Landcare Research, Private Bag 92170, Auckland, New Zealand; email: [email protected]
Abstract. Olive knot, caused by a pathogen or pathogens within the group of bacterial pathogens currently knownas Pseudomonas savastanoi, is described. The ecology, transmission and methods of control of the pathogens arediscussed. Strategies to minimise the effects of infection are recommended and these depend on attention to specificdetails in programs for pruning, irrigation and use of fertiliser. Introduction of the pathogens into previously oliveknot-free countries is most likely to occur through the importation of infected nursery stock. There is nocost-effective way to control knot in olive groves by using currently available bactericidal sprays. The use of knowndisease-resistant cultivars and future breeding programs to improve resistance will lead to effective control in thelong term. The distribution of the pathogen in Australasia is re-examined in the light of recent investigations of hostspecificity.AP03074Oli ve knotJ. M . Young
The first surviving record of the olive knot disease was inthe 4th century B.C. by the Greek, Theophrastus (Iacobellis2001). The pathogen appears to have been disseminated witholive (Olea europaea subsp. europaea) plants as they havebeen spread to, and propagated in, many regions in the world(Bradbury 1986).
In Australia, the oleander knot disease has been recordedin the eastern Australian states of New South Wales (Nobleet al. 1935), Tasmania (Sampson and Walker 1982) andVictoria (Adam and Pugsley 1934). In South Australia,Pseudomonas syringae is recorded as causing bacterialcanker on olive (Warcup and Talbot 1981). Moffett (1983),without giving primary references, recorded the pathogen onoleander in New South Wales, South Australia, Tasmania,Western Australia and Victoria. Recent surveys of olivegroves in New South Wales have failed to reveal indicationsof olive knot (L. Tesoriero, personal communication). At thetime of writing, there is no public record of olive knot inAustralia.
For more than a century, olive trees have been grown inNew Zealand, almost entirely as specimen ornamentals, withonly amateur production of pickled/preserved fruit.Commercial olive groves for oil and fruit have been a recentinitiative. Some years ago, the oleander knot pathogen,P. savastanoi (oleander strain) that may also attack olive, wasrecorded in New Zealand (Dye 1956). The olive knotpathogen, P. savastanoi (olive strain), was recently detected
in plants introduced through quarantine in 1997 (Braithwaiteet al. 1999). Although this source of the pathogen may havebeen successfully eradicated by the removal and destructionof all infected trees, olive knot has been reported in NorthIsland growing regions and may be evidence for earlierintroductions of the olive strain. At the time of writing (June2003) the pathogen has not been reported in the maingrowing areas of the South Island.
The pathogen
Until recently, a pathogen called P. syringae pv. savastanoiwas recognised as causing knot diseases, and it was thoughtthat this one pathogen was responsible for the condition inolive, oleander, ash and other hosts. Based on laboratory testsand comprehensive DNA–DNA re-association studies,Gardan et al. (1992) proposed that the pathogen bereclassified in the species P. savastanoi, as P. savastanoi pv.savastanoi. Based on field observations, laboratory studiesand pathogenicity tests, it has subsequently been proposedthat three closely related pathogens represented in the speciesP. savastanoi can be separately recognised – Pseudomonassavastanoi pv. fraxini (Janse 1982) Young et al. 1986,pathogenic to Fraxinus spp.; Pseudomonas savastanoi pv.nerii (Janse 1982) Young et al. 1996, pathogenic to oleanderand perhaps to olive; Pseudomonas savastanoi pv. savastanoi(ex Smith 1908) Gardan et al. 1992, pathogenic to olive. Inpathogenicity tests, the olive knot pathogen was specific toolive, whereas the oleander knot pathogen attacked oleander
34 Australasian Plant Pathology J. M. Young
and perhaps susceptible cultivars of olive. The olive knotpathogen appeared to be more virulent to olive than theoleander knot pathogen (unpublished data), but thisobservation has not been supported elsewhere (Iacobellis,personal communication). However, isolations of thepathogens in the field showed that olive strains only areisolated from olive, and oleander strains are isolated onlyfrom oleander (Caponero et al. 1995; Surico, personalcommunication), suggesting that each strain is specific to itsrespective host in nature. As yet, it has not been establishedif the oleander pathogen is specific to oleander in nature, orif it is also pathogenic to olive. In this text, the nameP. savastanoi (olive strain) is applied to the pathogen specificto olive, and the name P. savastanoi (oleander strain) is usedfor the pathogen, which primarily attacks oleander in the field,but may also be pathogenic to olive.
The knot-forming strains of P. savastanoi are similar toother members of this species and the closely related speciesP. syringae, in that they are specific in causing disease in asmall range of host genera. However, the knot-formingpathogens differ from almost all other bacterial plantpathogens in that they produce substantial quantities of planthormones (auxin and cytokinins). The effect of thesehormones is to induce unregulated cell multiplicationleading to galls or knots (Surico et al. 1985).
Mechanisms regulating host specificity are not fullyunderstood in any plant pathogens, although it seems thatthose for the olive knot pathogens are likely to be similar toother plant pathogenic pseudomonads. These entail avr/AVRand hrp gene interactions (Gabriel 1999; Keen 1996).
Common names of the disease
Common names in use are olive knot, olive gall andoleander knot.
Host range
The olive strains of P. savastanoi are pathogenic to somecultivated olives (Olea europaea subsp. europaea) and wildolives (Olea europaea subsp. oleaster, Olea europaea subsp.sativa). Oleander strains are pathogenic to oleander (Neriumoleander) and perhaps to some cultivated and wild olivecultivars (Bradbury 1986).
Geographic distribution of olive knot pathogens
The record below is based largely on the observation ofknot diseases (Bradbury 1986; CMI distribution maps ofplant diseases 1987). However, an unknown proportion ofrecords are applied to the pathogen on oleander because itwas assumed that the olive and oleander pathogens were thesame.
Europe: Austria, Cyprus, France, Germany, Greece, Italy,Netherlands, Norway, Portugal, Commonwealth ofIndependent States (Russian Federation), Spain, Sweden,Switzerland, United Kingdom, Former Yugoslavia.
Tunisia.North America: Mexico, USA (Arizona, Arkansas,
California, Texas).South America: Argentina, Brazil, Colombia, Peru,
Uruguay.Australasia: Australia (New South Wales, South
Australia, Tasmania, Victoria (all recorded on oleander),New Zealand (recorded on olive).
Symptoms and damage to olive
P. savastanoi characteristically produces raised ‘knots’ orgalls on branches of olive. Knots are primarily found onstems and branches, and on woody rather than herbaceoustissue (Varvaro and Surico 1978) (see Fig. 1). Although thepathogen has occasionally been isolated from olive roots,leaves and fruits, knots usually begin as small smooth lumpsat nodes or on the bark at internodes. Cutting through theseimmature knots reveals pale, apparently healthy tissuesurrounding a dark core. Knots develop for many months andcan expand to form rough-surfaced galls more than 2.5 cm indiameter (Iacobellis 2001). The main damage results whenknots occur early in tree development causing weaknesses bypartially girdling branches that may subsequently beintended to form the structure of mature trees. Severedamage to upper stems can lead to reduced fruit fill and totalyield (Schroth et al. 1973) and infection of fruiting branches,even in trees not considered to be severely infected. This isreported to cause ‘off’ tastes in fruit (Schroth et al. 1968).Fruit infection, as roughly circular brown spots 0.5–2.5 mmin diameter, is another form of the disease, though rare, thatdevelops during wet summers (Panagopoulos 1993).
Field inspection methods
Olive knot is relatively easily recognised when symptomsare well developed (see ‘Symptoms’ and Figures). In theirearly stages, knots can be confused with insect puncture(feeding or egg-laying) wounds. Usually, when the small,smooth, raised lumps that indicate incipient knots are firstdetected, more detailed searches will reveal clearlydeveloped knot symptoms.
Diagnosis of olive knot and identification of P. savastanoi
Isolation of pathogenic bacteria
Experience in this laboratory has indicated that isolationscould most easily be made from knots in their early stages,up to the first appearance of rough, exposed, unregulatedtissue. Older knots generally became invaded byfaster-growing secondary bacteria that made recognition ofthe pathogen more difficult. A selective medium (Ercolani1970) may be of value in these cases. Small sectors of theinterior knot tissue were excised from the outer edges,
Olive knot Australasian Plant Pathology 35
(a )
(c ) (d )
(b )
Fig. 1. (a) Natural infection of olive cv. Leccino (called Minerva); New Zealand showing knots at nodes and internodes.(b) Natural infection of olive (cv. unknown); France). (c) Knot development from wounds in stem (unknown cultivar); NewZealand. (d) Olive cv. Picholine showing knot development 10 months after inoculation with olive knot strain.
36 Australasian Plant Pathology J. M. Young
crushed in water to release the bacteria, and the suspensionspread on a surface-dry, solid medium such as King’smedium B (King et al. 1954) that both favoured bacterialgrowth and gave distinctive colony types. Characteristiccolonies of the small, slow-growing pathogen could bedifferentiated after incubation at 27°C for 2–3 days.Production of fluorescent pigments by colonies when viewedunder UV light is not reliable as a diagnostic observation(Panagopoulos 1993; unpublished data). Reference strains ofthe pathogen were necessary for comparison until familiarityallowed colonies to be recognised directly.
Confirmation of pathogenicity
Simple confirmation of pathogenicity is achieved byinoculating heavy suspensions of bacteria into the stems ofactively growing plants of susceptible olive and oleanderplants kept under controlled conditions in a glasshouse for aminimum of 42 days. The olive strains will cause knots insusceptible olive plants only. Oleander strains will causeknots in oleander and in some cultivars of olive. There is noreliable method of distinguishing between the olive andoleander knot pathogens from symptoms in olive.Pathogenicity tests are best done between spring andmidsummer and in autumn, when plants are most activelygrowing, but they can be done at all times of the year.
Identification of the pathogens
The olive and oleander knot pathogens can be identified(as P. savastanoi) using fingerprinting methods such asBiolog or determinative tests (Young and Triggs 1994) inaddition to pathogenicity tests. Janse (1991) showed that theknot-forming pathogens of Fraxinus (Pseudomonassavastanoi pv. fraxini) could be differentiated from the oliveand oleander strains of Pseudomonas savastanoi bydifferences in fatty acid composition. However, the fatty acidcomposition of the latter two pathogens was generally toosimilar for differentiation between them using this criterion.Differentiation of olive and oleander strains may be possibleusing molecular methods such as DNA restrictionfingerprinting (Mugnai et al. 1994). Other molecularmethods are in development (A. Sisto, personalcommunication; J. M. Young, unpublished data).
Biology and ecology
Variability in the pathogen
There is considerable variability in the response of plantsto different cultures of the pathogen (unpublished data).Some bacteria produce almost no reaction in inoculatedplants whereas others rapidly produce galls at the sites ofinoculation. So far there is no evidence that different levelsof aggressiveness are found in cultures from differentregions. Considerable variation in the severity of disease canoccur between localities (Osman et al. 1980a).
Influence of climate
High temperatures and high rainfall increase the effect ofbacterial pathogens in general. Olive knot appears to be mostsevere in spring and autumn (Krueger et al. 1999; Surico1977). This may be due to climatic influence but it may alsobe connected with the physiological state of trees at thosetimes.
Influence of crop management
Modern horticultural practice is to encourage rapid plantdevelopment in order to bring trees into early production andto deliver high yields. High nitrogen fertiliser regimes areparticularly likely to favour bacterial disease development(Baratta and Di Marco 1981; Young 1987). On the basis ofobservations in Sicily, the following (corrected for theSouthern Hemisphere) is recommended. Fertiliserapplications should be made in July–August at 1400–1500kg/ha. Olive blocks should be irrigated once beforeDecember and again ~30 days before harvest, at a total of1000–1200 m3/ha. Light applications of rapid action nitratesat 200–250 g N/plant should be carried out during thepre-harvest irrigation (Baratta and Di Marco 1981).
Survival and transmission
The olive strain of P. savastanoi lives in association witholive plants (Ercolani 1978). Populations of the bacterium donot survive away from infected plants and rapidly decline insoil. Knot induction is most prolific when plants are activelygrowing in spring (Surico 1977), when they are reacting toinduced wounds infected with the pathogen. The bacteriumis found on the leaf surfaces, with populations highest inspring and autumn (Ercolani 1978). The bacterium maysurvive within natural openings of the plant or in sub-clinicalinfections. Rain followed by high humidity favours infection(Teviotdale 1994).
P. savastanoi is present in infected plant material and isusually introduced into new regions in nursery stock. Thepathogen can be carried in aerosols and, therefore, can betransported in wind-driven rain. As a wound-infectingpathogen, P. savastanoi can also be transmitted on orchardequipment such as pruning implements. If olive knot isobserved in trees in an orchard block, it can be assumed thatthe entire block is at risk and that transmission of thepathogen to olive trees within a range of ~500 m willeventually occur in aerosols generated during storms.Removal of visibly diseased trees will not materially affectthis process. Effective control will depend on an informedapproach to disease management based on an understandingof the biology of the pathogen. Low-level populations of thepathogen can reside on leaves and in natural plant openings(Ercolani 1978) without immediately inducing symptoms ofdisease, but the observation of knot symptoms in an orchardis an indication of the presence of copious amounts of
Olive knot Australasian Plant Pathology 37
bacterial inoculum. Once knot symptoms have appeared in ablock it can be assumed that those trees will continue to beaffected by sporadic or prolonged outbreaks of the disease,and diseased trees will provide a source of inoculum that mayspread infection to other blocks. There is no reliable methodof eradication of the pathogen from orchards once it ispresent. P. savastanoi (like most bacterial pathogens) shouldnot be expected to express symptoms every year and shouldnot be expected inevitably to do serious damage; olive knotis likely to occur with varying degrees of intensity indifferent localities and to vary from year to year. Severedisease in one year may be followed by several seasonswithout significant damage. Irregular outbreaks of varyingseverity are characteristic of bacterial diseases.
Infection
Entry into susceptible plants, as evidenced by subsequentdisease development, is largely through wounds at leaf scars(Teviotdale 1994) and those caused by late spring freezingand hail, as well as pruning cuts (Iacobellis 2001; Sisto andIacobellis 1999; Teviotdale 1994), especially when leaf falloccurs or pruning is conducted in rainy weather or moistwinds. In exposed planted blocks, branch thrash in wind andrain is also a likely source of infection. The traditionalmethod of harvesting fruit by beating branches with stickscan lead to severe infections (Panagopoulos 1993).
Economic impact
There are no quantitative data on the impact of the diseaseon crop yield or crop quality (Iacobellis 2001), but extensiveresearch is reported in Italy and Spain. The disease isconsidered to ‘reduce productivity’ (Teviotdale 1994). Directobservation of disease development over several seasons willbe necessary to determine the impact of the pathogen inAustralasia.
Losses can be caused directly by localised infections thatinhibit flowering and affect fruit development and taste, andindirectly by weakening immature main leader branchesresulting in later damage to the tree frame. Because of thediffering climates, soil and topographic conditions in whicholives are grown, the extent of damage in New Zealand islikely to be highly variable from season to season and fromregion to region.
Control
Sanitation and cultural precautions
In countries and regions where the knot pathogen does notoccur, new olive groves should be established usingdisease-free nursery stock from pathogen-free sources. As aprecautionary measure, until the host specificity of olive andoleander strains is fully understood, the removal of nearby(within 500 m) oleander bushes should be considered as ameasure to eliminate possible sources of pathogenic bacteria
that could otherwise pose a threat to the new grove. Arecommended nursery practice (G. Surico, personalcommunication) is to maintain copper sprays on nurseryplants. Bordeaux mixture (copper sulphate, 1 kg; lime, 2 kg;water, 100 L), copper oxychloride (200–300 g/hL; a.i. 50%),or copper hydroxide (200–300 g/hL; a.i. 40%) may beapplied. Initial caution is advised until application is shownnot to cause leaf injury in local conditions.
Some reduction of infection caused by the practice ofharvesting by beating olive branches with sticks(Panagopoulos 1993) may be effected by using stickswrapped with cloth soaked in a copper solution (e.g. Kocide)at frequent intervals, especially when moving between trees.
Pruning
The most important control practices are those concernedwith pruning. As already stated, the pathogen cannot beeradicated from trees or orchards, but thoughtful pruning canminimise its worst effects. Attention to tree development inearly years offers the best approach to managing diseasedamage. Annual pruning should be done no later thanAugust to avoid the period of spring susceptibility. The goalfor pruning of young trees is to leave non-diseased branchesto form the scaffold of the mature tree. Individual assessmentshould form a guide to the removal of specific weakenedbranches. Infected young trees need not be removed unlessthey are so seriously infected that they show little prospect offorming a bearing tree. Pruning before expected rain shouldbe avoided.
The shape of crowns of very old trees damaged by hailand subsequently badly infected by bacterial knot can betransformed from the traditional inverted truncated conetapered to the base, to erect truncated cones tapered from thebase. Positive effects on tree health, growth and productivityhave been reported (Ruffaldi 1972).
Chemical spray control
There have been several reports of trials of the efficacy ofcopper spray compounds (e.g. copper hydroxide). These arenot always successful, and the cost-effective benefit is highlydoubtful (Sisto and Iacobellis 1999). To be effective, spraysmust be applied to maintain continuous bactericidal coverover a substantial part of the year, at the same time avoidingdamage from phytotoxic levels of copper spray. This isdifficult and not necessarily cost-effective.
Biological control
There is no documented proof for biological control ofany bacterial pathogen, such as P. savastanoi, that primarilyaffects the above ground structure of plants.
Cultivar resistance
Sisto and Iacobellis (1999) note the importance ofidentifying resistant cultivars of olive in order to contain the
38 Australasian Plant Pathology J. M. Young
disease and improve both the quantity and quality of fruit andoil yields. No olive cultivars are known that are completelyresistant to olive knot.
There have been few quantitative studies of resistanceoverseas. In Morocco, Gordale was considered to beresistant, Picholine Marocaine exhibited some symptoms,whereas Meslala was considered to be susceptible (Benjamaet al. 1987). An experimental study (Marcelo et al. 1999)indicated that Rendonil and Cobrancosa were relativelyresistant, Branquita and Santulhana expressed somesymptoms, and Cordovil de Serpa and Galga Vulgar weremost susceptible. Comparative studies indicated thatNocellara del Belice was highly susceptible, Leccino wassusceptible and Coratina was tolerant. In Iraq, Hawega-2 washighly resistant, whereas cvv. Ajrasi bazri, Ajrasi andBashiky were highly susceptible (Osman et al. 1980b).
A study of experimental inoculations by Sisto et al.(2001) showed that the cultivars Cellini di Nardo, Frantoio,FS-17, Morcana, Nociara, Ogliarola, and Pendolino weresusceptible, whereas Carolea, Bella di Spagna, Cerasela,Cima di Melfi, Coratina, Corniola, Dolce Agogia,Leucocarpa, Maiatica di Ferrandina, N3, Nolca and SanFelice gave a moderate response to the pathogen. A similarstudy (unpublished data) made here of the relative resistanceof olive cultivars favoured in New Zealand showed that themost susceptible cultivars were Manzanillo, Picholine andS.A. Verdale, and that the least susceptible were Carolea,Koroneiki and Pendolino.
Acknowledgements
The New Zealand Olive’s Association and the NewZealand Foundation for Research, Science and Technology(Contract C09X0201) for providing financial support for thedevelopment of this manuscript; S. R. Pennycook, LandcareResearch, Auckland, and D. R. W. Watson, Plant DiseasesDivision, DISR, Auckland (retired) for critically reading themanuscript and for their helpful suggestions.
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