Agriculture Reference
In-Depth Information
releases ethylene) prior to packing and storage developed
severe CI symptoms, expressed as mesocarp discolouration
after 3 weeks at 5°C. 'Fuerte' fruit treated with ethylene
gas (100 μl l
−1
) for 24 h at 20°C prior to storage at 5°C
exhibited mesocarp discolouration, which increased
dramatically during shelf life at 20°C. 'Fuerte' fruit treated
in cold storage with a continuous low-ethylene dose (4 μl
l
−1
) developed severe browning in the fruit pulp after 3
weeks at 5°C. 'Hass' fruit treated with 50 μl l
−1
ethylene,
for 12, 24 or 48 h at 5°C showed a gradual increase in
mesocarp discolouration after 3 weeks in cold storage plus
shelf life; the 48 h ethylene-treated fruit exhibited the most
severe pulp browning. Use of absorbent sachets that
removed ethylene from modified atmosphere (MA)
packages reduced mesocarp discolouration and decay
development in 'Hass' fruit after 5 weeks storage at 5°C.
Application of 1-methylcyclopropene (1-MCP), which
inhibits ethylene effects by competitive binding to ethylene
receptors, reduced mesocarp discolouration, decay devel-
opment and polyphenol oxidase (PPO) activity, whereas
this enzyme activity was induced in ethylene-treated fruit
that were cold stored for 4 weeks. 1-MCP (50-1000 nl l
−1
)
treated fruit were firmer following storage for 4 to 7 weeks
at 5.5°C and 6-24 h, at 6 or 15°C, had reduced skin
colouration (purpling) at removal from storage, increased
time to softening, and reduced physiological disorders
associated with long-term storage (Woolf
et al
. 2005).
Fruit conditioned at temperatures of 4, 6, 8, 10, 12 and
15 °C for a period of 0, 1, 2, 3, 4 or 5 days before 3 weeks
storage at 0°C, had reduced skin damage. The optimum
temperature/time combinations were 6 or 8°C for 3-5 days
prior to 0°C storage (Woolf
et al
. 2003).
may be covered with spore masses in the later stages of
infection. Decay penetrates through the flesh resulting in
discrete areas of discoloured flesh. In cultivars that darken
when ripe (such as Hass), rots may be less obvious exter-
nally. The most prevalent fungi responsible for post-harvest
diseases of avocado fruit are
Colletotrichum acutatum
,
C.
gloeosporioides
,
Botryosphaeria parva
,
B. dothidea
and
Phomopsis
(Hartill 1991). Apart from
Phomopsis
, which is
almost exclusively isolated from stem end rots, these fungi
can cause both stem end rots and anthracnose (a disease
usually characterised by necrotic lesions on the body of the
fruit) on 'Hass' avocados.
Botryosphaeria
spp. is generally
isolated in greater numbers from rots of avocados than are
any of the other fungi.
The most important post-harvest decays of avocados are
caused by the fungi
C. gloeosporides
, which causes
anthracnose or black spot decay, and
Diplodia natalensis
.
Also important are
Phomopsis
spp. and
Dothiorella
spp.
which cause stem-end rot (Ahmed & Barmore 1980).
Infection with
C
.
gloeosporides
occurs while the fruit is
developing on the tree. Fruit spot disease caused by
C. gloeosporioides
is the most commonly occurring dis-
ease of avocado. Infection of avocado fruits by
Fusarium
solani
and
F. sambucinum
causes accelerated softening of
fruits. Other diseases of avocados are cercospora spot
(
Cercospora purpurea
) and scab (
Sphaceloma perseae
),
which attack leaves as well as fruits (Kadam & Salunkhe
1995). Anthracnose, caused by
Glomerella cingulata,
of
which the conidial state is
Colletotrichum gloeosporioides,
is found in the United States, Israel (Prusky
et al
. 1983),
Argentina (Oste & Ramallo 1974), Australia (Peterson &
Inch 1980), New Zealand (Hartill 1991), India, South
Africa (Rowell 1983) and Puerto Rico (Nolla 1926).
Infection studies have identified
Colletotrichum gloe-
osporioides
as a weak pathogen. Anthracnose appears as
the fruit begins to soften as circular black spots covered
with pinkish spore masses in later stages. Decay can pen-
etrate through the flesh and induce browning and rancid
flavour. Infection is enhanced by wounding, artificially and
by the fruit spotting bug (Fitzell 1987). On the tree during
the season, spores of this fungus have been shown to ger-
minate, form an appressoria and a short infection peg
which penetrates about 1.5 μm into the skin (Coates
et al
.
1993). The fungus then remains quiescent until harvest,
when antifungal dienes in the skin of avocado fruit break
down due to degradation by lipoxygenase activity (Karni
et al
. 1989; Prusky
et al
. 1988), the fungus resumes growth
and invades the avocado fruit to cause post-harvest rots
(Prusky
et al
. 1988, 1984, 1983, 1990, 1991; Adikaram
et al
. 1992; Neeman
et al
. 1970; Sivanathan & Adikaram
DISEASES
Post-harvest diseases of avocados, an important problem
of this crop, are commonly developed during the latter
stages of fruit ripening, with symptoms first appearing
when fruit are minimally ripe but often becoming quite
severe before the fruit are over soft. Fruit ripened at 20°C
and assessed at the same stage of ripeness, just before the
flesh becomes over soft, had fewer post-harvest rots if they
had been previously stored at 4°C or 6°C, than if they had
been stored at either lower or higher temperatures. Diseases
of avocados are divided into two categories on the basis of
their location (Snowdon 1990). Stem end rots enter the
fruit at the stem, or peduncle end of the fruit and move
down the fruit resulting in discoloured flesh, often with
associated browning of the vascular strands (Johnson &
Kotze 1994). Body rots invade through the skin and are
generally manifested as circular brown to black spots that
