Everything You Need to Know About Botrytis Bud Rot in Cannabis

Bud rot is one of the most devastating things a grower can deal with. This day and age, when a positive microbial test can cause a grower to lose their crop, there is zero tolerance for fungal pathogens. Bud rot can be especially devastating indoors. If there are conducive conditions and susceptible varieties in close proximity, spores can quickly and easily spread throughout the entire grow groom.

What causes bud rot?

Bud rot is cause by Botrytis cinerea. which is the name for the anamorph (asexual form) of this fungus; sexual reproduction is rare in this species. It is an aggressive necrotrophic plant pathogen that causes disease on over 1,000 crops [1]. It is responsible for up to $100 billion in annual crop losses worldwide [2]. B. cinerea can infect a wide range of tissue types including fruits, flowers, leaves, stems, and storage tissues. It is a serious issue for both preharvest and postharvest (i.e. that characteristic fuzzy gray mold that grows on your strawberries that you get from the supermarket). However, sometimes this fungus can be desirable. Some grape growers utilize the fungus on wine grapes to produce ‘noble rot’ wines. These high value grapes have enhanced ripening responses and may have greater levels of sugars and flavor compounds. In Cannabis, bud rot is never desirable.

Luckily for us, B. cinerea is one of the best studies fungal organisms in the history of plant pathology. It is often used as the model organism for studying necrotrophic plant pathogens. B. cinerea is not just a mold that grows passively on your buds like Penicillium does on bread, it employs mechanisms to both suppress plant defenses and kill plant tissues.

Powdery Mildew and Bud Rot are Both Labeled as ‘Mold’. How do they Differ?

Let us compare B. cinerea to one of the other most damaging fungal disease of Cannabis: powdery mildew (PM). PM is a biotrophic fungus, meaning that it is an obligate parasite that requires living cells to extract nutrients from. Because of this, PM species are required to evolve strategies to specifically overcome the defenses of particular plant species and manipulate plant immune responses (this leads to relatively narrow host ranges for any given species of PM fungi). B. cinerea on the other hand, is much less precise in its pathogenicity strategies.

It tends to rely much more heavily on the secretion of plant toxins and enzymes to kill and digest plant tissues as opposed to suppressing cellular immune responses and maintaining host viability. The fungus can then feed on the dead tissue without having to defend itself against further attack by the plants. This partly explains the much wider host range of B. cinerea, as many of the toxins and cell wall degrading enzymes will ubiquitously kill a wide variety of plant tissues from a wide variety of plant species. As a rule of thumb, biotrophic plant pathogens rely most heavily on secreted effector proteins that manipulate the host plant’s defense response, while necrotrophic plant pathogens rely most heavily on phytotoxins, cell wall degrading enzymes, and other extracellular enzymes.

How does B. cinerea infect plants?

Though B. cinerea has long been considered a necrotroph, newer literature is beginning to show that B. cinerea might be better classified as a hemibiotroph, meaning that it begins its life as a parasite and later transitions to a necrotrophic lifestyle . In order to succeed as a necrotroph, a fungus first has to gain a foothold in the plant, and it does this by suppressing plant immune responses for a short period of time until enough fungal biomass has accumulated in the host plant to successfully switch to a necrotrophic lifestyle and kill surrounding plant cells. For Botrytis, this is not a long time, and the very first symptoms of infection by Botrytis are necrotic lesions that begin spreading, showing that the parasitic phase is quite short-lived indeed.

So how do we know that there is a parasitic phase? As described earlier, necrotrophs must kill plant cells to feed on. However, in initial infection events, Botrytis actually interferes with the plant’s programmed cell death immune function known as the hypersensitive response (HR). The hypersensitive response is a common way for plants to defend against pathogen invasion by killing cells under attack and bolstering the defenses of neighboring cells. One might think that this is beneficial to necrotrophs, but it appears that in order to initially establish itself in the host, Botrytis must suppress PCD by secreting effector proteins and small RNAs that interfere with normal plant responses [3]. Secreted small RNAs from Botrytis ‘hijack’ the RNA interference system in plants and help silence genes involved in plant immunity [4]. Another factor that challenges the notion of Botrytis as an obligate necrotroph is the fact that it can sometimes colonize plants asymptomatically, although I am not aware of this being demonstrated yet in Cannabis [5]. This raises the question of whether B. cinerea is a fairly ubiquitous endophyte that only causes serious disease when both the environment and host are conducive to disease development (there may be cases where a necrotrophic phase is not tiggered).

What is going on biochemically during plant infection?

After accumulating biomass within the host, Botrytis can switch to a necrotrophic lifecycle, and it employs a variety of pathogenicity tactics, including inducing the HR response in plant cells rather than suppressing it. For instance, it begins to produce macromolecular toxins that can induce plant cell death [6, 7]. One such metabolite, oxalic acid, may induce these responses through acidification of plant tissues, leading to production and activation of various fungal enzymes including pectinases (pectin degrading enzymes), laccases (lignin-degrading enzymes), and proteases (protein degrading enzymes) [8, 10]. Furthermore, oxalic acid can weaken cell walls by chelating calcium ions, which is necessary for forming calcium pectate in plant cell walls [10]. In a closely related necrotrophic species, Sclerotinia sclerotiorum, oxalic acid has been shown to trigger host HR response [9]. Botrytis has also been found to produce plant hormones and/or induce plant hormone changes including ethylene and abscisic acid levels, both of which have been found to make plants more susceptible to Botrytis infection [11, 12, 13, 14]. Furthermore, different effector proteins are expressed at different points of infection. BcSpl1 is one such protein that is more abundant in later infection stages and is an important virulence factor for B. cinerea, inducing cell death [15]. Another effector, BcIEB1, may help protect the fungus from a host-produced antifungal, osmotin [16]. Most putative effector genes in Botrytis are not well characterized, and some effectors may not contribute to virulence due to host plants evolving ways to recognize the effectors and trigger defense responses, such as is the case with BcNEP1 and BcNEP2 [17].

What is the life cycle of Botrytis?

Image result for botrytis life cycle
Image taken from https://media.nicks.com.au/media/imported-cms/image_200792512521151.gif

As previously mentioned, Botrytis usually functions as an asexual fungus. In the spring, fungal mycelium and sclerotia (defined later) begin to grow/germinate and make conidiophores that produce asexual spores known as conidia. Spores are usually dispersed through wind and water. In the presence of moisture (unlike PM, Botrytis spores require free water to germinate), the conidia (asexual spores) germinate and produce structures known as appressoria to penetrate plant cuticles through immense pressure buildup. The invasive hyphae can then grow within the extracellular space of plant tissues.

As previously discussed, they initially suppress plant responses and attempt to remain undetected while accumulating biomass. After a short period of growth, the fungus switches to a necrotrophic phase and begins to kill and rot proximal cells. After this initial foothold is established, the hyphae can continue to invade the host tissues and the fungus can produce more conidiophores on the plant tissue surface. This acts a secondary inoculum source that amplifies the spread of the disease within a given season (polycylclic disease). Come winter, the fungus begins to produce structures called sclerotia that are dense survival structures composed of highly melanized mycelium. Furthermore, mycelium can survive within dead plant tissue through the winter and produce conidia the following spring. The sexual phase is rare, but occurs when the sclerotia produce a fruiting body known as an ascocarp (analagous to a mushroom) that releases sexual spores known as ascospores.

What does bud rot look like in Cannabis? How do I diagnose it?

This disease displays both symptoms (visible effects on plant tissues) as well as signs (seeing the actual fungal tissue). However, long before you see a tuft of gray mold coming out of your buds, you will notice flagging of plant colas. This means that the tops of your colas will begin to dieback, leaving brown tissue as shown below:

Image result for botrytis on cannabis
Image taken from https://www.marijuanatimes.org/wp-content/uploads/2015/12/cannabis-fungus-640×401.jpg

You might also first notice symptoms on foliage. If your plant is not showing signs of nutrient burn or natural senescence of late flower, it can be easy to spot random leaves that have turned brown and dry, such as below:

https://www.icmag.com/ic/picture.php?albumid=50618&pictureid=1372226

The picture above shows signs of visible mycelium within the bud. However, if bud rot continues to progress, aerial mycelium will begin to grow as tufts out of your buds such as this:

Image result for botrytis on cannabis
https://www.growweedeasy.com/wp-content/uploads/2014/11/fluffy-white-bud-rot.jpg

I personlly lost a plant to bud rot when I first started growing because I attempted to grow in an unvented tent placed in a closet indoors without a humidifier, so I know how devastating it can be to see something like this on what you have worked so hard to produce.

How Do I Prevent Getting Bud Rot?

As with all plant diseases, it is important to keep in mind the disease triangle, which states that for a disease to develop, there needs to be a susceptible host, a conducive environment, and a virulent pathogen.

Virulent Pathogen

Unless you are in a perfectly enclosed environment, you have to assume that Botrytis spores are fairly ubiquitous in the environment. If you are within a contained grow, you have a bit of control over this factor, and you can do a few things to try to keep potential inoculum levels low.

  • UV lamps: Using supplemental UV lighting is recommended for increasing secondary metabolite production in plants (for more info on this, check out my post on grow lights under the Home Growing Made Easy page). It also has the added benefit of helping reduce spore inoculum levels. Beyond your supplemental UV lights, you can add UV-B lamps within the ducting in your sealed room to help sanitize the air.
  • HEPA filters: Using HEPA filters in your grow room will help remove spores from the air through active filtration.
  • Ozone: Ozone generators may be helpful in reducing the growth of Botrytis. One study found reduced growth rates in air with 1.5 uL/L of ozone [21]. However, ozone may have human health risks and may have negative effects on your plants at high concentrations.
  • Use dedicated clothing for your grow space can help prevent you from bringing in spores from the clothes you wear out in public. If you really want to take an extra step, you can invest in some Painters’ coveralls.
  • Have good cultural practices including sanitizing hands, tools, shoes etc. regularly. Always sterilize your tools frequently and sterilize your entire grow area after each harvest using techniques such as burning sulfur, spraying with 10% bleach, or Quat soaps. If you have infected tissues, do not mulch it into your soil at the end of the grow. cut off infected buds as soon as possible.

Susceptible Host

Most people do not select their plants based on their resistance to bud rot, though it can certainly be a factor. Growers (particularly indoor growers) generally choose what they are growing based on the market demand of what consumers want to smoke, and they rely on other practices to try to prevent their crop from getting bud rot. However, despite the lack of studies of this disease in Cannabis, one can look to community forums for discussion of strains that may show promise of being relatively resistant to bud rot.

In general, it is useful to consider what environments favor bud rot development. Landrace strains from regions of the world that have favorable conditions for bud rot likely experience the most pressure from Botrytis and are the most likely to have evolved resistance to the pathogen. Based on this, it is likely that Cannabis landrace strains from equatorial, moderately warm, humid, and wet regions of the world have developed greater resistance to bud rot than landrace strains from cold, drier climates. This is basically opposite of strains with higher levels of PM resistance. For instance, strains with Afghani heritage generally are more PM resistant than many equitorial sativa strains, whereas these equitorial strains generally are more resistant to bud rot than Afghani Cannabis plants.

One reason that I would recommend sativa strains that evolved in wet, moderate-warm climates is obvious from their plant structure: sativa buds are not as dense, internodal spacing is greater than indica plants, leaves are much thinner, and in general, the structure of these plants is conducive to high amounts of airflow and avoids wet microclimates within dense buds. Beyond the macro structure of the plant, there are likely more complex molecular interactions going on that contribute to a genotype’s resistance to bud rot.

It certainly is not a guarantee that growing a particular strain ensures bud rot resistance. It is also important to know that there can be genetic variability within a strain when it comes to disease resistance, and a bad enough environment may still be able to overcome resistant strains.

Examples of landrace strains with putative resistance to bud rot include:

  1. Durban Poison is a 100% inbred sativa plant from a wam, wet region of South Africa
  2. Brazil Amazonia is a landrace strain from one of the most conducive environments in the world to bud rot- the Amazon Jungle. However, it somewhat breaks the stereotype of what plants do best in these climates: it has an indica-like phenotype with denser buds and quicker flowering times than other strains on this list.
  3. Colombian Gold- Another landrace sativa from the tropics. Colombia is one of the most ecologically diverse regions in the world.
  4. Thai Sativa- from one of the most conducive regions in the world to bud rot, the Thai sativa is a very long-flowering strain with a classic sativa phenotype: lanky, thin leaves, large internodal spacing, buds not particularly dense.

These particular genetics are not really viable in a modern Cannabis market, aside from the occasional old-school stoner or a connoisseur of unique phenotypes. They are generally difficult to grow, low-yielding, and low-potency. However, there are many modern hybrid strains that have been bred from these landrace genetics.

Modern, commercially viable sativa strains:

  • Ghost Train Haze
  • Bruce Banner
  • Chernobyl
  • Amnesia Haze
  • Hawaiian Maui Wowie
  • Sour Diesel
  • Laughing Buddha
  • Bay 11
  • G13 Haze
  • Trainwreck
  • Casey Jones
  • Super Lemon Haze
  • Grapefruit
  • Red Dragon
  • Cannalope Haze
  • Destroyer
  • Jamaican Dream
  • Pineapple Express
  • AK-47
  • Hulkberry
  • Jack Herer
  • Chemdawg

Again, I am not making the claim that you will not get bud rot if you grow with these strains, but it certainly can make a difference to pick a strain with genetic history of sativa landrace from wet climates. Strain selection is most important for those growing outdoors in a moderate temperature, wet climate. If you have a dry environment or can control your environment, it should be possible to prevent bud rot with proper defoliation, training, and grow area design/IPM)

Conducive Environment

As mentioned previously, B. cinerea thrives in moderate temperature, humid, and wet environments. If moisture from dew or rain accumulates on plant buds, it is likely that there is a microclimate that develops in your buds with up to 100% relative humidity and free water that can stimulate Botrytis conidia germination. While Botrytis can infect foliage and stems, causing lesions, it is far less common than flower infections. This is likely due to the conducive microclimate in buds as compared to the microclimates surrounding leaves and stems, though floral tissues may also have less defensive abilities than these other tissue types.

There are a few basic tips to help prevent bud rot.

  1. Have high amounts of air circulation in your growing area. Not only will it help with drying out wet tissues quickly, it will help disrupt microclimates that may form where there is stagnant air, reducing local spikes in humidity and temperature. Have a good amount of fans, and do proper training and defoliation in order to maintain that breezes can reach every part of your plant.
  2. In my opinion, temperature can be important, but it is less important than controlling humidity, moisture and airflow. For instance, if you are in flowering stage and are supplementing CO2 in a commercial grow, it is important to maximize your yield and to make the most of high light and CO2 levels, a temperature around 80F is ideal for plant growth while maintaining most of the monoterpenes in your buds. This temperature is conducive to bud rot, but a lower temperature may be even more conducive. It seems that for Botrytis, moderate temperatures around 60-75F are most conducive for plant infection [18]. However, in greenhouse tomatoes, it was found that flower infections increased at higher temperatures (77F was the highest used in the study), whereas stem infections decreased. Based on this, it may be that Botrytis can thrive in Cannabis flowers at higher temperatures. I feel comfortable recommending that grow areas be kept at 77-82F during flower for the sake of plant evapotranspiration and growth, and I would not worry too much about temperatures dropping at night or reducing day temperatures in late flower to induce color changes and/or preserve some monoterpenes.
  3. Humidity: For those familiar with VPD (vapor pressure deficit), it is a figure that indicates the rate of evapotranspiration from plants dependent upon leaf temperature and local humidity. It is a good guide for grow room environmental settings to maximize plant growth, and a chart showing the ideal humidity level for different leaf temperatures is shown below:
https://assets.growell.co.uk/media/gene-bluefoot/v/p/vpd-chart.gif
https://assets.growell.co.uk/media/gene-bluefoot/v/p/vpd-chart.gif

After switching to flower, at 27C (around 80F), VPD recommendations would be to keep humidity around 55% until late flower, when it can be dropped to around 42%. For grapes, these recommendations should be sufficient to keep B. cinerea from taking hold. 65% RH or lower seems to be sufficient to prevent Botrytis in grape [25]. In a study done one rose petals, an RH of 92% at 15C was required to cause lesions within 24 hours [19]. However, it is imporant to keep in mid that Cannabis buds have a unique structure that can have very humid microclimates in the buds compared to these other plants.

In tomato, mild disease symptoms were found at humidity as low as 56% RH. Unlike in tomato, Cannabis should have a zero tolerance policy for bud rot. When inhaling spores, certain immunosuppressed individuals can actually develop infections from inhaling Botrytis spores. Furthermore, the microclimates formed within Cannabis buds can significantly raise the humidity of the air in the flowers above that found in the grow space. While it is not ideal on the VPD chart, I recommend keeping humidity at 50% RH during early flower, and 40% RH during the last few weeks of flower. It is not worth trying to gain a marginal yield increase while risking your entire crop to bud rot. I believe the quality/yield is still maintained at this RH, but if you would like to keep it higher, 50% RH is likely okay. I tend to recommend staying on the safe side when it comes to avoiding mold issues altogether.

Application-Based Control Methods

Given that there are few approved fungicides with a targeted mode of action, my recommendations will mostly be based on approved fungicides in California.

Plant oil

I am not a big fan of using neem oil in mid-late flower, mostly because of certain health risks associated with neem. However, I certainly believe in a good regimen of spraying neem in vegetative growth and early flower. In addition to spraying about every 10 days during vegetative growth, I recommend doing one application when you flip your light cycles to 12/12 and doing another application at around 2 weeks of flower. I would not apply neem after this point. However, one could continue using other oils including triglycerides such as cottonseed oil or soybean oil, or even a product such as Trifecta crop control that utilizes corn oil and essential oils from plants such as garlic, thyme, peppermint, and rosemary. It also contains citric acid which may help control fungi.

Personally, I prefer to stop using all oils about 2-3 weeks into flower depending on the strain, and I begin alternating a biofungicide such as Stargus or Serenade with a potassium bicarbonate product such as Green Cure. Every 5 days I spray one of the products, alternating between the two. However, for the last 2-3 weeks, I also stop applying the biofungicide and only spray potassium bicarbonate once per week excluding the last week.

Biofungicides

I believe that biofungicides are good to use for prevention of bud rot. They are not toxic and can be sprayed up to the day of harvest. We focus on soil health and the microbial community in plants’ rhizospheres, but we tend to not pay as much attention to the phylosphere of plants. In regards to premade products, I recommend spraying Bacillus amyloliquefaciens products such as Double Nickel 55 or Stargus during flower. I only say this because it is the only approved Bacillus spray to use in California, but Bacillus subtilis sprays such as Serenade are good. I would do the first spray at first sign of flower and reapply every 10 days for 3-5 applications. Essentially, this bacteria will be able to colonize the aerial portions of the plant and help prevent initial colonization from Botrytis.

pH Agents

I believe that all Cannabis growers should have a good spray schedule of either a citric acid-based product (i.e. Nuke Em by Flying Skull or Plant Therapy by Lost Coast) or a potassium bicarbonate product (i.e. Green Cure). These products help inhibit fungal spore germination by altering the surface pH of plant tissues. I would not use both products, since citric acid works by acidifying the surface while bicarbonate works by basifying the surface. Both citric acid and potassium bicarbonate have been found to inhibit Botrytis spore germination [22]. There is no research in Cannabis comparing these products, but both appear to be inhibitory in vitro. However, we also know that Botrytis functions partly by acidifying the plant tissues. We also have some evidence in postharvest rot of kiwi fruit, that citric acid may make disease incidence worse, while potassium bicarbonate is effective for control [23, 24]. For these reasons, I recommend using a potassium bicarbonate spray such as green cure weekly during flower, even up to the day of harvest.

  1. Fillinger, S., & Elad, Y. (2016). Botrytis: the fungus, the pathogen and its management in agricultural systems. Springer.
  2. Hua, L., Yong, C., Zhanquan, Z., Boqiang, L., Guozheng, Q., & Shiping, T. (2018). Pathogenic mechanisms and control strategies of Botrytis cinerea causing post-harvest decay in fruits and vegetables. Food Quality and Safety, 2(3), 111–119. https://doi.org/10.1093/fqsafe/fyy016
  3. Veloso, J., & van Kan, J. A. L. (2018). Many shades of grey in Botrytis–host plant interactions. Trends in Plant Science, 23(7), 613–622.
  4. Wang, M., Weiberg, A., Dellota Jr, E., Yamane, D., & Jin, H. (2017). Botrytis small RNA Bc-siR37 suppresses plant defense genes by cross-kingdom RNAi. RNA Biology, 14(4), 421–428.
  5. Ngah, N., Thomas, R. L., Shaw, M. W., & Fellowes, M. D. E. (2018). Asymptomatic Host Plant Infection by the Widespread Pathogen Botrytis cinerea Alters the Life Histories, Behaviors, and Interactions of an Aphid and Its Natural Enemies. Insects, 9(3), 80. https://doi.org/10.3390/insects9030080
  6. Huo, D., Wu, J., Kong, Q., Zhang, G. B., Wang, Y. Y., & Yang, H. Y. (2018). Macromolecular Toxins Secreted by Botrytis cinerea Induce Programmed Cell Death in Arabidopsis Leaves. Russian Journal of Plant Physiology, 65(4), 579–587. https://doi.org/10.1134/S1021443718040131
  7. Govrin, E. M., Rachmilevitch, S., Tiwari, B. S., Solomon, M., & Levine, A. (2006). An elicitor from Botrytis cinerea induces the hypersensitive response in Arabidopsis thaliana and other plants and promotes the gray mold disease. Phytopathology, 96(3), 299–307.
  8. Manteau, S., Abouna, S., Lambert, B., & Legendre, L. (2003). Differential regulation by ambient pH of putative virulence factor secretion by the phytopathogenic fungus Botrytis cinerea. FEMS Microbiology Ecology, 43(3), 359–366.
  9. Kim, K. S., Min, J.-Y., & Dickman, M. B. (2008). Oxalic acid is an elicitor of plant programmed cell death during Sclerotinia sclerotiorum disease development. Molecular Plant-Microbe Interactions : MPMI, 21(5), 605–612. https://doi.org/10.1094/MPMI-21-5-0605
  10. Petrasch, S., Knapp, S. J., van Kan, J. A. L., & Blanco-Ulate, B. (2019). Grey mould of strawberry, a devastating disease caused by the ubiquitous necrotrophic fungal pathogen Botrytis cinerea. Molecular Plant Pathology, 20(6), 877–892. https://doi.org/10.1111/mpp.12794
  11. Takino, J., Kozaki, T., Ozaki, T., Liu, C., Minami, A., & Oikawa, H. (2019). Elucidation of biosynthetic pathway of a plant hormone abscisic acid in phytopathogenic fungi. Bioscience, Biotechnology, and Biochemistry, 83(9), 1642–1649. https://doi.org/10.1080/09168451.2019.1618700
  12. Blanco-Ulate, B., Vincenti, E., Powell, A. L. T., & Cantu, D. (2013). Tomato transcriptome and mutant analyses suggest a role for plant stress hormones in the interaction between fruit and Botrytis cinerea. Frontiers in Plant Science, 4, 142.
  13. Valero-Jiménez, C. A., Veloso, J., Staats, M., & van Kan, J. A. L. (2019). Comparative genomics of plant pathogenic Botrytis species with distinct host specificity. BMC Genomics, 20(1), 203. https://doi.org/10.1186/s12864-019-5580-x
  14. Chague, V., Elad, Y., Barakat, R., Tudzynski, P., & Sharon, A. (2002). Ethylene biosynthesis in Botrytis cinerea. FEMS Microbiology Ecology, 40(2), 143–149. https://doi.org/10.1111/j.1574-6941.2002.tb00946.x
  15. Frías, M., González, C., & Brito, N. (2011). BcSpl1, a cerato-platanin family protein, contributes to Botrytis cinerea virulence and elicits the hypersensitive response in the host. New Phytologist, 192(2), 483–495. https://doi.org/10.1111/j.1469-8137.2011.03802.x
  16. González, M., Brito, N., & González, C. (2017). The Botrytis cinerea elicitor protein BcIEB1 interacts with the tobacco PR5-family protein osmotin and protects the fungus against its antifungal activity. New Phytologist, 215(1), 397–410. https://doi.org/10.1111/nph.14588
  17. Arenas, Y., Kalkman, E., Schouten, A., Vredenbregt, P., Dieho, M., Uwumukiza, B., & Kan. (2007). Functional analysis of Botrytis cinerea nep-like proteins.
  18. Greenhouse & Floriculture: Botrytis Blight of Greenhouse Crops | UMass Center for Agriculture, Food and the Environment. (n.d.). Retrieved March 5, 2020, from https://ag.umass.edu/greenhouse-floriculture/fact-sheets/botrytis-blight-of-greenhouse-crops
  19. Williamson, B., Duncan, G. H., Harrison, J. G., Harding, L. A., Elad, Y., & Zimand, G. (1995). Effect of humidity on infection of rose petals by dry-inoculated conidia of Botrytis cinerea. Mycological Research, 99(11), 1303–1310. https://doi.org/https://doi.org/10.1016/S0953-7562(09)81212-4
  20. EDEN, M. A., HILL, R. A., BERESFORD, R., & STEWART, A. (1996). The influence of inoculum concentration, relative humidity, and temperature on infection of greenhouse tomatoes by Botrytis cinerea. Plant Pathology, 45(4), 795–806. https://doi.org/10.1046/j.1365-3059.1996.d01-163.x
  21. Nadas, A., Olmo, M., & García, J. M. (2003). Growth of Botrytis cinerea and Strawberry Quality in Ozone-enriched Atmospheres. Journal of Food Science, 68(5), 1798–1802. https://doi.org/10.1111/j.1365-2621.2003.tb12332.x
  22. Fayza Tahiri Alaoui, Latifa Askarne, Hassan Boubaker, El Hassane Boudyach and Abdellah Ait Ben Aoumar, 2017. Control of Gray Mold Disease of Tomato by Postharvest Application of Organic Acids and Salts. Plant Pathology Journal, 16: 62-72.
  23. Pennycook, S. R. (1986). Citric acid dipping of kiwifruits promotes Botrytis storage rot. New Zealand Journal of Experimental Agriculture, 14(2), 205–207. https://doi.org/10.1080/03015521.1986.10426144
  24. Turkkan, M., Özcan, M., & Erper, İ. (2017). Antifungal effect of carbonate and bicarbonate salts against Botrytis cinerea, the casual agent of grey mould of kiwifruit. Akademik Ziraat Dergisi, 6, 107–114. https://doi.org/10.29278/azd.371066
  25. Ciliberti, N., Fermaud, M., Roudet, J., & Rossi, V. (2015). Environmental Conditions Affect Botrytis cinerea Infection of Mature Grape Berries More Than the Strain or Transposon Genotype. Phytopathology, 105(8), 1090–1096. https://doi.org/10.1094/PHYTO-10-14-0264-R

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