Pseudomonas savastanoi pv. savastanoi (oleander knot)
- Summary of Invasiveness
- Taxonomic Tree
- Notes on Taxonomy and Nomenclature
- Distribution Table
- Risk of Introduction
- Hosts/Species Affected
- Host Plants and Other Plants Affected
- Growth Stages
- List of Symptoms/Signs
- Biology and Ecology
- Means of Movement and Dispersal
- Plant Trade
- Impact Summary
- Detection and Inspection
- Prevention and Control
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- Pseudomonas savastanoi pv. savastanoi (ex Smith 1908) Gardan et al. 1992
Preferred Common Name
- oleander knot
Other Scientific Names
- Agrobacterium savastanoi (Smith) Starr & Weiss 1943
- Agrobacterium tonellianum (Ferraris) Starr & Weiss 1943
- Bacterium savastanoi E.F. Smith 1908
- Bacterium tonellianum Ferraris 1926
- Phytomonas savastanoi (Smith) Bergey et al. 1923
- Phytomonas tonelliana (Ferraris) Adam & Pugsley 1934
- Pseudomonas oleae (Arcangeli) Duggar 1909
- Pseudomonas savastanoi Smith & Petri 1908
- Pseudomonas syringae pv. savastanoi (Smith 1908) Young et al. 1978
- Pseudomonas syringae subsp. savastanoi (ex Smith 1908) Janse 1982
- Pseudomonas syringae subsp. savastanoi pv. oleae Janse 1981
- Pseudomonas tonelliana (Ferraris) Burkholder 1948
International Common Names
- English: bacterial blight of kiwi; bacterial canker of ash; canker of ash; oleander canker; olive canker; olive gall; olive knot
- Spanish: bacteriosis del laurel-rosado; chancro bacteriano del laurel-rosado; tuberculosis del fresno; tuberculosis del olivo
- French: bactériose de l'olivier; bactériose du laurier-rose; chancre bactérien du laurier-rose; galle du frene
Local Common Names
- Germany: Krebs: Esche; Krebs: Oleander; Krebs: Olive
- Italy: cancro batterico del frassino; rogna dell'oleandro; rogna dell'olivo; tubercolosi dell'olivo
- PSDMSA (Pseudomonas savastanoi pv. savastanoi)
Summary of InvasivenessTop of page Olive knot can become established if diseased plants are introduced to a new area and not promptly eradicated. Bacteria oozing from knots establish on the phylloplane and from there can spread to new areas by wind-driven rain, aerosols, agricultural practices (e.g. pruning or grafting) and perhaps by insect transfer; they can also be transported over indefinitely long distances in infected propagation material. Climates characterized by mild temperatures and a rainy autumn and spring favour the multiplication and dispersal of P. savastanoi pv. savastanoi in olive groves.
Taxonomic TreeTop of page
- Domain: Bacteria
- Phylum: Proteobacteria
- Class: Gammaproteobacteria
- Order: Pseudomonadales
- Family: Pseudomonadaceae
- Genus: Pseudomonas
- Species: Pseudomonas savastanoi pv. savastanoi
Notes on Taxonomy and NomenclatureTop of page The Greek philosopher Theophrastus first described olive knot disease in the 4th century BC. In 1885, G. Arcangeli suspected a bacterial cause for these abnormal growths and this was confirmed by Savastano (1886) who first succeeded in isolating the bacterium and reproducing disease symptoms by artificial inoculation of healthy olive plants. Smith (1908) recognized the priority of Savastano's studies and named the pathogen Bacterium savastanoi in his honour. Stevens (1913) allocated the bacterium to the genus Pseudomonas as P. savastanoi (Smith 1908) Stevens 1913. Subsequently, similar diseases were reported from Fraxinus (ash) (Brown, 1932) and Oleander (Peglion, 1905; Smith, 1928) caused by separate but similar bacteria, named as P. savastanoi var. fraxini (Brown 1932) Dowson 1943 and P. savastanoi var. nerii Smith 1928, respectively. When strains representing these varieties were compared they were not readily distinguishable one from another or from many other named pathogenic species. Furthermore, comparative pathogenicity testing indicated overlap of host range between the varieties. For these reasons, the species name was not included in the Approved Lists (Skerman et al., 1980), the pathogenic strains collectively being included in P. syringae as P. syringae pv. savastanoi.
On the basis of a study of strains from different hosts, Janse (1982b) proposed recognition of three pathovars of P. syringae subsp. savastanoi (ex Smith 1908) Janse 1982. These pathovar names were invalid when proposed (Young et al., 1991) and were only finally validated following the report of Gardan et al. (1992) and the proposal of recognition of the species P. savastanoi (Janse 1982) Gardan et al. 1992. Recognition of different pathogenic host ranges is formalized in the names P. savastanoi pv. savastanoi (Janse, 1982) Young et al. 1996, P. savastanoi pv. nerii (Janse 1982) Young et al. 1996 and P. savastanoi pv. fraxini (Janse, 1982) Young et al. (1996).
The three pathovars have been discriminated; pv. savastanoi causing parenchymatous galls on various species of Oleaceae and other hosts; pv. nerii causing parenchymatous galls or wart-like excrescences on Nerium oleander and various species of Oleaceae; and pv. fraxini causing wart-like excrescences on Fraxinus excelsior and (by inoculation) on Olea europea (Janse, 1981, 1982). The pathogenic differences are supported by the work of Mugnai et al. (1994) and Alvarez et al. (1998).
This pathovar classification formalizes the pathovar nomenclature of Janse (1982) and reflects the pathogenic features and other distinctive characters of strains isolated from the various host plants (Sutic and Dowson, 1963; Janse, 1981; Surico et al., 1985; Iacobellis et al., 1995, 1998). This datasheet includes information on pathovar savastanoi, affecting olive, and pv. nerii, affecting oleander, olive and ash. A separate datasheet on pv. fraxini, which is specific to ash, is available in this Compendium.
DescriptionTop of page P. savastanoi is a Gram-negative, rod-shaped bacterium with a polar flagella for motility. The majority of strains belong to the group Ib of the LOPAT identification scheme (Lelliott and Stead, 1987) but levan positive strains have also been reported (Iacobellis et al., 1993; Surico and Marchi, 2003).
DistributionTop of page The list of countries is based largely on the observation of knot disease (Bradbury 1986; CMI, 1987). However, an unknown proportion of records are applied to the pathogen on oleander because it was assumed that the olive and oleander pathogens were the same.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Algeria||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Egypt||Present||Ahmad et al. (2009)|
|Libya||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Morocco||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|South Africa||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Tanzania||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Tunisia||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Iran||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Iraq||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Israel||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Japan||Present||Tsuji et al. (2015)|
|Jordan||Present||Invasive||Rakan Hijazin and Hamid Khlaif (2005); Tehabsim et al. (1991)|
|Lebanon||Present||Bradbury (1986); UK, CAB International (1987)|
|Nepal||Present||Balestra et al. (2009)|
|Syria||Present||Alabdalla et al. (2009)|
|Turkey||Present||Invasive||Bradbury (1986); UK, CAB International (1987); Bozkurt et al. (2014)|
|Austria||Present, Localized||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Cyprus||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Czechoslovakia||Absent, Intercepted only||Bradbury (1986)|
|Union of Soviet Socialist Republics||Present||UK, CAB International (1987)|
|France||Present, Localized||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Greece||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Italy||Present, Localized||Invasive||Bradbury (1986); UK, CAB International (1987); Cinelli et al. (2013)|
|Netherlands||Present, Localized||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Poland||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Serbia and Montenegro||Present, Localized||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Slovenia||Present||Pirc et al. (2015)|
|Spain||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Sweden||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Switzerland||Present, Localized||Invasive||Bradbury (1986); UK, CAB International (1987)|
|United Kingdom||Present, Widespread||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Mexico||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|United States||Present||Invasive||Bradbury (1986)|
|-Alabama||Present||Conner et al. (2013)|
|-Arizona||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|-Arkansas||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|-California||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|-Texas||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Australia||Present||CABI (Undated)||Present based on regional distribution.|
|-New South Wales||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|-Queensland||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|-South Australia||Present||Invasive||Bradbury (1986); UK, CAB International (1987); Hall et al. (2004)|
|-Victoria||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|New Zealand||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Argentina||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Brazil||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Colombia||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Peru||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
|Uruguay||Present||Invasive||Bradbury (1986); UK, CAB International (1987)|
Risk of IntroductionTop of page P. savastanoi pv. savastanoi is included in the certification procedure of olive in some European countries (Martelli et al., 1995; Bertolini et al., 2003b).
HabitatTop of page Olive knot disease is present in all olive-growing regions. Climates characterized by mild temperatures and a rainy autumn and spring favour multiplication and dispersal of P. savastanoi pv. savastanoi in olive groves.
Oleander knot, caused by P. savastanoi pv. nerii, is widespread.
Hosts/Species AffectedTop of page P. savastanoi has been recorded as causing disease on: cultivated and wild olive (Olea europaea subsp. europaea, O. europaea subsp. oleaster, O. europaea subsp. sativa) (olive knots); Ligustrum spp. such as japanese privet (L. japonica) and privet (L. vulgare); Jasminus spp.; Forsythia intermedia; Phillyrea spp.; among Oleaceae; and oleander (Nerium oleander) (oleander knots) among the Apocynaceae. The pathogen has been reported (Bradbury, 1986) to cause symptoms when artificially inoculated on Achillea ptarmica, Chionanthus virginicus, Cucumis sativus, Datura stramonium, Foresteria acuminata, F. neomexicana, Forsythia suspensa, F. viridissima, Fraxinus velutina and F. angustifolia, F. floribunda, Jasminum primulinum [J. mesnyi], Ligustrum ovalifolium, Lycopersicon esculentum, Olea capensis, O. chrysophylla [O. europaea subsp. cuspidata], O. ferruginea [O. europaea subsp. cuspidata], O. laurifolia [O. capensis], O. verrucosa [O. europaea subsp. cuspidata], Osmanthus spp., O. americanus, O. acquifolium, O. fragrans, O. ilicifolia, Phaseolus vulgaris, Phllyrea decora [Osmanthus decorus] and P. media [P. latifolia var. media].
The record of host plants and geographic distribution of P. savastanoi was made over a long period before pv. savastanoi and pv. nerii were differentiated as separate pathogens and may refer to either pathovar.
Strains isolated from ash, olive and oleander differ in several characters (Iacobellis et al., 1995, 1998) including artificial inoculation on olive, oleander and ash (Sutic and Dowson, 1963; Janse, 1981; Surico et al., 1985; Iacobellis et al., 1998). Only a few strains isolated from olive or privet have been reported to cause overgrowths when artificially inoculated in oleander (Bottalico and Ercolani, 1971; Surico et al., 1984; Iacobellis et al., unpublished results). However, isolations of pathogens in the field have shown that oleander or olive strains are only isolated from oleander or olive suggesting that each pathovar is specific to its respective host in nature (Caponero et al., 1995; Iacobellis, unpublished results). These findings, if confirmed, justify the distinction of pathovars savastanoi and nerii in P. savastanoi.
P. savastanoi, as P. savastanoi pv. nerii, has been recorded on Fraxinus spp. (bacterial canker of ash) such as ash (F. excelsior), white ash (F. americana) and velvet ash (F. velutina).
Host Plants and Other Plants AffectedTop of page
|Actinidia deliciosa (kiwifruit)||Actinidiaceae||Main|
|Forsythia intermedia (Golden bells)||Oleaceae||Main|
|Nerium oleander (oleander)||Apocynaceae||Main|
|Olea europaea subsp. europaea (European olive)||Oleaceae||Main|
|Punica granatum (pomegranate)||Punicaceae||Other|
Growth StagesTop of page Vegetative growing stage
SymptomsTop of page Olive knot disease is characterized by the formation of neoplastic tissue (knots, galls) mainly on young stems and branches, but leaves, roots and other organs may occasionally be infected by P. savastanoi pv. savastanoi. Infections occur mainly through wounds on the plants, particularly cracks caused by late spring frost, hail storms, wind-blown sand, agricultural practices (e.g. pruning and crop harvesting) and leaf, blossom and raceme fall. Initially, the knots are small (a few millimetres in diameter), pale-green excrescences that expand, sometimes reaching several centimetres in diameter, and gradually turn greenish-brown or brown. Internally, the knots are compact, spongy tissues in which lysogenic cavities form that are filled with bacterial cells. With age, the knots crack, become partly necrotized, decay and die within 6-8 months after their formation. In some circumstances they can last for a longer period and increase in size. In the case of heavy infections, when knots partially or completely girdle branches, the affected limbs are dwarfed, defoliated or killed. On young plants in the field the knots may cause weakness in the plant by partially girdling branches that form the structure of the trees.
Although rare, infection of fruit may occur as neoplastic alteration of the mesocarp at the peduncle preventing fruit development and causing deformation, or numerous roughly circular, brown spots, 0.5-2.5 mm in diameter, initially raised and then depressed, at the lenticels. The effect of the disease on the olive crop is not well studied but reductions in yield can be expected where heavy infection has affected tree structure (Teviotdale, 1994). There are indications that heavy infection affects olive quality (Schroth et al., 1968, 1973).
On oleander, olive and the majority of Oleaceae, the typical symptoms are overgrowths, whereas on ash they are excrescences.
List of Symptoms/SignsTop of page
|Fruit / abnormal shape|
|Fruit / lesions: black or brown|
|Inflorescence / galls|
|Leaves / abnormal forms|
|Leaves / wilting|
|Roots / galls along length|
|Stems / dieback|
|Stems / galls|
Biology and EcologyTop of page Genetics
The virulence of strains of P. savastanoi pv. savastanoi and P. savastanoi pv. nerii is dependent on the production of phytohormones, indole-3-acetic acid and several cytokinins (Comai and Kosuge, 1982; Surico et al., 1985; Surico and Iacobellis, 1992; Iacobellis et al., 1994). These genes do not appear to be involved in the disease process on ash, which is not expressed as parenchymatous galls (Evidente et al., 1995; Iacobellis et al., 1998). Genes involved in the biosynthesis of both classes of phytohormone have been cloned and sequenced (Comai and Kosuge, 1982; Yamada et al., 1985; Powell and Morris, 1986). Recent studies on Tn5-induced mutants demonstrated the presence of the hrp gene cluster in P. savastanoi pv. savastanoi (Sisto et al., 1999). More recently some of the hrp/hrc genes (hrpF, hrpG, hrcC, hrpT and hrpV and hrpE) have been cloned and show homology with the corresponding genes in Pseudomonas syringae pv. syringae, P. syringae pv. glycinea and P. syringae pv. phaseolicola (Sisto et al., 2003). These results, together with the identification and characterization of the hrcC mutant of P. savastanoi pv. savastanoi, suggest that hrp/hrc genes play a key role in the pathogenicity of this.
Several studies mainly in southern Italy have shown that, in their saprophytic phase, P. savastanoi pv. savastanoi on olive and P. savastanoi pv. nerii on oleander, survive on the surfaces of leaves, twigs and fruits of host plants (Ercolani, 1971, 1983; Lavermicocca and Surico, 1987). The population density of P. savastanoi pv. savastanoi on host-plant phylloplanes reached their highest levels in the spring and autumn (Lavermicocca and Surico, 1987) when the plants were actively growing and highly susceptible, and infection occurred mainly during these seasons. Phylloplane colonization in olive appears to be correlated with leaf age, cultivar and agronomic practices (Ercolani, 1983; Varvaro and Ferrulli, 1983; Balestra and Varvaro, 1995). Although further investigation is necessary, epiphytic populations of P. savastanoi pv. savastanoi together with release from active knots are the main sources of inoculum, invading wounds on plants caused by leaf scars, frost injury, hail storm injury, agronomic practices, etc. Bacteria oozing from knots and/or resident on the phylloplane may be dispersed on the plant or to other plants in the same grove by rain and aerosol formed by wind-driven rain. Furthermore, pathogens resident on the phylloplane of healthy plants or causing sub-clinical infections can be transported on propagating material (plants, cuttings, buds, etc.). Transfer with planting material is the main pathway by which P. savastanoi is distributed over long distances.
Petri (1915) and Wilson (1935) proposed the possibility of latent infections and, in particular, the systemic movement of P. savastanoi in olive tissues, although this has never been demonstrated. Latent infections in olive might occur at leaf fall, when cuttings are prepared for rooting, or when the plants are grafted. The epidemiological importance and phytosanitary implications of latent infections will determine the need for further detailed investigations.
For P. savastanoi pv. nerii, the disease cycle is similar to that of the olive knot pathogen except that as an ornamental shrub, oleander is not subject to the continuous injurious management practices of olive. In this syndrome, the oleander knot bacterium moves through the laticifer vessels giving rise to secondary knots (Wilson and Magie, 1964; Azad and Cooksey, 1995). Pathogenicity tests show that oleander strains are virulent to oleander and at least some cultivars of olive (Caponero et al., 1995; Janse, 1982; Surico et al., 1985), whereas strains from olive are not virulent to oleander. By contrast, field isolations confirm that olive strains only are isolated from olive, and oleander strains only are isolated from oleander (Caponero et al., 1995; G. Surico, personal communication), suggesting that each strain is specific to its respective host in the field.
Means of Movement and DispersalTop of page The main sources of P. savastanoi pv. savastanoi inoculum are bacteria oozing from cracks in knots, or epiphytic bacteria on host plants. The short distance spread of inoculum is mainly mediated by wind-driven rain, but agricultural practices such as pruning, grafting, fruit harvesting and the use of infected propagation material also contribute to local spread. Insects may have a significant role in the dispersal of the pathogen, but evidence of this is lacking or contradictory. The olive fly (Bactrocera oleae) was previously considered important in the dissemination of P. savastanoi pv. savastanoi because the bacterium was thought to be symbiotically associated with this insect; however, studies have shown that the symbiotic bacterium is not P. savastanoi pv. savastanoi (Luthy, 1983a, b).
Movement in Trade
Whole plants or plant parts (i.e. cuttings, buds, etc.) showing knots are easily recognized and discarded in nursery practice. However, bacterial populations of P. savastanoi pv. savastanoi on the phylloplane and as latent and systemic infections make highly dubious the practice of permitting the transfer of plants cleared by inspection to be moved to disease-free localities.
Plant TradeTop of page
|Plant parts liable to carry the pest in trade/transport||Pest stages||Borne internally||Borne externally||Visibility of pest or symptoms|
|Leaves||Yes||Yes||Pest or symptoms usually invisible|
|Roots||Yes||Yes||Pest or symptoms usually visible to the naked eye|
|Seedlings/Micropropagated plants||Yes||Yes||Pest or symptoms usually visible to the naked eye|
|Stems (above ground)/Shoots/Trunks/Branches||Yes||Yes||Pest or symptoms usually visible to the naked eye|
|Plant parts not known to carry the pest in trade/transport|
|Fruits (inc. pods)|
|Growing medium accompanying plants|
|True seeds (inc. grain)|
Impact SummaryTop of page
|Fisheries / aquaculture||None|
ImpactTop of page Olive knot disease is endemic in several olive-growing areas, but the economic impact of the disease is poorly understood and generally under-estimated. The effects of the disease on production levels of olive trees are not clear and few studies have been published (Schroth et al., 1973; Michelakis, 1990). Schroth et al. (1973) reported that olive plants with moderate infections (0.5-1 knots/ft (about 30 cm) of fruitwood) had smaller fruits and 28% lower production than slightly infected plants (0.1-0.3 knots/ft of fruitwood) with a consequent reduction in farm income. The effects of the disease on oil yield and quality have not received much attention, although this has been suggested by several authors. However, green table olives from infected trees have been reported to have an off-flavour (bitter, salty, sour or rancid) (Schroth et al., 1968). Further detailed studies are necessary to define better the effects of infection on production levels and on the quality of fruits.
DiagnosisTop of page
Isolation is preferably made from early infection stages because older knots are generally invaded by fast-growing secondary bacteria, which can overwhelm colony formation of the pathogen. Small pieces of tissue are excised from the margins of lesions and comminuted in sterile water and streaked on surface-dried plates of nutrient agar or King's medium B. These are useful general purpose isolation media that do not favour fungal contamination. Pathogenic pseudomonads are generally slower growing than saprophytic bacteria, requiring 2-3 days before the appearance of small colonies. The development of largely unmixed colonies can be regarded as a presumptive indication of isolation of the pathogen. Yellow bacterial colonies usually produced by Pantoea agglomerans are frequently, though not always, found with P. savastanoi pv. savastanoi from olive and oleander knots and also from the phylloplane of diseased olive and oleander plants (Surico and Marchi, 2003). Semi-selective media for P. savastanoi pv. savastanoi described by Azad and Cooksey (1995) and Surico and Lavermicocca (1989) is probably efficacious if isolation must be made from old cankers or the phylloplane. Three selective media are available: ANS-S (Varvaro, 1983), PVF-1 (Surico and Lavermicocca, 1989) and OKA (Azad and Cooksey, 1995). Recent investigations have demonstrated limitations for each of these media in selectivity, recovery or colony morphology; however, PVF-1 was considered a suitable substrate for the isolation of P. savastanoi pv. savastanoi from knots and from the phylloplane of olive or oleander (Surico and Marchi, 2003).
Confirmation of the bacterium from knot symptoms on hosts of P. savastanoi in LOPAT Group 1 (Lelliott et al., 1966) would usually be all that is required to identify this pathogen. P. savastanoi pv. savastanoi is negative in tests for levan production, oxidase activity, pectate lyase and polygalacturonase (potato rot) activity, arginine dihydrolase activity, and positive in the tobacco hypersensitivity reaction. Some strains of P. savastanoi pv. savastanoi give a positive reaction in the test for levan (exopolysaccharide) production (Iacobellis et al., 1993). P. syringae pv. syringae gives the same reactions in these determinative tests. This pathogen can be discriminated by the tests referred to in Young (1991).
Confirmation is by pathogenicity test. Bacterial suspensions of not more than 10,000,000 c.f.u./ml are inoculated into wounds on stems of actively growing olive and oleander plants. Swellings at the inoculation sites are evident 10-20 days after inoculation, depending on the plant reaction and environment conditions, but virulence assays should last for at least 60 days. Olive strains (P. savastanoi pv. savastanoi) will only cause knots in olive plants, whereas oleander strains (P. savastanoi pv. nerii) will cause knots on both oleander and olive.
It is difficult to differentiate P. savastanoi pv. savastanoi from P. savastanoi pv. nerii. Janse (1991) showed that the knot-forming pathogens of Fraxinus (P. savastanoi pv. fraxini) could be differentiated from the olive and oleander strains of P. savastanoi by differences in fatty acid composition. However, the fatty acid composition of pv. savastanoi and pv. nerii strains was generally too similar for differentiation between them. Differentiation of olive and oleander strains may be possible using molecular methods such as DNA restriction fingerprinting (Mugnai et al., 1994).
Success using molecular methods such as DNA restriction fingerprinting has been reported (Mugnai et al., 1994; Sisto et al., 2002). A nested-PCR detection method has recently been developed (Bertolini et al., 2003a, b). Specific primers to the iaaL gene have been designed for PCR detection of P. savastanoi pv. savastanoi. IAALF/IAALR (Penyalver et al., 2000) and IAALN1/ IAALN2 (Bertolini et al., 2003a, b) were used as external and internal primers, respectively. This newly nested-PCR method, coupled with colorimetric detection and a pre-enrichment step using the PVF-1 medium, detected P. savastanoi. pv. savastanoi in asymptomatic nursery plants, confirming the presence of these bacteria as epiphytic and/or endophytic in asymptomatic olive plants. The method may be useful for sanitary selection and certification programmes for olive plants in schemes that include P. savastanoi pv. savastanoi, as well as for epidemiological studies.
These methods would only be used for research studies in which the differentiation of these two pathovars was necessary or when a high level of confidence in identification was necessary to support eradication programmes or quarantine restrictions that may involve compensation.
P. savastanoi pv. phaseolicola was identified using an ELISA-DAS test by González (2003).
The method of identification issued by the International Seed Federation in 2006 is successfully used in Balaz? et al. (2008). P. savastanoi pv. phaseolicola was isolated from bean seeds and isolated on a semiselective media. ELISA and PCR can then be used to confirm the identity of resulting isolates. Milk Tween Agar (MTA) and Modifies Sucrose Peptone Agar (MSPA) are both suitable for isolation of P. savastanoi pv. phaseolicola. Popovic´ et al. (2012) reported that, when isolated on MTA, P. savastanoi pv. phaseolicola colonies were creamy-white, flat and circular, whereas when cultivated on MSPA, colonies were light yellow, convex and shiny.
It has been suggested that the TaqMan real-time PCR-based method of pathogen diagnosis, as detailed in Cho et al. (2010), can be used for rapid detection of P. savastanoi pv. phaseolicola.
Detection and InspectionTop of page Bacterial knot disease on olive is easily recognized when the knots are well developed. However, in the early stages, the knots can be confused with insect puncture (feeding or egg-laying) wounds.
Prevention and ControlTop of page
Due to the variable regulations around (de)registration of pesticides, your national list of registered pesticides or relevant authority should be consulted to determine which products are legally allowed for use in your country when considering chemical control. Pesticides should always be used in a lawful manner, consistent with the product's label.
Olive knot can cause severe damage in most olive-growing regions and P. savastanoi pv. savastanoi is included in the certification procedure of olive in European countries (Martelli et al., 1995; Bertolini et al., 2003b).
Cultural Control and Sanitary Methods
In countries and regions where the knot pathogen does not occur, new olive groves should be established using disease-free nursery stock from pathogen-free sources. As a precautionary measure, until the host specificity of olive and oleander strains is fully understood, the removal of nearby (within 500 m) oleander bushes should be considered as a measure to eliminate possible sources of pathogenic bacteria that could otherwise pose a threat to the new grove. A recommended nursery practice is to maintain copper sprays on nursery plants. Bordeaux mixture (copper sulphate, 1 kg; lime, 2 kg; water, 100 litres), copper oxychloride or copper hydroxide may be applied. Initial caution is advised until application is shown not to cause leaf injury in local conditions (Young, 2004). The practice of harvesting by beating olive branches with sticks is a recognized way of transmitting the pathogen to wounded tissue (Panagopoulos, 1993). Some reduction of transfer of the pathogen and of infection may be effected by using sticks wrapped with cloth soaked in a copper solution (e.g. Kocide) at frequent intervals, especially when moving between trees (Young, 2004). The most important control practices are those concerned with pruning. As already stated, the pathogen cannot be eradicated from trees or orchards, but thoughtful pruning can minimize its worst effects. Attention to tree development in early years offers the best approach to managing disease damage. Annual pruning should be done no later than late winter to avoid the period of spring susceptibility. The goal for pruning of young trees is to leave non-diseased branches to form the scaffold of the mature tree. Individual assessment should form a guide to the removal of specific weakened branches. Infected young trees need not be removed unless they are so seriously infected that they show little prospect of forming a bearing tree. Pruning before expected rain should be avoided (Young, 2004). The shape of crowns of very old trees damaged by hail and subsequently badly infected by bacterial knot can be transformed from the traditional inverted truncated cone tapered to the base, to erect truncated cones tapered from the base. Positive effects on tree health, growth and productivity have been reported (Ruffaldi, 1972).
No completely resistant varieties are yet available, but there are several reports of useful tolerance (Benjama et al., 1987; Benjama et al., 1992; Benjama, 1994; Marcelo et al., 1999, Varvaro and Surico, 1978b; Young et al., 2005). Recent studies in Italy in which 30 olive cultivars were artificially inoculated with strains of P. savastanoi pv. savastanoi (Sisto et al., 2001) showed that cultivars Carolea, Bella di Spagna, Cerasella, Cima di Melfi, Coratina, Corniola, Dolce Agogia, Leucocarpa, Maiatica di Ferrandina, Nolca and San Felice had a moderate response to artificial infection, whereas Cellina di Nardò, Frantoio, Morcona, Nociara, Ogliarola and Pendolino showed a high response to infection. An intermediate response was shown by the cultivars Ascolana tenera, Cipressino, Itrana, Kalamata, Leccino, Manzanilla, Nocellara del Belice, Nocellara Etnea, Nostrale di Rigali, Pasola di Andria, Picholine, Toscanina and Termite di Bitetto. Another independent study confirmed some of these findings and found a genotype which was tolerant to the disease among the hybrid and open-pollinated seedlings studied (Hassani et al., 2003). In a comparative study, Young et al. (2005) reopted that the cultivars Carolea, Koroneiki, Leccino and Pendolino are the most tolerant, and that Barnea, Manzanillo, Picholine, Picual and a South Australian selection of Verdale are the least tolerant to P. savastanoi pv. savastanoi. Other similar studies (Marcelo et al., 1999) showed that the cultivars Rendonil and Cobrancosa were relatively resistant, Branquita and Santulhana expressed some symptoms, and Cordovil De Serpa and Galca vulgar were most susceptible to the disease. Field observations in Morocco indicated that cv. Gordale was resistant to P. savastanoi pv. savastanoi, cv. Picholine Marocaine exhibited some symptoms, and cv. Meslala was susceptible (Benjama et al., 1992; Benjama, 1994).
Chemical Spray Control
There have been several reports of trials of the efficacy of copper spray compounds (e.g. copper hydroxide). These are not always successful, and the cost-effective benefit is highly doubtful (Sisto and Iacobellis 1999). To be effective, sprays must be applied to maintain continuous bactericidal cover over a substantial part of the year, at the same time avoiding damage from phytotoxic levels of copper spray. This is difficult and not necessarily cost-effective. The possibility of using a bacteriocin of Pseudomonas syringae pv. ciccaronei for the control of olive knot was recently reported by Lavermicocca et al. (2002). Bacteriocin preparations of this bacterium are effective in the protection of infection niches and in reducing the density of P. savastanoi pv. savastanoi on the phylloplane.
ReferencesTop of page
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