Erwinia amylovora (fireblight)
- Summary of Invasiveness
- Taxonomic Tree
- Notes on Taxonomy and Nomenclature
- Distribution Table
- History of Introduction and Spread
- Risk of Introduction
- Habitat List
- Hosts/Species Affected
- Host Plants and Other Plants Affected
- Growth Stages
- List of Symptoms/Signs
- Biology and Ecology
- Natural enemies
- Notes on Natural Enemies
- Means of Movement and Dispersal
- Pathway Causes
- Pathway Vectors
- Plant Trade
- Wood Packaging
- Impact Summary
- Economic Impact
- Environmental Impact
- Impact: Biodiversity
- Social Impact
- Risk and Impact Factors
- Uses List
- Detection and Inspection
- Similarities to Other Species/Conditions
- Prevention and Control
- Links to Websites
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- Erwinia amylovora (Burrill 1882) Winslow et al. 1920
Preferred Common Name
Other Scientific Names
- Bacillus amylovorus (Burrill) Trevisan, 1889
- Bacterium amylovorum Chester, 1901
- Erwinia amylovora f.sp. rubi Starr et al., 1951
- Micrococcus amylovorus Burrill, 1882
International Common Names
- Spanish: fuego bacteriano
- French: feu bactérien
- Portuguese: fogo bacteriano
Local Common Names
- Bulgaria: ogne prigan
- Canada: brûlure bactérienne
- Czechoslovakia (former): spala
- Denmark: ildsot
- Germany: Feuerbrand
- Greece: vaktiriako kapsimo
- Hungary: tuzelhalas
- Israel: kerakhon
- Italy: colpo di fuoco
- Mexico: tizon de fuego
- Netherlands: bacterievuur
- Norway: paerebrann
- Poland: zaraza ogniowa
- Serbia: bakteriozna plamenjaca
- Spain: bakteri izurrua; foc bacteria
- Sweden: paronpest
- Turkey: ates yanikligi
- ERWIAM (Erwinia amylovora)
Summary of InvasivenessTop of page
The long distance spread of fire blight is a rare event which in most cases seems to be the result of plants or plant tissues being moved across the oceans. Short distance spread is the result of the characteristics of the pathogen, especially its ability to produce an exudate (bacteria embedded in exopolysaccharides) which is easily transported by wind, rain, insects or birds. This is very efficient; once the pathogen has moved into a new territory it almost always colonizes and becomes established. This is accompanied by economic losses in regions where apple, pear or loquat are grown commercially; it might prevent the survival of local cultivars and could disrupt international trade. To date fire blight has colonized most of North America, Western Europe and most of the countries around the Mediterranean Sea as well as New Zealand. Outbreaks of fire blight are irregular and difficult to control.
Taxonomic TreeTop of page
- Domain: Bacteria
- Phylum: Proteobacteria
- Class: Gammaproteobacteria
- Order: Enterobacteriales
- Family: Enterobacteriaceae
- Genus: Erwinia
- Species: Erwinia amylovora
Notes on Taxonomy and NomenclatureTop of page
The pathogen Erwinia amylovora is the type species for the genus Erwinia, a genus created in the Enterobacteriaceae to contain the Gram-negative, motile, aerobic to facultative anaerobic, non-sporulating bacteria ecologically associated with plants (Brenner, 1984).
Dye's classification system divided the genus Erwinia into four groups: amylovora, carotovora, herbicola and 'atypical' Erwinia (Dye, 1968, 1969a, b, c, respectively). Hauben et al. (1998) proposed, on the basis of 16S rRNA sequence homologies, that the four groups be split into the genera Erwinia, Pectobacterium, Pantoea and Brenneria, respectively. Although the groups are recognized as valid divisions, the recommended generic designations have not yet been uniformly adopted.
Although E. amylovora has been considered a highly homogeneous species, differences between strains of different geographic origins were detected based on pulsed-field gel electrophoresis (PFGE) (Jock et al., 2002; Jock and Geider, 2004) and on fragment length polymorphism in restriction digests of plasmid pEA29 PCR products (Lecomte et al., 1997). The polymorphism, caused by variation in the number of 8-bp DNA repeats in pEA29 (Schnabel and Jones, 1998; Kim and Geider, 1999), was shown to be unstable and therefore unreliable for strain typing (Schnabel and Jones, 1998). Using other molecular methods to assess the genetic diversity among strains from similar hosts, a few differences were detected but the strains still grouped together when the data were subjected to phylogenetic analyses (McManus and Jones, 1995b; Momol et al., 1997; McGhee et al., 2002).
Strains of E. amylovora pathogenic to Rubus sp. (brambles) were originally described as E. amylovora f.sp. rubi by Starr et al. (1951), a designation that is no longer used. Rubus strains do not show cross pathogenicity with Maloideae (pome or pip fruit and related ornamental) strains, but on the basis of high DNA-DNA homology the strains must be considered identical species (Gardner and Kado, 1972; Vanneste, 1995; McGhee et al., 2002). However, Rubus strains do differ from Maloideae strains in a number of molecular characteristics (Laby and Beer, 1992; McManus and Jones, 1995b; Momol et al., 1997; McGhee and Jones, 2000; McGhee et al., 2002; Jock and Geider, 2004; Braun and Hildebrand, 2005). Rubus strains have not been described outside North America (USA, Canada).
DescriptionTop of page
Cells of E. amylovora are Gram negative rods, 0.3 x 1-3 µm in size, occur singly, in pairs and sometimes in short chains, and are motile by two to seven peritrichous flagella per cell (see Paulin, 2000, for review).
E. amylovora forms colonies of characteristic colour and colony formation on most culture media (Bereswill et al., 1998). Colonies are domed, circular, mucoid on sucrose nutrient agar (Billing et al., 1961); red to orange on MS medium (Miller and Schroth, 1972); white, circular, mucoid on KB medium (Paulin and Samson, 1973); smooth large, pulvinate, light blue opalescent with craters on CCT medium (Ishimaru and Klos, 1984); and yellow, highly mucoid or less mucoid on MM2Cu media (Bereswill et al., 1998).
The bacteria are not visible to the naked eye, but when symptoms are present they would be visible to the naked eye.
DistributionTop of page
It is generally thought that fire blight originated on wild hosts (presumably Crataegus) in the north-eastern USA, where it has been described after the import and cultivation of European apple and pear varieties (van der Zwet and Keil, 1979). The first description outside the USA was in New Zealand (1919). In Europe, fire blight was first described in the UK (Kent) in 1957. From this year on, a permanent spread of the disease was assessed in Northern, Western and Central Europe. In 1998, all countries belonging to the European Union (except Portugal) had fire blight on pears, apples or ornamentals, either widespread (England, Belgium, Germany), localized (France, Switzerland) or in restricted spots, under control and local eradication (Spain, Italy, Austria). It can be said that Western Europe has been invaded by fire blight in the second half of the twentieth century. However, even today, wide areas of Europe remain free of fire blight (in Italy, Spain and the south-east of France). Fire blight invaded a large area around the Mediterranean Sea. It most probably spread from an initial outbreak detected in the Nile delta region of Egypt in 1964. The disease was later found in Greece (Crete), Israel, Turkey, Lebanon, Iran and countries of Central Europe. The introduction of E. amylovora in Egypt and England has resulted in one continuous zone infected by fire blight, which encompasses most of Western Europe and most of the Mediterranean region. Only countries in North Africa seem to be free of fire blight; although the disease has recently been described in Morocco.
A number of unconfirmed reports of fire blight (China, India, Korea, Saudi Arabia, Vietnam, Colombia) may rely on misdiagnosis, or insufficient description of the causal agent (confusion of fire blight with pear-blast symptoms caused by Pseudomonas syringae pv. syringae or with other Erwinia species reported on Asian pear). It must also be remembered that E. amylovora is a quarantine organism (list A2 OEPP), the economic consequences of a declaration of the presence of fire blight in a country may have costly consequences for the international trade of this country: it cannot be ruled out that the list of actually 'infected' countries is slightly longer than the list of officially declared areas.
In most cases, attempts to eradicate the pathogen in newly infected countries, only slows down the spread of the disease. Until fire blight is again detected in Australia, this country might be the only case where eradication has been successful. Fire blight-like symptoms were detected on cotoneaster in the Royal Botanic Gardens, Melbourne, Victoria, in April 1997, and diagnostic tests confirmed that the causal organism was E. amylovora (Rodoni et al., 1999). An intensive eradication programme was undertaken and national surveys conducted for 3 years following the detection of E. amylovora have confirmed the absence of the disease in all states of Australia (Rodoni et al., 2002). A record of E. amylovora in New South Wales, Australia, cited in previous editions of the Compendium, was included as a result of a database error and has now been removed. There has been no positive detection of E. amylovora in New South Wales.
Large areas of the world are still free of fire blight (South America, most of Africa and Asia) in spite of the fact that susceptible cultivars of European and American origin are grown in these areas, and that potentially susceptible host plants may be common in the environment.
See also CABI/EPPO (1998, No. 257).
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.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Armenia||Restricted distribution||Introduced||1989||Invasive||van der Zwet, 1996; CABI/EPPO, 2013; EPPO, 2014|
|Azerbaijan||Absent, unreliable record||EPPO, 2014|
|China||Absent, unreliable record||van der Zwet, 1996; CABI/EPPO, 2013; EPPO, 2014|
|India||Absent, unreliable record||CABI/EPPO, 2013; EPPO, 2014|
|-Maharashtra||Absent, unreliable record||Bradbury, 1986; CABI/EPPO, 2013; EPPO, 2014|
|Iran||Restricted distribution||Introduced||Invasive||Mazarei et al., 1994; Maroofi and Mostafavi, 1996; CABI/EPPO, 2013; EPPO, 2014; Seidghasemi et al., 2015|
|Israel||Widespread||Introduced||1985||Invasive||Beer et al., 1986; Zutra et al., 1986; Manulis et al., 1998; CABI/EPPO, 2013; EPPO, 2014|
|Japan||Absent, unreliable record||CABI/EPPO, 2013; EPPO, 2014|
|-Hokkaido||Absent, unreliable record||Beer et al., 1996; Kim et al., 1996; Momol et al., 1997; CABI/EPPO, 2013; EPPO, 2014|
|-Honshu||Absent, unreliable record||EPPO, 2014|
|Jordan||Present||Introduced||1990||Invasive||van der Zwet, 1996; CABI/EPPO, 2013; EPPO, 2014|
|Kazakhstan||Restricted distribution||CABI/EPPO, 2013; EPPO, 2014|
|Korea, Republic of||Transient: actionable, under eradication||Myung et al., 2016a; CABI/EPPO, 2013; EPPO, 2014; IPPC, 2015|
|Kyrgyzstan||Restricted distribution||CABI/EPPO, 2013; EPPO, 2014|
|Lebanon||Widespread||Introduced||1988||Invasive||CABI/EPPO, 2013; EPPO, 2014|
|Saudi Arabia||Absent, invalid record||CABI/EPPO, 2013; EPPO, 2014|
|Syria||Restricted distribution||Introduced||Invasive||Ammouneh et al., 2008; CABI/EPPO, 2013; EPPO, 2014|
|Taiwan||Absent, confirmed by survey||CABI/EPPO, 2013; EPPO, 2014|
|Turkey||Widespread||Introduced||1985||Invasive||Momol and Zeller, 1992; CABI/EPPO, 2013; EPPO, 2014|
|Vietnam||Absent, invalid record||CABI/EPPO, 2013; EPPO, 2014|
|Algeria||Present, few occurrences||EPPO, 2011; CABI/EPPO, 2013; EPPO, 2014|
|Egypt||Restricted distribution||Introduced||1960s||Invasive||El Goorani, 1973; Abo and El Dahab El Goorani, 1984; El Nasr et al., 1990; CABI/EPPO, 2013; EPPO, 2014|
|Morocco||Restricted distribution||Introduced||Invasive||Fatmi, 2008; CABI/EPPO, 2013; EPPO, 2014|
|Nigeria||Absent, reported but not confirmed||CABI/EPPO, 2013|
|Tunisia||Restricted distribution||CABI/EPPO, 2013; EPPO, 2014; Rhouma et al., 2014|
|Bermuda||Present||Introduced||1938||van der Zwet, 1993; CABI/EPPO, 2013; EPPO, 2014|
|Canada||Widespread||Introduced||1800s||Invasive||CABI/EPPO, 2013; EPPO, 2014|
|-Alberta||Present||Evans, 1996; CABI/EPPO, 2013; EPPO, 2014|
|-British Columbia||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Manitoba||Present||CABI/EPPO, 2013; EPPO, 2014|
|-New Brunswick||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Newfoundland and Labrador||Present||EPPO, 2014|
|-Northwest Territories||Present||EPPO, 2014|
|-Nova Scotia||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Ontario||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Prince Edward Island||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Quebec||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Saskatchewan||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Yukon Territory||Present||EPPO, 2014|
|Mexico||Restricted distribution||Introduced||Invasive||Mendoza and Teliz Ortiz, 1984; Lopez and Fucikovsky, 1990; Ramirez-Legarreta, 1990; CABI/EPPO, 2013; EPPO, 2014|
|USA||Widespread||1800s||Invasive||van and der Zwet Keil, 1979; CABI/EPPO, 2013; EPPO, 2014|
|-Alabama||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Arkansas||Present||CABI/EPPO, 2013; EPPO, 2014|
|-California||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Colorado||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Connecticut||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Delaware||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Florida||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Georgia||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Idaho||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Illinois||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Iowa||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Kansas||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Kentucky||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Louisiana||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Maine||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Maryland||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Massachusetts||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Michigan||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Minnesota||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Mississippi||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Missouri||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Montana||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Nebraska||Present||CABI/EPPO, 2013; EPPO, 2014|
|-New Hampshire||Present||CABI/EPPO, 2013; EPPO, 2014|
|-New Jersey||Present||CABI/EPPO, 2013|
|-New York||Present||CABI/EPPO, 2013; EPPO, 2014|
|-North Carolina||Present||CABI/EPPO, 2013; EPPO, 2014|
|-North Dakota||Present||CABI/EPPO, 2013|
|-Ohio||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Oregon||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Pennsylvania||Present||CABI/EPPO, 2013; EPPO, 2014|
|-South Carolina||Present||CABI/EPPO, 2013|
|-South Dakota||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Tennessee||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Texas||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Utah||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Virginia||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Washington||Present||CABI/EPPO, 2013; EPPO, 2014|
|-West Virginia||Present||CABI/EPPO, 2013; EPPO, 2014|
|-Wisconsin||Present||CABI/EPPO, 2013; EPPO, 2014|
Central America and Caribbean
|Guatemala||Present||Introduced||1966||van and der Zwet Keil, 1979; van der Zwet, 1993; CABI/EPPO, 2013; EPPO, 2014|
|Haiti||Absent, invalid record||CABI/EPPO, 2013; EPPO, 2014|
|Chile||Absent, never occurred||Bradbury, 1986; CABI/EPPO, 2013; EPPO, 2014|
|Colombia||Absent, invalid record||van der Zwet, 1993; CABI/EPPO, 2013; EPPO, 2014|
|Venezuela||Absent, unreliable record||CABI/EPPO, 2013; EPPO, 2014|
|Albania||Restricted distribution||Introduced||Invasive||Isufi and Myrta, 1996; CABI/EPPO, 2013; EPPO, 2014|
|Austria||Present, few occurrences||Introduced||1993||Invasive||Keck, 1994; Keck et al., 1997; CABI/EPPO, 2013; EPPO, 2014|
|Belarus||Present, few occurrences||CABI/EPPO, 2013; EPPO, 2014|
|Belgium||Restricted distribution||Introduced||1970s||Invasive||Veldeman, 1972; Samson et al., 1973; Verhoyen, 1983; Deckers and Daemen, 1992; CABI/EPPO, 2013; EPPO, 2014|
|Bosnia-Hercegovina||Restricted distribution||CABI/EPPO, 2013; EPPO, 2014|
|Bulgaria||Widespread||Introduced||1989||Invasive||van der Zwet, 1996; CABI/EPPO, 2013; EPPO, 2014|
|Croatia||Restricted distribution||CABI/EPPO, 2013; EPPO, 2014|
|Cyprus||Widespread||Introduced||1984||Invasive||Psallidas and Dimova, 1986; Psallidas, 1990; CABI/EPPO, 2013; EPPO, 2014|
|Czech Republic||Restricted distribution||CABI/EPPO, 2013; EPPO, 2014|
|Czechoslovakia (former)||Present||Introduced||Invasive||Kudela, 1988; Kudela et al., 1992|
|Denmark||Restricted distribution||Introduced||1968||Nilsson, 1969; Hockenhull, 1979; CABI/EPPO, 2013; EPPO, 2014|
|Estonia||Transient: actionable, under eradication||2012||EPPO, 2014b; CABI/EPPO, 2013; EPPO, 2014||Present, first found in 2012 in a small number of samples, under eradication.|
|Finland||Present||EPPO, 2014; Soukainen et al., 2015|
|France||Restricted distribution||Introduced||1972||Invasive||Samson et al., 1973; Fougeroux, 1981; LaRue and Vincent, 1990; CABI/EPPO, 2013; EPPO, 2014|
|-Corsica||Absent, confirmed by survey||EPPO, 2014|
|-France (mainland)||Restricted distribution||CABI/EPPO, 2013|
|Germany||Restricted distribution||Introduced||1971||Invasive||Fiebinger, 1986; Zeller, 1987; Brandt and Harzer, 1994; CABI/EPPO, 2013; EPPO, 2014|
|Greece||Widespread||Introduced||1984||Invasive||Panagopoulos and Panoutsos, 1987; Psallidas, 1990; CABI/EPPO, 2013; EPPO, 2014|
|-Crete||Restricted distribution||CABI/EPPO, 2013; EPPO, 2014|
|Hungary||Restricted distribution||Végh et al., 2012; CABI/EPPO, 2013; Végh and Palkovics, 2013; EPPO, 2014|
|Ireland||Present, few occurrences||van der Zwet, 1996; CABI/EPPO, 2013; EPPO, 2014|
|Italy||Restricted distribution||Introduced||Invasive||Cariddi, 1990; Cariddi and Piglionica, 1992; Finelli et al., 1996; CABI/EPPO, 2013; Pucci et al., 2013; EPPO, 2014|
|-Sicily||Present, few occurrences||CABI/EPPO, 2013; EPPO, 2014|
|Latvia||Present, few occurrences||IPPC, 2008; CABI/EPPO, 2013; EPPO, 2014|
|Lithuania||Restricted distribution||CABI/EPPO, 2013; EPPO, 2014|
|Luxembourg||Restricted distribution||CABI/EPPO, 2013; EPPO, 2014|
|Macedonia||Widespread||CABI/EPPO, 2013; Mitrev and Kostadinovska, 2013; EPPO, 2014|
|Moldova||Widespread||Introduced||1996||Invasive||Lukitsa and Verderevskaia, 1978; CABI/EPPO, 2013; EPPO, 2014|
|Montenegro||Widespread||Balaz et al., 2012; CABI/EPPO, 2013; EPPO, 2014|
|Netherlands||Widespread||Introduced||1966||Invasive||Kleijburg, 1979; CABI/EPPO, 2013; EPPO, 2014|
|Norway||Restricted distribution||Introduced||1986||Sletten, 1987; Sletten, 1990; CABI/EPPO, 2013; EPPO, 2014|
|Poland||Restricted distribution||Introduced||1966||Invasive||Borecki and Lyskanowska, 1968; Sobiczewski and Suski, 1988; CABI/EPPO, 2013; EPPO, 2014|
|Portugal||Absent, confirmed by survey||EPPO, 2014|
|Romania||Widespread||Introduced||1992||Invasive||Baicu et al., 1994; CABI/EPPO, 2013; EPPO, 2014|
|Russian Federation||Restricted distribution||CABI/EPPO, 2013; EPPO, 2014|
|-Central Russia||Restricted distribution||CABI/EPPO, 2013; EPPO, 2014|
|-Russia (Europe)||Present||Kharchenko, 2009|
|-Russian Far East||Present||CABI/EPPO, 2013|
|-Southern Russia||Restricted distribution||CABI/EPPO, 2013; EPPO, 2014|
|Serbia||Restricted distribution||CABI/EPPO, 2013; EPPO, 2014|
|Slovakia||Present, few occurrences||CABI/EPPO, 2013; EPPO, 2014|
|Slovenia||Restricted distribution||Introduced||2001||Invasive||Dreo et al., 2006; CABI/EPPO, 2013; EPPO, 2014|
|Spain||Restricted distribution||Introduced||1995||Invasive||de la Cruz Blanco, 1996; CABI/EPPO, 2013; EPPO, 2014|
|-Spain (mainland)||Restricted distribution||CABI/EPPO, 2013|
|Sweden||Restricted distribution||Introduced||1986||FAO, 1988a; CABI/EPPO, 2013; EPPO, 2014|
|Switzerland||Restricted distribution||Introduced||1989||Invasive||Grimm and Vogelsanger, 1989; Grimm et al., 1991; Hasler et al., 1996; CABI/EPPO, 2013; EPPO, 2014|
|UK||Restricted distribution||Introduced||1957||Invasive||Crosse et al., 1958; Lelliott, 1968; Glasscock, 1969; Stead, 1987; CABI/EPPO, 2013; EPPO, 2014|
|-Channel Islands||Eradicated||EPPO, 2014|
|-England and Wales||Widespread||EPPO, 2014|
|-Northern Ireland||Restricted distribution||EPPO, 2014|
|-Scotland||Restricted distribution||EPPO, 2014|
|Ukraine||Present||EPPO, 2014a; Bokshan and Sadlyak, 2009; CABI/EPPO, 2013; EPPO, 2014||Present, under official control.|
|-South Australia||Eradicated||Rodoni et al., 2002; CABI/EPPO, 2013; EPPO, 2014|
|-Victoria||Eradicated||Roberts, 1997; Rodoni et al., 2002; CABI/EPPO, 2013; EPPO, 2014|
|New Zealand||Restricted distribution||Introduced||1920s||Invasive||van and der Zwet Keil, 1979; CABI/EPPO, 2013; EPPO, 2014|
History of Introduction and SpreadTop of page
Fire blight was first noticed in Hudson valley, New York (USA) in the 1780s. Whether fire blight was native in the regions surrounding the Hudson valley, such as Quebec and Ontario, is not known. From this initial focus fire blight spread throughout North America. It was also accidentally imported into England and Egypt. From those two outbreaks it spread and became established in most of Europe and around the Mediterranean Sea. The introductions to New Zealand and Bermuda have not spread beyond these islands. E. amylovora has never been introduced intentionally; its presence is either the result of accidental introduction (England, New Zealand, Egypt and Bermuda) or due to the ability of the bacterium to spread locally relatively easily.
IntroductionsTop of page
|Introduced to||Introduced from||Year||Reason||Introduced by||Established in wild through||References||Notes|
|Natural reproduction||Continuous restocking|
|USA||New Zealand||1919||Nursery trade (pathway cause)||Yes||Bonn and Zwet (2000); Campbell (1920)||This is probably the first time E. amylovora was transported outside North America. Previous reports of E. amylovora in Japan cannot be confirmed.|
|USA||England and Wales||1956-57||Food (pathway cause)||Yes||Billing and Berrie (2002)||A very good analysis of the factors which might have led to fire blight getting in to England and the becoming established in the UK and subsequently in Western Europe has been published by Billing and Berrie in 2002.|
|USA||Egypt||early 1960s||Yes||El Helaly et al. (1964); Jock et al. (2002)||Strains isolated from Egypt show a different pattern by PFGE than those from England or New Zealand; this outbreak is due to a direct introduction from North America.|
|USA||Bermuda||before 1938||Yes||Bonn and Zwet (2000)|
Risk of IntroductionTop of page
E. amylovora is of quarantine concern in countries belonging to the following Regional Plant Protection Organizations: APPC (Asia and Pacific Plant Protection Commission), COSAVE (Comite Regional de Sanidad Vegetal para el Cono Sur), EPPO (European and Mediterranean Plant Protection Organization) and IAPC (Inter-African Phytosanitary Council). In addition, E. amylovora is quarantined in Belarus, Russia, Ukraine (EPPO, 1998) and South Africa (Erskine, 1975).
It is an EPPO A2 quarantine organism for Europe and EPPO countries and the specific quarantine for E. amylovora includes the requirement: 'that host plants should have been grown in areas where E. amylovora does not occur or else in a place of production found free from E. amylovora during the last growing season.' In the latter case, countries which consider themselves to be at high risk can specify that the field, as well as the surrounding zone of radius of at least 250 m, must be inspected at least once in July/August and once in September/October and that spot checks should be carried out in the surrounding zone of radius of at least 1 km in places where host plants are grown, at least once in July/October. For the southern hemisphere, equivalent periods would apply.
While these inspections are essentially visual, for symptoms of the disease, any suspect material will need to be tested for the presence of E. amylovora. In addition, exporting countries may need to perform random or systematic surveys of areas from which host plants are exported and in which the absence of E. amylovora has to be confirmed. Such surveys may involve sampling of apparently healthy host material in or on which E. amylovora may occur latently or 'epiphytically' (EPPO, 1992).
Habitat ListTop of page
|Terrestrial – Managed||Cultivated / agricultural land||Principal habitat||Harmful (pest or invasive)|
|Rail / roadsides||Present, no further details||Harmful (pest or invasive)|
|Urban / peri-urban areas||Present, no further details||Harmful (pest or invasive)|
Hosts/Species AffectedTop of page
E. amylovora is a pathogen of plants in the family Rosaceae; most of the natural hosts are in the subfamily Maloideae (formerly Pomoideae), a few belong in the subfamilies Rosoideae and Amygdaloideae (Momol and Aldwinckle, 2000). Genera in the subfamily Spiraeoideae have been reported as hosts on the basis of artificial inoculation (van der Zwet and Keil, 1979).
Strains of E. amylovora isolated from one host are pathogenic on most other hosts. This was the case for strains isolated from natural infections on Prunus salicina in the USA (Mohan and Thomson, 1996) and on Prunus domestica and Rosa rugosa in southern Germany (Vanneste et al., 2002a). Rubus strains (see Taxonomy and Nomenclature) are host specific; they are pathogenic on brambles but not on apple and pear (Starr et al., 1951; Braun and Hildebrand, 2005). Also, a few Maloideae strains exhibit differential virulence on apple; for example, strain Ea273 was not pathogenic across the same range of apple cultivars and rootstocks as common strain E4001A (Norelli et al., 1984, 1986).
Within each group of susceptible host plants, species or cultivars may be found with a high level of resistance; such plants may show no, or limited, symptoms under natural conditions or even following artificial inoculation (Forsline and Aldwinckle, 2002; Luby et al., 2002). Lists of resistant cultivars are published for important crops (van der Zwet and Keil, 1979; Zeller, 1989; Thomas and Jones, 1992; Berger and Zeller, 1994; van der Zwet and Bell, 1995; Bellenot-Kapusta et al., 2002).
Wild Pyrus (P. amygdaliformis, P. syriaca) in southern Europe and in the Mediterranean area, Crataegus (C. oxyacantha [C. laevigata], C. monogyna) in northern and central Europe, and ornamentals (Pyracantha, Cotoneaster, Sorbus) throughout Europe are important sources of inoculum for apple and pear orchards.
Host Plants and Other Plants AffectedTop of page
|Amelanchier alnifolia (saskatoon serviceberry)||Rosaceae||Other|
|Amelanchier canadensis (thicket serviceberry)||Rosaceae||Other|
|Aronia melanocarpa (black chokeberry)||Rosaceae||Other|
|Chaenomeles (flowering quinces)||Rosaceae||Other|
|Cotoneaster horizontalis (wall-spray)||Rosaceae||Other|
|Cydonia oblonga (quince)||Rosaceae||Main|
|Eriobotrya japonica (loquat)||Rosaceae||Main|
|Malus (ornamental species apple)||Rosaceae||Main|
|Malus domestica (apple)||Rosaceae||Main|
|Photinia davidiana (chinese stranvaesia)||Rosaceae||Other|
|Prunus armeniaca (apricot)||Rosaceae||Other|
|Prunus cerasifera (myrobalan plum)||Rosaceae||Other|
|Prunus domestica (plum)||Rosaceae||Other|
|Prunus salicina (Japanese plum)||Rosaceae||Main|
|Pseudocydonia sinensis (Chinese quince)||Rosaceae||Other|
|Pyracantha coccinea (Scarlet firethorn)||Rosaceae||Other|
|Pyrus communis (European pear)||Rosaceae||Main|
|Pyrus communis var. pyraster (poirier sauvage)||Rosaceae||Other|
|Pyrus pyrifolia (Oriental pear tree)||Rosaceae||Other|
|Rosa canina (Dog rose)||Rosaceae||Other|
|Rosa rugosa (rugosa rose)||Rosaceae||Other|
|Rubus (blackberry, raspberry)||Rosaceae||Other|
|Rubus fruticosus (blackberry)||Rosaceae||Other|
Growth StagesTop of page Flowering stage, Post-harvest, Vegetative growing stage
SymptomsTop of page
Fire blight's basic symptom is necrosis or death of tissues. Droplets of ooze on infected tissues are also an important symptom; they are the visible indication of the presence of fire blight bacteria. Except for minor differences, the symptoms of fire blight are basically the same on all host plants.
Infected blossoms initially become water-soaked and of a darker green as the bacteria invade new tissues. Within 5-30 plus days (commonly 5-10 days), the spurs begin to collapse, turning brown to black. Initial symptoms are often coincident with the accumulation of about 57 degree days, base 12.7°C, from the infection date (Steiner, 2000).
Infected shoots turn brown to black from the tip; shoots often bend near the tip to form a so-called 'shepherd-crook' shape. Shoots invaded from their base exhibit necrosis of basal leaves and the stem. Leaves and fruits may be invaded through petioles or stems or infected through wounds, resulting in discoloration followed by collapse of the leaves and fruit. During wet, humid weather, infected leaves and particularly the fruit often exude a milky, sticky liquid, or ooze containing bacteria.
From infected flowers and shoots, the bacteria may invade progressively larger branches, the trunk and even the rootstock. Infected bark on branches, scaffold limbs, trunk and rootstock turns darker than normal. When the outer bark is peeled away, the inner tissues are water-soaked often with reddish streaks when first invaded; later the tissues are dark brown to black. As disease progression slows, lesions become sunken and sometimes cracked at the margins, forming a canker.
Trees with rootstock blight may exhibit liquid bleeding from the crown at or just below the graft union in early summer. Water-soaked, reddish and necrotic tissues are visible when the outer bark is removed. Trees with infected rootstocks often exhibit yellow to red foliage about a month before normal autumn coloration. Rootstocks such as M.26, M.9 and relatives of M.9 often show these symptoms without evidence of infection in the trunk of the scion. Infection of M.7 and a few other rootstocks occurs following infection of suckers arising from the rootstocks; the infected suckers exhibit typical shoot blight symptoms. Many trees with rootstock blight will die in the first year after infection; the remaining rootstock-infected trees often die within 2-3 years.
Any plant tissues invaded by the bacteria can show ooze production on their surface. This exudate is a specific symptom of fire blight. Depending on weather conditions and on the time of the day, ooze may or may not be produced. It is most frequently observed early in the morning when the host water potential is positive. It may appear in different ways: droplets, threads or film on the plant's surface.
List of Symptoms/SignsTop of page
|Fruit / mummification|
|Leaves / necrotic areas|
|Leaves / wilting|
|Leaves / yellowed or dead|
|Stems / canker on woody stem|
|Stems / dieback|
|Stems / discoloration of bark|
Biology and EcologyTop of page
The life cycle of E. amylovora can be described as follows:
1. Infection through flowers. The entry of bacteria through natural openings in the floral cup (hypanthium) may take place after multiplication on the surface of stigmas.
2. Infection, later in the season. The entry of bacteria through small wounds produced by strong winds, hail, and insects may take place in young leaves and at the tips of growing shoots.
3. Internal invasion. Entry of E. amylovora into healthy shoots, branches and rootstocks may take place within trees by the systemic movement of bacteria from infected spurs and shoots.
4. Canker formation. The development of areas between infected and uninfected woody tissues were E. amylovora survives the dormant season.
Unlike some bacterial plant pathogens, E. amylovora is not an epiphytic bacterium; it is not able to multiply on the surface of healthy plants. The only stage where the bacteria multiply on the surface of the plant is on the stigmatic surfaces in the flower (Thomson, 1986). Pollinating and other flower-visiting insects are important for spreading the bacteria from both infested and infected flowers to healthy flowers. Other insects play a role in spread by visiting droplets of ooze exuding from cankers and then visiting healthy flowers. Free-water and high humidity in concert with temperature govern the rate of bacterial multiplication in the floral cup and the incidence and severity of flower infection (Pusey, 2000).
Climatic conditions during spring and summer play a key role in the occurrence and development of fire blight (Billing, 2000). The presence of bacteria on the stigmas of healthy flowers (epiphytic populations) is related to daily temperature (Thomson et al., 1982). Temperatures between 18 and 30°C with rain during bloom favour flower infection, frequent storms with wind-driven rain (with sufficiently high temperatures) during the period of growth elongation favour shoot and fruit infections and the rapid development of the disease.
Bacteria can be spread by wind and wind-driven rain within and between trees as ooze, strands (polysaccharide threads which may be present on the surface of infected plant) and aerosols (McManus and Jones, 1994). Secondary blossoms (rat-tails), which may be present on some hosts in late spring and summer, are often infected because weather conditions are more likely to be favourable when they are open. Severe infections may also take place in summer on shoots, leaves, fruits, following a hailstorm or any climatic event which wounds the plant surface, and is associated with rain.
Rootstock blight can develop from the internal spread of bacteria from an infected scion (Momol et al., 1998). Malling (M.) 9 and M.26 rootstocks are highly susceptible to internal invasion and rootstock blight (Momol et al., 1998; Norelli et al., 2003).
Dispersal of the pathogen may occur from the shipping of infected plant material. Latent infections may be present without any visible symptoms; the disease developing when the material is planted in the field. This mode of dispersal could introduce fire blight into new regions and countries.
ClimateTop of page
|C - Temperate/Mesothermal climate||Preferred||Average temp. of coldest month > 0°C and < 18°C, mean warmest month > 10°C|
|Cf - Warm temperate climate, wet all year||Preferred||Warm average temp. > 10°C, Cold average temp. > 0°C, wet all year|
|Cs - Warm temperate climate with dry summer||Tolerated||Warm average temp. > 10°C, Cold average temp. > 0°C, dry summers|
|Df - Continental climate, wet all year||Preferred||Continental climate, wet all year (Warm average temp. > 10°C, coldest month < 0°C, wet all year)|
Natural enemiesTop of page
Notes on Natural EnemiesTop of page
Bacterial microflora antagonistic to E. amylovora have been isolated and identified from the natural habitat of the pathogen (healthy and diseased plants, particularly stigmas) and from soil. Most bacteria found to exhibit antagonistic activity in vitro towards E. amylovora were Gram-negative bacteria (Pantoea agglomerans, Pseudomonas fluorescens) and new antagonists (yeasts, Gram-positive bacteria, bacteriophages and non-virulent strains of E. amylovora) are continually being found and characterized as possible control agents of fire blight (Johnson and Stockwell, 2000). P. agglomerans is a normal inhabitant of plant microflora and fire blight cankers. P. fluorescens is frequently found in the soil. Only some strains of these two species show an in vitro antagonistic effect towards E. amylovora.
Bacteriophages were initially isolated from soil or water (Billing, 1960). Generally, such phages are not strictly specific to E. amylovora (Vanneste and Paulin, 1990). Phages can also be isolated from fire blight infected plant tissues, but their host range is generally limited to E. amylovora and a few other species (Ritchie and Klos, 1979; Schnabel and Jones, 2001).
The list of natural enemies comprises antagonistic bacteria (P. agglomerans, P. fluorescens and Bacillus subtilis) and some antagonistic yeasts (Aureobasidium pullulans and Metschnikowia pulcherrima). All natural enemies compete with the pathogen for space and nutrients when it is growing on the stigmatic surface of the host plants. Some strains also produce an antibacterial compound that kills E. amylovora during this interaction.
Means of Movement and DispersalTop of page
By 1915, fire blight had spread throughout the USA; this was 135 years after it was first noticed in Hudson Valley in up-state New York, USA. Introductions outside North America were all accidental and rare. Such long distance spread most probably occurred with the transfer of infected plant material and, in at least one occasion (England 1950s), with the transfer of some crates contaminated by heavily infected fruit. Local spread of the disease is a consequence of the exudates (bacterial cells of the pathogen embedded in exopolysaccharides) produced by infected trees, which is easily transported by birds, insects, wind or rain. This is an efficient way to disperse the pathogen. The entire invasion of Western Europe and of countries around the Mediterranean Sea can be traced back to two initial outbreaks, which occurred less than 50 years ago.
Pathway CausesTop of page
|Botanical gardens and zoos||Fire blight has been found in Australia in a botanical garden. No plants outside the garden were fou||Yes||Bonn and Zwet, 2000|
|Breeding and propagation||Import of plant or plant material such as budwood for the purpose of breeding or propagation can lea||Yes||Yes||Bonn and Zwet, 2000|
|Hedges and windbreaks||Hawthorns are susceptible to fire blight but infection does not always result in highly visible symp||Yes||Bonn and Zwet, 2000|
|Horticulture||The movement of fire blight in the USA seems to have followed the introduction of apple and pear pro||Yes||Yes||Bonn and Zwet, 2000|
|Nursery trade||See introduction to Bologna (Italy) for example.||Yes||Yes||Bonn and Zwet, 2000|
|Smuggling||Smuggling of bud wood or other plant parts which may have harboured E. amylovora has been suspected||Yes||Yes|
Pathway VectorsTop of page
|Clothing, footwear and possessions||Transfer of germplasm.||Yes|
|Containers and packaging - non-wood||E. amylovora seems to be able to survive on some plastics but not on rigid high density polyethylene||Yes||Yes||Ceroni et al., 2004; Keck et al., 1996|
|Containers and packaging - wood||Containers/crates need to be contaminated with infected fruit producing copious amount of exudates.||Yes||Yes||Billing and Berrie, 2002|
|Host and vector organisms||Transfer of plants, honeybees and the movement of beehives.||Yes||Yes||Alexandrova et al., 2002|
|Transfer of germplasm.||Yes|
|Plants or parts of plants||Yes||Yes|
|Water||Rain, water||Yes||Thomson, 2000|
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|
|Bark||Yes||Yes||Pest or symptoms usually invisible|
|Flowers/Inflorescences/Cones/Calyx||Yes||Yes||Pest or symptoms usually invisible|
|Fruits (inc. pods)||Yes||Yes||Pest or symptoms usually invisible|
|Leaves||Yes||Yes||Pest or symptoms usually invisible|
|Seedlings/Micropropagated plants||Yes||Yes||Pest or symptoms usually invisible|
|Stems (above ground)/Shoots/Trunks/Branches||Yes||Yes||Pest or symptoms usually invisible|
|Wood||Yes||Yes||Pest or symptoms usually invisible|
|Plant parts not known to carry the pest in trade/transport|
|Growing medium accompanying plants|
|True seeds (inc. grain)|
Wood PackagingTop of page
|Wood Packaging liable to carry the pest in trade/transport||Timber type||Used as packing|
|Solid wood packing material with bark||No|
|Solid wood packing material without bark||poplar, oak, beech, spruce||Yes|
Impact SummaryTop of page
ImpactTop of page
Fire blight is a serious disease of plants in the subfamily Maloideae, especially apple, pear, quince and loquat. Epidemics, although sporadic, are often devastating depending on the occurrence of favourable climatic conditions, the amount of initial inoculum and virulence of the pathogen, and the susceptibility of the host species. Therefore, in any given site where fire blight is present, the disease can either be devastating or of secondary importance, according to the year and the varieties grown.
In addition, fire blight is a quarantine disease in most countries and, therefore, a single introduction, even of very limited importance in the field, may have a considerable economic impact in a newly infected country, due to the possible limitations in the international trade of plants.
It is generally considered that fire blight - with exceptions for particular years and cultivars - is unlikely to cause severe damage in Northern Europe (UK, Sweden, Norway and Denmark). In contrast, the threat is very serious for susceptible cultivars (pear, but also a number of recently released apple varieties and a number of ornamentals) in Southern and Central Europe.
Conversely, fire blight may be considered a disease of usually minor direct influence for a number of apple cultivars (such as Golden Delicious) and ornamentals in most areas. But the risk of unusual climatic conditions conducive to disease activity remains permanently present. This is illustrated, for example, by unexpected infections in UK cider apples in 1980 and 1982 (Gwynne, 1984), in pears and apples in Aquitaine and Anjou and Paris in France, in 1978 and 1984, respectively (Lecomte and Paulin, 1989) and in apple and pear flowers in Switzerland in 1995 (Mani et al., 1996).
In the Crimea, regional pear varieties are susceptible to E. amylovora, which can cause losses of 60-90% of flowers and buds in some years and reduce yields by a factor of 8-10 (Kalinichenko and Kalinichenko, 1983).
In Egypt, the first fire blight outbreaks since 1962 were recorded in 1982 and were associated with heavy rainfall during bloom. In 1983 and 1984, outbreaks also occurred and were associated with rainfall combined with wind storms during bloom and one 2-day rain during bloom, respectively. The severe occurrence of the disease was expressed mainly as flower blight and caused a loss of 10-75% flowers/tree (van der Zwet, 1986).
Fire blight is said to be at the origin of decreasing pear production in the eastern USA (van der Zwet and Keil, 1979). Similarly it caused, directly or indirectly, (following restrictive regulations) the progressive suppression of a number of cultivars in Europe: Laxton's Superb, Beurré Durondeau, Passe Crassane for pears, James Grieves and several cider-varieties for apples, and the ornamentals Cotoneaster salicifolius and Pyracantha atalantioïdes (Paulin, 1996).
In New York state, the potential economic loss of the rootstock phase in fire blight was estimated. Economic losses were estimated based on a 10% tree loss in high density apple orchards and were $8818/ha (Momol et al., 1999).
An epidemic in south-west Michigan apple orchards in 2000 was particularly severe and followed unusually warm, humid, wet weather in May. It was estimated that between 350,000 and 450,000 apple trees will be killed and 1500 to 2300 acres of apple orchards will be lost; the development costs of these orchards was over $9 million. Apple yields will be reduced by 35% over the region and some growers will experience losses of 100%. Out of the normal 4.5-7 million bushels produced in the region, the expected crop loss is 2.7 million bushels worth an estimated $10 million. It is estimated that the cumulative loss of yield will be $36 million since 5 years will be required for the region to recover. This will bring the total economic loss in the region to ca $42 million (Longstroth, 2000). The total loss might have surpassed those estimates that were made in 2000, as growers found out that partly infected orchards were not economical to run.
Economic ImpactTop of page
Global economical impact of fire blight is difficult to assess as often, outside major outbreaks, fire blight incidence is not reported. When it is reported it relates to the loss of crop for the year while the economic impact may last for up to 7 years (time for the new trees to be in full production). Furthermore, outbreaks are irregular and mostly unpredictable. Few publications assessed the cost of fire blight. In their review, Bonn and van der Zwet (2000) give the cost of fire blight, when it has been reported, for different parts of the world.
Environmental ImpactTop of page
E. amylovora does not modify any ecosystem. It is very destructive only to orchards of susceptible plant varieties. This situation could change if fire blight was introduced to Central Asia, the origin of the domestic apple tree, and where apple trees still grow wild.
Impact: BiodiversityTop of page
No plant species is threatened of extinction by fire blight. However, it could be interesting to look at whether some local cultivars of apple, pear and/or some ornamentals such as Pyracantha are, or could be, threatened due to fire blight.
Social ImpactTop of page
The presence of fire blight has rendered the culture of some very susceptible host plants very difficult or uneconomical (e.g. pears in the south-west of France, Emilia-Romagna in Italy and California, USA). Fire blight threatened the livelihood of pear growers in Emilia-Romagna, where growing pears is a traditional activity with some families having done so for several generations. In the south of Germany pear trees and some apple trees are part of the landscape. Those very old and very tall trees are extremely difficult to protect from the disease. Their disappearance changes the landscape and their replacement is expensive and takes time to grow and give the landscape its old look. Some of these 'ornamental-orchards' might have a value for the tourism industry.
Risk and Impact FactorsTop of page Invasiveness
- Invasive in its native range
- Proved invasive outside its native range
- Tolerates, or benefits from, cultivation, browsing pressure, mutilation, fire etc
- Highly mobile locally
- Fast growing
- Reproduces asexually
- Host damage
- Negatively impacts agriculture
- Negatively impacts cultural/traditional practices
- Negatively impacts livelihoods
- Highly likely to be transported internationally illegally
- Difficult to identify/detect as a commodity contaminant
- Difficult/costly to control
Uses ListTop of page
- Biological control
- Research model
DiagnosisTop of page
Diagnostic protocols for E. amylovora can differ between laboratories based on the methods, expertise and facilities available. A standardization of detection and diagnostic methods has been developed in Europe (López et al., 2002) and a laboratory guide has been prepared to assist in the identification of plant pathogenic bacteria including E. amylovora (Schaad et al., 2001).
Bacteria are readily recovered from fresh lesions using standard media such as Luria-Bertani (LB) agar, King medium B (KB), and nutrient agar + 5% sucrose (NAS). Cycloheximide (50-100 µg/ml) is often added to these media to inhibit fungal contaminants. Semi-selective media are used for recovery from specimens that potentially harbour significant populations of other bacteria in addition to E. amylovora. These media include: CG medium (Crosse and Goodman, 1973), CCT medium (Ishimaru and Klos, 1984), MS medium (Miller and Schroth, 1972), and MM2Cu medium (Bereswill et al. 1998). Some of these media are selective for E. amylovora; on others E. amylovora forms colonies that have a characteristic colour or colony type (see Description).
Once a pure culture is obtained, the determination of the species amylovora is possible using a combination of the following techniques:
The biochemical and physiological characteristics of E. amylovora used to differentiate it from other Erwinia species are listed in Bergey's Manual of Systematic Bacteriology (Holt et al., 1994); these are restated in part elsewhere (Paulin, 2000; Jones and Geider, 2001). A few key characteristics are that E. amylovora does not reduce nitrate to nitrite, does not produce a fluorescent pigment on KB medium and produces levan from saccharose.
A non-transferable plasmid called pEA29 was thought to be present in every wild type of E. amylovora (Vanneste et al., 1985). This discovery led to the development of molecular assays to identify colonies of E. amylovora and to detect E. amylovora in extracts from symptomatic and asymptomatic plants (Bereswill et al., 1992). Identification assays based on pEA29-PCR are the most widely used (McManus and Jones, 1995a; Llop et al., 2000; Merighi et al., 2000; De Bellis et al., 2007). However, PCR protocols using the specificity of chromosomal DNA have also been developed: ams region (Bereswill et al., 1995); a 187 bp fragment (Taylor et al., 2001); 23S rDNA gene (Maes et al., 1996); 16S/16S-23S rDNA region (Jeng et al., 2001). Some virulent strains of E. amylovora, which did not carry this plasmid pEA29 or its DNA sequence, have recently been found in Spain (Llop et al., 2006) and then in other European countries (Llop et al., 2008); the importance of assays relying on chromosomal DNA sequences might increase.
Other molecular methods
DNA hybridization assays are also available for identifying E. amylovora on the basis of chromosomal (Bereswill et al., 1995; Guilford et al., 1996; Maes et al., 1996) or plasmid pEA29 DNA (Bereswill et al., 1992; McManus and Jones, 1995a).
Some of the DNA-based techniques used for genomic fingerprinting (rep-PCR, PCR ribotyping, PFGE etc., see Notes on Taxonomy and Nomenclature) can also be used to characterize and identify E. amylovora.
Serological tests are used primarily in areas where reference strains can not be maintained or where molecular methods are not available. Polyclonal and monoclonal antisera have been produced against E. amylovora; some are available commercially. Antisera may be used in agglutination tests, double-diffusion tests, ELISA, immunofluorescence and immunodiffusion tests (Paulin and Samson, 1973; Roberts, 1980; Laroche et al., 1987; Gugerli and Gouk, 1994; Mraz et al., 1999). The use of polyclonal antibodies may lead to cross reactions with other bacteria (Roberts, 1980; Calzolari et al., 1982). Conversely, monoclonal antibodies may be too specific and not react with all the strains of E. amylovora (Lin et al., 1987).
Pathogenicity tests, hypersensitive reaction (HR)
It is always recommended to combine the techniques described above for the diagnosis of E. amylovora with some pathogenicity tests or at least a HR test to reduce the risk of wrong determination.
Pathogenicity tests involve inoculation of susceptible plants (growing apple or pear seedlings) or plant parts (flowers or green pears) (Ritchie and Klos, 1974; Pusey, 1997; Jones and Geider, 2001). A range of bacterial concentrations are often used as high inoculum concentrations (1000 million to 10,000 million c.f.u./ml) can result in false positives. Sterile water and known pathogenic strains are used as controls. Re-isolation and identification tests are conducted to confirm the identity of the bacterium. The HR reaction is determined by infiltration of tobacco leaf tissue with bacteria and evaluating the tissue for necrosis or complete collapse after 24 h (Klement, 1971; Jones and Geider, 2001).
Fatty acid analysis
The fatty acid profile of E. amylovora is specific and can be used for diagnosis when gas-liquid chromatographic equipment is available (van der Zwet and Wells, 1993). It was useful for confirming new introductions of the pathogen (van der Zwet and Wells, 1993; Keck et al., 1997) prior to the common availability of molecular techniques.
Detection and InspectionTop of page
Water-soaked flowers, spurs, or shoot tips accompanied by ooze production, followed quickly by necrosis, are early symptoms of fire blight. These symptoms can be detected in an orchard or nursery by experienced observers, but may be overlooked by the inexperienced.
A suitable period for inspection is 3-5 weeks after the blossom period. Look for necrotic leaves and branches, withered blossoms, crooked shoot tips, and ooze. Ooze is more likely to be present in the morning when air humidity is high and host water potential is positive; later in the day when the air is dry, ooze may be shiny and glassy.
Cankers may form on branches and trunks at the junction between infected and healthy bark tissues; therefore, inspections may be needed every 5-7 days throughout the summer or until no new infections are observed.
In autumn, mummified fruits and leaves hanging on dead branches is an indication of fire blight. In winter, the debris helps in locating cankers since the darker bark associated with old infection can blend in with the dormant healthy bark, particularly on older trees.
Similarities to Other Species/ConditionsTop of page
Erwinia pyrifoliae causes necrotic symptoms similar to fire blight on Asian pear trees (Pyrus pyrifoliae cv. Nashi) in South Korea (Rhim et al., 1999). The Asian-pear pathogen can be distinguished from E. amylovora by several microbiological and molecular tests including DNA-DNA similarity assays (Kim et al., 1999; McGhee et al., 2002; Jock and Geider, 2004). An Erwinia found on Asian pear trees in Japan resembles E. pyrifoliae more closely than E. amylovora (Kim et al., 2001; Jock and Geider, 2004); earlier doubtful records of E. amylovora in Japan (Beer et al., 1996; Kim et al., 1996; Momol et al., 1997) could refer to E. pyrifoliae.
An Erwinia isolated from necrotic pear blossoms in Spain differs from E. amylovora in PFGE analysis, in some physiological, serological, and PCR tests, and in pathogenicity on different hosts (Roselló et al., 2002, 2006). Recent taxonomic studies indicate that this pathogen belongs to a new species for which the name Erwinia piriflorinigrans has been proposed (Roselló et al., 2008).
Symptoms of fire blight may sometimes be confused with damage due to other bacteria or to fungi, insects or frost.
Flower infections on pear, caused by Pseudomonas syringae pv. syringae are initially similar to those caused by fire blight. Pseudomonas infections are often favoured by frost; therefore, all blossoms in the cluster and all spurs in the lower part of the tree and sometimes throughout the tree many show symptoms. Fire blight initially infects one or two blossoms per cluster and infected spurs are either scattered or clustered near cankers. Pseudomonas infections rarely extend from infected spurs into branches, and lesions in the bark develop a blister bark condition whereas fire blight infections commonly extend along branches to form large sunken cankers. Blackened pearlets, often seen after outbreaks of P. syringae pv. syringae (and frost), normally drop quickly. When cut they appear to be internally dry, whereas fruitlets invaded by E. amylovora are internally wet with ooze and bacterial growth. Monilia laxa causes blossoms and spurs to collapse but the disease rarely progresses down the branch.
The following insects may cause necrotic flowers and/or blackening of fruitlets: apple and pear weevils (Anthonomus pomorum, A. pyri); pear midges (Contarina pyrivora).
On young (growing) shoots
Young, succulent shoot tips may exhibit necrosis caused by P. syringae pv. syringae; but extension of the lesions beyond the current year's growth is rare. If cankers develop, they are superficial and do not produce ooze.
A number of pathogenic fungi cause cankers on mature shoots; girdling cankers can result in wilting and dieback of shoots, and even in the shepherd-crook symptom associated with fire blight. These fungi include: Nectria galligena, N. cinnabarina, Diaporthe perniciosa [D. eres], Phyalophora obtusa and Potebniamyces discolor [P. pyri]. A close examination of the base of the shoot will allow a clear distinction from fire blight shoot infection (fungal lesions are neatly limited, they do not produce ooze).
Some insects, due to wounds they cause at the base of young shoots, can cause a wilting and dieback of shoot tips suggestive of fire blight. Examples include attacks by leopard moth (Zeuzera pyrina), stem saw fly (Janus compressus) and bud curcullio (Rynchites ceruleus). Look for the presence of these insects and check for the absence of ooze.
A complete, and sometimes sudden, die-back of a tree resulting from fire blight infection in the rootstock may be confused with infection by several species of Phytophthora. Look for a bright-red lesion at the margin of cankers under the bark of fire-blight infected rootstocks (and/or ooze on the surface). Lesions due to Phytophthora are usually black, with clear-cut delimitation between healthy and diseased tissues.
Prevention and ControlTop of page
Legislative Control (Exclusion)
Fire blight is a quarantine disease in most countries and, therefore, shipments of plants, or parts of plants that can be host to fire blight, are under strict regulation. This regulation requires that only healthy plants produced in healthy environments are shipped. At the European level (EU), the genera relevant to quarantine regulation for fire blight are the following: Chaenomeles, Cotoneaster, Crataegus, Cydonia, Eriobotrya, Malus, Mespilus, Pyracantha, Pyrus, Sorbus (other than S. intermedia) and Stranvaesia.
In countries where fire blight is not yet detected, but exposed to permanent threat by nearby foci, a network for monitoring may be preventatively organized (Mazzucchi, 1994; Santos, 1995).
In the EU, a list (map) of so-called 'protected zones' in which fire blight is considered as absent is periodically published. In such protected zones, the import of host plants of fire blight from a contaminated country is forbidden (except from 'protected areas'). In non protected zones, where fire blight is likely to be endemic, specific 'protected areas' are settled (minimal surface: 50 km²) in which special surveys and official control guarantee the absence of fire blight on plants grown in nurseries. From these areas plants are allowed to be shipped (Petter and de Guenin, 1993). Heat treatment of plant propagation material has been proposed (Keck et al., 1995).
In some countries the production and commercialization of the most susceptible cultivars may be banned, or discouraged, particularly for certain cultivars of Cotoneaster, Pyrus, Malus and Crataegus.
As is the case with most bacterial diseases, cultural practices are very important to control fire blight. These practices will tend to reduce the frequency of infections, by decreasing the potential entry of bacteria into the plant: suppression of blossoms by severe trimming of Crataegus hedges has been recommended in the Netherlands (Meijneke, 1984b); suppression of secondary blossoms in pear orchards is a proposed control measure in France (Lecomte and Paulin, 1992).
A complementary strategy for reducing the severity of infection is to follow growing practices aimed at reducing tree vigour and the duration of shoot growth (also see Chemical Control/prohexadione calcium). Restricting nitrogen and water supply to the trees is the most common advice in this respect, together with a regular pruning of the trees.
Insect control is no longer believed to be a key factor in the limitation of movement of bacteria from tree to tree. Nevertheless, care should be taken with transportation of beehives to avoid movement from an infected to a healthy orchard. Similarly, overhead irrigation should be avoided in an orchard with a history of fire blight.
Cultural methods include the sanitation of trees, obtained by a prompt pruning out of symptoms as soon as they are detected in an orchard or a plantation (Steiner, 2000). The disinfection of tools (pruning shears) with chlorine or alcohol is probably useful (Teviotdale et al., 1991) during the growing season but not in winter when trees are dormant (Lecomte and Paulin, 1991).
The early detection of symptoms is important to the success of sanitation programmes. Surveys in orchards and nurseries are recommended in spring just before bloom (active cankers), after bloom (new flower infection), in summer after hailstorms and near the end of the period of shoot elongation (shoot infections and cankers). These surveys must be followed by the removal (cutting out) of all visible infections. In most cases, warning systems will provide an indication of the most suitable period when these surveys are useful (Billing, 2000).
Risking catastrophic tree losses from rootstock blight in high-density apple orchards can be avoided only by selecting trees propagated on resistant rootstocks for new orchards. Several promising highly resistant rootstocks have been released or will soon be released from rootstock-breeding programmes (Cline et al., 2001; Norelli et al., 2003). Some of these are dwarfing rootstocks suitable for high-density orchard systems; avoiding M.9 and M.26 rootstocks in favour of resistant rootstocks is the best control for rootstock blight. Rootstock blight has not been a problem on trees propagated on Budagovsky (B.) 9 and on some Japanese rootstocks (Bessho et al., 2001; Ferree et al., 2002).
Susceptible cultivars (and rootstocks) should be avoided when establishing new orchards and ornamental planting in regions with significant fire blight problems; unfortunately, this advice is seldom followed in practice. For example, many of the most commercially successful apple cultivars introduced in recent years (Braeburn, Fuji, Gala, Ginger Gold, Jonagold, and Pink Lady) are much more susceptible to fire blight than many older cultivars and planting of these cultivars, particularly when propagated on highly susceptible rootstocks, has resulted in devastating financial losses (due to fire blight) to individual apple growers and entire apple industries (Longstroth, 2000).
The number of chemicals of value for fire blight control is very limited; they belong to four categories: copper-containing compounds, antibiotics, growth regulators and elicitors.
Bordeaux mixture and fixed coppers were the first compounds used for control (Psallidas and Tsiantos, 2000). The number and timing of applications depend on the sensitivity of each cultivar to copper injury and the economic significance of the injury. Spring treatments at green tip may reduce the survival of E. amylovora around canker margins (Steiner, 2000); the value of such treatments needs to be established. More commonly, coppers are applied during bloom to prevent flower infection and in summer to prevent shoot infection.
Antibiotics (primarily streptomycin, also oxytetracycline, oxolinic acid and gentamicin) are used to prevent flower and shoot infections; they are more effective than, and not as phytotoxic as, coppers. A standard application schedule for streptomycin is two to three sprays in bloom and one to two sprays post-bloom for five sprays per year. Streptomycin has been used in North America since the 1950s and a few other countries such as New Zealand and Israel; more restrictive governmental regulation has limited and sometimes banned its use in other countries (McManus et al., 2002). Despite the selection of streptomycin-resistant strains in several countries (Jones and Schnabel, 2000; McManus et al., 2002) streptomycin use continues because alternative methods are less effective. In Israel, oxolinic acid, a synthetic quinolone antibiotic, has been used as an alternative to streptomycin (Shtienberg et al., 2001). However, strains of E. amylovora resistant to this antibiotic have been regularly isolated from Israel (Kleitman et al., 2005).
Warning systems, which provide information on risk periods (according to climate, to inoculum and to plant stages), are used in several countries for determining the need for chemical controls; timing of treatment based on warning systems often reduces the number of sprays without a reduction in effectiveness (Billing, 2000). Such systems have been developed in the USA (Thomson et al., 1982; Smith, 1993; Steiner, 2000), in Europe (Jacquart-Romon and Paulin, 1991; Berger et al., 1996; Berrie and Billing, 1997; Billing, 2000) and in Israel (Shtienberg et al., 2003). Some are available commercially. Warning systems have usually been developed for one climatic area; the use of these systems in another climatic area needs to be done very carefully, considering the influence of the different climatic parameters on the epidemiology of the fire blight pathogen (Billing, 2007).
The plant growth regulator prohexadione calcium (Apogee, Regalis) inhibits gibberellin biosynthesis and longitudinal shoot growth (Rademacker, 2000). When vegetative growth is inhibited by this regulator, it is less susceptible to fire blight (Sobiczewski et al., 2001); however, the chemical itself is not toxic to E. amylovora. In field studies, spread of fire blight during summer was reduced following the application of prohexadione calcium near the end of bloom period (Yoder et al., 1999; Costa et al., 2001). Recently, the two acylcyclohexanediones: prohexadione calcium and trinexapac ethyl, were shown to be able to reduce the incidence of fire blight on apple and pear flowers (Spinelli et al., 2007). Prohexadione calcium has been registered for growth and fire blight control in the USA and a few other countries.
Acibenzolar-S-methyl (ASM; tradenames Actigard, Bion) can stimulate the tree's natural defence mechanisms and provide a significant level of fire blight control (Brisset et al., 2000; Maxson-Stein et al., 2002). The highest level of control was obtained when sprays of ASM were initiated at the pink stage of bud development and repeated at weekly intervals, and the level of control increased as treatment rates were increased (Maxson-Stein et al., 2002). ASM was shown to stimulate the expression of pathogenicity related (PR) proteins in apple suggesting that resistance was induced through a systemic acquired resistance (SAR) pathway (Brisset et al., 2000; Maxson-Stein et al., 2002).
Many experiments with antagonistic bacteria have been performed to control fire blight. Extensive field trials have been conducted mainly with strains of Pseudomonas agglomerans and Pseudomonas fluorescens (Vanneste, 1996; Johnson and Stockwell, 1998, 2000; Mercier and Lindow, 2001; Vanneste et al., 2002b). A goal of many of these studies has been to assess factors that influence establishment and spread of the bacterial antagonist (Nuclo et al., 1998; Stockwell et al., 1998; Pusey 1999, 2002; Johnson et al., 2000). Other studies have emphasized the integration of bacterial antagonist with antibiotics (Lindow et al., 1996; Stockwell et al., 1996). In spite of encouraging results, consistency in the level of control has not been easy to obtain. This and the difficulties in registering biological control agents are probably the two main reasons why biological control of fire blight is not widely practiced at present.
Several studies on fire blight susceptibility of species, seedlings, cultivars and rootstocks have been carried out to identify resistant cultivars or sources of fire blight resistance; these sources of resistance are being used by breeding programmes in several countries for apple, pear and ornamentals (Lespinasse and Aldwinckle, 2000). In additional to the use of traditional breeding methods to produce new resistant cultivars, the feasibility of using genetic engineering methods to enhance the resistance of existing cultivars is being evaluated by several breeding programmes (Norelli and Aldwinckle, 2000).
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15/02/2008 Updated by:
Joel Vanneste, HortResearch Ruakura Research Centre, Bioprotection group, East Street, Private Bag 3123, Hamilton, New Zealand
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