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Black knot disease occurs on numerous cultivated and wild plums, prunes, and cherries. The disease is characterized by the presence of warty, black galls which may vary in size from 1/2 inch to more that 1 foot in length. The grotesque galls draw the attention from homeowners who want to improve the unsightly appearance of affected landscape trees. Black knot only affects certain types of trees, but once it takes hold, it can claim an entire tree within a couple of years.

Black knot has been reported on 24 species of Prunus but is most commonly found on wild and cultivated plums and cherries. Early publications from the 1950’s describing the disease report no cases affecting peach, but a few rare infections have been reported since that time. The disease can be found throughout North America but is most commonly found in the northeast.

Young, infected twigs may die during the first year of infection. Larger branches may take several years to display severe damage. The infected trees decline and become more symptomatic with each growing season. The infection stresses the entire tree causing it to weaken, decline, and possibly die. The stress placed on the tree may also make it susceptible to infections by other pathogens. Economically, the trees lose value after a few years. The portions of a branch distal to a knot become stunted, and occasionally knots enlarge to girdle a branch and possibly kill it. Trees with multiple infections become dwarfed and misshapen, markedly reducing their productivity and attractiveness.

Because of the long infection process and disease cycle, this disease is often overlooked by home gardeners and fruit producers. The leaves can mask the symptoms until firmly established infections are in place. Once established, it is very difficult to manage the disease. Commercial growers often discover the disease more quickly because they regularly inspect their trees during routine crop management. Awareness and strict monitoring of susceptible plants should be a priority for all home gardeners and commercial growers.


The disease is characterized by the presence of thick, black, irregular swellings on the twigs (Fig. 1). The presence of these symptoms is often first noticed in the winter season when they are unobscured by leaves. However, the fungal disease-causing agent has been present for quite some time. The pathogen’s presence disrupts the normal growth of the twigs and a tumor-like growth forms at the infection site. Infections may take place as much as a year or more prior to the development of these characteristic “knots”, therefore, the swellings are normally not noticed until the winter of the second season of infection. It takes a keen observer to notice the subtle, initial symptoms present during the first season of infection.

The first symptoms appear as small, light brown swellings of the current or previous season’s growth.. By the next season the swellings turn olive-green in color with a velvety texture. Over this growing season the knots darken and appear to have a hard, brittle texture (Fig. 2). The hard, black knots are the typical symptoms associated with the disease.


Disease Cycle

The fungus overwinters in the knots. About the time of bud emergence in the spring, the first ascospores are forcibly discharged from the ascostromata following a period of warm, wet weather. Apparently very short periods of wetness (only a few hours) are enough to prompt ascospore discharge. Temperatures between 16 and 27oC (60-80oF) are ideal for the dissemination, germination, and infection of new plant tissue. Recent studies have confirmed and concluded that rainfall and temperature are the key factors in the release of spores and that the duration of the rainfall or wet period is not a factor.

The ascospores are spread by air currents and rain splashing. Mainly the succulent green shoots and, occasionally, wounded tissues are most susceptible to infection by ascospores. Ascospore discharge continues to occur for 2-3 weeks after bloom. Infections take place during this time but may continue for a longer time period if susceptible host plant tissue is available. The germinating ascospores have the ability to penetrate unwounded surfaces of elongating, green shoots directly.

The knots develop very slowly, and by the end of the summer they appear only as small galls that might easily be overlooked (Fig. 3). Further development does not occur until the following spring when the knots enlarge very rapidly. They initially are quite soft in texture and become greenish-brown in color as conidia develop over their surfaces (Fig. 4). The conidia are disseminated by wind and splashing rain but probably do not figure as prominently as the ascospores in establishing new infections.

By the second summer after infection, the knots have enlarged considerably and begin to change to a hard, coal-black structure. The old knots enlarge every year by advancing at the margins. The fungus mycelium can also spread internally and give rise to new galls some distance from the original knot. The central, older portions of the knot eventually break down and are invaded by boring insects.

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