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New Zealand Journal of Experimental Agriculture

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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

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2/12

New Zealand Journal o Experimental Agriculture 1985,

Vol

13:

289-299 289

0301-5521/85/1304-0289 2.50/0 Crown copyright 1985

Review

Fungal fruit rots o

ctinidia deliciosa

(kiwifruit)

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-stor

age ripening.

Keywords plant diseases; fruit rots; post-har

vest 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 prob

lems have become more numerous and important

(Sale 1980). However, in comprehensive publica

tions dealing with the crop, information on kiwi

fruit 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, Depart

ment 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 Scler-

otinia 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 epi

demic in late January 1980 yielded 80%

S. sclero-

tiorum

and

20%

B

cinerea

(D. J. Beever

unpublished data). The presence of Botrytis in these

esions may have resulted from secondary infec

tion, possibly after the fruits had fallen to the

ground; over several years, I have isolated no fun

gus 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 depend

ent 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 Decem

ber. Blossoms and their pedicels tum pale brown

and wither. The symptoms are common on male

vines, and entire clusters of male blossoms degen

erate into a tangled mass (Fig. I); female buds and

blossoms are less frequently affected. Bud symp

toms could be confused with those

of

bacterial bud

rot (Young 1984), from which they differ in two

conspicuous ways: the characteristic bacterial slim

ing and darkening of the anthers is absent, and the


3/12

290

New Zealand Journal of Experimental Agriculture, 1985, Vol. 13

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 com

mon 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 scler

otia 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 t which either infected buds or

blossom debris (particularly senescing stamens nd

petals) are in contact with the fruit surface, or adja

cent 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,

Fig. 1 clerotinia sclerotiorum

blight

of

male kiwifruit blossoms.

Shoot lesions are arrowed.

lesions may dry out leaving the fruits badly scarred

Fig.

3) but otherwise unimpaired.

Etiology

clerotinia sclerotiorum

overwinters in kiwifruit

orchards as sclerotia in the soil. Some of the scler

otia will have developed on diseased kiwifruit blos

soms 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 ger

minate 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 trum

pet-shaped, off-white to fawnish-brown disc, usu

ally 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,

nd

December. Apothecial production usually termi

nates in mid summer as the soil dries out or as the

supply of overwintered sclerotia is depleted. How

ever, in some years nd in some

10ca1ities,

apothe

cial production may continue throughout the

summer.

There is frequent spore dispersal from the apoth

ecia. Changes in atmospheric humidity

or

pressure


4/12

Pennycook Fungal

fruit rots

of

kiwifruit

Fig. 2

Sclerotinia sclerotiorum field

rot

of

immature

kiwifruit. Sclerotium left) and adhering anthers right) are

arrowed.

trigger 'puffing', the simultaneous discharge of

thousands ofascospores from the upper, fertile sur

face 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 con

tact with an adequate food base

e

.g., senescing sta

mens and petals,

or

water droplets containing pollen

grains

or

pollen exudates) for saprophytic growth,

and

if

those infection sites subsequently remain wet

291

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 sta

mens

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.

scler-

otiorum

if their application is timed to coincide with

the deposition

of

ascospore showers. In some

seasons, a single, thorough application at late blos

som-early petal fall to prevent saprophytic colon

isation 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.

scler-

otiorum

in susceptible field crops (Hartill Camp

bell

1973;

KrUger 1973; Trutmann et al.

1980).

However, their efficacy has not been demonstrated

in kiwifruit orchards.

STORAGE R T

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 uni

form stem-end rots caused by the grey mould fun

gus,

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 path

ogens including

B. cinerea, Fusarium cumin tum

Ellis Everhart,

Cryptosporiopsis

spp., and

Phom-

opsis

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


5/12

292 New Zealand Journal o Experimental Agriculture 1985 Vol. 3

Fig. 3 Scarring

o

immature

kiwifruits resulting from dried out

lesions o


field rot.

Fig. 4


apothecia protruding above the

ground

in

a kiwifruit orchard.

Scale

is

indicated by a ballpoint

pen tip.


6/12

Pennycook-Fungal fruit rots

of

kiwifruit

Fig. 5 External 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 dif

ferent days.

Up

to

32

incidence

of

primary

Botry-

tis

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).

Symptoms

The symptoms

of

Botrytis

stem-end rot first begin

to appear after

c.

4 weeks

of

cold storage. A con

spicuous 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

293

Fig. 6 Internal symptoms of Botrytis cinerea stem-end

rot

of

cold-stored kiwifruit.

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 myce

lium may develop on the skin

of

the affected por

tion

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 sur

face

. External mycelium frequently spreads to adja

cent 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 tem

peratures

(M. J.

Muir &

S.

R. Pennycook unpub

lished data).


7/12

294

New Zealand Journal

of

Experimental Agriculture, 1985 , Vol. 13

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 80

90

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). t was initially assumed

by analogy with the etiology

of

Botrytis fruit rot

in strawberry) that Botrytis stem-end rots in kiwi

fruit 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 blos

som 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 cul

tured 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 contam

ination

of

the picking wound that is formed where

the fruit

is

snapped from its pedicel Pennycook

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 infec

tions 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.

Control

Because Botrytis infection occurs via the picking

wound that is created as the fruit is detached from

its pedicel during harvest, orchard fungicide appli

cations cannot directly control the disease. How

ever, 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 har

vesting and post-harvest handling

of

the fruits. The

dicarboximide fungicides iprodione and vinclozo

lin 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-har

vest 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 specifi

cally 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 treat

ments. Bulk methods

of

post-harvest fungicidal

treatment have not yet been tested, and commer

cial use

of

such methods would conflict with the

pesticide regulations of some importing countries.


8/12

Pennycook Fungal fruit rots of kiwifruit

295

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

RIP 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 fla-

vours in affected fruits, and indirectly, by the accel

erated ripening ofadjacent 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 fun

gal 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 path

ogens produce lesions only after the fruits have

already reached an advanced state of ripeness or

become disagreeably overripe.

Of

more commer

cial significance is a distinctive type of lesion,

caused by

otryosphaeria doth idea

(Mougeot ex

Fries) Cesati & de Notaris (anamorph:

Fusicoccum

aesculi

Corda), that develops at a relatively early

stage in the ripening process (Pennvcook 1981b; for

pathogen description and illustrations, see Penny

cook 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 var

iable 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 expand

ing 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).


9/12

296

New Zealand Journal

of

Experimental Agriculture,

1985,

Vol.

13

Fig. 9 External symptoms of Botryosphaeria doth idea

ripe rot of kiwifruit.

There

is

usually only one lesion per fruit, but occa

sionally 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 sur

face

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)

con

sisting

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 tis

sues 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 ripe

overripe 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 dis

tance from the trees S.

R

Pennycook unpublished

data). This distribution pattern suggests that infec

tions 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 n 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 t 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 pro

tectant fungicide programme. In one fungicide trial

in 1981-82, the greatest reduction in incidence of

B doth idea

ripe rot was achieved with a pro

gramme that included blossom, petal

fall,

and pre

harvest applications of dicarboximide fungicides;

programmes that lacked the blossom applications

gave smaller, but significant, reductions S. R. Pen

nycook unpublished data). However, the

1981

sur

vey data reported by Pennycook (198Ib) suggested

that pre-harvest dicarboximide sprays might be the

most effective. All these results may be measuring


10/12

Pennycook-Fungal fruit rots o kiwifruit

Fig. 1 upper) Surface view

skin peeled off o internal symp

toms

o

Botryosphaeria doth idea

ripe rot o kiwifruit.

Fig. lower) Internal symp

toms

o


ripe rot

o

kiwifruit.

Fig. 2 far right) Numerous

black pycnidia and ascomata o

Botryosphaeria dothidea develop

ing beneath the bark o a dead

twig in a poplar shelterbelt tree.

indirect effects. For example, a fungicide pro

gramme which reduces the incidence

o

Botrytis

stem-end rot will thus decrease ethylene produc

tion during cold storage see above), resulting in a

longer storage life and post-storage shelf-life for the

297

crop; the slower ripening o such fruits win delay

the development

o

ripe rot symptoms, resulting in

an apparent decrease in ripe rot incidence. Trays

repacked after removal

o

Botrytis-infected fruits

are probably at greatest risk

o

developing ripe rots


11/12

298

New Zealand Journal of Experimental Agriculture, 1985, Vol. 13

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

and trays that include some damaged fruits or fruits

of

more advanced maturity at picking. Conse

quently, 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 grad

ing and packing to improve the general storage

quality of the crop, and careful handling through

out the distribution chain to ensure that ripening

is not accelerated at too early a stage.

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