Post harvest diseases fruits and vegetables - Xavier University ...

FREEDOM PALESTINE FREEDOM PALESTINE FREEDOM PALESTINE
14 Postharvest Diseases of Fruits and Vegetables
G.E., 1975; Dickman and Alvarez, 1983; Binyamini and Schiffmann-
Nadel, 1972; Spalding and Reeder, 1986b), or by Colletotrichum musae in
banana fruits (Simmonds, 1941). The fungal conidia are found in large
quantities on the surface of the fruits during their development on the
tree. In the presence of free water upon the fruit, the spores germinate
and form an appressorium at the tip of the germ tube. The appressoria
function as resting spores on the fruit, since they resist environmental
conditions much better than the conidia; they remain vital for long
periods while embedded in the natural wax of the fruit or bound to its
surface. The binding can occur through a mucous secretion of the fruit, as
with C musae (Simmonds, 1941). Yet, the appressoria are infection
bodies capable of germinating, under suitable conditions, and forming
germinating tubes which penetrate into the tissues; they may even
develop fine "infecting hyphae" that penetrate under the cuticle or the
external layers of the epidermis. The appressoria themselves, or the
"infecting hyphae" which they form, comprise the quiescent stage of
fungal infection (Muirhead, 1981b; Prusky et al., 1990). Following
picking, when the fruit commences ripening, the quiescent infection
transforms into an active stage and initiates the development of the
typical anthracnose. In papaya, the penetration of the germ tubes occurs
through the stomata of the young, unripe fruit, while the appressoria can
remain dormant for a long period over the cuticle or in "caves" beneath
the stomata (Stanghellini and Aragaki, 1966).
Assumptions and explanations raised in connection with the
establishment of quiescent infections in unripe fruits were summarized
and classified into four categories by Simmonds (1963). Verhoeff (1974),
in his review of latent infections, had grouped these theories into three
groups (combining the nutritional and energetic requirements of the
pathogen into one group):
(1) The shortage in the young fruit of adequate substrate to meet with
nutritional and energetic requirements of the pathogen;
(2) The incapability of the pathogen to produce cell-wall degrading
enzymes in the young fruit;
(3) The presence of preformed antifungal compounds in the young fruit
that inhibit pathogen growth or enzymatic activity. Swinburne
(1983), in a later review, added the fourth category of theory:
(4) The accumulation of phytoalexins - antifungal compounds induced
by the host tissue as a result of actual or attempted fungal infection.
Following the description by Prusky and Keen (1995) of preformed
compounds that can be further induced in the host tissues, the third
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