Agriculture Reference
In-Depth Information
Stems are particularly susceptible to water loss due to
their high surface to volume ratio. The high rate of respira-
tion of stems may also be a contributor to stem browning,
as the respiration rate of the stems may be 15 times or more
that of berries. Although stem browning does not affect the
eating quality of the berries, it is a serious quality defect, as
it reduces the overall attractiveness of the bunch. Varieties
differ greatly in the rate at which post-harvest stem
browning occurs (Winkler et al . 1974).
There is a strong correlation between cluster water loss
and stem browning. A survey indicated that water loss
ranged from 0.5 to 2.1% based on the initial weight
(measured at harvest) within the 8-hour period before
cooling. The magnitude of the losses was directly related
to the length of delay, temperature during the delay before
cooling, and type of box material. Even a few hours
delay  at high temperatures can cause severe drying and
browning of cluster stems, especially on the hottest days.
When  cluster water loss reaches 2.0% or more for
'Perlette', 'Superior', 'Flame Seedless', 'Thompson
Seedless', 'Ruby Seedless', and 'Fantasy Seedless', stems
will show symptoms of browning approximately seven
days later in cold storage (Crisosto et al . 2001). In culti-
vars growing in France, water loss of as little as 3% can
cause a reduction in firmness and shrivelling of berries
(Chapon et al . 1991). In all the cases, excessive water loss
leads to berry shatter. A recent study shows that chloro-
phyll fluorescence is well correlated to water loss at the
cluster level (Wright et al . 2009).
Browning in both damaged and intact berries and stems
is almost certainly due to oxidation of phenolics via
quinones to brown pigments by the action of polyphenol
oxidase (Sapis et al . 1983a, 1993b). The severity may be
determined by the level of membrane permeability and
injury of cells (Burzo et al . 1998). Severe desiccation
causes the breakdown of cell membranes and the oxidation
of phenolics in the cell sap. Berries may suffer from skin
and pulp browning if they become bruised during handling.
Rachis and berry browning is inhibited by SO 2 treatment
(Morris et al . 1992). Berries that have not been treated with
SO 2 are also more susceptible to gradual browning of the
pulp over time (Luvisi et al . 1992). This may be exacer-
bated by the use of high levels of carbon dioxide during
storage for fungicidal or quarantine purposes (Ahumada
et al . 1996; Yahia et al . 1983; Crisosto et al . 2002c).
berries from Thompson Seedless have been linked to the
late (post fruit-set) application of gibberellin (GA3) before
harvest (Ben Tal 1990), however, GA3 treatments can have
opposite effects depending on the cultivar (Jeong et al .
1998). There appear to be three types of berry shatter:
physiological, pathological and mechanical. The first is
associated with the thickening and hardening of the pedicel
and production of an abscission layer (Ben Tal 1990;
Nakamura & Hori 1981; Xu et al . 1999). The presence of
fungi such as B. cinerea , Rhizopus stolonifer and Alternaria
spp. can cause wet abscission without an abscission layer
(Xu et al . 1999). Control of fungi with fungicides, acetic
acid or SO 2 fumigation reduces shatter in stored table
grapes (Xu et al . 1999; Sholberg et al . 1996; Morris et al .
1992). Some researchers reported that ethylene stimulates
berry shatter (Nakamura & Hori 1981; Lydakis & Aked
2003b). Cold storage, GA, NAA or aminooxyacetic acid
treatments were found to inhibit shatter (Wu et al . 1992).
In California, berry shatter is mainly triggered by mechan-
ical damage occurring during harvesting, packaging and
transportation (Luvisi et al . 1995).
Diseases and their control
Causal organisms
The primary cause of post-harvest loss in table grapes is
grey mould disease or Botrytis rot caused by Botrytis
cinerea (Pearson & Goheen 1988; Snowdon 1990) (Plate
9.1). This disease occurs wherever the crop is grown. The
fungus can grow at temperatures as low as −0.5°C (31°F)
and so may spread from one berry to another during storage
and transportation even if adequate pre-cooling is carried
out and suitable temperatures are maintained. Botrytis rot
can be identified by the characteristic 'slipskin' condition
that develops, and later, by 'nests' of decayed berries
encased in white mycelium.
Post-harvest berry infection is primarily caused by
conidial infection at or after veraison (Kock & Holz 1991a)
although some authors suggest it may happen at the flower
stage (Nair & Allen 1993). The fungus remains quiescent
in the developing fruit, with symptoms only appearing on
the mature fruit. It is thought that loss of berry resistance is
due to the decreasing ability of the maturing berry flesh to
synthesise antimicrobial stilbenes and also due to the fall in
proanthocyanidin concentration during development (Hill
et al . 1981; Creasy & Coffee 1988). Berry cracking in
certain cultivars also encourages infection.
Other less important fungal post-harvest diseases of
table grapes include: Aspergillus rot ( Aspergillus niger )
which doesn't grow below 5°C, blue mould rot, ( Penicillium
spp), Rhizopus rot ( Rhizopus oryzae; R. stolonifer ),
Berry Shatter
Berry loss or shatter can be a significant problem with
certain cultivars of table grapes such as Thompson Seedless
(Wagener 1985; Berry & Aked 1996). The high losses of
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