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[SANET-MG] Hosema ceranea and CCD

27 April 2007
Prof. Joe Cummins
A Parasitic Fungus Nosema ceranea and Honey Bee Decline
The decline of honey bees has become a global issue of grave concern. The common features of the decline, designated colony collapse disorder (CCD), include failure of foraging bees to return to their hive, the inability of infected hives to attract healthy bees and the infection of bees from inflicted hives with parasites and viruses. A United States National Research Council report focused on introduced parasitic mites, the bacterial foul brood disease and viruses but made cursory mention of pesticides, genetically modified (GM) crops and no consideration of electromagnetic radiation from cell phones that are capable of disrupting bee behaviour or compromising their immune system (1). The sub lethal effects on bees of pesticides , GM crops(2,3) and radiation from mobile phone base station (4) were discussed and the need to include them in fuller investigation of CCD was made clear. Recently a parasitic fungus was implicated as a potential key to CCD but those results were admittedly highly preliminary. The fungus, Nosema ceranea, a single celled parasite was found in affected hives from around the USA as well as in some hives where bees survived (5). Nosema is a single celled obligate parasite belonging to the Microsporidia which infect invertebrates and vertebrates including humans. Nosema infection of honey bees has been known for over one hundred years as it was caused by Nosema apis which is relatively benign. The oriental honey bee Apis cerana was infected with Nosema ceranea but in 2005-2006 the infecting microsporidium was found in Apis mellifera in a highly virulent form(6,7).Nosema ceranea was identified in Apis mellifera honey bees collected from around the world and its importance as an emerging pathogen for beekeeping was stressed (8). The increase in virulence of Nosema ceranae shifted from cerana bees to mellifera bees may be related to mutations in the microsporidium or to environmental factors such as pesticides which decreased immunity in melifera bees. Microsporidia infections in humans, for example, are associated with suppression of the immune system by viruses or drugs. Nosema ceranea causes bees to die within eight days after infection. Foraging bees seem to be the most infected and to leave the colony but be too weak to return, leaving behind a small cluster and a weak colony. The antibiotic fumagillin is the only effective treatment of infected hives (9). Fumagillin treatment is applied using antibiotic dissolved in sugar solution Pollen and hive frames should be irradiated with electron beams (10). Fumagillin has genotoxic (chromosome damaging) effects on humans (11). In spite of the genotoxic potential fumagillin is the drug of choice for the treatment of microsporidia infection in AIDS patients, organ transplant recipients , contact lens wearers and the elderly(12) Fumagillin is also used as a cancer treatment drug because it inhibits angiogenesis (blood flow )to tumours (13). Until 2006 microsporidia were often deemed to be protozoa but in 2006 they were demoted to the kingdom of the fungi. The basis for the demotion was molecular data from a number of genes (14). Microsporidia are obligate intracellular parasites, their spores have thick walls and are highly resistant Within the spores a polar extrusion tube is coiled , when the spore contacts a cell the extrusion tube is uncoiled and pierces the membrane of the target cell injecting spore plasma and initiating uptake of the spore into the cell initiating the reproductive cycle and release of spores (15). The parasite cells lack mitochondria and depend on their hosts for aerobic respiration. However, some mitochondrial genes are present in the nuclei of the parasite and in some cases mitochondrial relics made up of tiny double membrane vesicles containing enzymes but lacking respiratory functions are present (16). Nosema ceranea may be a major contributor to CCD but it seems likely that the virulence of the parasite may depend upon the compromise of the bee’s immune system by pesticides such as the systemic insecticides and fungicides used as seed treatment or as sprays by virus infections or by a combination of exposures that create immunodeficiency. It is time for government agencies to be willing to consider pollution as a contributor to CCD.
1. Committee on the Status of Pollinators in North America American National Research Council Status of Pollinators in North America 2006 ISBN:978-0-309-10289-6 2. Ho,M-W. and Cummins,J. Mystery of disappearing honeybees Science in Society 2007, 34 in press
3. Cummins,J. Requim for the honeybee Science in Society 2007, 34 in press
4. Ho,M-W. Mobile phones and vanishing bees Science in Society 2007, 34 in press 5. Chong.J. and Maugh,T. Experts may have found what's bugging the bees Los Angeles Times 2007 http://www.latimes.com/news/la-sci-bees26apr26,0,2135129,print.story 6. Higes M, Garcia-Palencia P, Martin-Hernandez R and Meana A. Experimental infection of Apis mellifera honeybees with Nosema ceranae (Microsporidia). J Invertebr Pathol. 2007 Mar;94(3):211-7 7. Higes M, Garcia-Palencia P, Martin-Hernandez R and Meana A. Experimental infection of Apis mellifera honeybees with Nosema ceranae (Microsporidia). J Invertebr Pathol. 2007 Mar;94(3):211-7 8. Klee J, Besana AM, Genersch E, Gisder S, Nanetti A, Tam DQ, Chinh TX, Puerta F, Ruz JM, Kryger P, Message D, Hatjina F, Korpela S, Fries I and Paxton RJ. Widespread dispersal of the microsporidian Nosema ceranae, an emergent pathogen of the western honey bee, Apis mellifera. J Invertebr Pathol. 2007 Mar 12; [Epub ahead of print] doi:10.1016/j.jip.2007.02.014
9. Wikepedia Nosema ceranae 2007 http://en.wikipedia.org/wiki/Nosema_ceranae
10. Mantitobia Agriculture, Foods and Rural Initiatives Recommendations for administering antibiotics to honey bee colonies 2006 http://www.gov.mb.ca/agriculture/crops/honey/bha01s00.html 11. Stanimirovic Z, Stevanovic J, Bajic V and Radovic I. Evaluation of genotoxic effects of fumagillin by cytogenetic tests in vivo. Mutat Res. 2007 Mar 30;628(1):1-10 12. Didier ES, Maddry JA, Brindley PJ, Stovall ME and Didier PJ. Therapeutic strategies for human microsporidia infections. Expert Rev Anti Infect Ther. 2005 Jun;3(3):419-34. Review. 13. Chen GJ, Weylie B, Hu C, Zhu J and Forough R FGFR1/PI3K/AKT signaling pathway is a novel target for antiangiogenic effects of the cancer drug Fumagillin (TNP-470). J Cell Biochem. 2007 Feb 12; [Epub ahead of print] 14. James TY, Kauff F, Schoch CL, Matheny PB, Hofstetter V, Cox CJ, Celio G, Gueidan C, Fraker E, Miadlikowska J, Lumbsch HT, Rauhut A, Reeb V, Arnold AE, Amtoft A, Stajich JE, Hosaka K, Sung GH, Johnson D, O'Rourke B, Crockett M, Binder M, Curtis JM, Slot JC, Wang Z, Wilson AW, Schussler A, Longcore JE, O'Donnell K, Mozley-Standridge S, Porter D, Letcher PM, Powell MJ, Taylor JW, White MM, Griffith GW, Davies DR, Humber RA, Morton JB, Sugiyama J, Rossman AY, Rogers JD, Pfister DH, Hewitt D, Hansen K, Hambleton S, Shoemaker RA, Kohlmeyer J, Volkmann-Kohlmeyer B, Spotts RA, Serdani M, Crous PW, Hughes KW, Matsuura K, Langer E, Langer G, Untereiner WA, Lucking R, Budel B, Geiser DM, Aptroot A, Diederich P, Schmitt I, Schultz M, Yahr R, Hibbett DS, Lutzoni F, McLaughlin DJ, Spatafora JW and Vilgalys R. Reconstructing the early evolution of Fungi using a six-gene phylogeny. Nature. 2006 Oct 19;443(7113):818-22. 15. Franzen,C. How do microsporidia invade cells Folia Parasitologica 2005, 52,36-40 16. Roger AJ and Silberman JD. Cell evolution: mitochondria in hiding. Nature. 2002 Aug 22;418(6900):827-9.

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