New Zealand Journal of Experimental Agriculture

ISSN: 0301-5521 (Print) (Online) Journal homepage: http://www.tandfonline.com/loi/tnzc19

Fungal fruit rots of Actinidia deliciosa (kiwifruit)

S. R. Pennycook
To cite this article: S. R. Pennycook (1985) Fungal fruit rots of Actinidia deliciosa
(kiwifruit), New Zealand Journal of Experimental Agriculture, 13:4, 289-299, DOI:
10.1080/03015521.1985.10426097
To link to this article: http://dx.doi.org/10.1080/03015521.1985.10426097

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New Zealand Journal of Experimental Agriculture, 1985, Vol. 13: 289-299

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Review

Fungal fruit rots of Actinidia deliciosa (kiwifruit)

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S. R. PENNYCOOK
Plant Diseases Division, DSIR
Private Bag, Auckland, New Zealand
Abstract
Current knowledge of the symptoms,
etiology, and control of the three main fungal fruit
rots of kiwifruit in New Zealand is reviewed. Field
rot, caused by Sclerotinia sclerotiorum, affects
immature fruits on the vines. Storage rot, caused
by Botrytis cinerea, affects harvested fruits during
cold storage. Ripe rot, caused by Botryosphaeria
doth idea, affects harvested fruits during post-storage ripening.
Keywords
plant diseases; fruit rots; post-harvest diseases; kiwifruit; Sclerotinia sclerotiorum;
Botrytis cinerea; Botryosphaeria dothidea; field rot;
storage rot; ripe rot
INTRODUCTION
The kiwifruit, Actinidia deliciosa (Chevalier) Liang

& Ferguson (1984; syn. A. chinensis Planchon var.

hispida Liang), is now established as New Zealand's

major horticultural export crop (Weston & Bollard
1984). During the early years of its commercial
development, the crop was regarded as virtually
disease-free (Bailey 1950, 1961; Bailey & Topping
1951; Schroeder & Fletcher 1967), but, with the
increasing duration of kiwifruit monoculture and
the rapid expansion of production, disease problems have become more numerous and important
(Sale 1980). However, in comprehensive publications dealing with the crop, information on kiwifruit diseases and their control has remained sparse

This paper was first presented on 23 November 1983 at

a seminar in honour of Professor F. J. Newhook on his
retirement from the Chair of Plant Pathology, Department of Botany, University of Auckland, Auckland, New
Zealand.
Received 30 May 1985; revision 29 July 1985

and rudimentary (Fletcher 1971; Ford 1971; Sale

1981, 1983, 1984).

This paper reviews our current knowledge in New

Zealand of field rot, storage rot, and ripe rot, the
three main fungal diseases that directly affect the
marketable product - the fruit.
FIELD ROT
The major rot that affects immature fruits while
they are growing on the vines is caused by Sclerotinia sclerotiorum (Libert) de Bary (Pennycook
1982; for pathogen description and illustrations, see
Kohn 1979). Field rot has often in the past been
mistakenly attributed to infection by Botrytis
cinerea Persoon : Fries (Fletcher 1971; Ford 1971;
Sale 1981). Isolations from lesions on fruits that
had dropped from the vines during a field rot epidemic in late January 1980 yielded 80% S. sclerotiorum and 20% B. cinerea (D. J. Beever
unpublished data). The presence of Botrytis in these
!esions may have resulted from secondary infection, possibly after the fruits had fallen to the
ground; over several years, I have isolated no fungus other than S. sclerotiorum from numerous field
rot lesions on fruits that had not yet fallen from
the vines. Seasonal incidence of field rot is dependent on the frequency and duration of periods of
summer rain conducive to the establishment of
infection by Sclerotinia ascospores. An estimated
5% loss of immature fruits was reported from the
Te Puke district after a severe Sclerotinia infection
period in late December 1980.
Symptoms
The earliest symptom of Sclerotinia field rot is a
blossom blight during late November and December. Blossoms and their pedicels tum pale brown
and wither. The symptoms are common on male
vines, and entire clusters of male blossoms degenerate into a tangled mass (Fig. I); female buds and
blossoms are less frequently affected. Bud symptoms could be confused with those of bacterial bud
rot (Young 1984), from which they differ in two
conspicuous ways: the characteristic bacterial sliming and darkening of the anthers is absent, and the

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Fig. 1 Sclerotinia sclerotiorum

blight of male kiwifruit blossoms.
Shoot lesions are arrowed.

withered brown tissues are not confined to the bud

but usually include the full length of the pedicel as
well.
In a dry season, the withered blossoms become
dry and crisp with little or no mycelium apparent.
No secondary spread of infection occurs.
In a wet season, the rotting blossoms remain soft
and mushy, and become covered with copious white
mycelium. The mycelium often aggregates into
dense knots c. 1-3 mm in diameter, which may
darken and harden to form sclerotia. The rot lesions
frequently progress from the pedicels into the shoots
(Fig. 1), and destructive secondary spread is common where rain-sodden infected blossoms adhere
to shoots, leaves, and petioles.
Fruit rot symptoms can develop at any time from
fruit set onwards, but occur most commonly during
December and January. Fruit lesions are watery,
sunken, and more or less whitish (depending on the
degree of superficial mycelial growth); black sclerotia often develop amongst the mycelium on the
surface of the lesions (Fig. 2). Lesions rarely occur
on clean, exposed fruit surfaces, but are usually
centred on sites at which either infected buds or
blossom debris (particularly senescing stamens and
petals) are in contact with the fruit surface, or adjacent fruits are in contact with each other so that
they retain a water droplet between them.
Fruits affected by large, deeply penetrating lesions
usually drop from the vines within a week or two
of infection. However, if dry weather intervenes,

lesions may dry out leaving the fruits badly scarred

(Fig. 3) but otherwise unimpaired.
Etiology
Sclerotinia sclerotiorum overwinters in kiwifruit
orchards as sclerotia in the soil. Some of the sclerotia will have developed on diseased kiwifruit blossoms and fruits during the previous summer, but
probably their major source is saprophytic growth
of the fungus on grass and weed debris and other
ground litter.
After a period of winter dormancy, sclerotia 'germinate' during spring and summer in response to
moisture and rising soil temperatures (Willetts &
Wong 1980). Apothecia (sexual fructifications) grow
from the sclerotia up through the soil and litter,
and flare out just above ground level into a trumpet-shaped, off-white to fawnish-brown disc, usually c. 5-6 mm in diameter (Fig. 4). In the Te Puke
district, the earliest apothecia have been found in
kiwifruit orchards in late September; they become
plentiful during late October, November, and
December. Apothecial production usually terminates in mid summer as the soil dries out or as the
supply of overwintered sclerotia is depleted. However, in some years and in some 10ca1ities, apothecial production may continue throughout the
summer.
There is frequent spore dispersal from the apothecia. Changes in atmospheric humidity or pressure

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for several hours (Willetts & Wong 1980). There is

no secondary spread from fruit lesions because the
pathogen does not produce conidia (asexual spores).
Control
The risk of Sclerotinia infection can be reduced by
removal of senescent blossom tissues from the
vines. A vigorous air-blast spray application at petal
falI will help dislodge the senescent petals and stamens ofthe female flowers from the newly set fruits.
Male vines should be pruned as soon as possible
after pollination, to eliminate the senescent male
blossoms. General pruning for a relatively open
canopy will also reduce the risk of infection by
allowing the vines to dry more quickly after rain.
The dicarboximide fungicides registered for use
on kiwifruit, iprodione (Rovral) and vinclozolin
(Ronilan), are extremely effective against S. sclerotiorum if their application is timed to coincide with
the deposition of ascospore showers. In some
seasons, a single, thorough application at late blossom-early petal fall to prevent saprophytic colonisation of senescing blossom tissues may be
sufficient. However, in a wet season, additional
applications may be necessary during blossom and
after petal fall.
Ground applications of fungicides, herbicides,
fumigants, and hyperparasitic fungi have been used
to destroy either sclerotia or apothecia of S. sclerotiorum in susceptible field crops (Hartill & Campbell 1973; KrUger 1973; Trutmann et al. 1980).
However, their efficacy has not been demonstrated
in kiwifruit orchards.

Fig. 2 Sclerotinia sclerotiorum field rot of immature

kiwifruit. Sclerotium (left) and adhering anthers (right) are
arrowed.

trigger 'puffing', the simultaneous discharge of

thousands of ascospores from the upper, fertile surface of an apothecium (Hartill & Underhill 1976).
This phenomenon can sometimes be observed as
a transient, cigarette smoke-like wisp rising a few
centimetres from the orchard floor as the litter is
disturbed. Discharged ascospores are dispersed by
wind and deposited on the vines as ascospore
'showers'.
Fruit infections result only if ascospores are
deposited at infection sites that are in direct contact with an adequate food base (e.g., senescing stamens and petals, or water droplets containing pollen
grains or pollen exudates) for saprophytic growth,
and if those infection sites subsequently remain wet

STORAGE ROT

Harvested fruits that have been graded and packed

as healthy and unblemished will often develop rot
symptoms while being held in commercial cold
storage at Oe. During the normal storage life of
the fruits, these symptoms consist of strikingly uniform stem-end rots caused by the grey mould fungus, Botrytis cinerea Persoon : Fries (Scapin et al.
1983; Beever et al. 1984; Pennycook 1984; for
pathogen description and illustration, see Ellis
1971). Later, when the storage life of the fruits is
coming to an end, more variable symptoms
develop, associated with a number of fungal pathogens including B. cinerea, Fusarium acuminatum
Ellis & Everhart, Cryptosporiopsis spp., and Phomopsis spp. The Botrytis rot of kiwifruit reported from
California (Opgenorth 1983; Sommer et al. 1983)
appears to belong in this category of late-storage
diseases; the symptoms and etiology described for
the Californian disease differ from those of Botrytis
stem-end rot in New Zealand. Botrytis stem-end

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Fig. 3 Scarring of immature

kiwifruits, resulting from dried out
lesions of Sclerotinia sclerotiorum
field rot.

Fig. 4 Sclerotinia sclerotiorum

apothecia protruding above the
ground in a kiwifruit orchard.
Scale is indicated by a ballpoint
pen tip.

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293

Fig. 5 External symptoms of Botrytis cinerea stem-end

rot of cold-stored kiwifruit.

Fig. 6 Internal symptoms of Botrytis cinerea stem-end

rot of cold-stored kiwifruit.

rot first became a problem in New Zealand in 1978

(Beever et al. 1984), when the overall loss to the
industry was estimated as c. 2-3%. Incidence is
unpredictable and highly variable, not only from
year to year and from orchard to orchard, but even
between fruits picked from the same vines on different days. Up to 32% incidence of primary Botrytis stem-end rots has been recorded in New Zealand
kiwifruit (S. R. Pennycook unpublished data), and
an incidence of> 50% has been reported from Italy
(Bisiach et al. 1984; Bisiach & Minervini 1984).

water-soaked, and often has a faint pinkish-fawn

discoloration.
Initially, there is little or no visible fungal growth
on the outside of the rotting fruit. Later, however,
an uneven, fluffy, dull white layer of Botrytis mycelium may develop on the skin of the affected portion of the fruit. This white mycelium usually
resembles the typical 'white mould' of Sc/erotinia
sc/erotiorum. rather than the 'grey mould' usually
associated with Batrytis infections. After prolonged
cold storage, the mycelium may assume a grey,
fuzzy appearance, because of the growth of tufts of
dark conidiophores bearing numerous, powdery,
grey conidia; in other instances, the mycelium may
aggregate to form small, flat, irregularly shaped,
black sclerotia, closely appressed to the fruit surface. External mycelium frequently spreads to adjacent fruits within the tray, ultimately causing
secondary infections ('nesting'). At 1C, Botrytis
lesions on kiwifruit produce only a small amount
of ethylene (an hourly rate of c. 0.2 J-lgjkg fruit),
although they are capable of prolific production (an
hourly rate of up to 135 J-lg/kg) at ambient temperatures (M. J. Muir & S. R. Pennycook unpublished data).

Symptoms

The symptoms of Botrytis stem-end rot first begin

to appear after c. 4 weeks of cold storage. A conspicuous external darkening commences at the stem
end of the fruit, and advances with a straight,
sharply defined front (Fig. 5). The affected area
retains the normal shape of the fruit, and feels soft
but resilient. The unaffected area remains firm and
does not differ from healthy fruits. The rot advances
more or less evenly through all the internal tissues
of the fruit (Fig. 6); after several weeks it may have
spread throughout the fruit, but often the distal end
remains unaffected. The affected flesh is glassy and

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1984 and unpublished data). Symptoms first begin

to appear after c. 4 weeks of cold storage. After c.
12 weeks, the remaining healthy fruits are unlikely
to develop primary Botrytis stem-end rots during
continued cold storage, although secondary infections (nesting) may continue to develop.
The low concentrations of ethylene produced by
Botrytis rots during cold storage may reduce the
storage life of healthy fruits within the same tray.
Such fruits also tend to have a reduced post-storage
shelf-life and a more rapid onset of ripe rots (see
below) compared with similar fruits from trays
unaffected by Botrytis storage rots.

Fig. 7 Sporulation (arrowed) of Botrytis cinerea on

senescent petal of a kiwifruit blossom at fruit set.

Etiology
Botrytis cinerea often becomes conspicuous in
kiwifruit orchards during late blossom and petal
fall (late November-December). On unsprayed
vines, profuse sporulation may be visible on 8090% of blossoms that have senescing petals (Fig.
7). During wet weather, leaf lesions may develop
from secondary spread via adhering debris from
infected blossoms (Fig. 8). It was initially assumed
(by analogy with the etiology of Botrytis fruit rot
in strawberry) that Botrytis stem-end rots in kiwifruit were the result of latent infections established
on the fruits during the blossom period (Beever
1979). Subsequent experimental data (Pennycook
1984 and unpublished data) have indicated that this
assumption was incorrect, and that kiwifruit blossom infections have only an indirect influence on
stem-end rots by increasing the amount of Botrytis
inoculum present in the orchards.
Through the remainder of the growing season
(January-May), Botrytis sporulation is rarely
observed on kiwifruit vines, except on wounded
tissues. However, the fungus can be readily cultured from apparently healthy, undamaged sepals
and fruits; the nature of this Botrytis population is
unclear, but it appears to be predominantly
epiphytic.
Fruit infection occurs during harvesting, grading,
and packing operations, by direct Botrytis contamination of the picking wound that is formed where
the fruit is snapped from its pedicel (Pennycook

Control
Because Botrytis infection occurs via the picking
wound that is created as the fruit is detached from
its pedicel during harvest, orchard fungicide applications cannot directly control the disease. However, they can contribute indirectly, by reducing the
level of Botrytis inoculum present at harvest. The
two critical periods for this purpose are: (a) late
blossom-early petal fall, to prevent the build up of
heavy Botrytis sporulation on senescing petals; and
(b) pre-harvest, to minimise the risk of Botrytis
contamination of the picking wounds during harvesting and post-harvest handling of the fruits. The
dicarboximide fungicides iprodione and vinclozolin are currently recommended for both these
applications. The pre-harvest application should be
a thorough wetting with a high volume, dilute spray,
to achieve maximum fungicide penetration to the
specific target area, the stem end of the fruits,
including the sepals. The residues from the pre-harvest application also prevent the growth of external
mycelium on infected fruits during storage, thus
eliminating nesting and confining losses to those
fruits with primary, picking wound infections.
Incidence of Botrytis stem-end rot in unsprayed
fruits has been significantly decreased by the use
of techniques which reduce the opportunities for
Botrytis contamination of the picking wounds
(Pennycook 1984 and unpublished data). However,
such techniques have not yet been translated into
practical, commercial methods.
Incidence of Botrytis stem-end rot in unsprayed
fruits has also been decreased to a very low level
by experimental applications of dicarboximide
fungicide immediately post-harvest, either specifically to the picking wounds, or as a general fruit
dip (S. R. Pennycook unpublished data). A delay
of 24 h between harvest and fungicide application
significantly reduced the efficacy of such treatments. Bulk methods of post-harvest fungicidal
treatment have not yet been tested, and commercial use of such methods would conflict with the
pesticide regulations of some importing countries.

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Fig. 8 Secondary infection of kiwifruit leaf by Botrytis cinerea growing from adhering, infected blossom debris.

RIPE ROT

Kiwifruits develop ripe rots as they are ripening at

ambient temperatures, either immediately after
harvest or after removal from cold storage. The
presence of ripe rots reduces the crop's shelf-life
directly, by the deterioration of flesh Quality and
the development of unpleasant odours and flavours in affected fruits, and indirectly, by the accelerated ripening of adjacent fruits because of ethylene
evolution. However, it is not clear to what extent
either the onset of the rots is a result of the ripening
process, or the developing rots are themselves a
primary cause of accelerated ripening. Several fungal pathogens have been isolated from various ripe
rot symptoms (Beraha 1970; Sommer & Beraha
1975; Pennycook 1981 a; Hawthorne et al. 1982;
Hawthorne & Reid 1982), but most of these pathogens produce lesions only after the fruits have
already reached an advanced state of ripeness or
become disagreeably overripe. Of more commercial significance is a distinctive type of lesion,
caused by Botryosphaeria doth idea (Mougeot ex
Fries) Cesati & de Notaris (anamorph: Fusicoccum
aesculi Corda), that develops at a relatively early
stage in the ripening process (Pennvcook 1981 b; for

pathogen description and illustrations, see Pennycook & Samuels 1985). In samples of kiwifruits
from the Te Puke district, up to 15% of fruits have
been affected with the distinctive, early symptoms
of B. doth idea ripe rot, while the total incidence of
this fungus (including later developing, more variable symptoms) has been up to 32% (Pennycook
1981 b). B. dothidea ripe rot is also a major disease
affecting kiwifruits grown in Japan (S. Takaya pers.
comm.).
Symptoms

An occasional early symptom of B. dothidea ripe

rot is the development of shallow, brown dimples,
c. 2-5 mm in diameter, on the surface of the fruits;
the skin within each dimple is unbroken, with a
thin layer of dry, yellowish flesh beneath. Some,
but not all, of these dimples develop into expanding rot lesions as the fruits ripen, whereas, in other
instances, identical rot lesions develop without a
preliminary dimple having been observed.
Lesions of B. dothidea ripe rot expand rapidly
into large, pale brown ovals up to c. 30 mm long
with a narrow, glassy, dark green margin (Fig. 9).

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Fig. 9 External symptoms of Botryosphaeria doth idea

ripe rot of kiwifruit.

There is usually only one lesion per fruit, but occasionally up to three may develop simultaneously.
In some years the lesions occur mainly on the side
of the fruits, but in other years mainly at the distal
end, centred on the senescent styles. The lesion surface is soft and squashy; it usually conforms to the
normal outline of the fruit, but is slightly depressed
in some instances; the skin is unbroken. Internally,
the fruit tissues are macerated so that the skin peels
back easily to expose a zonate lesion (Fig. 10) consisting of a narrow, water-soaked, green margin
surrounding a water-soaked, gas-suffused, whitish
oval, often with a small, hard, yellowish, central
core corresponding to the tissues underlying the
dimple symptom (see above). The macerated tissues extend deep into the fruit in a cone or lens
sharply delimited from the unaffected flesh (Fig. II).
Lesions of B. doth idea developing in fully ripeoverripe fruits are smaller and more variable than
the earlier developing lesions. On each fruit there
are usually numerous, sometimes confluent, lesions,
most of which yield fungi other than B. doth idea;
lesions caused by the various pathogens cannot be
distinguished reliably on the basis of their
appearance.

Etiology
Botryosphaeria dothidea is a cosmopolitan fungus
with a wide host range (Punithalingam & Holliday
1973; as B. ribis Grossenbacher & Duggar). In
kiwifruit orchards, the most abundant source of
inoculum is in the numerous dead twigs and
branches in poplar shelterbelt trees. The bark of
these twigs and branches is often riddled with black,
asexual and sexual fructifications (pycnidia and
ascomata) of B. dothidea (Fig. 12). Ascomata and
pycnidia have also been found occasionally in the
bark of kiwifruit prunings that have been left to lie
on the ground in the orchard.
In samples of kiwifruits picked from a block
sheltered by heavily infected poplars, incidence of
B. doth idea ripe rot decreased with increasing distance from the trees (S. R. Pennycook unpublished
data). This distribution pattern suggests that infections are caused by wind-borne ascospores which
are discharged into the air during warm, wet
weather (Sutton 1981). (The conidia, an alternative
potential source of inoculum, are produced in slimy
masses that are distributed over only relatively short
distances by rain splash.) There is no unequivocal
evidence of when the fruits become infected; warm,
wet weather, conducive to ascospore dispersal and
infection, can occur at any period of the growing
season, but some experimental data suggest that
infections become established as early as blossom
or fruit set (see below).
Whenever they may occur, the infections remain
completely latent until the fruits begin to ripen.
Factors which accelerate the ripening process not
only accelerate the onset of ripe rot symptoms but
also appear to increase their severity. However, the
development of ripe rot lesions may itself be a
cause, rather than an effect, of accelerated ripening.
Control
Fungicide applications to shelterbelt trees, and
elimination of kiwifruit prunings (either by removal
or by mulching) could be used to reduce the amount
of inoculum of B. doth idea present in the orchard.
Because the time of infection of the kiwifruits is
unknown, it is difficult to design an effective protectant fungicide programme. In one fungicide trial
in 1981-82, the greatest reduction in incidence of
B. doth idea ripe rot was achieved with a programme that included blossom, petal fall, and preharvest applications of dicarboximide fungicides;
programmes that lacked the blossom applications
gave smaller, but significant, reductions (S. R. Pennycook unpublished data). However, the 1981 survey data reported by Pennycook (198Ib) suggested
that pre-harvest dicarboximide sprays might be the
most effective. All these results may be measuring

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297

Fig. 10 (upper) Surface view

(skin peeled off) of internal symptoms of Botryosphaeria doth idea
ripe rot of kiwifruit.
Fig. 11 (lower) Internal symptoms of Botryosphaeria doth idea
ripe rot of kiwifruit.

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Fig. 12 (far right) Numerous

black pycnidia and ascomata of
Botryosphaeria dothidea developing beneath the bark of a dead
twig in a poplar shelterbelt tree.

indirect effects. For example, a fungicide programme which reduces the incidence of Botrytis
stem-end rot will thus decrease ethylene production during cold storage (see above), resulting in a
longer storage life and post-storage shelf-life for the

crop; the slower ripening of such fruits win delay

the development of ripe rot symptoms, resulting in
an apparent decrease in ripe rot incidence. Trays
repacked after removal of Botrytis-infected fruits
are probably at greatest risk of developing ripe rots

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in the market place, together with late-picked crops,

and trays that include some damaged fruits or fruits
of more advanced maturity at picking. Consequently, the best method of avoiding the potential
economic damage from B. doth idea infections may
be a combination of effective control of Botrytis
storage rot, scrupulous quality control during grading and packing to improve the general storage
quality of the crop, and careful handling throughout the distribution chain to ensure that ripening
is not accelerated at too early a stage.

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Bailey, F. L. 1950: The culture of Chinese gooseberry
vines. New Zealand journal of agriculture 80:
223-231.
- - - - 1961: Chinese gooseberries: their culture and
uses. New Zealand Department of Agriculture. bulletin 349 (revised). 24 p.
Bailey, F. L.; Topping, E. 1951: Chinese gooseberries: their
culture and uses. New Zealand Department of
Agriculture. bulletin 349. 23 p.
Beever, D. J. 1979: Botrytis storage rot of kiwifruit. In:
Proceedings of kiwifruit seminar held at Tauranga,
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Beever, D. J.; McGrath, H. J. W.; Clarke, D. L.; Todd,
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