Phomopsis vaccinii (Phomopsis twig blight of blueberry)

In susceptible blueberry cultivars, blighting of 1-year-old woody stems with flower buds is the predominant symptom in North Carolina, USA. Systemic invasion has also been reported (Milholland, 1982). Infected succulent, current-year shoots wilt in 4 days and become covered with minute lesions. The fungus continues to travel downward through the stem at a rate averaging 5.5 cm in 2 months, killing major branches (Wilcox, 1939; Daykin and Milholland, 1990). If it reaches and encircles the crown, the plant may wilt and die. Regardless of age of stems, cankers are long and narrow, and are covered by the bark or epidermis (Weingartner and Klos, 1975). On blueberry stems over 2 years old, D. vaccinii causes a brown discoloration of the stem xylem below wilt symptoms (Weingartner and Klos, 1975). Direct inoculation of woody stems only produces localized lesions. Infected leaves show spots enlarging to 1 cm with pycnidia/conidiomata appearing in 2 weeks. The fungus may also remain dormant until favourable conditions permit it to resume growth (Wilcox, 1939). Wilt of (symptomless) blueberries stems occurs in July-August and continues until October in Michigan, USA. Pycnidia appear from August to October mostly on dead stems 3-5 years old (Weingartner and Klos, 1975). In Arkansas, USA, twig blight symptoms at early fruit set include blighting of 1-year-old woody stems with flower buds and occasional blighting of new, young, succulent growth without flower buds (Ames et al., 1988). Infected fruits turn reddish-brown, soft, mushy, often splitting and causing leakage of juice (Milholland and Daykin, 1983).In cranberry, D. vaccinii principally causes a viscid rot of the fruits, which become softened and discoloured. In some cases, a viscous substance can be strung out from the cut surface of the berry (Kusek, 1995). The fungus also causes a dieback of the upright stems ('upright dieback'), which become yellow, then orange and brown, before dying back (Boone and Caruso, 1995).

All cultivars of V. corymbosum and V. macrocarpon are susceptible to D. vaccinii (Wilcox, 1939; Weingartner and Klos, 1975; Milholland and Daykin, 1983; Ames et al., 1988), though some variation in susceptibility has been reported (Teodorescu et al., 1988). Bordeaux mixture with a suitable spreader was first used, as a spray at the late flower-bud stage (Wilcox and Bergman, 1945). Ferbam has also been tested and reported to give as good control as Bordeaux mixture applied before the flower buds opened. More recently, chlorothalonil and benomyl have given good reduction of canker in field trials (Parker and Ramsdell, 1977). The spray regimes recommended on blueberry are relatively intensive: at budbreak and at 14-day intervals through full bloom to control twig blight, then at 14-day intervals through berry development to control the fruit rot phase.

Since D. vaccinii occurs as an endophyte in apparently healthy vines, only vines known to be disease-free should be marketed and in particular exported. Certification schemes for Vaccinium should be followed as appropriate (OEPP/EPPO, 1997).

The disease is widely established in the USA on blueberry and cranberry, wherever these crops are grown (Friend and Boone, 1968; Farr et al., 1989; Caruso and Ramsdell, 1995). On blueberry, it was formerly considered to be of minor importance (Wilcox, 1939). The disease became serious in a few marshes in Wisconsin in 1966 and in isolated instances caused serious losses (Friend and Boone, 1968). In 1975, Phomopsis dieback was reported epidemic in the centre of the blueberry-producing area in Indiana and southern Michigan and D. vaccinii was then considered to be a serious pathogen under favourable conditions (Weingartner and Klos, 1975). In the southeastern USA, particularly in North Carolina, the disease has recently "increased tremendously in importance and severity" (Caruso and Ramsdell, 1995). Twig blight of susceptible blueberry cultivars has been estimated to cause fruit loss of 2-3 pints per bush in North Carolina (Milholland, 1982). In New York supermarkets in 1978 and 1979, Phomopsis fruit rot accounted for 0.5% loss of the 15.2% defective fruits (Milholland and Daykin, 1983).In cranberry, D. vaccinii does not cause the twig blight disease seen on blueberry. It occurs on the shoots and leaves, without apparently causing any significant damage. Occasionally, shoots die back, in the so-called 'upright dieback'. However, this is a minor disease, "not causing appreciable economic loss except in Massachusetts" (Caruso and Ramsdell, 1995). Since the other pathogen implicated in the disease (Synchronoblastia crypta) has only been reported in this state (and New Jersey), while D. vaccinii is widespread in the USA, it may be that the role of D. vaccinii is in any case much less than that of S. crypta. Damage to fruits by D. vaccinii is rather more important. D. vaccinii was responsible for a reduction of 18-35% of the cranberry crop in several plots in 1933 in Massachusetts (Bergman and Wilcox, 1936). In Wisconsin, loss of up to 65% of cranberries in storage due to Godronia cassandrae (end rot), D. vaccinii (viscid rot) and Ceuthospora lunata (=Apostrasseria lunata) (black rot) have been reported (Carlson, 1963). However, Caruso and Ramsdell (1995) consider the storage fruit-rot to be generally minor, with moderate losses locally.