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MANAGING MUMMY-BERRY DISEASE OF BLUEBERRIES IN MASSACHUSETTS 



D. R. Cooley, W. J. Manning, and S. J. McCouch 

 Department of Plant Pathology 



Mummy-berry disease is caused by the fungus Monolinia vaccinii- 

 corymbosi. It is probably the most serious blueberry disease in Massa- 

 chusetts, though no accurate loss estimate is available. 



In order to manage the disease, the disease cycle as shown on 

 the following page must be understood. The fungus is an Ascomycete 

 and produces two types of spores: ascospores and conidia. These 

 spores disseminate the fungus. 



The disease gets its name from the so-called mummy berry which 

 allows the fungus to overwinter. This mummy is actually a 'fungal 

 mass which winters on the ground, and in the spring produces apothecia, 

 which look like small mushrooms. In the apothecia, ascospores are 

 formed. These ascospores are discharged in moist weather during early 

 spring, and land on leaves and twigs, where infections start. This 

 is called the leaf and twig blight stage, or bud and twig blight stage, 

 of mummy berry. As symptoms develop, conidia form in diseased tissues. 

 These secondary spores are disseminated by rain, wind and bees to 

 blossoms and other new tissues. The fungus grows into the blossoms 

 and tissue, invading the developing fruit. This is the blossom blight 

 stage of the disease. The fruit turns salmon-colored or grey by mid- 

 summer, and drops to the ground. There it becomes a mummy of mycelia. 

 The fungus overwinters in the mummified fruit. 



Researchers (Ramsdell et al . , 1974, 1975) have found that ascospore 

 release is not closely correlated with the stage of the blueberry 

 plant's growth. Ascospores are generally present when the first green 

 tissue appears in the spring, and continue to be present through bloom. 

 Conidial release overlaps the end of ascospore release and continues 

 until after bloom. Ascospore release is inversely correlated with 

 relative humidity; conidia release is inversely correlated with leaf 

 wetness. A combination of drying and wetting stimulates release; max- 

 imum release periods come during dry periods following free moisture, 

 usually rain, on the leaves. After release, spores can travel at 

 least 1000 ft. 



It has been concluded that inoculum is generally present in such 

 large amounts that protective chemical controls applied throughout 

 both primary and secondary infection periods are necessary to effect- 

 ively manage the disease (Ramsdell et al . , 1976). Since this strategy 

 is protective, it is based almost entirely on plant growth stages. 

 Cover spra s begin just before bud break, and continue until just 

 after petal fall. Early infections are effectively inhibited by tri- 

 forine (Funginex), applied at or just prior to bud break, and continuing 



1 

 Extension Technician, Associate Professor, and Graduate Assistant, 

 respectively. Department of Plant Pathology, University of Massa- 

 chusetts, Amherst, 01003 



