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This 45% reduction in honey beecolonies has been a slow declinemarked at points by disaster.Disasters include widespread honeybee deaths due to pesticides, mites,diseases, and recently, colony col-lapse disorder (see below).

By William Quarles

About one-third of all the foodwe eat requires animal polli-nation, and most of our

fruits, vegetables, and nuts are pol-linated by bees. Due to increaseddevelopment, pesticides, and habi-tat destruction, native bees thatpollinated many of our crops are indecline (Buchmann and Nabhan1996). Crop production in the U.S.has shifted to large monocultures,pollinated almost entirely by com-mercially managed colonies of thehoney bee, Apis mellifera. Largebeekeepers transport thousands ofbee colonies long distances to pro-vide crop pollination throughout theU.S. (USHR 2007; 2008; NAS 2007).Large numbers of bees are needed

for pollination, and availablecolonies are overworked. About halfthe honey bees in the U.S. areneeded just to pollinate the 650,000acre (263,000 ha) California almondcrop. Honey bees are trucked likemigrant workers into California forthe almond crop, then to Washing-ton and Oregon for apples, toFlorida for citrus, and into theNortheast for blueberries. In transit,bees are fed poor diets of cornsyrup and soy proteins. Pollinationof diverse crops at a large numberof locations increases exposure topesticides, mites, and diseases(Delaplane and Mayer 2000; USHR2007; Cannell 2008; Covina 2007).Honey bee pollination is big busi-

ness, and its crop value has beenestimated at $14.6 billion. If thevalue of animals fed on forage cropsare added to the estimate, honeybee pollination is worth about $19billion each year (NAS 2007; Morse

and Calderone 2000; Losey andVaughn 2006).

Decline of the Honey BeeDespite our dependence on honey

bees, we have lost about 45% ofthem over the past 60 years.According to the USDA, there were5.9 million colonies in 1947 andabout 2.4 million today. However,since 1985, beekeepers with fewerthan five colonies have not beencounted. This change results in anundercount of about 0.86 millioncolonies each year. So we haveabout 3.3 million colonies today,and have lost at least 45% of ourbees (NAS 2007).

In This Issue

Honey Bee Collapse 1

ESA Report 11

Calendar 12

Volume XXX, Number 9/10, September/October 2008

Pesticides and Honey BeeColony Collapse Disorder

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University of California, Davis researcher and beekeeper Michael “Kim”Fondrk is shown tending bees in the Roy Gill almond orchard, Dixon,California. The boxes are beehives, and more than a million of thesecolonies are needed to pollinate California almonds.

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2 Box 7414, Berkeley, CA 94707IPM Practitioner, XXX(9/10) September/October 2008

UpdateThe first round of major losses

was due to the careless use of pes-ticides, development, loss of forage,and other factors. Honey beecolonies declined from 5.9 millionin 1947 to 4.1 million in 1972—aloss of about 30%. This first crisiswas mentioned by Rachel Carson inSilent Spring (NAS 2007; Carson1962). In California alone, pesti-cides killed about one million beecolonies between 1966 and 1979.Large numbers of bees were killedby organochlorine, carbamate,pyrethroid, and organophosphatepesticides. In the 1970s, farmersadjusted application methods tohelp protect bees. Efforts weremade to restrict pesticide applica-tions while crops are in bloom, andduring times when honey bees areactively foraging. However, residualpesticides have undoubtedly keptbees under stress (NAS 2007;Atkins 1992; Johansen 1977; Morse1975).

Mites and PesticidesDisaster struck again in the

1990s. The weakened bees wereattacked starting in 1984 by thetrachael mite, Acarapis woodi, andby the “vampire mite” Varroadestructor in 1987. Tracheal mitesinterfere with bee respiration.Varroa mites are lethal to a colonybecause they interfere with repro-duction and carry pathogens thatinfect and destroy the bees. Bee lar-vae and pupae are parasitized, andthose that live to become adults areweakened. They are starved, show-ing low weight, low serum proteins,severe wing deformations, andreduced longevity. Varroa infesta-tions are fatal to a colony within sixmonths if untreated, and honey beecolony losses of 30-80% were seenin some states in 1995-1996 (NAS2007; Sammataro et al. 2000;Benjamin and McCallum 2008).The mites were bad, the reaction

also bad. Beekeepers treated miteinfestations with pesticides intro-duced directly into the hive. First,the pyrethroid tau-fluvalinate(Apistan®), then the organophos-phate coumaphos (CheckMite®)were used to control the parasitic

mites. Exposure to these pesticidesdepresses bee immune systems andmakes them even more susceptibleto varroa transmitted pathogens(Desneux et al. 2007; Morse 1975).The mite-pesticide combination hascaused a drop from 4.2 millionhoney bee colonies in 1981 to 2.4million colonies in 2005. This is adecline of about 43% using rawUSDA data. When this figure is cor-rected for a change in USDA count-ing methodology in 1985, the esti-mate of colony losses due to pesti-cides and mites is 22% (NAS 2007).

Pesticide ResistancePesticide treatments were effective

for a time, but varroa mites are nowresistant to both fluvalinate andcoumaphos. Replacement pesti-cides, including biocontrol fungihave been studied, but have notbeen widely adopted. Many expertsbelieve that IPM management,including resistant queens may benecessary in the future (Baxter etal. 1998; Delaplane et al. 2006;Oliver 2007; Elzen and Westervelt2002; NAS 2007).Other stresses contributing to

U.S. honey bee decline includeinvasion of Africanized bees in1990, pathogens such as Nosemaand Paenibacillus larvae, and pestssuch as the small hive beetle,Aethina tumida, and the wax moth,Galleria melonella (NAS 2007;Quarles 1994).

Massive Losses of BeesIn the last ten years, we have

seen large, dramatic losses of honeybees both in the U.S. and else-where. Massive honey bee deathshave been seen in France,Germany, Belgium, and the UK.Problems were first noticed inFrance in 1994. Beekeepers thereblamed the sudden deaths onGaucho®, a new systemic pesticidewith the active ingredient imidaclo-prid. Gaucho was used to protectsunflower seeds against pests.Treated seeds grow into sunflowerscontaining imidacloprid in flowers(8 ppb), pollen (3 ppb) and nectar(1.9 ppb). Perhaps coincidentally,the French honey bee population

The IPM Practitioner is published six timesper year by the Bio-Integral ResourceCenter (BIRC), a non-profit corporationundertaking research and education in inte-grated pest management.Managing Editor William QuarlesContributing Editors Sheila Daar

Tanya DrlikLaurie Swiadon

Editor-at-Large Joel GrossmanBusiness Manager Jennifer BatesArtist Diane Kuhn

For media kits or other advertising informa-tion, contact Bill Quarles at 510/524-2567,birc@igc.org.

Advisory BoardGeorge Bird, Michigan State Univ.; SterlingBunnell, M.D., Berkeley, CA ; Momei Chen,Jepson Herbarium, Univ. Calif., Berkeley;Sharon Collman, Coop Extn., Wash. StateUniv.; Sheila Daar, Daar & Associates,Berkeley, CA; Walter Ebeling, UCLA, Emer.;Steve Frantz, Global Environmental Options,Longmeadow, MA; Linda Gilkeson, CanadianMinistry of Envir., Victoria, BC; JosephHancock, Univ. Calif, Berkeley; HelgaOlkowski, William Olkowski, Birc Founders;George Poinar, Oregon State University,Corvallis, OR; Ramesh Chandra Saxena,ICIPE, Nairobi, Kenya; Ruth Troetschler, PTFPress, Los Altos, CA; J.C. van Lenteren,Agricultural University Wageningen, TheNetherlands.ManuscriptsThe IPMP welcomes accounts of IPM for anypest situation. Write for details on format formanuscripts or email us, birc@igc.org.

CitationsThe material here is protected by copyright,and may not be reproduced in any form,either written, electronic or otherwise withoutwritten permission from BIRC. ContactWilliam Quarles at 510/524-2567 for properpublication credits and acknowledgement.

Subscriptions/MembershipsA subscription to the IPMP is one of the bene-fits of membership in BIRC. We also answerpest management questions for our membersand help them search for information.Memberships are $60/yr (institutions/libraries/businesses); $35/yr (individuals).Canadian subscribers add $15 postage. Allother foreign subscribers add $25 airmailpostage. A Dual membership, which includesa combined subscription to both the IPMPand the Common Sense Pest ControlQuarterly, costs $85/yr (institutions); $55/yr(individuals). Government purchase ordersaccepted. Donations to BIRC are tax-deductible.FEI# 94-2554036.

Change of AddressWhen writing to request a change of address,please send a copy of a recent address label.© 2008 BIRC, PO Box 7414, Berkeley, CA94707; (510) 524-2567; FAX (510) 524-1758.All rights reserved. ISSN #0738-968X

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started to crash as the treated sun-flowers began to bloom and nectarbegan to flow. The manufacturerdenied that there was any relation-ship between seed treatments anddeaths of the bees (Bonmatin et al.2005; Schmuck et al. 2001).Bees in France had definitely

been exposed to pesticides. Onestudy used traps to collect pollensamples at 125 widely separatedcolonies throughout the country.They analyzed for 36 different pesti-cides and found residues of 19,including fipronil, imidacloprid, car-baryl, aldicarb, cypermethrin,chlorpyrifos and others. Pesticidesfound in largest concentrationswere coumaphos and tau-fluvali-nate—the chemicals used to treatvarroa mite infestations. The mostfrequent residues found were imida-cloprid (49.4%), imidaclopridmetabolites (44.4%), and fipronil(12.4%). Imidacloprid or itsmetabolites were found in 69% ofthe samples. Pollen was contami-nated with 1-5 pesticides. The con-tamination was seasonal only withfipronil, with fipronil maxima inMarch and April (Chauzat et al.2006).

French Pesticide BanPressure from the French bee-

keeping industry led to a ban onthe use of imidacloprid on sunflow-ers and corn, but honey bees con-tinued to die. Finally, in 2004France also banned the pesticideRegent®, which has the activeingredient fipronil. According toSchacker (2008), the bees started torecover in 2005 and even largernumbers were seen in 2006.There is no doubt that these

potent new pesticides can kill beesif bees are exposed. Just 3.7 bil-lionths of a gram of imidaclopridwill likely kill a bee (oral LD50= 3.7to 81 ng/bee). Another pesticide,fipronil, is also potent with an oralLD50 of 3.7 to 6 ng/bee. For com-parison, the oral LD50 of cyperme-thrin is 160 ng/bee and for theorganophosphate dimethoate 152ng/bee (Colin et al. 2004; Schmucket al. 2001; Suchail et al. 2001ab).In May of 2008, about 50% of

honey bees in the German state of

Baden-Wurttemberg were killed.The problem was traced to theapplication of the systemic pesti-cides clothianidin and imidaclopridto seeds. According to the manufac-turer, farmers applied these pesti-cides without using the adhesivesrecommended to keep the pesticideslocalized to seeds. Germany bannedthe use of these pesticides for seedtreatment after this incident (ENS2008; EPA 2008).

Large Losses in the U.S.Large losses have also been seen

in the U.S. According to a NationalAcademy of Science report (NAS2007), “During the winter of 1995-1996, northern U.S. beekeepersexperienced their largest losses inhistory; in some states, 30 to 80%of colonies were lost. Similar losseswere observed in the winters of2000-2001 and 2004-2005. Data oncolony losses are derived frominformal surveys of beekeepers, andthe exact causes of colony deathshave not been established.” Possiblecauses were a combination of pesti-cides, mites, and pathogens (NAS2007).Even larger losses have been seen

in the last two years. About 33% ofthe managed honey bee colonies inthe U.S. were lost in the winter of

2006-2007. Another 36% were lostduring the winter of 2007-2008.Some of the loss was due to over-wintering stress, but many coloniesthat died showed a strange, newbehavior. Entomologists studyingthese large losses called the phe-nomenon colony collapse disorder(CCD) (USHR 2007; 2008)

Colony Collapse DisorderColony collapse disorder (CCD)

was first noticed in November of2006, although it may have startedabout two years earlier. Normally,a large number of bee colonies, per-haps 15-25%, die due to overwin-tering stress, including starvation.During the winter of 2006-2007,some beekeeping operations lost30-90% of their colonies, and aver-age overall losses of about 33%were about 10-15% larger thanusual (USHR 2007; Bee 2007;Henderson et al. 2007).Adult bees were not dying in

their hives or near their hives, theysimply disappeared. They left andnever came back. Beekeepers inPennsylvania with CCD lost anaverage of 75% of their colonies in2006, while those free of CCD lostabout 25% (Bee 2007). Losses fromCCD also occurred in the winter of2007-2008, when about 36% of allbee colonies were lost (USHR 2008).

3IPM Practitioner, XXX(9/10) September/October 2008 Box 7414, Berkeley, CA 94707

Update

A honey bee is headed toward an almond blossom. Honey beepollination is essential for the California almond crop.

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UpdateSymptoms of CCD include:•Foraging adult bees leave the

hive and do not return.•Decline is rapid, and the colony

goes from a large, strong colonywith no signs of mite infestation toa dead one within a couple ofmonths.•No dead bees are found in, or

near the hive.•Adult bees left in the hive show

signs of a depressed immune sys-tem.•Queen and apparently healthy

brood remain in the hive.•Nearby bees wait weeks before

they enter the hive to remove food.•Predators such as the small hive

beetle or the wax moth also delayentry.•When a dead hive is placed on

top of a healthy one, so that thehealthy bees are forced to occupythe hive, those bees also disappear(USHR 2007; 2008; USDA 2008;Hayes 2007).

Extent of the ProblemAccording to an online National

Bee Survey through June of 2007,CCD is widespread throughout thecountry, and has been reported inat least 35 states. Both large com-mercial beekeepers that transporttheir bees from state to state andsmall non-migratory beekeepers arereporting the problem (USHR 2007).Both large and small beekeepersare reporting severe losses, butoperations with 1,000-10,000colonies are reporting extreme loss-es more often. These are beekeepersthat focus on migratory crop polli-nation. Their bees are exposed totransportation stress, and are morelikely to encounter pesticides (Bee2007).

Is it Real?Hard data about honey bees is

hard to get. The USDA counts thenumber of honey producingcolonies every year. However, thisestimate is somewhat unreliablebecause colonies used only for polli-nation are not counted. Starting in1985, beekeepers that maintainfewer than five colonies have notbeen included in the count. Since

colonies are moved from state tostate, colonies are sometimescounted more than once.Furthermore, health of honey beecolonies is not monitored, and beesare not systematically checked forexposure to pesticides andpathogens (NAS 2007).Most of the information about

CCD has been obtained from casestudies of individual beekeepers, byonline surveys completed by bee-keepers (625 of them), and by sur-veys conducted by trade magazines.

This information is not comprehen-sive and may not reflect the totalextent of the problem. Though com-prehensive data is not available, itis clear that very large numbers ofbees are dying in the U.S. (Bee2007).

Colony ReplacementIf we had not replaced them, we

would have lost 55% of our honeybee colonies over the last two years.Fortunately, colonies are replacedin the spring either by ordering“package bees” from suppliers or bysplitting existing colonies andadding new queens. All the replace-ment activity is expensive, and thenumbers of U.S. bees are limited. In2005, U.S. beekeepers were forcedto import bees for the first timesince 1922. Over 100,000 colonies

were imported from Australia.Increased expense has forced manybeekeepers out of business, andhas driven a steady downwardtrend in the number of colonies.The overall loss of 45% of our beessince 1947 has occurred despiteconstant colony replacements (NAS2007).At the same time that honey bee

numbers are decreasing, plantedacreage requiring pollination hasincreased. Increasing need plusdecreased supply has resulted in

higher prices for pollination. In2007, the average rental cost for abee colony for almond pollinationwas $150, about double what it wasthe year before (USHR 2007).

Effect of the SeasonMost of the massive bee kills in

the U.S. are occurring during over-wintering. This is not too surprisingdue to the basic biology of thehoney bee. Honey bees live inperennial colonies, but the natureof the colony changes with the sea-sons (see Box A Honey Bee Biology).Queens live 1-3 years, worker beeslive about 6 weeks in the summerand 6 months during the fall andwinter. Large numbers of foragerscollect nectar and pollen during thesummer. Foraging kills a lot ofthem, and colony numbers drop in

Closeup of a hive suffering from colony collapse disorder. Note thatbrood is present, but that adult bees have disappeared.

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5IPM Practitioner, XXX(9/10) September/October 2008 Box 7414, Berkeley, CA 94707

Updatethe fall. A smaller colony overwin-ters, then queens start laying eggsin late December, and the colonystarts to expand in January(Winston 1987; Langstroth 1923;Morse 1975).Adult winter bees are old bees,

and are physiologically differentfrom summer bees. Because of theirrelatively long lifetime, winter beeshave had more time to be exposedto pesticides and pathogens. Winterbees are often more susceptible topesticides. This may be becausethey have greater fat deposits,allowing pesticides to accumulate.For instance, winter bees are 4xmore sensitive to the chronic lethaleffects of imidacloprid than aresummer bees. Cold temperaturesalso make pyrethroids andorganophosphates more toxic tobees (Decourtye et al. 2003;Johansen 1975; Belzunces et al.2001b).In Northern states, overwintering

bees must cluster for warmth, andeat massive amounts of storedhoney. Consumption ranges from30-80 lbs (13.6-36.3 kg) per hive(Farrar 1952). Clustering beesrarely defecate, so any pesticideresidue in the honey could build upin their bodies (Morse 1975;Langstroth 1923). They are exposedall winter to any pesticides in thehoneycomb from mite treatments.Unprecedented amounts of fluvali-nate, up to 400 ppm, have beenfound in CCD hives (USHR 2008).Winter colonies are also smaller,typically 10,000 workers versus40,000 workers found in the sum-mer. Since there are fewer bees inthe winter, loss of smaller numberscan lead to colony collapse (Morse1975; Winston 1987).Because of the problems of over-

wintering in cold climates, manybeekeepers transport their bees towarmer climates to overwinter.These colonies are allowed to forageand are sometimes fed corn syrupor sucrose solutions. Even thesepampered bees are still exposed toany toxins or pathogens present inthe hive, and CCD was actually firstobserved in colonies transportedfrom Pennsylvania to overwinter inFlorida (USHR 2007).

According to an online survey of625 beekeepers, most of them donot feed their overwintering bees.But providing food does not stopCCD. When colonies are fed sucrosesyrup, about half these colonies stillget CCD. Feeding of this sort doesnot stop ingestion of stored pollenand exposures to pesticides in waxand honeycomb (see below) (Bee2007).

What is Causing CCD?The exact cause of CCD has not

yet been determined. A CCD taskforce has been established, and anumber of possibilities are beinginvestigated (USDA 2008).Pathogens are known to kill honeybees, and pathogens are beinginvestigated as a cause of CCD.Many of the colonies are infectedwith Israeli Acute Paralysis Virus(IAPV). However, this virus isbelieved to be a marker, not acause. Also, this pathogen does notfit the specifics of the disorder. Beesdying from pathogens are thrownout of the hive by housekeepingbees, and dead bees accumulate infront of the hive. Certainly miteswill kill bees, but again deaths frommites are well characterized. CCDcolonies start out healthy and mitefree. Surviving bees do not showmite infestations (USHR 2007;Schacker 2008).

Pesticides as a Cause ofCCD

The surviving bees are showingsigns of stress. Pesticides and otherchemicals are known to kill beesand depress their immune systems(Morse 1975; Desneux et al. 2007).Many currently used pesticidessuch as imidacloprid, clothianidin,fipronil, chlorpyrifos and others areextremely toxic to bees. Pesticidescan also exert sublethal effects thatinclude disorientation and loss ofshort term memory that may pre-vent bees from returning to thehive. So pesticide exposure andpesticide contamination of the hivecould explain most of the symptomsof CCD (USHR 2007; Decourtye etal. 2003; Suchail et al. 2001ab;Chauzat et al. 2006). One observa-

tion that seems to implicate pesti-cides is that organic beekeepers donot seem to have CCD (Schacker2008).Bees can come into contact with

pesticides when foraging or whenthe hive is treated with pesticides tokill mites. Foragers can collect con-taminated pollen and nectar andbring it back to the hive. Some ofthe nectar and pollen is mixedtogether with enzymes to form beebread. In the hive bees evaporatewater from nectar to producehoney. Any pesticide in the nectaris concentrated at least 4x in thehoney, which is stored for later use.So bees can be exposed both in thefield and in the hive (Bonmatin etal. 2005; Kievits 2007).

Pesticides in the HiveDespite the importance of honey

bees, colony health and pesticideexposure has not been systemati-cally monitored, and EPA registra-tion of a pesticide does not requirea measurement of sublethal effectson honey bees (NAS 2007). Pesticidecontamination of bees is only nowbeing systematically studied. Re-searchers at Penn State Universityanalyzed bees, pollen, and waxhoney combs for pesticide residuesin 2008. Some of the samples camefrom CCD colonies, others camefrom colonies that showed no symp-toms. All of the bees tested werecarrying at least one pesticide. Atotal of 108 pollen samples showedresidues of 56 pesticides andmetabolites. Each pollen sampleaveraged 6 pesticides, and one sam-ple showed 31. In 88 wax samples,residues of 22 pesticides andmetabolites were found. The miti-cides coumaphos and fluvalinatewere found in all wax samples. Thisdiverse contamination opens thequestion of synergism. Mixtures ofpesticides are known to be moretoxic to bees than individual prod-ucts. Some fungicides, for instance,are known to increase the toxiceffects of insecticides (Johansen1977; Atkins 1992; PA 2008; USHR2008; Pilling and Jepson 1993;Schmuck et al. 2003).According to David Mendes, Vice

President of the American Bee-

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Update

A beehive is dynamic, with rapidpopulation turnover, especially in thesummer. A summer hive has typically40-45% of its population as eggs, lar-vae and pupae. About 55-60% areadult workers that live about 6weeks, spending their first 3 weeksworking in the hive, and then 3weeks foraging. It takes about 3weeks for an egg to become an adult,so as the foraging population dies, itis replaced by hive workers, and hiveworkers are replaced by new adults.Every 3 weeks in the summer there isa new foraging population, and every6 weeks there is a completely newgeneration of adults (Wilson 2004).Numbers of honey bees in colonies

vary by the season. A winter colonyhas about 10,000 workers, a summercolony 40,000. Foragers feed on nec-tar and collect pollen. The pollen ismade into bee bread, which is a com-bination of pollen, nectar andenzymes. This is used to feed larvae.Up to 100 kg (220 lbs) of nectar iscollected by individual foragers, about50 mg at a time. This is made intoabout 30 kg (66 lbs) of honey, whichis used as food for overwintering(Kievits 2007).The fate of the colony depends on

the workers. Workers in the summerlive 15-38 days; spring and fall 30-60days. Winter bees live an average of140 days, but as long as a year. Beesdrink large amounts of water. Theycollect water, propolis, which isresinous glue used for construction,nectar, which is used to make honey;and pollen, which is especially usedto feed developing larvae. Nectar is 5-80% sugars, mostly sucrose, fructoseand glucose. Foragers transfer nectarto nurse bees that add enzymes,reduce the water content to less than18%, then store it in the honey combas a food source for the whole colony.Most of the honey bee nutritioncomes from pollen, which containsprotein, fat, vitamins, minerals andsteroids (Winston 1987).

Life StagesLife stages include eggs, larvae,

pupae and adults. Adults includemales (drones), female workers, and aqueen. The queen starts laying eggsin December. Over a period of 3 days

the egg membrane slowly dissolves,revealing the larva. Larvae are fed bynurse bees a combination of glandu-lar secretions and honey over the firstfour days, and larvae molt daily. Foodis often just dumped into the cell andlarvae are exposed to the food by con-tact and ingestion. Larvae are fedhundreds of times by nurse bees.Pollen is fed starting on the 3rd day.By the 6th day of the larval stage and9 days after egglaying, the cell iscapped. Over a period of 3-5 daysafter the cell is capped, larvae standupright in the cell, defecate and spina cocoon for the pupal stage. Thepupal stage lasts about 8-9 days,then the pupae molts, becoming anadult. The process for development ofa new worker takes about 21 days(Winston 1987).Adults eat honey and pollen. Honey

is obtained from storage or by beggingand trophallaxis. Lack of pollen andprotein during the first 10 days ofadult life reduces life span. Some pol-lens are more nutritious than others,but bees must obtain 10 essentialamino acids to continue living(Winston 1987).

Hives and SwarmsWild honey bees swarm with a

queen looking for a nest. When theyfind an appropriate space, they startbuilding the waxy honey comb.Hexagonal cells for worker brood andhoney are the same size, drone cellsare larger; queens are raised in thim-ble sized appendages to the comb.Comb construction takes about 45days. Several combs are constructed,spaced about 0.95 cm (3/8 in) apart.Combs are glued to the nest site withbee glue or propolis, which is alsoused to cement cracks, and insulatethe nesting cavity (Winston 1987).Domestic beehives are based on the

Langstroth principle. Wooden framescontaining beeswax or plastic hexago-nal cell templates are suspended in awooden box about 0.95 cm (3/8 in)apart. These boxes are called supers,and they can be stacked vertically.Supers are placed on a wooden foun-dation, and the top super has one ortwo wooden lids. This simple arrange-ment makes it easy to move the hivesaround. Honey is produced in the top

supers, brood in the lower ones.Honey laden frames can be removed,uncapped with a knife, and honey isremoved with a centrifuge. Framesare reused for years (Langstroth1923; Winston 1987).

Age and WorkJobs inside the hive are done by

young adults, older adults act asguards and foragers. Hive jobsinclude first cleaning, then acting asnurses, food processing and combbuilding. These jobs are age relatedbecause they rely on glandular devel-opment. Nurses are about 7-13 daysold. Adults start foraging when theyare about 23 days old. Variations areseen in these ages according to com-plex factors and the needs of thecolony. When there are large colonylosses, workers start foraging atyounger ages (Winston 1987).Bees spend very roughly 10-15

days collecting nectar; 15-20 dayscollecting pollen; 30 days eatingpollen; about 30 days processing andstoring nectar; and about 10 daysfeeding larvae. So adults are exposedto nectar for 45 days, to pollen about50 days of their adult lives. Finally,there is extensive trophallaxis so thatfood collected by a few bees is distrib-uted throughout a colony within 24hours (Winston 1987)

Foraging BehaviorHoney bees specialize in their forag-

ing. They tend to collect either nectaror pollen from a single species offlowers until the food source isdepleted. For instance, one studyshowed 58% of foragers collected onlynectar, 25% only pollen, and 17%both nectar and pollen. Good nectarproducers are maple, milkweed,phacelia, sage, thyme, acacia and fig-wort. Colonies need 15-30 kg (33-66lbs) of pollen every year, but may col-lect up to 55 kg (121 lbs). Coloniesneed 60-80 kg (132-176 lbs) of honeyeach year. Workers must make one tofour million trips a year to managethis supply. Relatively few resourcesare used for scouting. A few scoutsfind a rich resource, and communi-cate its location through a dance thatrecruits large numbers of foragers(Winston 1987)

Box A. Biology of the Honey Bee

keeping Federation, 18 of his hiveswere used in the above study.Samples of pollen from Florida cit-rus showed high levels of imidaclo-prid and aldicarb. In Massachusettscranberries, fungicide levels as highas 7000 ppb were found in pollen.Only four hives were still alive 10months later (USHR 2008).

Are Systemic PesticidesCausing CCD?

Though many pesticides canstress bees, some U.S. beekeepersbelieve that CCD is caused by beeexposures to new pesticides, suchas imidacloprid (IMD), clothianidin,fipronil, and others (USHR 2007).For instance, imidacloprid is usedextensively in the U.S. on cropssuch as blueberries, citrus, cran-berries, strawberries, pecans, stonefruits, cotton, corn, melons, vegeta-bles, forests, ornamentals, and turf.Some of these are crops commer-cially pollinated by bees. Accordingto David Hackenberg, the beekeeperwho discovered CCD, “beekeepersthat have been most affected so farhave been close to corn, cotton,soybeans, canola, sunflowers,apples, vine crops, and pumpkins.So what is it about these crops thatare killing the bees?”(USHR 2007).Hackenberg’s idea is that foragers

“may bring pollen and nectar backto the hive and store it in theircomb to use later. It is usually sev-eral months later when naturalsources of pollen and nectar slowdown in the field that the beeswould use this store of pollen andnectar to raise brood that the symp-toms appear....What may finally killthe hive are two things: first, theloss of most of the adult beesbecause when sick bees leave thehive to collect food they do notreturn (disappearing disease) andsecond the remaining young bees inthe hive may have such a weakenedimmune system that normalpathogens found in the hive suchas fungus easily overwhelm them”(USHR 2007).The best way to test this hypothe-

sis is with nationwide monitoring ofbee colonies. A number of migratorycolonies should be monitored

through a season, and levels of pes-ticides checked on a regular basis.If the colony starts to collapse, andsignificant pesticide residues arefound in bee bread and honey, thenthe hypothesis is confirmed. Asmentioned above, these kinds ofexperiments are now underway(USDA 2008; USHR 2008).We already know that pesticide

contamination of bee food canoccur. Bayer researchers fed honeybees sugar syrup containing 10 ppbIMD, and the resulting honey con-tained 5-8 ppb (Schmuck et al.2001). Wallner et al. (1999) andWallner (2001) exposed honey beesto Phacelia tanacetifolia that hadbeen treated with IMD. Concen-tration in collected nectar rangedfrom 3-10 ppb, and similar concen-trations were found in bee bread.

Field Levels ofImidacloprid

Imidacloprid can be applied as aseed treatment, a soil drench, or asa foliar spray. According to theCalifornia EPA, where IMD is beingused, models suggest expected con-centrations in surface water of 17ppb, and 2 ppb is expected ingroundwater. When IMD treatedseeds are planted, seed residue canbe blown offsite by planting equip-ment. Residues on plants near acrop site can be 14-54 ppb (Fossen2006). Sunflower seed treatments

can lead to concentrations of 13ppb in sunflower pollen (Laurentand Rathahao 2003). Other experi-ments show 3.9 ppb in sunflowerpollen, 8 ppb in flowers, and 1.9ppb in nectar. Rape has 4.4 to 7.6ppb in pollen. Corn can have aver-age concentrations of 2.1 ppb inpollen and 6.6 ppb in flowers. Somecorn plants show concentrations of18 ppb in pollen. Leaves of sugarbeets can have 15.2 ppm (Fossen2006; Bonmatin et al. 2005). Beescould ingest IMD in pollen, nectar,and water. They could be exposedby contact on flowers and leaves oftreated plants.Treated plants metabolize IMD to

toxic metabolites, and one of themis twice as toxic to bees as IMD.Chauzat et al. (2006) found IMDmetabolites in 44% of pollen sam-ples collected in France. Bayerresearchers found that about 15%of IMD in sunflower pollen hadmetabolized (Sur and Stork 2003).Imidacloprid is used extensively

in California, and was the 6th mostcommonly used insecticide(162,254 lbs) according to acreage(788,402 acres) in 2005. It is usedon citrus, almonds, and other cropspollinated by bees. Large numbersof CCD colonies have been found inCA (DPR 2006; Bee 2007;Henderson et al. 2007).According to Schacker (2008),

colony collapse disorder is not seenin states such as Nevada where imi-

7

Box 7414, Berkeley, CA 94707IPM Practitioner, XXX(9/10) September/October 2008 7

Update

Susan Cobey, University of California bee breeder andSusan Cobey, University of California bee breeder andgeneticist, is holding a “frame” of healthy bees. Eachgeneticist, is holding a “frame” of healthy bees. Eachbeehive contains several of these frames.beehive contains several of these frames.

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Other experiments have shownthat mortality starts at feeding lev-els between 24-48 ppb (Decourtyeet al. 2004). Bees probably do notreceive this level of exposure intreated fields. However, other pesti-cides and especially fungicides havebeen shown to lower toxic thresh-olds through synergism (Johansen1977; Pilling and Jepson 1993;USHR 2007; Schmuck et al. 2003).Sublethal effects such as reduced

feeding have been found at levels of

2001ab) (see Box B). This fact couldexplain why some colonies get CCD,while others in the same area donot (Hayes 2007). Reasonable esti-mates of bee IMD exposure throughpollen and nectar in treated fieldsare 3 to 10 ppb (Bonmatin et al.2005; Wallner et al. 1999). Toxicityis cumulative, and one experimentshowed 50% mortality when beeswere fed 0.1 to 10 ppb IMD for 10days (Suchail et al. 2001ab). (SeeBox B.)

dacloprid is not used. This observa-tion, however, does not prove thatimidacloprid causes CCD, becausethose states also have few crops topollinate, and few migratory bees.

Can Field Levels of IMDHarm Bees?

Some bees are extremely sensitiveto IMD, and acute toxicity levelscan vary by a factor of 100(Schmuck et al. 2001; Suchail et al.

Box 7414, Berkeley, CA 94707Box 7414, Berkeley, CA 94707

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IPM Practitioner, XXX(9/10) September/October 2008 Box 7414, Berkeley, CA 947078

Update

Exposure to a lethal dose of imida-cloprid causes immediate excitation,including trembling and tumbling.After several hours, workers slowdown and become inactive. Deathoccurs 4 to 96 hours after poisoning(Suchail et al. 2001ab; 2003). Thereis a 100 fold variation in acute toxici-ty according to the kind of bee andthe season. The LD50 has been meas-ured at 3.7 ng/bee in bees from theUK, and 40.9 ng/bee for Germanbees. The acute oral LD50 is some-where between 3.7 and >80 ng/bee.The LD50 by contact is 81 ng/bee.This large variation in sensitivitycould explain why some colonies diefrom CCD and others do not(Decourtye et al. 2003; Suchail et al.2001ab; Schmuck et al. 2001).Imidacloprid is metabolized by bees

into toxic metabolites. Bees metabo-lize 50 µg/kg (5 ng/bee) acute dosesof IMD quickly, the half life is about4.5 hrs, and it is completely goneafter 24 hours. The toxic metabolitespeak about 4 hours after oral inges-tion of IMD. One of these metabolites,an olefin derivative, is twice as toxicto bees as IMD. Since death occurs 4-96 hours after exposure, mortalitymay be due mostly to metabolites(Suchail et al. 2003; 2004).

Chronic ToxicityToxicity accumulates, so repeated

feeding of doses lower than the LD50is also lethal. Large variations havebeen seen in chronic toxicity (Suchailet al. 2001ab). Decourtye et al. (2004)found mortality occurred at imidaclo-prid feeding concentrations in therange 24-48 ppb after 11 days. Bayer

researchers found no effect on beemortality at feeding concentrations of20 ppb (Schmuck et al. 2001).Suchail et al. (2001ab) found veryhigh chronic toxicity for imidacloprid.Half of bees fed sugar solutions of 0.1to 10 ppb imidacloprid over a 10 dayperiod died. Concentration levels ofimidacloprid similar to this are foundin nectar and pollen of plants receiv-ing IMD seed treatment. The discrep-ancy between the work of Suchail andothers may be due to the “large vari-ability in effects induced by imidaclo-prid.” Suchail also used a feedingsolution that contained dimethylsul-foxide (DMSO) that might have actedas a synergist. There is known syner-gism between imidacloprid and fungi-cides, and maybe DMSO is also asynergist.

Sublethal EffectsConcerns have also been raised

about sublethal effects. Variousexperiments have shown that learn-ing in bees can be confounded bypesticides. Homing flight durations,food intake, odor learning, and bee tobee communication can be affected(Pham-Delegue et al. 2002; Colin etal. 2001; Bortolotti et al. 2003;Medrzycki et al. 2003; Colin et al.2004; Desneux et al. 2007). Con-centrations as low as 6 ppb of IMDand 2 ppb of fipronil have causedobserved sublethal effects (Colin et al.2004).For instance, doses of deltamethrin

27x lower than the LD50 caused 80%of foragers to lose their way back tothe hive (Colin et al. 2001a). Sub-lethal doses of IMD have been shown

to affect bumble bee foraging. After 9days of foraging in sunflowers treatedwith IMD, about 10% more bumblebees were lost in the field comparedto bumble bee foragers in untreatedfields (Taséi et al. 2001).Curé et al. (2001) found that the no

effect level of imidacloprid in sugarsyrup was 20 ppb. Kirchner (1999)found that a dose above 20 ppb,“causes not only a reduction in theforaging activity of treated bees, butalso induces trembling dances thatdiscourage other worker bees fromforaging. The waggle dance that com-municates foraging direction becomesless precise.”Decourtye et al. (2004) found that

24 ppb IMD reduced honey bee num-bers foraging at a feeder, and reducedsyrup intake by a factor of three. Thisconcentration also reduced olfactorylearning, which correlates with find-ing food supplies.Sublethal doses of 6 ppb may cause

bees to eat less. Colin et al. (2004)found that 6 ppb concentrations ofIMD did not reduce the number offoragers at a sugar feeder, but fewerforagers ingested the contaminatedsyrup. If honey bees have an aversionto eating their food stores, resultingstarvation and forced foraging in win-tertime could manifest as CCD.

SynergismToxic, chronic and sublethal

thresholds can be lowered by syner-gism. Toxic effects of pyrethroids,neonicotinoids such as IMD, andfungicides are synergistic (Brobyn2001; Schmuck et al. 2003; USHR2007; Iwasa et al. 2004).

Box B. Toxicity of Imidacloprid

9

2006. A survey of pesticide residues inpollen loads collected by honey bees inFrance. J. Econ. Entomol. 99(2):253-262.

Colin, M.E., Y. LeConte and J.P. Vermandere.2001. Managing nuclei in insect-proof tun-nels as an observation tool for foragingbees: sublethal effects of deltamethrin andimidacloprid. In: Belzunces et al., 2001a,pp. 259-268.

Colin, M.E., J.M. Bonmatin, I. Moineau, C.Gaimon, S. Brun and J.P. Venmandere.2004. A method to quantify and analyzethe foraging activity of honey bees: rele-vance to the sublethal effects induced bysystemic pesticides. Arch. Environ.Contam. Toxicol. 47:387-395.

Covina, G. 2007. Nobody home. Terrain39(2):22-25.

Curé, G., H.W. Schmidt and R. Schmuck.2001. Results of a comprehensive fieldresearch programme with the systemicinsecticide imidacloprid (Gaucho®). In:Belzunces et al., 2001a, pp. 49-59.

Decourtye, A., M. LeMetayer, H. Pottiau, M.Tisseur, J.F. Odoux and J.H. Pham-Delegue. 2001. Impairment of olfactorylearning performances in the honey beeafter long term ingestion of imidacloprid.In: Belzunces et al., 2001a, pp. 113-117.

Decourtye, A., E. Lacassie and M.-H. Pham-Delegue. 2003. Learning performances ofhoneybees (Apis mellifera) are differentiallyaffected by imidacloprid according to theseason. Pest Manag. Sci. 59:269-278.

Decourtye, A., J. Devillers, S. Cluzeau, M.Charreton and M.H. Pham-Delegue. 2004.Effects of imidacloprid and deltamethrinon associative learning in honey beesunder semi-field and laboratory condi-tions. Ecotoxicol. Environ. Saf. 57:410-419.

Delaplane, K.S. and D.F. Mayer. 2000. CropPollination by Bees. CABI Publishing,Wallingford, Oxon, UK. 344 pp.

Delaplane, K.S., J.D.Ellis and J.A. Berry.2006. Profitability of a varroa IPM system.Am. Bee J.146:438

Desneux, N., A. Decourtye and J.M. Delpuech.2007. The sublethal effects of pesticides onbeneficial arthropods. Annu. Rev. Entomol.52:81-106.

DPR (California Department of PesticideRegulation). 2006. Top 100 pesticides byacres treated in 2005. CADPR,Sacramento, CA. www.cdpr.gov

Elzen, P.J. and D. Westervelt. 2002. Detectionof coumaphos resistance in Varroadestructor in Florida. Am. Bee J.142:291292.

ENS (Environment News Service). 2008.German coalition sues Bayer over pesticidehoney bee deaths. www.ens-newswire.com

EPA (Environmental Protection Agency). 2008.EPA acts to protect bees.www.epa.gov/pesticides

Farrar, C.L. 1952. Ecological studies on over-wintered honey bee colonies. J. Econ.Entomol. 45(3):445-449.

Fossen, M. 2006. Environmental fate of imida-cloprid. CA Dept. of Pesticide Regulation,Sacramento, CA. 16 pp.

Hayes, J. 2007. Florida workshop discussescolony collapse disorder. Am. Bee J.147:295-297.

methods to control mites. Thesemethods are more labor intensive,but pesticide resistance can beminimized.If we do not take better care of

our bees, there could be a signifi-cant impact on crop production.Some foods could become scarceand expensive. We should also treatour bees better because they areour friends, they enrich our planet,and it is the right thing to do.

William Quarles, Ph.D., is an IPMSpecialist, Executive Director of theBio-Integral Resource Center(BIRC), and Managing Editor of theIPM Practitioner. He can be reachedby email, birc@igc.org.

ReferencesAtkins, E.L. 1992. Injury to honey bees by poi-

soning. In: The Hive and the Honey Bee,rev. ed., J.M. Graham, ed. Dadant andSons, Hamilton, IL. 1324 pp.

Baxter, J., F. Eischen, J. Pettis, W.T. Wilsonand H. Shimanuki. 1998. Detection of flu-valinate resistant varroa mites in U.S.honey bees. Am. Bee J. 138:291.

Bee. 2007. Online survey by Bee AlertTechnology. www.oardc.ohio-state.edu/agnic/bee/ccd.htm

Benjamin, A. and B. McCallum. 2008. A Worldwithout Bees. Guardian Books, London.298 pp.

Belzunces, L.P., C. Pélissier and G.B. Lewis,eds. 2001a. Hazards of Pesticides to Bees.INRA, Paris. 308 pp.

Belzunces, L.P., R. Vandame and X. Gu.2001b. Joint effects of pyrethroid insecti-cides and azole fungicides on honey beethermoregulation. In: Belzunces et al.,2001a, pp. 297-298.

Bonmatin, J.M., P.A. Marchand, R. Charvet, I.Moineau, E.R. Bengsch and M.E. Colin.2005. Quantification of imidaclopriduptake in maize crops. J. Agric. FoodChem. 53:5336-5341.

Bortolotti, L., R. Montanari, J. Marcilino, P.Medrzycki, S. Maini and C. Porrini. 2003.Effects of sub-lethal imidacloprid doses onthe homing rate and foraging activity ofhoney bees. Bull. Insectology 56(1):63-67.

Brobyn, P.J. 2001. Possible synergistic effectson honeybees of pyrethroids and fungi-cides: the UK regulatory consideration. In:Belzunces et al., 2001a, pp. 97-111.

Buchmann, S.L. and G.P. Nabhan. 1996. TheForgotten Pollinators. IslandPress/Shearwater Books, Washington,D.C. and Covelo, CA. 243 pp.

Cannell, E. 2008. A world without bees.Pesticides News 81:21-23.

Carson, R. 1962. Silent Spring. Fawcett,Greenwich, CT. 304 pp.

Chauzat, M.P., J.P. Faucon, A.C. Martel, J.Lachaize, N. Cougoule and M. Aubert.

6 ppb. Reduced feeding could leadto poor nutrition, which could con-tribute to CCD. Longterm feeding of4-40 ppb impairs olfactory learning,which is associated with findingfood (Decourtye et al. 2001; 2004).Other sublethal effects on foragingstart at 24 ppb (Kirchner 1999).Again, pesticide synergism couldlower the toxic thresholds.Because bees can mix pollen from

treated plants with that fromuntreated plants, exposure dependson percent of food obtained fromtreated crops. But bee recruitmenttends to concentrate foragers fromthe same hive on the same plants(see Box A). If migratory bees arepollinating a treated crop, much ofthe collected pollen should be con-taminated (Bonmatin et al. 2005).The situation is complicatedbecause bee exposure variesaccording to life stage and jobtasks. Despite the complications,French researchers believe thatconcentrations of IMD found in thefield are large enough to put bees atrisk (Halm et al. 2006; Rortais et al.2005; Bonmatin et al. 2005).

ConclusionColony collapse disorder is proba-

bly caused by stress, and pesticidesare definitely one of those stresses.Preliminary data suggest that CCDhives are contaminated with anumber of pesticides, including imi-dacloprid. Imidacloprid has pro-found effects on honey bee mortali-ty and behavior. Toxic thresholdsare low, and can be lowered furtherthrough synergism with other pesti-cides. Bees show a wide range ofsensitivity, and this fact couldexplain why some colonies collapse,others do not. Though the evidenceis suggestive, it will take a nation-wide monitoring program to confirmor deny the role of pesticides incolony collapse disorder.If colony collapse disorder has

taught us anything, it is to takebetter care of our bees. The EPAshould require sublethal toxicitytests. Bee colonies should be sys-tematically monitored on a regularbasis for diseases and pesticideexposures. Beekeepers should avoidtoxic miticides and switch to IPM

Box 7414, Berkeley, CA 94707IPM Practitioner, XXX(9/10) September/October 2008 9

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ed amounts of contaminated pollen andnectar consumed by different categories ofbees. Apidologie 36:71-83.

Sammataro, D., U. Gerson and G. Needham.2000. Parasitic mites of honey bees: lifehistory, implications, and impact. Annu.Rev. Entomol. 45:519-548.

Schmuck, R., R. Schoning, A. Stork and O.Schramel. 2001. Risk posed to honeybees(Apis mellifera: Hymenoptera) by an imida-cloprid seed dressing of sunflowers. PestManag. Sci. 57:225-238.

Schmuck, R., T. Stadler and H.W. Schmidt.2003. Field relevance of a synergistic effectobserved in the laboratory between an EBIfungicide and a chloronicotinyl insecticidein the honeybee, Apis mellifera. PestManag. Sci. 59:279-286.

Schacker, M. 2008. A Spring without Bees:How Colony Collapse Disorder HasEndangered our Food Supply. The LyonsPress, Guilford, CT. 292 pp.

Suchail, S., D. Guez and L.P. Belzunces.2001a. Toxicity of imidacloprid and itsmetabolites in Apis mellifera. In: Belzunceset al., 2001a, pp. 121-126.

Suchail, S., D. Guez and L.P. Belzunces.2001b. Discrepancy between acute andchronic toxicity induced by imidaclopridand its metabolites in Apis mellifera.Environ. Toxicol. Chem. 20(11):2482-2486.

Suchail, S., L. Debrauwer and L.P. Belzunces.2003. Metabolism of imidacloprid in Apismellifera. Pest Manag. Sci. 60:291-296.

Suchail, S., G. DeSouza, R. Rahmani and L.P.Belzunces. 2004. In vivo distribution andmetabolism of 14C-imidacloprid in differ-ent compartments of Apis mellifera. PestManag. Sci. 60:1056-1062.

Sur, R. and A. Stork. 2003. Uptake, transloca-tion and metabolism of imidacloprid inplants. Bull. Insectology 56(1);35-40.

Taséi, J.N., G. Ripault and E. Rivault. 2001.Effects of Gaucho® seed coating on bum-blebees visiting sunflower. In: Belzunces etal. 2001a, pp. 207-212.

USDA (United States Department ofAgriculture). 2008. Colony CollapseDisorder Action Plan.www.ars.usda.gov/is/br/ccd

USHR (United States House ofRepresentatives). 2007. Colony CollapseDisorder and Pollinator Decline.Subcommittee on Horticulture andOrganic Agriculture. March 29, 2007.http://agriculture.house.gov

USHR (United States House ofRepresentatives). 2008. Pollinator Healthand Colony Collapse Disorder.Subcommittee on Horticulture andOrganic Agriculture. June 26, 2008.http://agriculture.house.gov

Wallner, K., A. Schur and B. Stürz. 1999.[Tests regarding the danger of the seeddisinfectant, Gaucho, for honey bees].Apidologie 30:423.

Wallner, K. 2001. Tests regarding effects ofimidacloprid on honey bees. In: Belzunceset al., 2001a, pp. 91-94.

Wilson, B. 2004. The Hive: the Story of theHoneybee and Us. John Murray, London.308 pp.

Winston, M.L. 1987. The Biology of the HoneyBee. Harvard University Press, Cambridge,MA. 281 pp.

Halm, M.P., A. Rortais, G. Arnold, J.N. Taseiand S. Rault. 2006. New risk assessmentapproach for systemic insecticides: thecase of honey bees and imidacloprid(Gaucho). Environ. Sci. Technol. 40:2448-2454.

Henderson, C., L. Tarver, D. Plummer, R.Seccomb, S. Debnam, S. Rice and J.Bromenshenk. 2007. U.S. National BeeLoss Survey: Preliminary Findings withRespect to Colony Collapse Disorder. Am.Bee J. 147(5):381-384.

Iwasa, T. et al. 2004. Crop Prot. 23(5):371-378.Johansen, C.A. 1977. Pesticides and pollina-

tors. Annu. Rev. Entomol. 22:177-192.Kievits, J. 2007. Bee gone: colony collapse dis-

order. Pesticides News 76:3-5.Kirchner, W.H. 1999. Mad bee disease?

Sublethal effects of imidacloprid (Gaucho)on the behavior of honey bees. Apidologie30:422.

Kraus, B. and R.E. Page 1995. Effect of Varroajacobsoni on feral Apis mellifera(Hymenoptera: Apidae) in California.Environ. Entomol. 24:1473-1480.

Laurent, F.M. and E. Rathahao. 2003.Distribution of 14C imidacloprid in sun-flowers, Helianthus annus, following seedtreatment. J. Agric. Food Chem. 51:8005-8010.

Langstroth, L.L. 1923. On the Hive and theHoney Bee, 22nd ed., rev. C.P. Dadant,The American Bee Journal, Hamilton, IL.438 pp.

Losey, J.E. and M. Vaughn. 2006. The eco-nomic value of services provided byinsects. BioScience 56:311-323.

Medrzycki, R., R. Montanari, L. Bortolotti, A.G.Sabatini, S. Maini, and C. Porrini. 2003.Effects of imidacloprid administered insub-lethal doses on honey bee behaviour.Laboratory tests. Bull. Insectology56(1):59-62.

Morse, R.A. 1975. Bees and Beekeeping.Cornell University Press, Ithaca, NY. 295pp.

Morse, R.A. and N.W. Calderone. 2000. Thevalue of honey bees as pollinators of U.S.crops in 2000. Bee Culture 128(3):1-15.

NAS (National Academy of Sciences). 2007.Status of Pollinators in North America.National Academy Press, Washington, DC.300 pp.

Oliver, R., 2007. Fighting varroa: silver bulletor brass knuckles. Am Bee J. 147:526-530.

PA (Penn State Press Release). 2008. Pesticidebuildup could lead to poor honey beehealth. Penn State Press Release, August18, 2008.http://live.psu.edu/story/3389/rss30

Pham-Delégue, M.H., A. Decourtye, L. Kaisrand J. Devillers. 2002. Behavioural meth-ods to assess the effects of pesticides onhoney bees. Apidologie 33:425-432.

Pilling, E.D. and P.C. Jepson. 1993. Synergismbetween EBI fungicides and a pyrethroidinsecticide in the honey bee (Apismellifera). Pesticide Sci. 39:293-297.

Quarles, W. 1994. Living with Africanized bees.Common Sense Pest Control Quarterly1(4):5-14.

Rortais, A. G. Arnold, M.P. Halm and F.Touffet-Briens. 2005. Modes of honeybeesexposure to systemic insecticides: estimat-

IPM Practitioner, XXX(9/10) September/October 2008 Box 7414, Berkeley, CA 9470710

Update

Pastoral Beneficials“Pastured dairy and beef cattle provide

a critical link in the food supply systemby utilizing marginal land,” said PhillipKaufman (Univ of Florida, PO Box110620, Gainesville, FL 32611; pkauf-man@ifas.ufl.edu). Pastured systems canprovide positive environmental impactsto watersheds and nutrient recycling.Dung burying beetles play a valuablerole in pasture ecosystem sustainabilityby reducing pasture fouling, nitrogenvolatilization, parasitism and pest flies,with averted losses estimated at $0.38billion.“Current active IPM efforts for pas-

tured cattle include monitoring animalsfor populations of harmful fly pests, andpreemptive use of cultural and chemicalcontrols,” said Kaufman. “Augmentativebiological control of pasture pests is inits infancy.”In a baited pitfall trap survey in

Florida, the major dung beetle speciesstabilizing pasture ecosystems, account-

By Joel Grossman

T hese Conference Highlights arefrom the Dec. 9-12, 2007,Entomological Society of America

(ESA) annual meeting in San Diego,California. ESA’s next annual meeting isNovember 16-19, 2008, in Reno, Nevada.For more information contact the ESA(10001 Derekwood Lane, Suite 100,Lanham, MD 20706; 301/731-4535;http://www.entsoc.org).

Poinsettia IPM Ecology“Competition among herbivores can

impact pest management practices, thusit is important to understand these rela-tionships for successful integration ofmanagement tactics,” said ClaudiaKuniyoshi (Ohio State Univ, 1680Madison Ave, Wooster, OH 44691;kuniyoshi.1@osu.edu). In poinsettiasthere is an interaction between above-ground pests such as silverleaf whitefly,Bemisia argentifolii,and belowgroundpests such as darkwinged fungus gnats,Bradysia impatiens. There are alsointeractions from high nitrogen fertilizerlevels.At high nitrogen levels, whitefly sur-

vival is higher than at low nitrogen lev-els. High nitrogen levels also encouragefungus gnat populations, and whiteflyegg laying increases. Eventually, whiteflypopulations suppress belowground fun-gus gnat populations. These ecologicaleffects may in part be caused by pestmodification of plant quality.

Pumpkin IPMJim Jasinski (Ohio State Univ, 1512 S

US Hwy 68, Ste B100, Urbana, OH43078; jasinski.4@osu.edu) talked abouta survey of pumpkin growers in Indiana,Illinois, Ohio, Michigan, Minnesota,Wisconsin and Ontario, Canada. About52% called disease control the numberone management problem; 18% saidweeds; and 14% insects. Among the IPMpractices adopted: 73% scout for plantdiseases; 76% cultivate for weed controluntil the vines close the row; 65% moni-tor for squash bugs; and 84% of growersapply pesticide sprays in early morningor evening to reduce impacts on honeybees.

ing for 26% of the beetles collected,included brown dung beetle,Onthophagus gazella ;bull-headed dungbeetle, O. taurus; and Euoniticellusintermedius.

Camp Ant IPMIn South Carolina state parks, where

the Argentine ant, Linepithema humile,is invading campsites, tents, public facil-ities and recreational vehicles, “approxi-mately 70% of the campers used theirown pesticides to treat for L. humile,”said Brittany Russ (Clemson Univ, 114Long Hall, Clemson, SC 29634; brit-tar@clemson.edu). “Campers were typi-cally found to be over-treating theircamping areas or were proactively treat-ing areas against potential ant infesta-tions.” Despite the ad hoc insecticidespray and dust onslaught, the numberof ant trails remained constant in stateparks, indicating “a need for better con-trol strategies.”“Establishing baiting areas by park

ESA 2007 Annual MeetingHighlights—Part 5

Everett “Deke” Dietrick, entomologistand pioneer in the field of biological pestcontrol, died at his home in Ventura onDecember 23. His scientific training inentomology and his boundless interest ininsect ecology on farms led him to collabo-rate in founding Rincon-Vitova Insectaries.Through his encouragement and advicemany hundreds of farmer clients rejectedconventional chemical control and transi-tioned to biological control methods.After returning from the war in 1947, he

eagerly took an opening with the UCStatewide Department of BiologicalControl, led by one of his most cherishedmentors, Professor Harry Smith. Twelveyears of university field research observinginsect ecology, pesticide resistance, andthe phenomenal success of classical bio-control projects led him to believe thatchemical pesticides usually cause moreproblems than they solve.He left the university to pioneer the new

profession of pest control advisor. In part-nership with Ernest “Stubby” Green, andthen later Jack Blehm, he establishedinsectaries in Ventura and Riverside togrow various insect predators and para-sites for commercial use against croppests. The two companies merged in 1971

to form Rincon-Vitova Insectaries, Inc. nowowned and managed by daughter JanDietrick.Deke was a Board Certified Entomo-

logist and an Emeritus Member of theEntomological Society of America. In 1972he served as an expert witness atCongressional hearings in Washington, DCthat led to the banning of DDT in theUnited States.For over 40 years Deke mentored scores

of individuals who wanted to be part of hiswork. He labored to teach people in letters,articles, talks, and papers (some of whichare posted at www.rinconvitova. com/diet-rick_papers.htm). Interviews of Dekebetween 1994 and 1997 can be found atwww.rinconvitova.com/ dietrick_inter-views.htm. He was increasingly hopeful inthe last several years, seeing the rise inenvironmental awareness and the growthof the organic industry.Expressions of remembrance and sup-

port for Deke and his work may be direct-ed in the form of tax-deductible donationsto the Dietrick Institute for Applied InsectEcology, www.dietrick.org, a non-profitorganization offering training in ecological-ly based pest management, PO Box 2506,Ventura, CA 93002.

Everett “Deke” Dietrick

11

Box 7414, Berkeley, CA 94707IPM Practitioner, XXX(9/10) September/October 2008 11

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12 Box 7414, Berkeley, CA 94707IPM Practitioner, XXX(9/10) September/October 2008

personnel for foraging L. humile early inthe camping season may be beneficialfor quelling larger infestations fromoccurring as the camping season pro-gresses,” said Russ. “We expect theimproved control measures to decreasethe number of complaints by campersabout L. humile and reduce the misuseor overuse of cleaning powders, insecti-cide powders and broadspectrum insec-ticide sprays used by visitors and parkpersonnel.”

Ozone Hive Fumigation“Ozone (O3) is a powerful oxidant that

has the ability to disinfect, eliminateodors, taste, and color, and remove pes-ticides,” said Rosalind James (USDA-ARS, 5310 Old Main Hill, Logan, UT84322; rosalind.james@ars.usda.gov).“Ozone can potentially be used to treatold comb and bee equipment. It isalready used as an agricultural fumigantfor stored products. O3 also breaksdown quickly to H20 (water) and O2(molecular oxygen), so it will not persistin wax comb, wood, or plastic.”Ozone fumigation can potentially elim-

inate pests of old honeycomb such asgreater wax moth, Galleria mellonella,which creates a large amount of webbingas it feeds on old comb, plus pesticidessuch as coumaphos (Checkmite™) andfluvalinate (Apistan™) that persist inhives after varroa mite treatment. Theprototype ozone generator (O3ZoneCompany, ID) fed 500-1,000 ppm ozonein one side of a gas incubator and outthe other side, creating 215-430 ppm O3inside the test chamber.At 77-95°F (25-35°C), ozone fumiga-

tion degraded coumaphos faster thanfluvalinate. Though pesticide degrada-tion products need to be tested, decont-amination of low pesticide levels shouldtake no more than 13 hours. Small waxmoth larvae were killed in 1-2 hours bythe lowest O3 concentrations. Wax mothadults were killed within 6 hours. Eggswere most resistant, requiring 48 hoursat 33.7°C (93°F) for complete kill. “Onemethod to avoid the long exposure timesrequired to kill all the eggs may be totreat twice,” said James. “Once to killadults and any larvae or pupae that maybe present, and then a second shorttreatment 5-6 days later to kill the newlyemerged larvae that hatched from anyeggs that survived the first treatment.”

Woody Plant TermiteReservoirs

Formosan subterranean termites,Coptotermes formosanus, have causedan estimated $300 million in damages in

the city of New Orleans from 1966 to1996, and $500 million in damage in thestate of Louisiana. An areawide IPM pro-gram using bait stations and non-repel-lent termiticides was begun in NewOrleans’ French Quarter in 1998. “Treesand woody plants may be reservoirs forFormosan subterranean termites toinfest structures,” said Dennis Ring(Louisana State Univ, 404 Life Sci Bldg,Baton Rouge, LA 70803; dring@agctr.lsu.edu). Thus, trees and woody plantswere inspected visually and using anacoustical probe.A total of 1,026 properties on 35 city

blocks with 1,873 trees and woodyplants were inspected. First, “aerial pho-tographs of each block of the FrenchQuarter in the test area were obtained,”said Ring. “Then visual inspections weremade to locate trees by walking blocks.Property owners were contacted andappointments were made to inspecttrees. Inspections consisted of visuallyinspecting around the trunks of trees fortermites, mud tubes or packs of soil. Anacoustical probe was used to detect ter-mites in trees. The soil around trees wasprobed with the distance between probesno more than 12 in (30 cm) apartbecause 12 in is the upper limit to theeffectiveness of the acoustical probe.”The termite infestation rate for trees

was about 2% (17 properties; 39 trees).Pest management professionals treated13 of the infested properties with baitstations and 4 with liquid termiticides.Only one tree was reinfested and retreat-ed. “Trees and woody plants infested bytermites will be re-inspected periodicallyand infested trees will be retreated,” saidRing. “Continued inspection of trees andwoody plants in other blocks included inthe program are ongoing.”

Predatory Mite SugarSupplements

“Sugary supplements (M-30; 30%solution of 1:1 fructose & glucose)enhance Phytoseiulus persimilis survivaland fecundity even in the presence ofprey,” said Guadalupe Rojas (USDA-ARS, 59 Lee Rd, Stoneville, MS 38776;grojas@msa-stoneville.ars.usda.gov).“The presence or absence of extra floralnectaries may significantly impact theperformance of P. persimilis in the field.Mass rearing of the predator may beenhanced by providing sugary supple-ments in addition to prey.”

Globalization ofWoodboring Beetles

“Wood and wood products used tosupport, brace or package commodities

CalendarDecember 4-6, 2008. Acres USA Eco-FarmConference. St. Louis, MO. Contact: 800/355-5313; www.acresusa.com

December 5-6, 2008. Sustainable AgriculturePest Management Conference. San LuisObispo, CA. Contact: CCOF, 831/423-2263;www.ccof.org

December 8-11, 2008. Annual Meeting, NorthCentral Weed Science Soc. Indianapolis, IN.Contact: 217/352-4212; www.ncwss.org

January 19-23, 2009. 21st Annual AdvancedLandscape IPM Short Course. College Park,MD. Contact: U. Maryland, 301/405-3913 Ex3911; www.raupplab.umd.edu/conferences/adv-landscape

January 21-24, 2009. Annual EcologicalFarming Conference: United We Grow.Asilomar, CA. Contact: www.eco-farm.org

January 24, 2009. 32nd Annual Bay AreaEnvironmental Education Resource Fair. SanRafael, CA. Contact: K. Hanley, 510/657-4847;www.baeerfair.org

January 28, 2009. 11th Annual San FranciscoIPM Conference. Presidio, San Francisco.Contact: SF Dept. of Environment, 11 GroveSt., San Francisco, CA 94102; 415/355-3776;jessian.choy@sfgov.org

February 10-12, 2009. Pacific NorthwestSustainable Agriculture Conference. Richland,WA. Contact: KCCD, 6-7 E. Mountain ViewAvenue, Ellensburg, WA 98962; 509/525-3389.

February 24, 2009. 10th Annual Organic TurfTrade Show. Farmingdale, NY. Contact:Neighborhood Network, 7180 RepublicAirport, East Farmingdale, NY 11735;631/963-5454, www.neighborhood-network.org

February 26-28, 2009. 20th Annual OrganicFarming Conference. La Crosse, WI. Contact:MOSES, PO Box 339, Spring Valley, WI54767; www.mosesorganic.org

March 1-3, 2009. California Small FarmConference. Sacramento, CA. Contact:www.californiafarmconference.com

March 24-26, 2009. Sixth International IPMSymposium. Portland, OR. Contact: TomGreen, IPM Institute, 608/232-1410; www.ipm-centers.org/IPMsymposium09/

December 13-17, 2009. Entomological Societyof America Annual Meeting. Indianapolis, IN.Contact: ESA, 9301 Annapolis Road, Lanham,MD 20706; Fax 301/731-4538;www.entsoc.org

Conference Notes

13IPM Practitioner, XXX(9/10) September/October 2008 Box 7414, Berkeley, CA 94707

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during shipment provide the major path-way for global transport of woodboringbeetles, a well-known group that causessignificant ecological and economicimpacts to forests,” said CharlesBellamy (CDFA, 3294 Meadowview Rd,Sacramento, CA 95832; cbellamy@cdfa.ca.gov). “Annual losses to forest-derived products attributed to introduc-tions of non-native insect species intothe U.S. are about $2.1 billion per year,”and “as globalization continues we arelikely to see an increase in introductionsof non-native organisms.”“Approximately 93% of all insects

intercepted on wood articles at U.S.ports of entry between 1985 and 1998were beetles, making an urgent case fordeveloping diagnostic tools associatedwith this large group of insects,” saidBellamy. “Because of the potential cata-strophic damage that could be causedby the introduction and spread of non-native invasive wood-boring beetle taxa,it is of no surprise that an identificationresource is the most frequently request-ed tool by Plant Pest Quarantine.”Lucid3 (CBIT, Univ of Queensland,

Australia; www.lucidcentral.org), a Java-based program running on varied oper-ating systems (e.g. Windows, Macintosh,LINUX), is being used to build a series ofwoodboring beetle identification keys forscientists, the general public and quar-antine and plant protection personnel.

Biocontrol Aromas“Herbivore-induced plant volatiles

have been shown to attract natural ene-mies,” said Christina Harris (Penn StateUniv, 121 Chem Ecol Lab, Orchard Rd,University Park, PA 16802; cmh347@psu.edu). On DPL90 cotton, feeding ofcabbage looper, Trichoplusia ni, but notbeet armyworm, Spodoptera exigua,induces cotton plants to release beta-farnesene.Beet armyworm (BAW) feeding, but

not cabbage looper (CL) feeding, inducesthe release of the sesquiterpene volatilesalpha-humulene and gamma-bisabolene.“Terpene emission was quantitativelyhigher for BAW-infested relative to CL-damaged and intact plants,” said Harris.“These findings may explain field obser-vations that CL is more heavily para-sitized by the generalist parasitoid waspCotesia marginiventris in the presence ofBAW.”

Hotel Bed Bugs“Generally commercial clients, hotels

in particular, have a great understand-

ing of the liability issues associated withbed bugs,” and their cooperation withpest control efforts is above average,said Judith Black (Steritech Group, Inc,5742 W 114th Pl, Broomfield, CO80020; judy.black@steritech.com).“The process we go through is an

extremely thorough inspection and treat-ment” using basic detection tools likebright flashlights and putty knives, saidBlack. “We are ripping the room apart,taking off outlet covers, taking picturesoff the walls, taking down curtain rods,all that kind of thing. We are basicallydismantling the room. We are havingthem quarantine linens, and then getthem laundered separately. We do askthat the mattress and box spring be dis-posed of.” Encasement of old mattressesand box springs could potentially harborlive bed bugs and present a liabilityissue. But encasements are recommend-ed when installing new beds, to avoidfuture replacement.Within hotels, the number of treated

rooms ranged from none to 23%; theaverage was 2.5%. The total number ofrooms treated for bed bugs went from 7in 2003 to over 700 rooms in 293 hotelsin 2007. Over the five year period, over60% of the 700 mid-range hotels weretreated for bed bugs, though over 99% ofthe 75,000 rooms did not have bed bugproblems in any given year. About halfthe time, a hotel with a problem calledback only once or twice, indicating bedbugs were not being reintroduced.However, 8% called more than 10 times.About 20% of the time, the “secondary

rooms” which are above, below andbeside the infested “primary” room alsowere infested; the former secondaryroom becomes a primary room if aninfestation is found, and then a new setof secondary rooms are inspected. About70% of the time the infested secondaryroom is next door to the primary room;10% of the time it is above, and 18% ofthe time it is below.“Bed bugs have legs” and they use

wall voids to move within a facility.When moving from the primary room,bed bugs typically move into the adja-cent secondary room sharing the wallwith the bed headboard. In 2006 retreat-ments went up dramatically, and therewere many field reports of pyrethroidresistance. So, in 2007 a switch wasmade from synthetic pyrethroid-basedliquid residuals and dusts to non-syn-thetic pyrethroid products and encase-ments were introduced; and the numberof retreatments decreased.

Conference Notes

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Box 7414, Berkeley, CA 94707Box 7414, Berkeley, CA 94707IPM Practitioner, XXX(9/10) September/October 2008 15

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