1Department of Biology, Valdosta State University, Valdosta, GA 31698, USA; 2Rutgers University Blueberry and Cranberry Research Center, Chatsworth, NJ 08087, USA

Background and objectives
Cranberry fruit rot is a limiting factor for cranberry production in New Jersey, USA. Glomerella cingulata, Physalospora vaccinii, and Botryosphaeria vaccinii are three of the major species of pathogens involved in this complex disease that can infect and remain latent in cranberry tissue [1]. The objectives of these studies were to determine aspects of the life histories of these pathogens including overwintering reservoirs, timing of infection, and latent periods.

Results and conclusions
In greenhouse studies, G. ;cingulata (anamorph Colletotrichum gloeosporioides) was recovered from rotted cranberry fruits, 5-6 ;months after open flowers or immature green berries were inoculated with a conidial suspension. This is the first reported attempt to obtain diseased berries in artificial inoculation tests, thus completing Koch's postulates for G. ;cingulata as a causal agent of cranberry fruit rot. These studies indicate that flowers or immature green berries can be infected without showing symptoms of rot for 4-5 months.

In field studies in 1995 and 1996, G. cingulata was recovered from older portions of the stem tissues [2]. In contrast, P. ;vaccinii was found in both leaves and stems, while B. ;vaccinii was found primarily in leaves but rarely in stems. G. cingulata and P. ;vaccinii were also found in senescent fruit pedicels from the previous years. The three fungi were rarely recovered from open flowers or from immature berries prior to August.

To resolve the timing of infection by these pathogens, field studies were carried out in 1996 and 1997. The fungicide chlorothalonil (Bravo 720, 5 ;pints/acre) was applied to field plots in five two-spray cassettes, with each two-spray cassette staggered by 10-14 ;days. The flowering and fruiting phenology of plants was determined throughout the season. Plots were harvested at the end of September and the percentage fruit rot was determined. Incidence of fruit rot increased in treatments where the two-spray cassettes were started after 190 Julian days. The amount of infection leading to rot for each time period was calculated by subtraction of the per cent rot from the treatment immediately following it. This calculated infection period corresponds to a time period when plants were out-of-bloom, indicating that infection takes place later in the season, rather than during flowering, as previously described [3].

These findings contribute to proposed life cycles for these pathogens, in which the fungi survive endophytically in different parts of the plant. G. ;cingulata survives in older stem tissue, senescent pedicels from previous years, or possibly senescent tissue in the duff layer. Sporulation may occur on these tissues, allowing splash-dispersal of conidia to immature fruit. The role of sexual reproduction is unknown, as perithecia of G. ;cingulata have not been observed in the field. B. ;vaccinii overwinters in fallen leaves [1] and in 2-year-old leaves on uprights. Infections are believed to begin in the spring via conidia and ascospores from fruiting bodies in senescent tissue [1]. P. ;vaccinii survives in both leaves and stem tissue, and may produce ascospores that can infect developing fruit later in the season.

1. Caruso FL, Ramsdell DC, eds., 1995. Compendium of Blueberry and Cranberry Diseases. St Paul: APS Press.
2. Stiles CM, Oudemans PV, 1997. Phytopathology 87, S94.
3. Zuckerman BM, 1958. Plant Disease Reporter 42, 1214-1221.