Sclerotinia, caused by the fungus Sclerotinia sclerotiorum, is a disease capable of causing significant fruit loss in kiwifruit orchards at flowering and during the months that follow. Research into the environmental conditions required for Sclerotinia to infect kiwifruit flowers and fruitlets is currently being undertaken at Ruakura Research Centre. This research, also aims to establish the significance of floral tissue infection as a pre-requisite for disease of blossoms and fruit.

This disease has three distinct phases:

• The first sign of Sclerotinia disease in your kiwifruit orchard might be when male blossoms become infected, sometimes producing visible white mycelia on rotted flower masses.

• Secondly, infection during or soon after petal-fall, on female vines, causes the developing fruitlet and its stalk to quickly rot and turn brown. These usually dry up, and remain attached to the vine for several weeks or months.

• Thirdly, field rot can occur during December, January and February. This will initially appear as a small pale green, soft lesion on the fruit surface. These infections are usually associated with floral tissues adhering to the fruit. Continuously wet conditions will allow this rot to progress and cause fruit drop. However, in many instances the progress of this rot is halted, possibly due to changing environmental conditions and/or defence mechanisms within the plant. This produces scarring of the fruit surface, which may range from superficial scars only 3-4 mm across, to severe, deep scarring, 20-40 mm in length.

Life Cycle

Sclerotia are special structures formed by this fungus within cavities of infected blossoms and on the surface of infected fruit. Sclerotinia allow the fungus to survive in the soil through the winter months. Tiny mushrooms (2-10 mm dia.) called apothecia, emerge from sclerotia from September through to January/February, and release spores (ascospores). Dry conditions at the soil surface will delay apothecia emergence. Apothecia can survive for several days or weeks depending on the prevailing environmental conditions, and can be revived with rainfall, after being dry and shrivelled.

Ascospores are the primary inoculum for all Sclerotinia infections and disease. The process of spore release from apothecia is called 'puffing' . This active ejection of ascospores enables them to travel the short distance from the orchard floor into turbulent air. Little is known about the daily or seasonal fluctuations in ascospore numbers or their dispersal and survival in kiwifruit orchards.

Several years ago, data were obtained from a spore trap operating in a Te Puna orchard for the purpose of Botrytis research . This data indicates that spores were present on most days from late November to early May, although there was considerable fluctuation from day to day. Also, during some weeks, spore numbers were very low. This pattern is likely to vary from year to year and between orchards.

Management

Firstly, do you know if you have Sclerotinia in your orchard, and how bad is it? It might be easy to find, but it is difficult to measure what your losses are. You should look carefully for dried blossoms on the vines 1-2 weeks after petal fall and fruit scarring and field rot later in the season. The best means of estimating your total losses from Sclerotinia is to carry out regular (2-3 weeks) assessments of marked samples of fruit, starting soon after petal-fall. An easy way to do this, is by tagging two fruiting canes on each of several vines within a block and repeatedly assess these for disease incidence, by counting the number of infected fruit out of the total number.

Sclerotinia blossom rot needs to be distinguished from bacterial bud/blossom rot. Severe bacterial rot of buds and flowers causes these structures to abort at the base of the flower stalk, initially leaving a green stalk still attached to the vine. Less severe infections may cause mis-shapened fruit, but will not cause a lesion on the fruit surface. Sclerotinia blossom rot, on the other hand, will leave a dried brown blossom and brown stalk. These are often overlooked by orchardists, yet losses at this early stage are typically much greater than losses from field rot later in the season, and can be as high as 20%.

Once you know what your fruit losses have been in previous seasons, you can better estimate the potential value of spray applications to control this disease. The most effective time to apply fungicides (Benlate, Rovral or Ronilan) is mid-flowering to petal-fall, which is when the floral tissues are at greatest risk from infection. Wet weather conditions are obviously important in determining risk from Sclerotinia infection during flowering and later in the season. Currently these tricky, and somewhat subjective, spray timing decisions have to be made without the benefit of objective guidelines. There is clearly a need to define infection conditions in New Zealand kiwifruit growing regions.

The choice of fungicide for Sclerotinia control can influence Botrytis management due to the effect of increasing fungicide resistance within Botrytis populations. Sclerotinia does not develop resistance to these fungicides. However since both fungi can be very active during flowering there is a need to integrate the management of these two diseases.

Sclerotinia infection

Infection of floral tissues by Sclerotinia is a pre-requisite for this disease to develop in many of its 400 host plants, because ascospores can not directly infect healthy green tissue such as leaves, pods (in legumes) and fruit. On the other hand, senescing or dying tissues during petal-fall, such as petals and stamens, are rapidly infected in wet conditions. This allows the fungus to establish mycelia within this tissue, and it is from here that it is able to penetrate and infect adjacent tissues. This is probably the case in kiwifruit, since infection usually occurs soon after flowering and where floral tissues have adhered to the calyx end of the fruit.

There are several factors relating to infection and biology of Sclerotinia which are not fully understood in kiwifruit :

• The precise environmental conditions required for infection

• The time required for infection

• Whether or not, ascospores can directly infect immature kiwifruit?

• How long Sclerotinia can survive within floral tissue?

Increasing our knowledge of these aspects will assist disease management decisions, by more clearly identifying the sources of fruit infections, and providing improved weather-based prediction of disease risk.

Other factors, such as competition from other naturally occurring fungi (including Botrytis), bacteria and yeasts may influence the successful establishment of Sclerotinia within floral tissues. HortResearch scientists, Dr Phil Elmer and Stephen Hoyte, are investigating opportunities for utilising the ability of selected beneficial micro-organisms to colonise floral tissues, thereby excluding both Sclerotinia and Botrytis.

Proposed Studies

Currently, research at the Ruakura Research Centre is focused on establishing the infection pathways for blossom and fruitlet infection, including the role of adhering floral tissues. In addition, the environmental conditions required for ascospores of Sclerotinia to infect flower tissues, and for fruitlets to become infected via adhering floral tissues, will be investigated. The conditions required for lesion development on fruit will be studied to increase our understanding of why fruit infections either form scars or continue to develop as soft field rots. One of the techniques being employed includes fluorescent microscopy to study infection sites. Figure 1 shows petal tissue 24 hours after inoculation with Sclerotinia ascospores.

The longer term goal is to incorporate data on previous disease records, inoculum levels, crop growth stage and environmental conditions, into a disease-risk prediction model identifying both the need for sprays, and the most effective time of application. This could be made available to growers through the Orchard 2000 system, which is currently used in the pipfruit industry.

I would specially like to thank the New Zealand Kiwifruit Marketing Board for supporting this research through their Research Scholarship fund.

References: Hoyte, S. M., R. J., and Gouk, S. C. (1992). Field observations of Sclerotinia sclertiorum: Apothecial development and sclerotial production. In: Proceedings 45th NZ Plant Protection Society Conference. pp 188-192.

Pak, H., and Manning, M. (1995). How does spraying for Sclerotinia in kiwifruit affect Botrytis. New Zealand Kiwifruit October 1995. pp 19-20.

NOTE

The choice of fungicide for Sclerotinia control can influence the level of Botrytis in the orchard. Although Benlate can be used in addition to a single dicarbomide (Ronilan, Rovral) application, there may be serious consequences for the management of Botrytis in the orchard. Botrytis has been shown to select for dual resistance to the Benlate and dicarboximade fungicides and this may increase the incidence of Botrytis in the orchard. Rovral and Ronilan should be used as the preferred means of managing Sclerotinia and Benlate should only be used on orchards where there has been a history of very low Botrytis levels.