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acarapisosis of honey bees

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Datasheet

acarapisosis of honey bees

Summary

  • Last modified
  • 26 September 2017
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • acarapisosis of honey bees
  • Overview
  • This datasheet is about acarapisosis of honey bees as defined by the World Organisation for Animal Health, or OIE (OIE, 2012...

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Identity

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Preferred Scientific Name

  • acarapisosis of honey bees

International Common Names

  • English: acarapisosis; acarine disease; bee acariasis
  • Spanish: acariosis
  • French: acariose

Overview

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This datasheet is about acarapisosis of honey bees as defined by the World Organisation for Animal Health, or OIE (OIE, 2012), i.e. a disease of the adult honey bee, Apis mellifera, and possibly of other Apis species (such as Apis cerana). The disease is caused by the tarsonemid mite Acarapis woodi; it is on the list of diseases notifiable to the OIE.

A. woodi, also called the tracheal mite, is an internal obligate parasite of the respiratory system of adult bees, which feeds on haemolymph whilst living and reproducing mainly in the large prothoracic trachea of the bee (OIE, 2012).

Acarapisosis has been found in North and South America, Europe and the Middle East. Mortality rates of bees vary, but a high mortality can be caused by a heavy infestation. The mites can spread by direct contact of bees and newly-hatched adults are most susceptible. Acarapisosis may remain in a colony for years with little damage, and worker bees and queens become less susceptible to infestation with age. Severe infestations cause severe mortality and whole apiaries may be lost (Woodward and Quinn, 2011).

Acarapis is a genus of minute mites that are mainly parasitic on insects. Males and nymphs are difficult to separate from other known species (Denmark et al., 2000) such as Acarapis externus and Acarapis dorsalis. Such similarities indicate a need for diagnostic tests based on genetics such as that documented by Evans et al. (2007) or simple dissection techniques for finding A. woodi in honey bees (Sammataro, 2006).

Hosts/Species Affected

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A. woodi infests European honey bees (Apis mellifera), Africanized honey bees (Apis mellifera scutellata) and Asian honey bees (Apis cerana). Bees may rob honey from other hives, and can come into contact with A. woodi then. Colonies weakened by mite infestation are more vulnerable to robbing. Adult bees less than 24 h old are more susceptible to attack from A. woodi than older bees are (Woodward and Quinn, 2011).

An association between the honey bee behavior of grooming and mite infestation has been recorded. Danka and Villa (2005) reported a 4-fold greater frequency of tracheal mites on the thoraxes of grooming bees compared to non-grooming bees.

Theophilidis et al. (2002) reported that one of the Apis mellifera strains from Greece displayed a morphological feature that could be a resistance mechanism against A. woodi. The authors studied the morphology of prothoracic spiracles in 3 Apis mellifera strains, namely, Apis mellifera carnica, Apis mellifera macedonica and Apis mellifera ligustica. They found that A. m. macedonica showed a smaller area of the atrium and smaller diameter of the trachea, compared to the other strains.

Other reports indicate the importance of brood pupation temperature in A. woodi infestations. McMullan and Brown (2005) compared the performance of newly-emerged bees raised at 30°C with those raised at 34°C, which is a more ‘normal’ brood temperature. The newly-emerged bees raised at 30°C contained over twice the level of mites. The authors concluded that the increased susceptibility to tracheal mites resulting from reduced brood temperature may help to explain the mortality, in the temperature-stressed late winter/early spring period, of colonies with a moderate mite infestation in autumn.

Distribution

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The native range of A. woodi is uncertain. The mites were first reported from dying bee colonies in the Isle of Wight, UK, in 1921 (Woodward and Quinn, 2011), although later evidence suggested that the so-called “Isle of Wight” disease could not be attributed to them (Bailey, 1964, in Denmark et al., 2000).

Widespread bee mortality was attributed to the mites in early twentieth-century Europe. They were first discovered in the USA in Hidalgo County, Texas in early July 1984 and had spread to 17 American states by 1985 (Woodward and Quinn, 2011). The species is now present throughout the continental USA, except Alaska, in both managed and feral honey bee colonies (Woodward and Quinn, 2011).

Acarapisosis has been found in North and South America, Europe and the Middle East (OIE, 2012).

Distribution Table

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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/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

AfghanistanNo information availableOIE, 2009
ArmeniaDisease not reportedOIE, 2009
AzerbaijanDisease not reportedOIE, 2009
BahrainDisease never reportedOIE, 2009
BangladeshNo information availableOIE, 2009
BhutanDisease not reportedOIE, 2009
CambodiaNo information availableOIE, 2009
ChinaNo information availableOIE, 2009
-Hong KongNo information availableOIE, 2009
IndiaPresentEPPO, 2009; OIE, 2009
IndonesiaDisease not reportedOIE, 2009
IranPresentOIE, 2009
IraqDisease never reportedOIE, 2009
IsraelPresentOIE, 2009
JapanDisease not reportedOIE, 2009
JordanNo information availableOIE, 2009
KazakhstanDisease not reportedOIE, 2009
Korea, Republic ofNo information availableOIE, 2009
KuwaitDisease not reportedOIE, 2009
KyrgyzstanDisease not reportedOIE, 2009
LaosNo information availableOIE, 2009
LebanonPresentOIE, 2009
MalaysiaDisease never reportedOIE, 2009
MongoliaNo information availableOIE, 2009
MyanmarNo information availableOIE, 2009
NepalNo information availableOIE, 2009
OmanNo information availableOIE, 2009
PakistanPresentEPPO, 2009; OIE, 2009
PhilippinesNo information availableOIE, 2009
QatarNo information availableOIE, 2009
Saudi ArabiaNo information availableOIE, 2009
SingaporeDisease never reportedOIE, 2009
Sri LankaDisease never reportedOIE, 2009
SyriaNo information availableOIE, 2009
TajikistanDisease not reportedOIE, 2009
ThailandNo information availableOIE, 2009
TurkeyNo information availableOIE, 2009
United Arab EmiratesDisease not reportedOIE, 2009
VietnamNo information availableOIE, 2009
YemenNo information availableOIE, 2009

Africa

AlgeriaDisease not reportedOIE, 2009
AngolaNo information availableOIE, 2009
BeninNo information availableOIE, 2009
BotswanaDisease never reportedOIE, 2009
Burkina FasoNo information availableOIE, 2009
ChadNo information availableOIE, 2009
CongoNo information availableOIE, 2009
Congo Democratic RepublicPresentEPPO, 2009
DjiboutiDisease not reportedOIE, 2009
EgyptPresentRashad et al., 1985; OIE, 2009
EritreaNo information availableOIE, 2009
EthiopiaDisease never reportedOIE, 2009
GabonNo information availableOIE, 2009
GambiaNo information availableOIE, 2009
GhanaNo information availableOIE, 2009
GuineaNo information availableOIE, 2009
Guinea-BissauNo information availableOIE, 2009
KenyaNo information availableOIE, 2009
LesothoDisease never reportedOIE, 2009
MadagascarDisease never reportedOIE, 2009
MalawiNo information availableOIE, 2009
MaliNo information availableOIE, 2009
MauritiusDisease never reportedOIE, 2009
MoroccoNo information availableOIE, 2009
MozambiqueNo information availableOIE, 2009
NamibiaNo information availableOIE, 2009
NigeriaNo information availableOIE, 2009
RwandaNo information availableOIE, 2009
SenegalNo information availableOIE, 2009
South AfricaDisease never reportedOIE, 2009
Spain
-Canary IslandsPresentEPPO, 2009
SudanDisease never reportedOIE, 2009
SwazilandNo information availableOIE, 2009
TanzaniaNo information availableOIE, 2009
TogoNo information availableOIE, 2009
TunisiaDisease not reportedOIE, 2009
UgandaNo information availableOIE, 2009
ZambiaNo information availableOIE, 2009
ZimbabweNo information availableOIE, 2009

North America

CanadaPresentOIE, 2009
GreenlandDisease not reportedOIE, 2009
MexicoRestricted distributionEPPO, 2009; OIE, 2009
USAWidespreadIntroduced1994EPPO, 2009; OIE, 2009; Woodward and Quinn, 2011Found throughout continental USA except Alaska

Central America and Caribbean

BelizeDisease never reportedOIE, 2009
Costa RicaPresentOIE, 2009
CubaPresentOIE, 2009
Dominican RepublicDisease never reportedOIE, 2009
El SalvadorDisease not reportedOIE, 2009
GuadeloupeNo information availableOIE, 2009
GuatemalaDisease not reportedOIE, 2009
HaitiNo information availableOIE, 2009
HondurasNo information availableOIE, 2009
JamaicaDisease never reportedOIE, 2009
MartiniqueDisease never reportedOIE, 2009
NicaraguaDisease not reportedOIE, 2009
PanamaNo information availableOIE, 2009

South America

ArgentinaPresentEPPO, 2009; OIE, 2009
BoliviaNo information availableOIE, 2009
BrazilPresentEPPO, 2009; OIE, 2009
ChilePresentEPPO, 2009; OIE, 2009
ColombiaPresentEPPO, 2009; OIE, 2009
EcuadorDisease never reportedOIE, 2009
French GuianaDisease never reportedOIE, 2009
ParaguayPresentEPPO, 2009
PeruDisease never reportedOIE, 2009
UruguayPresentEPPO, 2009; OIE, 2009
VenezuelaPresentEPPO, 2009; OIE, 2009

Europe

AlbaniaPresentLeka, 1986; OIE, 2009
AustriaPresentEPPO, 2009; OIE, 2009
BelarusDisease never reportedOIE, 2009
BelgiumPresentEPPO, 2009; OIE, 2009
BulgariaNo information availableOIE, 2009
CroatiaDisease never reportedOIE, 2009
CyprusDisease never reportedOIE, 2009
Czech RepublicDisease not reportedOIE, 2009
DenmarkPresentBitidningen, 1991; OIE, 2009
EstoniaDisease not reportedOIE, 2009
FinlandPresentBitidningen, 1991; OIE, 2009
FrancePresentEPPO, 2009; OIE, 2009
GermanyPresentEPPO, 2009; OIE, 2009
GreeceRestricted distributionOIE, 2009
HungaryPresentEPPO, 2009; OIE, 2009
IcelandDisease never reportedOIE, 2009
IrelandPresentEPPO, 2009; OIE, 2009
ItalyPresentEPPO, 2009; OIE, 2009
LatviaDisease not reportedOIE, 2009
LiechtensteinDisease not reportedOIE, 2009
LithuaniaDisease not reportedOIE, 2009
LuxembourgDisease not reportedOIE, 2009
MacedoniaAbsent, reported but not confirmedOIE, 2009
MaltaAbsent, reported but not confirmedOIE, 2009
MontenegroDisease not reportedOIE, 2009
NetherlandsPresentEPPO, 2009; OIE, 2009
NorwayDisease not reportedOIE, 2009
PolandPresentEPPO, 2009; OIE, 2009
PortugalPresentEPPO, 2009; OIE, 2009
RomaniaDisease not reportedOIE, 2009
Russian FederationPresentEPPO, 2009; OIE, 2009
SerbiaDisease not reportedOIE, 2009
SlovakiaDisease not reportedOIE, 2009
SloveniaDisease not reportedOIE, 2009
SpainPresentEPPO, 2009; OIE, 2009; Garrido-Bailón et al., 2012
SwedenDisease never reportedOIE, 2009
SwitzerlandPresentEPPO, 2009; OIE, 2009
UKRestricted distributionEPPO, 2009; OIE, 2009
UkraineDisease not reportedOIE, 2009

Oceania

AustraliaDisease never reportedOIE, 2009
French PolynesiaDisease never reportedOIE, 2009
New CaledoniaDisease never reportedOIE, 2009
New ZealandDisease never reportedOIE, 2009

Diagnosis

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Acarine disease caused by A. woodi infestation may be in a colony for years and cause little damage. Older worker bees and queens are less susceptible to infestation than younger bees. Under conditions of severe infestation, bees are unable to fly, honey production declines and sudden death of the hive occurs in winter (Woodward and Quinn, 2011).

Detection of A. woodi requires dissection of honey bees followed by microscopic observation of the tracheal sacs (FERA, 2010; Kojima et al., 2011). Kojima et al. (2011) developed a PCR method to detect A. woodi thus aiding rapid and sensitive detection in honey bee samples. Brown tracheae signify the presence of mites, as opposed to clear or white ones in healthy bees (OIE, 2012).

Disease Course

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The symptoms in bee colonies infested with A. woodi are few until infestation is severe. Bees may develop disjointed, “K” wings making it impossible for them to fly. Other symptoms include decline of honey production; sudden death of the hive during winter; and brown tracheae instead of healthy clear or white ones (Woodward and Quinn, 2011; OIE, 2012). Diagnosis of acarapisosis is achieved by observing the mites in the tracheae (OIE, 2012).

Pathogenic effects result from mechanical injuries to the tracheae and from physiological disorders caused by obstructions to the air ducts, lesions in the tracheal walls and depletion of haemolymph (OIE, 2008). Worker bees and queens become less susceptible with age (Woodward and Quinn, 2011).

It is considered that in the UK, if 30% of bees in a coloony are infested, the colony will die in the following spring. However, generally in Europe a realistic threshold could be set at 10% (FERA, 2010).

Epidemiology

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The following description of the life cycle is based mostly on information in Woodward and Quinn (2011):

A. woodi passes through four life cycle stages: egg, larva, resting nymph stage and adult. The gravid female mite enters a bee shortly after the bee emerges from the cell, and moves through the first thoracic spiracle into the breathing tubes.

The mite remains in the host for the rest of its life or until the bee dies. The female mite lays 5-7 eggs, 3-4 days after arriving in the host. The adult male mites mature in 11-12 days and the females are mature after 14-15 days.

A. woodi is reported to have an ‘enormous’ egg size, which is said to be due to the fact that it has a quiescent, apodous nymphal stage. The larva receives an ‘abnormal amount’ of energy at the time of hatching, in the form of ‘egg substance’ (Ewing, 1922).

Following mating, gravid females of the next generation crawl to the tip of a bee hair and enter a new host via the spiracles. Bees that are less than 24 hours old tend to be attacked. The heaviest infestations occur when the bees are confined to the hive and under crowded conditions, in the winter. They then show signs of decline during the summer.

Mites can be spread by bee-to-bee contact within a colony and movement between hives, for example swarming or robbing of honey (Woodward and Quinn, 2011), although Korpela (2002) found in Finland that non-infested apiaries near an infested experimental apiary ‘remained non-infested for years’, suggesting a low risk of natural transmission from one apiary to another.

The rapid spread of the mites observed in the USA was facilitated by migratory beekeepers, who moved bee colonies from southern states northwards for crop pollination. Sales of queens and package bees by commercial bee businesses also assisted in dispersing the mites (Woodward and Quinn, 2011).

The movement of bees, equipment and supplies worldwide has assisted in spreading bee diseases to all areas where bees are raised (OIE, 2012).

Impact

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Economic Impact

Beekeepers and commercial bee suppliers could suffer an economic impact due to A. woodi. Bee mortality caused by infestations of A. woodi varies; if infestations are high, mortality can be high and entire apiaries have reportedly been lost. In particular, when A. woodi was introduced to the USA, widespread losses of bee colonies and entire apiaries were reported. However, most honey bee colonies in the USA have developed some resistance to or tolerance of mite infestations and acarine disease is not as severe as it was in the 1980s and 1990s; the introduction of the varroa mite (Varroa destructor) in 1987 overshadowed the impact of A. woodi (Woodward and Quinn, 2011).

Honey bees are important to the agricultural and horticultural sectors as pollinators, so any disease causing decline in bee populations will have a significant impact on their role in these industries.

Environmental Impact

Impact on habitats

Jyothi (2004) studied factors affecting pollinators, pollination and seed production of sunflowers in Karnataka, India during 1996-97. The aim of the study was to look at the effects of endosulfan and parasitic mites, including A. woodi, on Apis mellifera, Apis cerana, Apis florea, Apis dorsata and Trigona iridipennis (they also studied fly and butterfly pollinators). As well as reporting a significant decrease in seed yield and pollinator population after insecticide application, they also found a decrease in targets returning with pollen load at mite-infested colonies compared with normal colonies. Obviously factors affecting pollinators will also have an impact on pollination and thus ultimately affect an ecosystem that relies on pollination for development.

Impact on biodiversity

A. woodi is listed as one of the causes of the decrease of honey bees in the world by Kadowaki (2010).

Social Impact

The effect of acarapisosis outbreaks on honeybee health will also have a significant impact on honey products and thus the livelihood of beekeepers.

Disease Treatment

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See Prevention and Control section.

Prevention and Control

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Movement Control

The federal Honey Bee Act of 1922 was passed in the USA after the initial discovery of A. woodi in the UK in 1921. This Act prohibited the importation of any honey bee into the USA, although in more recent years it has been relaxed somewhat (Woodward and Quinn, 2011).

Chemical Control

In addition to regulating the movement of bees from countries known to have A. woodi, chemical and resistance methods are available (FERA, 2010). Chemical control may involve fumigation with menthol crystals (Woodward and Quinn, 2011).

Underwood and Currie (2009) described a method to fumigate bee colonies with formic acid for the control of A. woodi and Nosema sp. However, regarding A. woodi control, the results were unclear (FERA, 2010). Although it was shown that indoor winter fumigation of honey bee colonies with formic acid was effective in killing a high percentage of mites, it did not significantly reduce the proportion of bees with infested tracheae over the duration of the experiments, which meant that the results were affected by the method used to determine the efficacy of the treatment. According to Woodward and Quinn (2011), evaporating formic acid is also very effective, not only against A. woodi but also against Varroa destructor.

Eischen and Vergara (2004) studied natural products as fumigants for the control of A. woodi. They reported a low but significant mite mortality caused by smoke from pine needles, mesquite, corncobs and coffee beans.

Woodward and Quinn (2011) documented that the smell of bees can be altered, making them less attractive to mites. This is done by the use of grease patties (vegetable shortening and sugar), which keep mites from infesting young bees.

Host Resistance

The Buckfast bee, and some other honey bee stocks, are resistant to tracheal mites. Mites are still able to infest the bees, but the level of infestation is too low to cause significant damage (see Danka and Villa, 1994).

Theophilidis et al. (2002) reported that one of the Apis mellifera strains from Greece displayed a morphological feature that could be a resistance mechanism against A. woodi. The authors studied the morphology of prothoracic spiracles in 3 Apis mellifera strains, namely, Apis mellifera carnica, Apis mellifera macedonica and Apis mellifera ligustica. They found that A. m. macedonica showed a smaller area of the atrium and smaller diameter of the trachea, compared to the other strains.

Destruction of heavily infested bee colonies has benefits in that it removes mites ttat could infest other colonies, and over time will select stocks of acarine-tolerant bees (FERA, 2010).

According to Woodward and Quinn (2011), most honey bee colonies in the USA have developed some resistance to or tolerance of mite infestations and acarine disease is not as severe as it was in the 1980s and 1990s.

References

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Bailey L, 1985. Acarapis woodi: a modern appraisal. Bee World, 66(3):99-104.

Bitidningen, 1991. The acarine [tracheal] mite is now also in Denmark and Finland. (Även trakékvalstret finns nu i Danmark och Finland.) Bitidningen, 90(11):352.

Danka RG; Villa JD, 1994. Resistance to infestation by tracheal mites in Buckfast honey bees: field test and investigations of mechanisms. In: American Bee Journal, 134(12). 831.

Danka RG; Villa JD, 2005. An association in honey bees between autogrooming and the presence of migrating tracheal mites. Apidologie, 36(3):331-333. http://www.edpsciences.org/journal/index.cfm?edpsname=apido

Delfinado-Baker M; Baker EW, 1982. Notes on honey bee mites of the genus Acarapis Hirst (Acari: Tarsonemidae). International Journal of Acarology, 8(4):211-226.

Denmark HA; Cromroy HL; Sanford MT, 2000. Featured Creatures: honey bee tracheal mite, Acarapis woodi. Florida: University of Florida. http://entnemdept.ufl.edu/creatures/misc/bees/tracheal_mite.htm

Donovan BJ; Paul F, 2005. Pseudoscorpions: the forgotten beneficials inside beehives and their potential for management for control of varroa and other arthropod pests. Bee World, 86(4):83-87.

Eischen FA; Vergara CH, 2004. Natural products smoke and its effect on Acarapis woodi and honey bees. Apidologie, 35(4):341-349. http://www.edpsciences.org/journal/index.cfm?edpsname=apido

EPPO, 2009. PQR database. Paris, France: European and Mediterranean Plant Protection Organization. www.eppo.org.

Evans JD; Pettis JS; Smith IB, 2007. A diagnostic genetic test for the honey bee tracheal mite, Acarapis woodi. Journal of Apicultural Research, 46(3):195-197.

Ewing HE, 1922. Studies on the taxonomy and biology of tarsonemid mites, together with a note on the transformations of Acarapis (Tarsonemus) woodi Rennie (Acarina). Canadian Entomologist, 54:104-113.

FERA (Food and Environment Research Agency), 2010. IPM and Acarine. Sand Hutton, UK: Food and Environment Research Agency, 2 pp. https://secure.fera.defra.gov.uk/beebase/downloadDocument.cfm?id=208

Garrido-Bailón E; Bartolomé C; Prieto L; Botías C; Martínez-Salvador A; Meana A; Martín-Hernández R; Higes M, 2012. The prevalence of Acarapis woodi in Spanish honey bee (Apis mellifera) colonies. Experimental Parasitology, 132(4):530-536. http://www.sciencedirect.com/science/journal/00144894

Jyothi JVA, 2004. Factors affecting the pollinators, pollination and seed production of sunflower. Journal of Entomological Research, 28(3):265-268.

Kadowaki T, 2010. Current situations and causes of the decrease of honey bees in the world. Kagaku to Seibutsu, 48(8):577-582. http://www.jsbba.or.jp/02/kaseiindex.html

Kojima Y; Yoshiyama M; Kimura K; Kadowaki T, 2011. PCR-based detection of a tracheal mite of the honey bee Acarapis woodi. Journal of Invertebrate Pathology, 108(2):135-137. http://www.sciencedirect.com/science/article/pii/S0022201111001601

Korpela S, 1998. Pest status and incidence of the honey bee tracheal mite in Finland. Agricultural and Food Science in Finland, 7(4):469-476.

Korpela S, 2002. Honey bee tracheal mite in Finland: population dynamics, natural transmission between apiaries and impacts of introductions via bee trade. In: Bees without frontiers: Sixth European Bee Conference, Cardiff, UK, 1-5 July 2002 [ed. by Jones, R.]. Cardiff, UK: International Bee Research Association, 66-72.

Leka A, 1986. Some parasitoses of bees. (Disa parazitoza në bletët tona.) Buletini i Shkencave Zooteknike e Veterinare, 4(1):39-44.

McMullan JB; Brown MJF, 2005. Brood pupation temperature affects the susceptibility of honeybees (Apis mellifera) to infestation by tracheal mites (Acarapis woodi). Apidologie, 36(1):97-105. http://www.edpsciences.org

Morse RA; Eickwort GC, 1990. Acarapis woodi, a recently evolved species? In: Proceedings of the International Symposium on Recent Research on Bee Pathology, Ghent, Belgium, September 5-7, 1990. 102-107.

OIE (World Organisation for Animal Health), 2008. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. Paris, France: World Organisation for Animal Health. http://www.oie.int/fileadmin/Home/eng/Health_standards/tahm/A_index.htm

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

OIE, 2012. World Animal Health Information Database. Version 2. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int/wahis_2/public/wahid.php/Wahidhome/Home

Rashad SE; Eweis MA; Nour ME, 1985. Studies on the infestation of honeybees (Apis mellifera) by Acarapis woodi in Egypt. In: Proceedings of the Third International Conference on Apiculture in Tropical Climates, Nairobi, Kenya, 5-9 November 1984. 152-156.

Sammataro D, 2006. An easy dissection technique for finding the tracheal mite, Acarapis woodi (Rennie) (Acari: Tarsonemidae), in honey bees, with video link. International Journal of Acarology, 32(4):339-343.

Theophilidis G; Hatjina F; Gregorc A; Pappas N; Zacharioudakis S; Thrasyvoulou A, 2002. Morphological differences in prothoracic spiracles between three strains of Apis mellifera (L). existence of a resistance mechanism against Acarapis woodi. In: Bees without frontiers: Sixth European Bee Conference, Cardiff, UK, 1-5 July 2002 [ed. by Jones, R.]. Cardiff, UK: International Bee Research Association, 62-65.

Underwood RM; Currie RW, 2009. Indoor winter fumigation with formic acid for control of Acarapis woodi (Acari: Tarsonemidae) and Nosema disease, Nosema sp. Journal of Economic Entomology, 102(5):1729-1736. http://docserver.ingentaconnect.com/deliver/connect/esa/00220493/v102n5/s1.pdf?expires=1264653331&id=0000&titleid=10264&checksum=6C4DFB902969BA9E6A493690CCC09F5C

Woodward SL; Quinn JA, 2011. Encyclopedia of Invasive Species. California, USA: ABC-CLIO, LLC, xlii + 764 pp.

Organizations

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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

Contributors

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23/03/2012: Original text by:

Dr Claire Beverley, CABI, Nosworthy Way, Wallingford, OX10 8BU, UK

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