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 Australasian Plant Disease Notes
Disease notes, new records and quarantine interception reports are published in Australasian Plant Disease Notes.

 

Article << Previous     |     Next >>   Contents Vol 35(1)

Postharvest infection of Freesia hybrida flowers by Botrytis cinerea

A. I. Darras A B E, D. C. Joyce C, L. A. Terry A, I. Vloutoglou D

A Plant Science Laboratory, Cranfield University, Silsoe, Bedfordshire, MK45 4DT, UK.
B Current address: Department of Floriculture, School of Agricultural Technology, Technological Educational Institute of Kalamata, 24100 Antikalamos, Kalamata, Greece.
C The Centre for Native Floriculture, Department of Agronomy and Horticulture, The University of Queensland, Gatton, Qld 4343, Australia.
D Benaki Phytopathological Institute, Plant Pathology Department, 8 S. Delta Street, 145 61 Kifissia, Athens, Greece.
E Corresponding author. Email: tassosdarras@yahoo.co.uk
 
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Abstract

‘Specking’ on harvested freesia (Freesia hybrida) flowers is a problem worldwide. The disease is caused by the fungal pathogen Botrytis cinerea. This disease symptom detracts from appearance and reduces marketability of the flowers. Unlike other important cut flower crops (e.g. gerbera), the mode of infection and epidemiology of postharvest freesia flower specking caused by B. cinerea has not been reported. Epidemiological studies were carried out under simulated conditions typical of those occurring during postharvest handling of freesia flowers. Infection of freesia flowers by B. cinerea occurred when a conidium germinated, formed a germ tube(s) and penetrated epidermal cells. Fungal hyphae then colonised adjacent cells, resulting in visible lesions. Different host reactions were observed on freesia ‘Cote d’ Azur’ petals at 20°C compared to 5°C. The infection process was relatively rapid at 20°C, with visible lesions produced within 7 h of incubation. However, lesion expansion ceased after 24 h of incubation. Infection was slower at 5°C, with visible lesions produced after 48 h of incubation. However, lesion development at 5°C was continuous, with lesions expanding over 4 days. Light microscopy observations revealed increased host defence reactions during infection. These reactions involved production of phenolic compounds, probably lignin and/or callose, around infection sites. Such substances may play a role in restricting petal colonisation and lesion expansion. Disease severity and lesion numbers on freesia flowers incubated at 12°C were higher, but not significantly higher (P > 0.05), than on those incubated at 20°C. Disease severity and progression were differentially mediated by temperature and relative humidity (R.H.). Infection of freesia flowers was severe at 100% R.H. for all three incubation temperatures of 5, 12 and 20°C. In contrast, no lesions were produced at 80 to 90% R.H. at either 5 or 20°C.

Keywords: cut-flower, histopathology, inoculum level, relative humidity, temperature.


   
    


 
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