Sudden Death Syndrome in Kaki Persimmon: Some Observations

Gregory L. Reighard1 and Jerry A. Payne2

 

1Associate Professor of Horticulture, Clemson University, Clemson, SC 29634-0375
2Research Entomologist, USDA Southeastern Fruit and Tree Nut Laboratory, P.O. Box 87, Byron, GA 31008
 

        The Japanese, oriental, or kaki persimmon (Diospyros kaki L.) is native to China, but has been cultured in Japan for at least 1100 years.  Kaki persimmon cultivars were introduced to the United States in the late 1800s where small commercial plantings were started in California, Louisiana, and Florida. By 1930, California, Florida, Alabama, and Texas had the most acreage under production (Griffith and Griffith, 1982).  Today, the majority of commercial acreage remains in California (about 1200 acres) with another 20 acres in Florida.  Interest in producing kaki persimmon in the southeastern United States is increasing because new cultivars are becoming available, and the fruit can be grown with little or no pesticides.  Furthermore, increased consumer knowledge of persimmons and an increasing population of Asian-Americans has created a small market in the southeastern United States.
        Kaki persimmons are preferred over our native American persimmons (Diospyros virginiana L.) by most consumers because of their large size, few seeds, and the absence of (or easily removed) astringency from pulp tannins that pucker the mouth when not neutralized through coagulation during ripening.  However, little cultural information is available for growing kaki persimmons in the Southeast. Moreover, the cultivar performance information given in nursery catalogs or university bulletins is often based on limited observations from small plantings and can often be misleading since a number of genetically different but morphologic ally similar (especially fruit shape) persimmon cultivars are sold under the same name. Hence, this erroneous information can lead to confusion when cultivar recommendations are given to potential kaki growers in the Southeast.
        To better observe the adaptability of a number of kaki persimmon cultivars sold in the southern United States, cultivar trials were established at Byron, Georgia and Columbia, South Carolina, in the 1980s.  However, many bearing trees died suddenly in specific years at both locations from 1986 to 1991.  Therefore, this report will describe the symptoms exhibited by these dying trees so that more can be learned from other growers about this puzzling death syndrome.
 

Planting History

        In 1984, 17 Kaki persimmon cultivars grafted to American persimmon rootstock were planted at the Southeastern Fruit and Tree Nut Research Laboratory near Byron, Georgia.  These cultivars were 7 non-astringent types (FL 11-72-10, ‘Fuyu’, ‘Hana Fuyu’, ‘Hanagosho’, ‘Ichikikei Jiro’, ‘Jiro’, ‘Shogatsu’) and 10 astringent types (Aizumishirazu’, ‘Eureka’, ‘Giombo’, ‘Hachiya’, ‘Hiratanenashi’, ‘Korean’ ‘Saijo’, ‘Sheng’, ‘Tamopan’, ‘Tanenashi’).  Fourteen trees of each cultivar were planted. In 1987, 23 Kaki and 4 American persimmon cultivars all budded on American persimmon rootstock were planted on a deep Lakeland sand at the Sandhill Research and Education Center near Columbia, South Carolina. The 27 cultivars were as follows: (23 Kaki) ‘California Fuyu’, ‘Chocolate’, ‘Eureka’, FL 11-72-10, ‘Fuyu’, ‘Gailey’, ‘Giombo’, ‘Gosho’, ‘Great Wall’, fla~chiya’, ‘Hana Fuyu’, ‘Hanagosho’, ‘Hiratanenashi’, ‘Homestead’, ‘Jiro’, ‘Korean’, ‘Maru’, ‘Saijo’, ‘Sheng’, ‘Shogat-su’, ‘Tamopan’, ‘Tanenashi’, unknown sporadic pistillate, and (4 American) ‘Early Golden’, ‘Garretson’, ‘Meader’, and ‘Ruby’.  Each variety was represented by 1-3 trees.  Adequate fertilizer, weed control, and water were provided at both locations.  No fungicides were used, and the trees showed no nutrient deficiency symptoms.  Trees at both locations also fruited during the years of evaluation.
 

Disease Symptoms

        In 1986 and 1987 at Byron and in 1990 and 1991 at Columbia, kaki persimmon trees collapsed and died within weeks after normal leafout and shoot growth.  Trees continued to die each spring at Byron during the late 1980s from the same symptoms.  Each of these periods of sudden tree death was preceded by either extremely low winter temperatures at Byron or by a very late spring freeze at Columbia.  The symptoms were the same at both locations, and onset of symptoms and subsequent tree death was often delayed for a year or more after cold stress.  Rootstocks never died, and vigorous sprouting often occurred just below the graft line.
        The first symptoms on trees at Columbia appeared in mid-April approximately 2-3 weeks after shoot elongation began and progressed rapidly for another 2-3 weeks during the flowering period of late April and early May.  Progression of the disease symptoms ended by mid-May, and those trees not killed recovered sufficiently to set and mature fruit.  The symptoms first appeared as a blackening discoloration of the leaf veins of the juvenile non-ligninized leaves.  Next, these affected leaves began to abscise at the leaf petiole scar followed by the flowers which abscised at the distal end of the peduncle.  Soon after, the young green shoots started showing black streaking and subsequently shriveled and died.  Death progressed from the tops of major branches of scaffolds downward until the main trunk was killed to the graft union with the rootstock.  When the bark of older wood from the branches and trunk was peeled back from the soft xylem, black vertical streaks were found throughout the cambial tissues and most recently formed xylem.  The intensity of the streaking increased during the progression of the symptoms and was greater in trees killed than those that only had branches killed.  These black streaks might be depositions in the vascular tissue of the same or similar tannins found in the fruit.
        This rapid decline appeared to follow winters with unusually or record cold temperatures such as -5o F on January 21, 1985, at Byron and freezing temperatures of 24o F at Columbia on March 21, 1990, following an unusually early spring.  Disease symptoms were first observed at Byron in April 1986, approximately 14 months after the subzero temperatures in 1985.  The March 21 freeze at Columbia killed all emerged shoots and green buds (bud scales shed).  All current shoot growth was killed as well as some 2-year-old wood.  Sunken cankers developed at the base of a few branches on some trees, and a few small weak trees developed the black discoloration symptoms and died.  However, all the surviving trees produced vigorous healthy shoots from epicormic buds originating near the shoot bases.  After a mild winter and spring in 1991, these shoots emerged, elongated, and foliated normally for a few weeks before the symptoms of this syndrome again began to appear and kill large healthy trees.
 

Pathogen isolation

        Tissues from declining trees were cultured and inspected for bacterial, fungal, and viral pathogens. No known pathogenic organisms were isolated.  However, Scott and Payne (1988) found isometric viruses in embedded tissue from leaves.  A similar disease syndrome has been reported for kaki persimmon in Italy and Brazil (Mazzetti 1956, Herbas 1969).  In both these cases, a latent virus inherent in kaki persimmon was suspected as the casual agent. Mazzetti (1956) hypothesized that unfavorable growing conditions (i.e., environmental stress) may trigger the replication of the virus leading to the symptoms.  Italy experienced an epidemic of this disease from 1945-1950 during which time cold winters occurred especially in 1947.  Differences in cultivar suscep-tibility were also noted.
This information suggests that environmental stresses such as severe cold injury lead to the symptoms observed in Georgia and South Carolina.  If these symptoms are directly attributed to reactivation of a latent virus, then virus-free material must be made available to test this hypothesis to determine if persimmon cultivars should be virus-free before planting in the Southeast.  In addition, American persimmon should be assayed for this virus to determine if it is a transmissible host.
 

Cultivar Susceptibility

        Since American persimmon was the rootstock for the Byron and Columbia plantings, it is not known if kaki persimmon as a rootstock would reduce or increase stress on the scion cultivar.  This needs further investigation as well as cultiyar selection.  At both Byron and Columbia, the astringent varieties ‘Korean’ and ‘Sheng’ showed less injury than all other cultivars.  These cultivars are generally more cold hardy and leafout later than other cultivars.  ‘Giombo’ and ‘Hana Fuyu’ also had slightly higher survival.  Other cultivars such as FL 11-72-10 (Florida selection), ‘Hachiya’, and ‘Eureka’ were extensively injured or killed by this disease and should not be recommended in areas where cold injury might occur.
        Future work on this problem needs to be directed at isolating the causal agent of this syndrome so that recommendations as to cultivar and virus-free scionwood and rootstock can be made with confidence.  Furthermore, caution should be emphasized whenever extension specialists and consultants are asked for recommendations concerning the commercial potential of kaki persimmon in the southeastern United States because of this uncertainty about tree longevity due to cold stress.
 

Literature Cited

Griffith E. and M.E. Griffith.  1982.  Persimmons for everyone. Publ. North American Fruit Explorers. 145 p.

Herbas R.  1969.  El mosaico del caqui (Diospyros kaki) y algunas propiedades fisicas de su agente causual. Turrialba 19(4): 480-490.

Mazzetti, A.  1956.  A new disorder of Oriental persimmon in Italy.  FAO Plant Protection Bulletin 4(12):181-183.

Scott, S. W and I. A. Payne.  1988.  Decline of Oriental persimmon. Phytopathology 78(12):1568. (Abstr.)