Agriculture Reference
In-Depth Information
Diplodia stem-end rot
Diplodia
stem-end rot is an important citrus post-harvest
disease in warm and humid growing regions of the world.
In a typical summer-rainfall production area, 13-42% of
untreated fruit may develop stem-end rot symptoms
(Eckert & Brown 1986). All citrus cultivars are susceptible
to this disease. The incidence and severity of stem-end rot
can be increased by ethylene de-greening treatments
(Brown 2003d).
only in advanced stages of infection at high relative
humidity levels.
Ethylene de-greening significantly enhances stem-end rot
due to the stimulation of abscission by ethylene (Barmore &
Brown 1985). The temperature and relative humidity used
in de-greening also favours fungal growth and disease
development (Brown 2003d). After harvest it was shown
that
Phomopsis
stem-end rot was a more common cause of
decay than
Diplodia
stem-end rot when oranges were not
treated with ethylene (Brooks 1941). In addition, it was
observed that
Diplodia
was almost always the cause of
decay on fruit when ethylene de-greening was used.
Morphology
Pycnidia (spore producing structures) are subglobose to
globose and 300-700 μm in diameter. The young spores
are hyaline, nonseptate and granular, whilst the mature
spores (17-43 μm × 10-18 μm) are striated with one
septum (Timmer
et al
. 2000).
Control
Preventative measures
Good agricultural practices that produce healthy trees with
minimal amounts of deadwood or removal of deadwood
by pruning can aid in the control of stem-end rot. Proper
ethylene concentrations of 5-10 ppm needed for de-greening
should be maintained, since higher levels will not enhance
de-greening, but will significantly increase the incidence
of
Diplodia
stem-end rot. Spot picking or delayed harvest
for better natural fruit colour development, will signifi-
cantly reduce the time of de-greening required and the
occurrence of decay (Brown 2003d).
Disease cycle and epidemiology
Spores of the fungus are produced in specialized structures
called pycnidia, which are formed on the surface of dead
wood on the tree. Initial infection of deadwood is caused
by airborne spores that are produced on debris found in the
soil. These spores are dispersed to the fruit during the
warm, rainy, summer months. The fungus colonizes dead
tissue of the button surface where it remains dormant until
after harvest. After harvest, the fungus invades the stem
end of the fruit when the button abscises, which provides a
temporary natural opening for the hyphae to penetrate the
cells of the fruit core and rind (Brown & Wilson 1968).
Chemical control
Treatments applied prior to de-greening are much more
effective than ones applied after. Zhang and Swingle (2005)
illustrated that temperatures of 30-35°C significantly
reduced green mould, but increased stem-end rot. In addi-
tion, it was indicated that fruit drenched with thiabenda-
zole, followed by curing at 35°C for 48 h before packing,
was effective in controlling both green mould and stem-end
rot (Zhang & Swingle 2005).
Transmission
Sporulation rarely occurs on infected fruit and contamina-
tion of handling and packing equipment by the fungus is
therefore not a major source of transmission (Brown
2003d). The decay also does not spread from infected to
healthy fruit in packed containers.
Phomopsis stem-end rot
Phomopsis stem-end rot is caused by the fungus
Diaporthe
citri
F.A. Wolf (anamorph
Phomopsis citri
H. Fawc. non
Sacc. Traverso & Spessa). Phomopsis decay becomes more
prevalent after the de-greening season and is more preva-
lent in humid subtropical and tropical regions (Timmer
et al
. 2000). All types of citrus are susceptible and no other
hosts for this fungus have been identified yet (Kucharek
et al
. 2000).
Symptomology
Initial symptoms (i.e. lesions) of
Diplodia
stem-end rot are
similar to that of
Phomopsis
stem-end rot. Infection occurs
more frequently at the stem end of the fruit but occasion-
ally occurs through injuries on the side or stylar end of the
fruit. The fungus grows rapidly through the spongy central
axis of the fruit and unevenly through the rind, which pro-
duces finger-like projections of brown tissue on the infected
fruit (Syngenta 2007). Decay forms at both ends of the fruit
before covering the entire fruit. A sour, fermented odour
is usually present and sometimes the fruit will become
black (Brown 2003d). Decayed tissue is initially firm but
later becomes watery and soft. Surface mycelia appear
Morphology
Pycnidia (200-450
m
m) are scattered, dark, ovoid, thick
walled and erumpent. Alpha conidia (2.5-4 × 5-9
m
m) and
beta conidia (0.7-1.5 × 20-30
m
m) are produced. The alpha
