wind and splashing water.<ref name=":02" /> The tissue is then penetrated either directly with a [[germ tube]] or using an [[appressorium]], thus initiating a new infection.<ref name=":84">{{Cite journal|last=Bowen|first=Joanna K.|last2=Mesarich|first2=Carl H.|last3=Bus|first3=Vincent G. M.|last4=Beresford|first4=Robert M.|last5=Plummer|first5=Kim M.|last6=Templeton|first6=Matthew D.|date=2011|title=Venturia inaequalis: the causal agent of apple scab|url=https://bsppjournals.onlinelibrary.wiley.com/doi/abs/10.1111/j.1364-3703.2010.00656.x|journal=Molecular Plant Pathology|language=en|volume=12|issue=2|pages=105–122|doi=10.1111/j.1364-3703.2010.00656.x|issn=1364-3703|pmc=PMC6640350|pmid=21199562}}</ref> Shortly after penetration, light green [[lesions]] develop on the infected tissue and gradually darken, expand, and pucker as the infection progresses.<ref name=":0" /> Older foliar lesions are typically brown-green in colouration and irregularly shaped<ref name=":1" />. Older foliar lesions are typically brown-green in colouration and irregularly shaped.<ref name=":12">{{Cite web|url=https://www2.gov.bc.ca/gov/content/industry/agriculture-seafood/animals-and-crops/plant-health/insects-and-plant-diseases/tree-fruits/apple-scab#cycle|title=Apple Scab Management in British Columbia - Province of British Columbia|last=Agriculture|first=Ministry of|website=www2.gov.bc.ca|access-date=2020-02-18}}</ref> 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.<ref name=":1" /> Within 10 days of infection, asexual [[Conidium|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<ref name=":1" />. At the end of the season, heavily-infected fruit and foliage will fall from the canopy, allowing for the development of [[Pseudothecia|pseuothecia]], which serve as a source of primary inoculum for the next spring.
[[Image:Apple scab SEM.jpg|thumb|The reproductive conidia of ''Venturia inaequalis'' erupting through the cuticle of a crabapple leaf.]]
[[Image:Apple scab SEM.jpg|thumb|The reproductive conidia of ''Venturia inaequalis'' erupting through the cuticle of a crabapple leaf.]]
[[File:Apple scab in Tashkent region.jpg|thumb|Apple scab]]
[[File:Apple scab in Tashkent region.jpg|thumb|Apple scab]]

Revision as of 15:27, 22 March 2020

Not to be confused with Applecrab.
Apple scab
Apple scab
Common namesAlso: sooty blotch
Causal agentsVenturia inaequalis
HostsApple
EPPO CodeVENTIN

Apple 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][6] 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.[7][8] 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.[7][8] 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.[9]

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.[10] However, genetic studies have indicated that apple scab likely emerged in Central Asia.[11] 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.[11][12] 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.[12]

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.[13] It may also be noted that the release of ascospores is synchronized with budbreak and the unfurling of the host plant's first leaves.[14] 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.[15] 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.[16] 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.
Apple scab


Control

In affected orchards, new infections can be reduced by removing leaf litter and trimmings containing infected tissue from the orchard and incinerating them. This will reduce the amount of new ascospores released in the spring. Additionally, scab lesions on woody tissue can be excised from the tree if possible and similarly destroyed.

Chemical controls can include a variety of compounds. Benzimidazole fungicides, e.g., Benlate (now banned in many countries due to its containing the harmful chemical benzene) work well but resistance can arise quickly. A number of other chemical classes including sterol inhibitors such as Nova 40, and strobilurins such as Sovran are used extensively; however, some of these are slowly being phased out because of resistance problems.

Contact fungicides not prone to resistance, such as Captan, are viable choices. Potassium bicarbonate is an effective fungicide against apple scab, as well as powdery mildew, and is allowed for use in organic farming.[17][18][19][20] Copper and Bordeaux mixture are traditional controls but are less effective than chemical fungicides, and can cause russeting of the fruit. Wettable sulfur also provides some control. Timing of application and concentration varies between compounds.

An apple scab prognostic model called RIMpro was developed by Marc Trapman, which numerically grades infection risk and can serve as a warning system. It allows better targeted spraying. Parameter for calculation are wetness of leaves, amount of rain fall and temperature.[21][22]

Fifteen genes have been found in apple cultivars that confer resistance against apple scab. Researchers hope to use cisgenic techniques to introduce these genes into commercial cultivars and therefore create new resistant cultivars. This can be done through conventional breeding but would take over 50 years to achieve.[23]

Of the known resistance genes, only the Vf gene has been widely introgressed into new apple cultivars (such as Red Prima and Katrina). However, apple scab has shown that it can evolve to render the vf gene ineffective.[24]

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. ^ admin (2015-03-06). "Apple Scab". Center for Agriculture, Food and the Environment. Retrieved 2020-03-09.
  4. ^ a b c d 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. ^ "Apple Disease - Apple Scab". Penn State Extension. Retrieved 2020-02-02.
  7. ^ a b 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
  8. ^ a b "Apple scab". Apple scab. Retrieved 2020-02-18.
  9. ^ 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.{{cite journal}}: CS1 maint: PMC format (link)
  10. ^ 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
  11. ^ 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.
  12. ^ a b 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.{{cite journal}}: CS1 maint: PMC format (link)
  13. ^ 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
  14. ^ 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.{{cite journal}}: CS1 maint: PMC format (link)
  15. ^ 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.{{cite journal}}: CS1 maint: PMC format (link)
  16. ^ Agriculture, Ministry of. "Apple Scab Management in British Columbia - Province of British Columbia". www2.gov.bc.ca. Retrieved 2020-02-18.
  17. ^ "Archived copy". Archived from the original on 2010-05-07. Retrieved 2014-11-17.{{cite web}}: CS1 maint: archived copy as title (link)
  18. ^ "Powdery Mildew - Sustainable Gardening Australia". Archived from the original on 2016-03-03. Retrieved 2014-11-17.
  19. ^ "Organic Fruit Production in Michigan". Archived from the original on 2012-02-16. Retrieved 2014-11-17.
  20. ^ Tamm, Lucius; Amsler, Thomas; Schaerer, Hansjakob; Refardt, Mathias (2006). "Efficacy of Armicarb (potassium bicarbonate) against scab and sooty blotch on apples". In Boos, Markus (ed.). Ecofruit: 12th International Conference on Cultivation Technique and Phytopathological Problems in Organic Fruit-growing (PDF). pp. 87–92. Retrieved 10 August 2015.
  21. ^ RIMpro Scab forecast model Fruitwebinfo. not dated, retrieved 25 October 2015
  22. ^ R. Rancane, M. Eihe, L. Jankovska Adaptation of the apple scab simulation model RIMpro in integrated plant protection in Latvia 25 November 2008, doi 10.17660/ActaHortic.2008.803.7
  23. ^ http://www.cisgenesis.com/content/view/7/35/lang,english/ Resistance to apple scab
  24. ^ Breakdown of the Scab Resistance Gene Vf in Apple Leads to a Founder Effect in Populations of the Fungal Pathogen Venturia inaequalis, doi:10.1094/PHYTO.2004.94.4.364
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