European foul brood
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IdentityTop of page
Preferred Scientific Name
- European foul brood
International Common Names
- English: EFB; European foulbrood; European foulbrood disease; European foulbrood of honey bees; Infection of honey bees with Melissococcus plutonius
OverviewTop of page
This datasheet is about European foul brood (EFB) disease of honey bees as defined by the World Organisation for Animal Health, or OIE (OIE, 2013b), i.e. a disease of the larval and pupal stages of honey bees caused by the bacterium Melissococcus plutonius (formerly Melissococcus pluton or Streptococcus pluton). It is found on all continents where Apis mellifera is kept, and also affects A. cerana; it causes significant damage to the beekeeping industry, and is on the list of diseases notifiable to the OIE.
Hosts/Species AffectedTop of page
European foul brood is a disease of honey bees (genus Apis) (OIE, 2013b) and has been reported from colonies of Apis cerana (Ansary et al., 2001; Rana et al., 2004) as well as A. mellifera (FAO, 2006).
Wardell (1982) reported that bee midgut pH may be a factor affecting disease incidence. Studies carried out in Michigan, USA, to investigate the high incidence of EFB in colonies taken to pollinate Vaccinium corymbosum found that midgut pH rose to 6.0-6.5 in larvae fed on blueberry pollen. This is the optimum pH for development of Streptococcus pluton [M. plutonius]; control was effective using a soyabean supplement with an acidifying agent. It was also found that blueberry pollen contained 10 times as much manganese as non-blueberry pollen, and contents of other minerals were also higher, although it is not known whether this is linked to EFB.
DistributionTop of page
European foul brood disease is distributed worldwide (Forsgren et al., 2013) on all continents where Apis mellifera is kept; it also affects A. cerana (FAO, 2006). The Distribution table contains records only for those countries where records are readily available, so it should not be taken as an exhaustive list of where the disease is present.
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|
|Afghanistan||No information available||OIE, 2009|
|Armenia||Disease not reported||OIE, 2009|
|Azerbaijan||Disease not reported||OIE, 2009|
|Bahrain||Disease never reported||OIE, 2009|
|Bangladesh||No information available||OIE, 2009|
|Bhutan||Disease not reported||OIE, 2009|
|Cambodia||No information available||OIE, 2009|
|China||No information available||OIE, 2009|
|-Hong Kong||No information available||OIE, 2009|
|India||Present||Singh and Garg, 2000; OIE, 2009; Rana et al., 2012||First recorded in 1989 in Himachal Pradesh|
|Indonesia||Disease not reported||OIE, 2009|
|Iran||Restricted distribution||OIE, 2009|
|Iraq||Disease never reported||OIE, 2009|
|Japan||Present||OIE, 2009; Okumura et al., 2012|
|Jordan||No information available||OIE, 2009|
|Kazakhstan||Disease not reported||OIE, 2009|
|Korea, Republic of||No information available||OIE, 2009|
|Kuwait||Disease not reported||OIE, 2009|
|Kyrgyzstan||Disease not reported||OIE, 2009|
|Laos||No information available||OIE, 2009|
|Malaysia||Restricted distribution||OIE, 2009|
|Mongolia||No information available||OIE, 2009|
|Myanmar||No information available||OIE, 2009|
|Nepal||No information available||OIE, 2009|
|Oman||No information available||OIE, 2009|
|Pakistan||No information available||OIE, 2009|
|Philippines||No information available||OIE, 2009|
|Qatar||No information available||OIE, 2009|
|Saudi Arabia||No information available||OIE, 2009|
|Singapore||Disease never reported||OIE, 2009|
|Sri Lanka||Disease never reported||OIE, 2009|
|Syria||No information available||OIE, 2009|
|Tajikistan||Disease not reported||OIE, 2009|
|Thailand||Present||Neramitmansook et al., 2003; OIE, 2009|
|Turkey||Present||OIE, 2009; Yalçinkaya and Keskin, 2010|
|United Arab Emirates||Disease not reported||OIE, 2009|
|Vietnam||No information available||OIE, 2009|
|Yemen||No information available||OIE, 2009|
|Angola||No information available||OIE, 2009|
|Benin||No information available||OIE, 2009|
|Botswana||Disease never reported||OIE, 2009|
|Burkina Faso||No information available||OIE, 2009|
|Chad||No information available||OIE, 2009|
|Congo||No information available||OIE, 2009|
|Djibouti||Disease not reported||OIE, 2009|
|Egypt||No information available||OIE, 2009|
|Eritrea||No information available||OIE, 2009|
|Ethiopia||No information available||OIE, 2009|
|Gabon||No information available||OIE, 2009|
|Gambia||No information available||OIE, 2009|
|Ghana||No information available||OIE, 2009|
|Guinea||No information available||OIE, 2009|
|Guinea-Bissau||No information available||OIE, 2009|
|Kenya||No information available||OIE, 2009|
|Lesotho||Disease never reported||OIE, 2009|
|Madagascar||Disease never reported||OIE, 2009|
|Malawi||Present||Mwale, 1992; OIE, 2009|
|Mali||No information available||OIE, 2009|
|Mauritius||Disease never reported||OIE, 2009|
|Morocco||No information available||OIE, 2009|
|Mozambique||No information available||OIE, 2009|
|Namibia||No information available||OIE, 2009|
|Nigeria||No information available||OIE, 2009|
|Rwanda||No information available||OIE, 2009|
|Senegal||No information available||OIE, 2009|
|South Africa||Disease never reported||OIE, 2009|
|Sudan||Disease never reported||OIE, 2009|
|Swaziland||No information available||OIE, 2009|
|Tanzania||No information available||OIE, 2009|
|Togo||No information available||OIE, 2009|
|Tunisia||Disease not reported||OIE, 2009|
|Uganda||No information available||OIE, 2009|
|Zambia||No information available||OIE, 2009|
|Zimbabwe||No information available||OIE, 2009|
|Greenland||Disease never reported||OIE, 2009|
|Mexico||Disease not reported||OIE, 2009|
|USA||Present||Wardell, 1982; OIE, 2009|
Central America and Caribbean
|Belize||Disease not reported||OIE, 2009|
|Costa Rica||Present||OIE, 2009; Calderón and Sánchez, 2011|
|Dominican Republic||Disease not reported||OIE, 2009|
|El Salvador||Present||OIE, 2009|
|Guadeloupe||No information available||OIE, 2009|
|Guatemala||Disease not reported||OIE, 2009|
|Haiti||No information available||OIE, 2009|
|Honduras||No information available||OIE, 2009|
|Jamaica||Disease not reported||OIE, 2009|
|Martinique||No information available||OIE, 2009|
|Nicaragua||No information available||OIE, 2009|
|Panama||No information available||OIE, 2009|
|Argentina||Present||Schotman, 1989; OIE, 2009|
|Bolivia||Present||Schotman, 1989; OIE, 2009|
|Brazil||Present||Bailey, 1984; Schotman, 1989; OIE, 2009|
|Chile||Present||Schotman, 1989; OIE, 2009|
|Colombia||Present||Schotman, 1989; OIE, 2009|
|Ecuador||Disease never reported||OIE, 2009|
|French Guiana||Disease not reported||OIE, 2009|
|Peru||Present||Schotman, 1989; OIE, 2009|
|Uruguay||Present||OIE, 2009; Invernizzi et al., 2011|
|Venezuela||Present||Schotman, 1989; OIE, 2009|
|Albania||No information available||OIE, 2009|
|Austria||Disease not reported||OIE, 2009|
|Belarus||Present||Al'bert et al., 2002; OIE, 2009|
|Belgium||Disease not reported||OIE, 2009|
|Bulgaria||Disease not reported||OIE, 2009|
|Croatia||Disease not reported||OIE, 2009|
|Cyprus||Disease not reported||OIE, 2009|
|Czech Republic||Disease not reported||OIE, 2009|
|Denmark||Disease not reported||OIE, 2009|
|Estonia||Disease not reported||OIE, 2009|
|Finland||Disease not reported||OIE, 2009|
|France||No information available||OIE, 2009|
|Germany||Disease not reported||OIE, 2009|
|Greece||Disease not reported||OIE, 2009|
|Hungary||Restricted distribution||OIE, 2009|
|Iceland||Disease never reported||OIE, 2009|
|Ireland||Disease not reported||OIE, 2009|
|Italy||Present||Greatti, 2005; OIE, 2009|
|Latvia||Disease not reported||OIE, 2009|
|Liechtenstein||Disease not reported||OIE, 2009|
|Lithuania||Disease not reported||OIE, 2009|
|Luxembourg||Disease not reported||OIE, 2009|
|Macedonia||Absent, reported but not confirmed||OIE, 2009|
|Malta||Absent, reported but not confirmed||OIE, 2009|
|Montenegro||Disease never reported||OIE, 2009|
|Netherlands||Disease not reported||OIE, 2009|
|Norway||Disease not reported||OIE, 2009|
|Poland||Disease not reported||OIE, 2009|
|Portugal||Disease not reported||OIE, 2009|
|Romania||Disease not reported||OIE, 2009|
|Russian Federation||Present||OIE, 2009|
|Serbia||No information available||OIE, 2009|
|Slovakia||Disease not reported||OIE, 2009|
|Slovenia||Disease not reported||OIE, 2009|
|Spain||Present||Flores et al., 2000; OIE, 2009|
|Switzerland||Present||OIE, 2009; Fried, 2012|
|UK||Present||OIE, 2009; Budge et al., 2010|
|Ukraine||Disease not reported||OIE, 2009|
|Australia||Present||Schotman, 1989; Witte, 2003; OIE, 2009|
|French Polynesia||No information available||OIE, 2009|
|New Caledonia||Present||OIE, 2009|
|New Zealand||Disease never reported||OIE, 2009|
DiagnosisTop of page
It is unreliable to identify the presence of European foul brood (EFB) by signs of the disease in the field (OIE, 2013a). The most usual and obvious sign of EFB is larval death shortly before they are due to be sealed in their cells, but the cause of this can vary and is not necessarily EFB. Most infected colonies display few visible signs and in any case these often quickly subside before the end of the active season.
Diagnosis of EFB can be carried out by microscopy of suitable cultures, tube agglutination tests on the isolated bacterium, polymerase chain reaction (PCR) and hemi-nested PCR. Hemi-nested PCR can be used to analyse larvae, adults and honey bee products (Djordjevic et al., 1998; McKee et al., 2003; OIE, 2013a).
Diagnosis of the disease is well-documented by the OIE Terrestrial Manual (OIE, 2013a), which should be consulted for techniques in the areas of microscopy, immunological and culture methods, and PCR.
Disease CourseTop of page
As documented by the OIE (2013a), larvae that are infected, but not removed from the colony by nursery bees, become flaccid and light yellow, turning brown, and at the same time they decay into a semi-liquid mass. This then dries out, and forms a dark brown scale that is easily removed from the cells. Bee larvae usually die of this disease 1-2 days before being sealed in their cells, or occasionally shortly afterwards, but always before pupal development. However, Rana et al. (2004) found that Apis cerana larvae died at the prepupal-pupal stage.
Infected larvae die because they have been deprived of food by competition from the bacteria in their guts (FERA, 2013). A study by Kanbar et al. (2004) found that M. plutonius isolated from wounds of honey bee pupae caused by Varroa destructor produced a toxic compound, tyramine, and concluded that this was the causative agent of the observed toxic symptoms in bee larvae.
EpidemiologyTop of page
The OIE (2013a) states that European foul brood is most prevalent when colonies are growing quickly. Bee larvae usually die of this disease 1-2 days before being sealed in their cells, or occasionally shortly afterwards, but always before pupal development. However, Rana et al. (2004) reported a destructive foul brood disease in Himachal Pradesh, India, which attacked native bees, Apis cerana, in March 2002-November 2003 and resulted in death of the brood at the prepupal-pupal stage (like Thai sacbrood virus/American foul brood/ectoparasitic mite infestation rather than European foul brood), but nevertheless was shown on isolation of the causative organism to be M. plutonius infection. Conventional treatment with oxytetracycline failed to control the disease in A. cerana colonies and so this disease was tentatively designated as ‘Cerana’ European foul brood.
Nurse bees often detect sick larvae and remove them from the colony, but if the larvae go undetected, some may survive and develop through to adulthood. Defecation by these surviving larvae serves to propagate the bacteria because their faeces are infected (OIE, 2013a). Voiding of their gut contents at the time of pupation also contaminates the comb (FERA, 2013).
As documented by the OIE (2013a), larvae that are infected, but not removed from the colony by nursery bees, become flaccid and are light yellow, turning brown, and at the same time they decay into a semi-liquid mass. This then dries out, and forms a dark brown scale that is easily removed from the cells. If brood are severely affected, they may give off a very stale or sour odour, sometimes acidic. Contamination of the honeycombs enables the disease to persist from year to year (OIE, 2013a, b).
The disease can be spread by natural movement of bees, but the main cause of spread is the movement of bees and equipment by beekeepers (FERA, 2013).
Studies have implicated Varroa destructor as playing a role in European foul brood infection (Kanbar et al., 2004). Bacteria isolated from wounds of honey bee pupae caused by V. destructor were found to be M. plutonius. The bacteria were grown to produce a toxic compound, tyramine. The authors stated that this indicated that tyramine is the causative agent of the observed toxic symptoms in bee larvae.
ImpactTop of page
Honey bees are important to agriculture and horticulture as pollinators, and European foul brood is a very serious and infectious disease (FERA, 2013). The value of pollination is estimated to exceed the value of products from beehives many-fold (Delaplane and Mayer, 2000). Any disease that causes a significant decrease in honeybee population will have an adverse effect on the beekeeping industry and agricultural production.
The effect of European foul brood outbreaks on honeybee health will also have a significant impact on honey products and thus the livelihood of beekeepers.
Impact on habitats
Bee decline will have a significantly negative affect on pollination in habitats that rely on these insects for development. The value of pollination is estimated to exceed the value of products from beehives many-fold (Delaplane and Mayer, 2000; Cuthbertson and Brown, 2006).
Impact on biodiversity
A decline in native bees, such as A. mellifera, due to the spread of European foul brood, will have a negative effect on bee biodiversity; Cuthbertson and Brown, 2009).
Disease TreatmentTop of page
In the UK at least, weak colonies infected with M. plutonius or those with a high proportion of diseased brood are usually destroyed, but lightly diseased colonies may in certain circumstances be treated with an antibiotic (FERA, 2013).
The use of antibiotics has been studied to control M. plutonius. Brazilian beekeepers were advised to use streptomycin in syrup after studies showed that while Streptococcus plutonius [M. plutonius] was resistant to terramycin, it was sensitive to streptomycin at concentrations over 50 μg/ml and to amplacylin at 2.5 μg/ml (Machado and Lemos, 1974).
In vitro tests using six antibiotics (ciprofloxacin, chlortetracycline, penicillin, oxytetracycline, cloxasillin [cloxacillin?] and tetracycline) against M. plutonius were carried out by Bahman and Rana (2003). They found that oxytetracycline was the most effective in inhibiting the growth of the bacterium. When this antibiotic was added to concentrated sugar syrup and used to treat a diseased colony, suppression of EFB was observed after the 8th day of treatment. The treatment continued to be effective 6 months later.
Unfortunately the use of tetracyclines to control foul brood can lead to traces of the antibiotic in honey. Bonta et al. (2007) determined a method for detecting residues in honey, using reversed-phase high performance liquid chromatography (HPLC) with UV detection.
Other in vitro tests have looked at plant products, namely Ecophil-P and Green TM, for use against the causative agents of brood diseases, including M. plutonius. Gurgulova et al. (2008) reported that Ecophil-P had adequately-expressed antibacterial and antifungal activity against the microorganisms tested. The minimum inhibitory concentration (MIC) of Green TM against M. plutonius, Paenibacillus larvae and P. alvei was comparatively low. The authors concluded with the recommendation that the investigated plant products were suitable for use in beekeeping.
M. plutonius was one of several bee disease and mycoses studied by Al’bert et al. (2002) in Belarus. They found that Bacillus cereus 494, B. subtilis 30043 and B. circulans showed the best probiotic properties.
Studies by Manning (2001) suggested that pollens with a high lipid concentration, dominated by linoleic, linolenic, myristic and dodecanoic acids, play a significant role in inhibiting growth of M. plutonius (amongst other spore-forming bacteria).
Wardell (1982) found that among larvae fed on blueberry pollen, which raises the pH in the midgut to the optimal level for development of M. plutonius, control was effective using a soyabean supplement with an acidifying agent, or terramycin extender patties, or both.
Recent research suggests that the ‘Shook Swarm’ method, in which the colony is transferred to entirely new uncontaminated combs in one operation, is very effective at combating EFB (FERA, 2013).
Integrated Pest Management using a variety of methods as appropriate is recommended by FERA (2013).
Prevention and ControlTop of page
It is important that beekeepers are vigilant and learn to recognise the signs of foul brood, and are careful not to risk introduction of the disease to their apiaries (Tomkies et al., 2009; FERA, 2013).
Spread between colonies can be restricted by quarantine systems and disinfection of equipment (FERA, 2013). Movement of bees and equipment from infected apiaries may be prohibited, for example in the UK (FERA, 2013). The OIE Terrestrial Animal Health Code (OIE, 2013b) regulates the movement of bees, equipment and bee products from countries or zones where the disease is present -- adult bees must come from apiaries meeting certain conditions including an absence of local outbreaks, eggs, larvae and pupae must be inspected by a method in the OIE Terrestrial Manual (OIE, 2013a), equipment must be sterilised, and products must be sterilised or inspected.
Gamma radiation is used in the beekeeping industry to sterilize hive equipment contaminated with the causative agent of American foul brood, Paenibacillus larvae. Although studies have shown that gamma radiation significantly reduced numbers of M. plutonius (Hornitzy, 1986), Hornitzy (1994) reported that combs exposed to up to 8 kGy of gamma radiation still contained viable M. plutonius and the dose required for decontamination has not yet been determined. Irradiation and treatment with sodium hypochlorite solution are both recommended for sterilization of equipment by the OIE Terrestrial Animal Health Code (OIE, 2013b).
Integrated Pest Management using a variety of methods as appropriate is recommended by FERA (2013).
(See also the 'Disease Treatment' section).
ReferencesTop of page
Al'bert RS, Birman BYa, Beznos TV, Lysak VV, Baeva IA, 2002. Investigations into probiotic preparations used in prevention of purulent diseases and mycoses in bees. Veterinarnaya Nauka - Proizvodstvu, No.36:219-226
Belloy L, Imdorf A, Fries I, Forsgren E, Berthoud H, Kuhn R, Charrière JD, 2007. Spatial distribution of Melissococcus plutonius in adult honey bees collected from apiaries and colonies with and without symptoms of European foulbrood. Apidologie, 38(2):136-140. http://www.edpsciences.org/journal/index.cfm?edpsname=apido
Bonta V, Marghitas LA, Dezmirean D, Moise A, Bobis O, Maghear O, 2007. Optimization of HPLC method for quantifying tetracycline residue in honey. Bulletin of University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca. Animal Science and Biotechnologies, 63/64:186-190. http://www.usamvcluj.ro
Budge GE, Barrett B, Jones B, Pietravalle S, Marris G, Chantawannakul P, Thwaites R, Hall J, Cuthbertson AGS, Brown MA, 2010. The occurrence of Melissococcus plutonius in healthy colonies of Apis mellifera and the efficacy of European foulbrood control measures. Journal of Invertebrate Pathology, 105(2):164-170. http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WJV-50BJNX2-1&_user=10&_coverDate=10%2F31%2F2010&_rdoc=9&_fmt=high&_orig=browse&_origin=browse&_zone=rslt_list_item&_srch=doc-info(%23toc%236888%232010%23998949997%232316759%23FLA%23display%23Volume)&_cdi=6888&_sort=d&_docanchor=&_ct=18&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=91d936109212dd95909050ba15c116c6&searchtype=a
Calderón RA, Sánchez LA, 2011. Diagnosis of bee diseases in Africanized honey bees in Costa Rica: prevalence and distribution from September to November 2007. (Diagnóstico de enfermedades en colmenas de abejas africanizadas en Costa Rica: prevalencia y distribución de Setiembre a Noviembre del 2007.) Agronomía Costarricense, 35(2):49-60. http://www.mag.go.cr/rev_agr/index.html
Cuthbertson AGS, Brown MA, 2006. Vital Pollinators: honey bees in apple orchards. The Biologist, 53:78-81
Cuthbertson AGS, Brown MA, 2009. Issues affecting British honey bee biodiversity and the need for conservation of this important ecological component. International Journal of Environmental Science and Technology, 6(4):695-699. http://www.ceers.org/ijest
FAO (Food and Agriculture Organization of the United Nations), 2006. Honey bee diseases and pests: a practical guide. Rome, Italy: Food and Agriculture Organization of the United Nations, viii + 33 pp. [FAO agricultural and food engineering technical report 4.]
FERA (Food and Environment Research Agency), 2013. Foulbrood disease of honey bees and other common brood disorders. Sand Hutton, UK: Food and Environment Research Agency, 37 pp. https://secure.fera.defra.gov.uk/beebase/downloadDocument.cfm?id=7
Forsgren E, Budge GE, Charrière JD, Hornitzky MAZ, 2013. Standard methods for European foulbrood research. Journal of Apicultural Research, 52(1):52.1.12. http://www.ibra.org.uk/articles/The-COLOSS-BEEBOOK-European-foulbrood
Glinski Z, 1972. Properties and antigenic structure of Streptococcus pluton. I. Morphological and cultural characteristics. (Badania nad wlasciwosciami i budowa antygenowa Streptococcus pluton. I. Wlasciwosci morfologiczne i hodowlane.) Medycyna Weterynaryjna, 28(7):399-405
Gurgulova K, Zhelyazkova I, Malinova K, Takova S, 2008. Investigation of Ecophil-P and Green TM biological activity against the causative agents of infectious brood diseases. In: Sbornik dokladi ot nauchnata konferentsiya: Traditsii i s'vremenhost v'v veterinarnata meditsina. Sofia, Bulgaria: Lesotekhnicheski Universitet, 306-316
Invernizzi C, Antúnez K, Campa JP, Harriet J, Mendoza Y, Santos E, Zunino P, 2011. Health status of honey bees in Uruguay. (Situación sanitaria de las abejas melíferas en Uruguay.) Veterinaria (Montevideo), 47(181):15-27. http://www.smvu.com.uy
Kanbar G, Engels W, Nicholson GJ, Hertle R, Winkelmann G, 2004. Tyramine functions as a toxin in honey bee larvae during Varroa-transmitted infection by Melissococcus pluton. FEMS Microbiology Letters, 234(1):149-154
Kardakov VP, 1974. Morphological, cultural and biochemical properties of micro-organisms in collective and state-farm apiaries in Odessa province. Zaraznye i nezaraznye zabolevaniya sel'skokhozyaistvennykh zhivotnykh na yuge Ukrainy, editor I. A. Izmailov and 5 others. Odessa, Ukrainian SSR: Odesskii Sel'skokhozyaistvennyi Institut., 28-33
Machado JO, Lemos MVF, 1975. Isolation of, and control measures for, Streptococcus pluton, in apiaries in Igarapava, Jardinopolis and Ribeirao Preto (SP). (Streptococcus pluton, seu isolamento e combate nos apiarios de Igarapava, Jardinopolis e Ribeirao Preto - Estado de Sao Paulo.) In: Anais do terceiro Congresso Brasileiro de Apicultura, 1974. Piracicaba, SP., Brazil 199-203
OIE (Office International des Epizooties), undated. Diseases of bees. Paris, France: Office International des Epizooties, 6 pp. http://www.oie.int/fileadmin/Home/eng/Media_Center/docs/pdf/Disease_cards/BEES-EN.pdf
OIE (World Organisation for Animal Health), 2013. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. Paris, France: World Organisation for Animal Health. http://www.oie.int/en/international-standard-setting/terrestrial-manual/access-online/
OIE (World Organisation for Animal Health), 2013. Terrestrial Animal Health Code, edition 22. Paris, France: Office International des Epizooties. http://www.oie.int/international-standard-setting/terrestrial-code/access-online/
OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int
Okumura K, Arai R, Okura M, Kirikae T, Takamatsu D, Osaki M, Miyoshi-Akiyama T, 2012. Complete genome sequence of Melissococcus plutonius DAT561, a strain that shows an unusual growth profile and is representative of an endemic cluster in Japan. Journal of Bacteriology, 194(11):3014. http://jb.asm.org/content/194/11/3014.full
Rana BS, Rana R, Gulshan Kumar, Sharma HK, Gupta JK, Kiran Dayal, 2004. 'Cerana' European foulbrood causing havoc to the native bee, Apis cerana F., in Himachal Pradesh. Pest Management and Economic Zoology, 12(1):109-111
Rana BS, Rao KM, Chakravarty SK, Sapna Katna, 2012. Characterization of Melissococcus plutonius causing European foulbrood disease in Apis cerana F. Journal of Apicultural Research, 51(4):306-311. http://www.ibra.org.uk
Tomkies V, Flint J, Johnson G, Waite R, Wilkins S, Danks C, Watkins M, Cuthbertson AGS, Carpana E, Marris G, Budge G, Brown MA, 2009. Development and validation of a novel field test kit for European foulbrood. Apidologie, 40(1):63-72. http://www.edpsciences.org/journal/index.cfm?edpsname=apido
Trüper HG, Clari L de', 1998. Taxonomic note: erratum and correction of further specific epithets formed as substantives (nouns) 'in apposition'. International Journal of Systematic Bacteriology, 48:615
OrganizationsTop of page
World: IBRA, International Bee Research Association, Unit 6, Centre Court, Main Avenue, Treforest, RCT, CF37 5YR, UK, www.ibra.org.uk
World: OIE (World Organisation for Animal Health), 12, rue de Prony, 75017 Paris, France, http://www.oie.int/
UK: British Beekeepers’ Association, National Beekeeping Centre, Stoneleigh Park, Stoneleigh, Warwickshire, CV8 2LG, UK, www.britishbeekeepers.com
ContributorsTop of page
23/03/2012: Original text by:
Dr Claire Beverley, CABI, Nosworthy Way, Wallingford, Oxfordshire, OX10 8DE, UK.
Distribution MapsTop of page
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