Pseudomonas syringae pv.

actinidiae in New Zealand

preliminary conclusions

Summary
The virulent strain Pseudomonas syringae pv. actinidiae (Psa-v) is present in New Zealand
and cannot be eradicated. It causes very serious losses in Italy but has not yet caused the same
damage in New Zealand. This difference in disease severity is almost certainly due to differences in
climate between European and New Zealand growing regions. The Italian experience therefore
gives only general guidance as to the behaviour of the pathogen in New Zealand.
Pruning to remove dead wood is a standard hygiene practice. However, pruning is not a
control measure for bacteria. ‘Aggressive containment’, very heavy pruning to remove all kiwifruit
leaves, canes and vines, leaving the stumps of trunks in affected blocks and orchards, will almost
certainly be counter-productive. Repeated re-infection from vines expressing low-level infections
makes local containment impossible.
Copper sprays are too toxic for application in the growing season and are unlikely to be
efficacious. Intense copper cover over leaf fall may reduce cane infection in autumn, reducing
disease development in spring and improving fruit yields.
This pathogen will cause unwanted losses in kiwifruit, but its severity will only be accurately
known after detailed surveys are conducted over several seasons.
Introduction
The Italian strain of P.s. actinidae has been studied for 3–4 years in Italy and for half a year in
NZ. This is an extremely small research and observational base. Nevertheless, there is enough
information in the literature, from past general experience, and in local observations, to draw
preliminary conclusions.
At present, the virulent strain of P.s. actinidiae (Psa-v) is localized to an area near Te Puke. It
cannot be eradicated from New Zealand but its spread can be slowed by restricting the movement of
kiwifruit material from regions where the disease is found.
Some studies must wait until the pathogen/disease is stably established and its distribution
determined accurately so that the conditions that favour the pathogen and host can be established.
P.s. actinidiae strains
Three populations of the pathogen have been reported. The first was recorded in Japan and in
Italy more than 30 years ago. This pathogen caused sporadic losses but formed the basis of the
pathovar name and preliminary epidemiological findings. Subsequently, a second population that
causes a more serious form of the disease has been recorded in gold kiwifruit in Italy since 2008
and in New Zealand in November 2010. These two populations are genetically very similar and are
considered to be members of the same ‘haplotype’. These virulent and weakly virulent populations
are now referred to as Psa-v and Psa-lv, respectively. The third population has only been identified
in New Zealand so far (Chapman et al., 2011). This is a distinct genetic haplotype of the pathogen
but it is weakly virulent. Differentiating these populations by name is cumbersome, but the most
accurate terminology, until further studies clarify matters, is to recognise the pathovar, P. syringae
pv. actinidiae haplotype 1, which includes Psa-v and Psa-lv, as well as haplotype 2 (Psa-lv). In the
following note, only haplotype 1 Psa-v will be discussed here.
Kiwifruit cultivars
Observations in Italy show that gold kiwifruit cultivars (Actinidia chinensis) are more
susceptible than ‘Hayward’ (A. deliciosa). A significant difference between the two species may be
their susceptibility to frost. A. chinensis has a shorter period of winter hibernation and can therefore
be expected to suffer tissue injury in the longer periods of winter cold.
Differences in the behaviour of Psa-v in Italy and New Zealand
Unfortunately, practically all literature on Psa concerns the behaviour of Psa-lv in Japan and
Psa-v in Italy. Growing conditions in New Zealand are very different from those in the Northern
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Hemisphere growing regions and this literature does not accurately describe the behaviour of the
pathogen here.
In Italy, cankers in trunks and leaders are the most serious symptom because they girdle
whole limbs and can kill entire vines. The probable main cause of this serious condition is the
severe winter cold that occurs in Italy’s Mediterranean climate. This winter symptom also occurs in
‘Hayward’ in Japan where it is caused by haplotype 1 Psa-lv. These cankers usually die out in
spring-summer when temperatures rise above 200C. Die-back and lesion development in vegetative
and fruiting canes occurs in spring.
In New Zealand, cankers in trunks and leaders are rare. There are occasional cankers in
leaders but they seem to be so undeveloped that they very rarely girdle vines. Losses here are
primarily due to infections of vegetative and fruiting canes. These develop in spring and summer.
Symptoms in canes could be the result of leaf scar infections that occur in autumn. The
pathogen probably rests during winter, becoming active in spring, and spreading in first and second
year canes. Infected canes lead to girdling and wilting of flowering shoots.
Spread of the pathogen is mainly through the tissue underlying the bark (the parenchyma) but
outside the circulatory cylinder (the cortex). The pathogen may invade the cortex of young canes,
blocking the flow of xylem sap to outer stems and canes and cause wilting. However, there is little
if any evidence that movement in xylem is a pathway for long distance migration of the pathogen
from leaves to canes. Careful dissection and isolation will be necessary to clarify the matter further.
Leaf spots are the most common and easily observed symptom. Their role seems to be only of
creating inoculum that is dispersed by rain.
Epidemiology
The occurrence and severity of epidemics is primarily determined by seasonal weather. It is
only when climatic conditions particularly favour the pathogen, sometimes after several years of
relative quiescence, that an epidemic causing significant regional losses may occur. Such outbreaks
do not inevitably presage future epidemics. The micro-climate in orchards is critical in determining
the local severity and extent of disease. This means that, while it may be possible to determine the
extent to which an area is at risk, more detailed predictions of local infection are impossible.
Weather conditions that favour infection are sporadic, occur at times when vines are
susceptible, and are closely associated with rainy, wet, humid, conditions. Once vines are infected,
disease development is largely determined by temperature.
In this first season, canker development in leaders has been rare. Psa is limited mainly to leaf
infection and to the infection of first and second year canes. However, these infections are confined
to relatively small localized pockets, representing a small proportion of blocks. Leaf-spots in
summer are usually trivial but they are probably the main source of next season’s inoculum; the
pathogen being carried over autumn in and on leaves to leaf scars at leaf-fall. Leaves appear to
remain infected into autumn. Infections of leaf scars appear to remain dormant until early spring
when the pathogen becomes active and infects new season’s growth. It would be very unusual for
cane infections to be carried over into the next season.
The preliminary results of Max & Max (2011) indicate an association between leaf spots and
cicada feeding injury. They suggest that feeding wounds are sites of infection of Psa, the pathogen
migrating from wounds into leaves and causing leaf spots. If this were the case then visible
infection of the leaf veins would be expected. This association is interesting but there is no evidence
that cicada nest wounds penetrate to the cortex. Careful dissection and isolation will be necessary to
clarify the matter further.
The symptoms expressed this season should not be expected to cause major losses and it will
only be after detailed surveys are made over several seasons that the significance of the disease will
be known. Growers with infected orchards can make a very tentative estimate of loss by comparing
the quantity and quality of yields this season with those of past seasons.

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Dispersal
The pathogen is largely spread within orchards and locally as aerosols raised by wind-driven rain.
Other pathogens have been reported to be carried hundreds of metres in rain and this is the case for
Psa. If the disease is visible in a block, then it is practically certain that every vine is contaminated
by the pathogen and that it is present in all adjacent apparently healthy blocks and orchards.
Spread in orchards on implements can occur, but it will be secondary in importance to natural
spread. Courtesy requires that orchardists observe sensible hygienic measures moving equipment
between orchards.
Other kiwifruit pathogens in NZ
Three other pathogens of kiwifruit have probably been present in New Zealand since the
introduction of kiwifruit and before. These are P. syringae pv. syringae, P. viridiflava and
Pseudomonas sp. (causes bacterial bud rot). They cause leaf spots similar to P.s. actinidiae. None of
these cause significant damage but their leaf symptoms can be indistinguishable from those of Psa.
Diagnosis based on leaf symptoms alone is unreliable.
Climate
Serious outbreaks occur under precisely prescribed conditions, usually occurring regionally or
sub-regionally. The national climate is so variable between regions that it is unlikely a pathogen
would cause nationwide epidemics. Southern growing regions are likely to be at greater risk.
Several important questions about the behaviour of Psa should be framed in terms of NZ’s seasonal
conditions compared with those in Italian regions. A study of historical daily temperatures and
rainfall may indicate to what extent conditions mimic those of Italy and Japan and hence likely
regional severity. Only when the pathogen is distributed more widely, in a wider climatic range,
will it be possible to establish the best areas for future planting and those to avoid.
Management and Control
Any proposed control protocol must be cost-effective; the return in crop yield from the
treatment must exceed labour and material costs. It is only by crop surveys that the regional severity
of a disease and the success of a control measure can be described accurately.
Pruning
Pruning was introduced to control fungal diseases in the 19thC when it was realized that spore
production occurred mainly after plant tissue was killed. Spore production and dispersal in this way
was a main source of further fungal infection. This practice has since been recommended for
bacterial control and for Psa in particular:
1. To prevent further spread in canes
The pathogen moves rapidly in canes. The Italian advice is to cut 70 cm beyond visible
infection. This assumes that further advance of the disease will be greater than this. If such pruning
entails the removal of extensive healthy canes with flowers and fruits, then consideration should be
given to waiting to see the infection outcome.
2. To remove inoculum in infected vines to reduce future infection in subsequent years.
Compared with inoculum still present in living plants, infected prunings are only likely to be a
secondary source. Pruning should be part of normal orchard practice. Disposal by mulching,
fertilizing, wetting prunings and covering them for a few months should be adequate.
3. To prevent further spread of disease in blocks and orchards (aggressive pruning; the removal of
all leaders, canes and leaves, shortening the vine to leader and trunk stumps).
Apparently, the present aggressive pruning programme is based on the assumption that Psa is
a systemic pathogen, moving in the circulatory system of the vine from infected leaves into canes
and leaders and that the removal of infected leaves will reduce the severity of the disease. There is
little evidence for this.

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 In blocks that are pruned back to the stumps of leaders and trunks, disease will inevitably
reappear with any new growth, arising from inoculum in the block itself or from adjacent blocks.
Aggressive pruning appears to arise from a confusion between eradication and management.
Recovery of vines that have been aggressively pruned in this way may be doubly difficult because
the gross imbalance between roots and shoots means that sprouts and grafted scions, the most
susceptible of all young tissue, are now are confronted with a virulent pathogen. Unless a leader is
clearly girdled it is inadvisable to remove a canker - the leader may regenerate.
Pruning wounds are sites for infection that may be reduced if pruning can be done in dry
weather.
There have been many attempts to control bacterial pathogens by pruning. There have been
few, if any, claims of success. Pruning is for general hygiene, not for bacterial control.
Comprehensive trials should be conducted to determine the most effective pruning protocols.
Spray control
Once disease is visible in leaves in an orchard, it cannot be reached by sprays and will already
be widespread in adjacent blocks and orchards. There is little efficacy in spraying after rain.
Because very low levels of infection will have spread much more widely without detection, it is
impossible to prevent further spread. Copper sprays, even at low concentrations, are too toxic for
continuous cover over the growing season and will stunt leaf growth, causing seriously reduced
yields. However, copper sprays may be a cost effective preventive measure if applied only at leaf-
fall.
If leaf scars represent the main sites for winter carry-over, as seems possible, there may be a
brief seasonal window in autumn, in which a cost-effective copper programme might be effective
for economic control. A small number of high concentration copper sprays, applied over leaf-fall
may significantly reduce leaf scar infection and hence disease development in canes in spring.
Formal trials are essential.
Literature
Chapman J, Taylor R, Alexander B. Second report on characterization of Pseudomonas
syringae pv. actinidiae (Psa) isolates in New Zealand. Report of the Ministry of Agriculture and
Fisheries. March, 2011 10 pp.
Max S, Max W, 2011. Cicadas – a major threat for Psa spread? NZ Kiwifruit Journal May–
June, 15–19.

John M. Young
Mt Albert
Auckland 1025

18 May 2011

youngj@clear.net.nz

John Young was recruited into Plant Diseases Division, DSIR, in 1967, qualified PhD from
Aberdeen University in 1972, and transferred to Landcare Research in 1992, retiring in 2006. For
his entire career, he studied the epidemiology, management, control, and identification of plant
pathogenic bacteria, principally the pathovars of P. syringae of significance to horticultural and
arable crops. For seven years, he studied other bacterial pathogens of kiwifruit.