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Natural Bee Husbandry / Archives for No.16 Summer 2020

No.16 Summer 2020

A Brief History of Foulbrood: from superstitions to veterinary medicine and back

14 August 2020 by

by Sofia Croppi and Erik Tihelka. No.16 August 2020

Beekeeping belongs among the oldest agricultural activities of man. Since at least 9,000 years before the present, humans have regularly collected honey and wax, an avocation that later developed into true beekeeping as we know it today. The long history of human interest in the life of honey bees is documented in ancient manuscripts such as Columella’s (4 – c. 70 AD) monumental work De re rustica, which also includes vivid descriptions of honey bee diseases. In the aforementioned book, Columella discusses, among others, disorders and diseases such as starvation, dysentery, poisoning from plants, and possibly also conditions that we know today as European and American foulbrood, and tracheal mite infestation. However, it was not until much later that the earliest scientific enquiries into the causes of foulbrood were first made. 

The first use of the word ‘foulbrood’ has been traced back to the German apiculturist and clergyman Adam Gottlob Schirach (1724 – 1773) in 1769 [1]. Schirach argued that the disease is caused by malnutrition and by a disorder of the queen that causes her to lay brood the wrong way into the cell. Thus, in 2020, 251 years have elapsed since the first modern attempt at explaining foulbrood in bees, albeit retrospectively a somewhat naïve one. 

Looking back at the history of bee diseases before the age of modern veterinary medicine offers us a unique insight into the history of beekeeping but understanding how our ancestors dealt with this serious disease can also be inspiring for organic beekeepers today. In this article, we briefly examine the history of American and European foulbrood in central European apiculture at the turn of the 19th and 20th centuries as viewed through the lens of the beekeeping press of the time. 

American foulbrood, also abbreviated to AFB, is a disease of honey bees that hardly requires an introduction. The causative agent of AFB is the destructive Gram-positive, spore-forming, rod-shaped bacterium Paenibacillus larvae. The equally destructive European foulbrood,  EFB, is caused by the Gram-positive Melissococcus pluton which, unlike the former, affects open brood. It was not until 1885 that Cheshire and Cheyne demonstrated that the causative agent of the latter disease is the bacterium Bacillus alvei, which was subsequently reclassified as Melissococcus pluton [2],[3]. The disease became known as European foulbrood, since it was first described in Europe. The causative agent of American foulbrood, Paenibacillus larvae, was not discovered until 1907 in the USA, but despite their somewhat misleading names both diseases have a cosmopolitan distribution [4]. Before this date, beekeepers had to rely largely on their intuition and trial-and-error to combat the disease. 

Early beekeeping authors used terms such as “foulbrood”, “bee plague”, “brood decay”, or “sour disease” interchangeably, while others developed specific nomenclatural systems. For example, Jan Dzierżon (1811 – 1906), the influential Polish beekeeper and one of the first modern European beekeepers to use a movable frame hive, distinguished between two types of foulbrood – ‘mild and curable’ which affected open brood (possibly European foulbrood) and ‘malignant and incurable’ foulbrood which affected capped and uncapped brood, (possibly American foulbrood [5], but it is possible that other non-infectious conditions were included under these umbrella terms as well. The fact that foulbrood used to be defined so vaguely and that it was probably used to refer to several different diseases of the brood presented a massive complication, for it was hardly possible to study the disease without clearing the problem of naming it first. Today it is often impossible to know whether the authors were dealing with American or European foulbrood, or if they encountered a totally different condition, especially when their descriptions are brief. An overview of diseases, at least passingly similar to American and European foulbrood, is given in Tab. 1.  

DiseaseSimilarities to FoulbroodDifferences from Foulbrood
Sacbrood.Discoloured larvae, perforated capping, unpleasant smell.Pupal stage never effected infected larvae show clear segmentation. The dead larvae have a raised head infected larva appears baggy-like, if punctured a watery fluid escape dried scales can be easily removed from the cell.
Chalkbrood.Perforated cappings.Diseased larvae become white to grey and chalky in appearance mummies can easily be removed affected larvae never rope.
“Half-moon syndrome”.Discoloured larvae unpleasant smell.Many eggs in one cell drone brood in worker cells affected larvae do not rope.
Brood dying from malnutrition.Discoloured and decaying brood, perforated capping.Symptoms similar to European foulbrood.
Brood dying from cold.If not removed quickly by bees the dead brood decays, becomes discoloured and produces an unpleasant smell.Symptoms similar to foulbrood.
Tab. 1: Overview of diseases of the brood that may have be confused with American and European foulbrood [6].

Enigmatic causes

Many conflicting ideas about the possible causes of foulbrood have been voiced throughout the last 250 years. Reverend Schirach, who coined the disease’s name in the mid-18th century, attributed foulbrood to malnutrition and the queen placing bee eggs head inwards into the cells. Numerous authors after him, proposed their own hypotheses, a selection of which is provided in Tab. 2. 

AuthorCause
Schirach (1769)Malnutrition and placing bee larvae head inwards into the cells
Leuckhart (1860)Fungi
Muhlfeld (1868)Parasitic wasp, genus ichneumon
Preuss (1868)Fungus, genus Cryptococcus
Geilen (1868)Bees bringing decaying matter home from animal corpses
Lambrecht (1870)Fermentation of bee bread
Hallier (1870)Fungi
Cornallia (1870)Fungus, genus Cryptococcus
Fischer (1871)Malnutrition
Tab. 2: Some early hypothesis on the origin of the foulbrood disease [7], [8].

Due to the wide range of conditions historically considered under foulbrood, it should not be surprising that the disease was traditionally thought to have many causes. A popular explanation in the latter half of the 19th century claimed that a combination of malnutrition and neglect of the brood by nurse bees could result in foulbrood (9). Some believed that foulbrood outbreaks coincided with the honeydew flow and that honeydew can contains pathogenic fungi that may cause the disease (10). Others thought that foulbrood was caused by insufficient protein in the bee’s diet (11) and some observed that foulbrood was especially prevalent in years with poor honey yields (12). Others even believed that foulbrood resulted from “poisoned honey” (13) pointing to the plant Daphne mezereum as the possible culprit (14,15). While this plant is indeed poisonous to humans, similar effects have not been reported in bees. Moreover, poisoning by toxic nectar or pollen typically affects the adult bee population and not the brood alone (16).

Similarly, it was claimed that “foul” or “fermented” honey and pollen could be the cause of foulbrood (14 – 17). Honey and pollen collected in late autumn can start fermenting during the winter and in spring beekeepers often found conspicuous moulds overgrowing the combs. But could fermenting honey and pollen cause foulbrood? The Prussian beekeeper Emil Hilbert designed an experiment in 1878 in which he fed two strong colonies with fermented honey and pollen. The colonies weakened quickly, losing a considerable portion of the adult population and much of their brood died. In 20 days, all that what was left of the two colonies was just the queen surrounded by a small cohort of workers. However, the experimental feeding failed to induce foulbrood symptoms. Hilbert therefore concluded that fermenting honey and pollen could not be the sole cause of foulbrood (18). 

Another oft-cited hypothesis was that foulbrood outbreaks are triggered by cold spells that cause the brood to die; it was suspected that if a beekeeper inspects his hive too frequently the brood may succumb to the cold. Likewise, frosty nights in early spring may cause large amounts of brood to die and if the bees don’t remove all the dead brood in time, a foulbrood outbreak may result (11, 19). To prevent brood from dying when inspections had to be done on cold days, some placed a hot brick onto the bottom board to compensate for the lost heat (17). 

The Czech beekeeper and priest Ferdinand Liška carried out a series of experiments on air circulation inside the hive in the 1870s. He concluded that CO2-rich air leaves the hive only very slowly and that bees must therefore fan vigorously to facilitate gas exchange between the hive and its surroundings. He used several anecdotal observations of other beekeepers and of himself to suggest that foulbrood is caused by “foul” or “depleted” air. When bee brood dies, due to cold for instance, it would undergo a process of decay that would presumably produce various poisonous gases responsible for the characteristic smell associated with foulbrood. Liška advised that a well-ventilated hive can best prevent the disease (9).

By the 1880s, some French beekeepers came to believe that the disease was caused by “foul” water. It was advised that beekeepers provide their colonies with clean water and change it daily. Some boiled the water and added thyme twigs. According to reports from the time, these measures were very efficient in some cases (20). The traditional practice of adding thyme twigs to water is certainly very interesting, since essential oils and extracts from thyme have been shown to possess strong antimicrobial properties against P. larvae in laboratory trials (21, 22).

By the end of the 19th century, most beekeepers came to believe that foulbrood was in fact a microbe-borne disease (17, 23) Janklo (15) wrote in 1905: “The most frequent cause of bacteria is with greatest certainty the uncleanness of the bee’s dwelling and the air in the beehive. Hives that are not ventilated well can cause foulbrood, because foul air provides ideal conditions for bacterial life. These then start to swirl and multiply as soon as they find a dead larva in the comb.” 

Beekeepers in the 19th century believed that mismanagement and various mistakes on behalf of the beekeeper could contribute to a foulbrood outbreak. Several authors, starting with Schirach in 1769, have emphasised the role of malnutrition in the development of the disease. This view seems to be corroborated by recent findings. Malnourished bees are indeed more susceptible to disease (24b -26). When P. larvae is ingested, it resides in the bee larval gut and competes with the developing bee for food (27). If food is plentiful, the larvae will most probably develop normally, pupate, and excrete the pathogen during development. But if food is in short supply, P. larvae will eventually kill the larva and produce typical AFB symptoms (28). Therefore, the old observation that foulbrood and bee nutrition are linked seems to be based on truth. 

The location of the hive was thought to play an important role in foulbrood outbreaks. Beehives located in shaded and damp places were supposedly more likely to develop foulbrood. Beekeepers were advised to keep their apiaries clean and pick up any dead bees. Beekeeping tools had to be cleaned frequently, beehives kept well-ventilated, the combs changed frequently, and the colonies kept strong all year around to prevent foulbrood (15, 29). Another widespread belief claimed that foulbrood outbreaks only occur when the weather is unfavourable; a cold spell would first kill larvae and if not cleaned quickly the condition would soon spread to the rest of the brood (30). The bee genotype was another factor taken into account. Some beekeepers observed that Italians (A. m. ligustica) were especially susceptible to the disease compared to the native dark honey bees (A. m. mellifera). 

Surprisingly, early writings from the middle of the 19th century indicate that foulbrood was originally not very prevalent. In 1840, the Czech beekeeper and clergyman Josef Stern called foulbrood a “rare disease” (13). The Prussian bee journal Eichstadt Bienenzeitung in 1868 published an account of a local beekeeper that kept bees since his early childhood but never came across foulbrood until one of his colleagues purchased a movable frame hive (31). In Germany, there was a popular saying “Dzierzonstöcke, Faulbrutstöcke”(30) which very roughly translates as “Dzierżon hives, foulbrood thrives”, referring to Jan Dzierżon’s early movable frame hive. The observation that many beekeepers only started experiencing problems with foulbrood when they switched from primitive straw and log hives to modern movable frame hives is surprisingly prevalent in apicultural literature of the timeas well as the claim that early on, affected colonies would often recover spontaneously (13)

Caution is needed when interpreting these observations. It is possible that since before the introduction of movable comb hives beekeepers were hardly able to inspect their colonies, they would rarely see foulbrood and therefore considered it a rare disease. But perhaps the prevalence of foulbrood during the 19th century before the introduction of movable frame hives was, at least in central Europe, lower than today. Foulbrood is absent or present at very low levels across much of Africa where intensive beekeeping is not practised and where beekeepers replenish their stock from captured swarms (33). Likewise, studies in New Zealand have demonstrated that the prevalence of American foulbrood in feral colonies is low (34). 

Do we have any hard data to show how prevalent foulbrood was in Europe in the past? Quantitative surveys of bee diseases provide valuable data for understanding the historical development of bee health, but studies of this kind are rare over the past 250 years. In Bohemia (western historical region of the present day Czech Republic), the State Federation of Beekeeping Societies (SFBSB, Zemské ústředí včelařských spolků pro Čechy) acted as a union of several hundreds of smaller beekeeping clubs so that over 85% of Bohemian beekeepers were affiliated with the Federation. The SFBSB monitored honey bee losses between 1936 and 1941 by sending out questionnaires to its local constituent organisations (35). Although the survey does not capture the state of honey bee health before the introduction of ‘modern’ beekeeping practices, its scale and age make it of a special interest nonetheless. Between 1936 and 1941, reported annual colony mortality averaged 8.1% (2.1% – 23%; Tab. 3). High loses were experienced during the war years when winter feed was scarce, so the figure is likely an overestimate of what the normal bee mortality rates would be like. In either way, an 8.1% colony loss rate is almost half the colony mortality beekeepers in Austria, Czech Republic, Slovakia, Poland, Germany, Switzerland and Slovenia are experiencing today, at least based on data collected by the COLOSS between 2008 and 2016 (36-38). Although caution should be exercised when comparing these two bee health surveys since they used different methodologies, it should also be pointed out that central Europe is still enjoying one of the lowest colony mortality rates on the continent (36). Assuming that beekeepers were faithful in reporting their colony losses, then during the five years of the SFBSB survey, foulbrood incidence was low and accounted for merely 1% of colony losses. The leading causes of colony death were the so-called ‘obstipatio apium’ and ‘obstipatio pollinaris’ (syndromes associated with dysentery and loss of adult workers, respectively), nosematosis, and tracheal mite disease. All in all, the results of this historical and indeed rather unique bee survey show that bee losses were probably much lower before the introduction of Varroa, and that foulbrood was not a major contributor of colony mortality at the time. 

Year193619371938193919401941Average
Winter mortality1.6%2.9%1.6%1.4%21.5%10.5%6.7%
Total losses2.1%4.0%2.3%2.3%23.0%14.9%8.1%
Tab. 3a: Percent colony mortality in Bohemia (1936-1941) during the winter and during the entire year based on data published by SFBSB35.

Why did pre-modern beekeepers experience low foulbrood incidence? This could have been due to the beekeepers restocking capturing wild swarms, which are subject to higher selection pressures than managed colonies and so are presumably more resistant to the disease (39). Studies in New Zealand confirmed that wild colonies have lower P. larvae spore loads than managed colonies (40). Traditional skep beekeepers would often kill their best colonies in autumn to extract honey and this barbaric practice possibly prevented the build-up of spores in hive material. Another factor that may have aided the presumed resistance or tolerance to foulbrood was that in the past, colonies were seldom treated by beekeepers, placing them under stronger selective pressures. Consequently, colonies were under a much higher pressure to develop resistance compared with today (39). Old apiaries were small and dispersed (41) reducing the likelihood of bees drifting or robbing and exchanging pathogens; this limited the transmission of foulbrood and would probably lead pathogens to evolve avirulence (39). Moreover, before movable frame hives became widespread in Europe in the mid-19th century, beekeepers could not transfer combs between hives which probably significantly limited the spread of the disease. Beekeepers allowed and encouraged their colonies to swarm because before the introduction of modern queen rearing methods and advances in making splits, swarming used to be the only way beekeepers could multiply their stocks. Swarming probably decreases the spore load of individual colonies and thus lowers the chance of a foulbrood outbreak (42,43). Before the invention of the honey extractor in 1865, beekeepers in Europe had to extract honey either by immersing honeycombs into warm water or by using presses. Both methods damaged the comb to the extent that it could not be reused. This meant that bees had to draw fresh comb every year, likely reducing the pathogen load. 

Chart by Visualizer

Janko (15) cites two ways of foulbrood transition: primary and secondary. Primary transmission, as he called it, occurs when the bees themselves bring pathogens into their hive. Secondary transmission occurs when the apiculturist brings the pathogen with contaminated beekeeping equipment. Some beekeepers believed that foulbrood could be transmitted by wax moths (20). An interesting note regarding the transmission of foulbrood was made by McLain (44). He suggested that the causative agent of foulbrood may be transmitted via the beekeeper’s contaminated clothes. He also observed that the disease spreads in the direction of the prevailing wind. This caused him to believe that wind could play an important role in transmitting foulbrood as well. Today it is understood that most beekeeping equipment, perhaps with the exception of the hive tool, plays a negligible role in foulbrood transmission, but the observation of foulbrood spreading downwind may be associated with the direction of drifting bees (6).

Even in the 19th century, many beekeepers relied on some form of a quarantine system for their colonies. Quarantine zones were set up as soon as unhealthy colonies were detected to protect the uninfected ones. Foulbrood positive hives would be carried to a separate apiary, far away from healthy stock. To prevent cross-contamination, beekeepers had to use dedicated tools and clothes for work at the quarantined colonies (15). Once a quarantine was established, the treatment could start. Many different treatment methods were designed in the past but unfortunately few empirical studies were carried out to test their efficiency. 

Before the discovery and widespread introduction of antiseptics in the 1860s, it was apparently widely believed that hives with bees that suffered from foulbrood should be emptied and let to air for two years. It was believed that like this the disease would “leave the hive” (14). Later, many practitioners of beekeeping recognised that in order to avoid infection in the future, the hive and the associated tools must be disinfected. One recipe suggested that hives should be washed with 10% sulphuric acid, rinsed thoroughly with water, and then placed into a pre-heated oven for several hours. Meanwhile frames with dead brood were to be burned and dead bees buried. The soil in front of the hive had to be dug up and sprinkled with 10% sulphuric acid (31). Some suggested that there is no need to burn all the combs, but the beekeepers should manually remove dead larvae from the cells and then return them into the hive. Some beekeepers even summoned birds to clean their frames of dead bees. Not all beekeepers were willing to burn their equipment or spend long hours cleaning the combs and so some took this advice more lightly than others, which undoubtedly helped amplify and even spread the disease further. 

In Britain, Frank Richard Cheshire (1833?–1894) suggested mixing phenol with sugar water in a 1:500 ratio and feeding the resulting solution to diseased colonies (40). The effects of the treatment have been disputed, some beekeepers reported that the procedure was totally inefficient, and later various alleged improvements were made to the method (45). However, more recent studies have shown that phenolic phytochemicals do display strong antimicrobial activities against P. larvae (46). 

Others recommended feeding colonies with a mixture of salicylic acid or beta naphthol with sugary water in a 1:1,000 ratio. Emil Hilbert made extensive experiments with using salicylic acid to treat foulbrood and constructed a burner to evaporate the acid. The burner was loaded with 0.5-1g of salicylic acid powder, ignited, and placed into the hive. After all acid evaporated, the bees were fed with honey or sugar mixed with more salicylic acid in a 1:935 ratio. The whole procedure was then repeated five times. The chemical was apparently nontoxic to young brood. Formic acid and thymol were also endorsed. These treatments were reportedly the most efficient if the disease was only in its infancies, late-stage foulbrood was difficult to treat (8, 10, 12, 47).         

Different variants of the shook swarm method were also popular. This approach involves the transfer of adult bees into a new disinfected hive, while leaving the old combs and brood behind (13). The old hive was then burned or disinfected thoroughly with phenol and formaldehyde. The combs from old hive were immersed in a 4% formaldehyde solution for 24 hours. The wax was then extracted and sold for industrial uses. Beekeepers were warned not to reuse wax from infected colonies (15, 29, 48). Indeed, P. larvae spores are heat-resistant and survive when wax is boiled in water. Only when left at 120°C for half hour and under pressure are all spores killed (49). 

Some beekeepers observed that replacing the queen may help cure the disease (50,70) but it is more likely that the alleviation of disease symptoms was due to brood interruption resulting from queen replacement rather than the superior qualities of the new queen. 

Interestingly, some traditional European beekeepers during the 19th century believed that foraging on certain plants such as spiraea shrubs, poplar trees, and other conifers could help colonies suffering from foulbrood to overcome the disease. Some beekeepers that had colonies with advanced foulbrood noticed that their colonies recovered spontaneously after foraging on willow trees (12,51). This observation is likewise interesting, since laboratory studies have found that the pollen of some plants contains saturated fatty acids that have antimicrobial properties against P. larvae and M. pluton (52). Plants with pollen high in these bioactive compounds have been highlighted as potentially important resources for honey bee self-medication (53). 

Not everyone believed, however, that foulbrood can be efficiently cured. Some held the opinion that no efficient treatment exists and advocated the destruction of all affected colonies by burnin (17,54). 

Although beekeeping law has its origins in the ancient world, few restrictions regarding bee diseases were in place in Europe during the 19th century. It was not until 1914 that American and European foulbrood became notifiable veterinary diseases under the Austro-Hungarian law (55). When a beekeeper suspected American or European foulbrood in his colonies, he had to notify the mayor. He would then call a veterinarian or a beekeeping expert who would inspect the colonies and decide on the next steps. A sample of the infected comb would be sent for laboratory analysis. All diseased colonies were quarantined; moving the hives or selling bee products was strictly prohibited. If the disease was severe and affected many colonies, the bees had to be killed with sulphur and the hives and equipment stored away carefully so they would not be come into contact by forager bees from other uninfected apiaries. If the progression of the disease was mild, the shook swarm method would be used. Contaminated materials had to be either burned or disinfected where possible. Failure to comply with the law would result in a fine ranging from 1 to 1,000 Austro- Hungarian Krones (i.e. €4 to €8,180 in 2019 value) or into imprisonment for 1 day to 3 years (56). 

Some of the traditional methods of foulbrood treatment, namely moving colonies to self-medicate on certain plants or providing extracts of aromatic plants may find a surprising resonance with organic beekeepers today. It would be interesting to speculate that our ancestors took advantage of the antimicrobial and anti-AFB properties of fatty acids and essential oils of plants long before they have been re- discovered and studied empirically in the several past decades. Perhaps it is time to re-examine the traditional practices of European beekeepers in a new light. 

We thank Ioannis Anagnostopoulos for valuable comments on an earlier version of this manuscript. 

Sofia Croppi.
Erik Tihelka.

Sofia Croppi was first introduced to beekeeping by her mother as a teenager. Her interest in bees was furthered through her passion for veterinary medicine and ecological sustainability thanks to a number of collaborations that brought her closer to apiological research. She is currently collaborating with the Food and Agriculture Organization of the United Nations (FAO) in Rome to study antimicrobial resistance in bees. Sofia will be commencing her studies at the Veterinary School of the University of Bristol in September 2020.

Erik Tihelka comes from a family with a long tradition of beekeeping managing 40 colonies in the Kutná hora region of the Czech Republic. The key focus of their beekeeping is apitourism and public outreach regarding bee conservation. He is interested in integrating molecular data and fossil evidence to elucidate questions in insect evolution. Erik will be commencing his studies in evolutionary biology at the University of Bristol in the Fall of 2020.

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[33] Hussein M.H. (2000) Beekeeping in Africa, Apiacta 1, 32–48.; Fries I., Raina S. (2003) American Foulbrood and African Honey Bees (Hymenoptera: Apidae), J. Econ. Entomol. 96, 1641–1646.
[34] GOODWIN, R. M., HOUTEN, A. T., PERRY, J. H. Incidence of American foulbrood infections in feral honey bee colonies in New Zealand. New Zealand Journal of Zoology 21(3), pp. 285-287, 1994. 
[35] Nepraš J. (ed) (1941). – Zpráva zemského ústředí včelařských spolků pro Čechy v roce 1935 (Annual Report of the State Federation of Beekeeping Societies for Bohemia for 1941). [in Czech]. Prague, State Federation of Beekeeping Societies for Bohemia. Dietemann, V., Pirk, C. W. W., & Crewe, R. (2009). Is there a need for conservation of honeybees in Africa?. Apidologie, 40 (3), 285-295. 
[36] BRODSCHNEIDER, R., GRAY, A., ZEE, R. VAN DER, ADJLANE, N., BRUSBARDIS, V., CHARRIÈRE, J.-D., CHLEBO, R., COFFEY, M.F., CRAILSHEIM, K., DAHLE, B., DANIHLÍK, J., DANNEELS, E., GRAAF, D.C. DE, DRAŽIĆ, M.M., FEDORIAK, M., FORSYTHE, I., GOLUBOVSKI, M., GREGORC, A., GRZĘDA, U., HUBBUCK, I., TUNCA, R.İ., KAUKO, L., KILPINEN, O., KRETAVICIUS, J., KRISTIANSEN, P., MARTIKKALA, M., MARTÍN-HERNÁNDEZ, R., MUTINELLI, F., PETERSON, M., OTTEN, C., OZKIRIM, A., RAUDMETS, A., SIMON-DELSO, N., SOROKER, V., TOPOLSKA, G., VALLON, J., VEJSNÆS, F., WOEHL, S. Preliminary analysis of loss rates of honey bee colonies during winter 2015/16 from the COLOSS survey. Journal of Apicultural Research 55(5), pp. 375-378 (2016). 
[37] ZEE, R. VAN DER, PISA, L., ANDONOV, S., BRODSCHNEIDER, R., CHARRIÈRE, J.-D., CHLEBO, R., COFFEY, M.F., CRAILSHEIM, K., DAHLE, B., GAJDA, A., GRAY, A., DRAZIC, M.M., HIGES, M., KAUKO, L., KENCE, A., KENCE, M., KEZIC, N., KIPRIJANOVSKA, H., KRALJ, J., KRISTIANSEN, P., HERNANDEZ, R.M., MUTINELLI, F., NGUYEN, B.K., OTTEN, C., ÖZKIRIM, A., PERNAL, S.F., PETERSON, M., RAMSAY, G., SANTRAC, V., SOROKER, V., TOPOLSKA, G., UZUNOV, A., VEJSNÆS, F., WEI, S., WILKINS, S. Managed honey bee colony losses in Canada, China, Europe, Israel and Turkey, for the winters of 2008–9 and 2009– 10. Journal of Apicultural Research 51(1), pp. 100-114, 2012. 
[38] ZEE, R. VAN DER, BRODSCHNEIDER, R., BRUSBARDIS, V., CHARRIÈRE, J.-D., CHLEBO, R., COFFEY, M.F., DAHLE, B., DRAZIC, M.M., KAUKO, L., KRETAVICIUS, J., KRISTIANSEN, P., MUTINELLI, F., OTTEN, C., PETERSON, M., RAUDMETS, A., SANTRAC, V., SEPPÄLÄ, A., SOROKER, V., TOPOLSKA, G., VEJSNÆS, F., GRAY, A. Results of international standardised beekeeper surveys of colony losses for winter 2012–2013: analysis of winter loss rates and mixed effects modelling of risk factors for winter loss. Journal of Apicultural Research 53(1), 19-34, 2014. 
[39] SEELEY, T. D., TARPY, D. R., GRIFFIN, S. R., CARCIONE, A., DELANEY, D. A. A survivor population of wild colonies of European honeybees in the northeastern United States: investigating its genetic structure. Apidologie 46(5), pp. 654-666, 2015. 
[40] GOODWIN, R. M., HOUTEN, A. T., PERRY, J. H. Incidence of American foulbrood infections in feral honey bee colonies in New Zealand. New Zealand Journal of Zoology 21(3), pp. 285-287, 1994. 
[41] BAILEY, L. The Effect of the Number of Honey Bee Colonies on their Honey Yields and Diseases. Ilford: Central Association of Bee-Keepers, 1984, 16 p. 
[42] DUNHAM, W. E., KING, P. E. Treating Colonies Affected with American Foulbrood with a Bacteriological Verificaton. Journal of Economic Entomology 27(3), pp. 601-607, 1934. 
[43] MUNAWAR, M. S., RAJA, S., WAGHCHOURE, E. S., BARKAT, M. Controlling American Foulbrood in honeybees by shook swarm method. Pakistan Journal of Agricultural Research 23(1-2), pp. 3-58, 2010. 
[44] MCLAIN, N. W. Report on experiments in apiculture. Report of the Commissioner of Agriculture for 1886. Washington: Government Printing Office, 1887, pp. 583-591. 
[45] SCHRÖTER, K. O nové léčbě plodmoru [About a new foulbrood cure]. Včela brněnská 22(9), pp. 137-138, 1888. 
[46] MĂRGHITAŞ, L., DEZMIREAN, D., CHIRILĂ, F., FIŢ, N., BOBIŞ, O. Antibacterial activity of different plant extracts and phenolic phytochemicals tested on Paenibacillus larvae bacteria. Scientific Papers Animal Science and Biotechnologies 44, pp. 94-99, 2011. 
[47] ANON, J. R. Domácí zprávy včelařsé: z okolí Prahy [Regional beekeeping news: Prague]. Český včelař 11(1), pp. 13-14, 1878. 
[48] ŠPAČEK, F. Kterak léčím hniloplod [My foulbrood treatment method]. Český včelař 9(7), pp. 92-93, 1875. 
[49] MACHOVÁ, M (1993) Resistance of Bacillus larvae in beeswax. Apidologie 24(1), pp. 25-31, 1993. 
[50] CHESHIRE, F. E. Queen and eggs containing Bacillus alvei— foul brood? British Bee Journal 12(152), pp. 276-277, 1884. 
[51] TADMAN, J. Medical herbs for bees – an experiment. The Australasian Beekeeper 115(5), pp. 450-451, 2014. 
54 LOVEČEK, J. (ed.) Řehoř Mendl včelařem [Gregor Mendel as a Beekeeper]. Olomouc: Kroužek lidových včelařských výzkumníků v Olomouci, 1964, 23 p. 
55 SCHÖNFELD, A. Nemoci a nákazy včel [Honey Bee Diseases]. Kladno: Svaz zemských ústředí včelařských spolků v ČSR, 1938, p. 56. 
56 ADAMEC, F. Zákon o nákazách včelího plodu [Bee Brood Disease Act]. Brno: Zemský ústřední spolek včelařský v Brně, 1914, 30 p. 
52 MANNING, R. Fatty acids in pollen: a review of their importance for honey bees. Bee World, 82(2), pp. 60-75, 2001
53 TIHELKA, E. The immunological dependence of plant-feeding animals on their host’s medical properties may explain part of honey bee colony losses. Arthropod-Plant Interactions 12(1), pp. 57-64, 2018. 

Filed Under: No. 17, Uncategorised

Progress report on three years of treatment-free beekeeping

13 August 2020 by

Including a test of three types of queen: Wild Colony, Webster Russian, and VSH Italian

In the Spring of 2017, I decided to attempt treatment-free beekeeping of colonies managed for honey production.  To do so, I stopped giving miticide treatments to the colonies that I keep in one of my apiaries and I started keeping detailed records on the fates of these colonies.  Now, three years later, I am making an initial report on my progress toward having colonies that grow large, make honey, and survive without being treated with miticides.  In addition, I will report on a one-year study conducted in 2019-2020 in which I compared colonies headed by three types of queen (wild caught in New York, Webster Russians from Vermont, and VSH Italians from California) regarding their suitability for treatment-free beekeeping.

My three-year (so far) study of treatment-free beekeeping

I am conducting this study near the small city of Ithaca, in New York State. It sits 170 miles northwest of New York City, at the southern end of Cayuga Lake. The surrounding landscape consists of rolling, open farmland to the north, and rugged, wooded hills to the south. The apiary that I have devoted to this study is located five miles east of Ithaca, and is tucked in a small valley called Ellis Hollow, which is where I have lived for most of my life.  Ellis Hollow is a horseshoe-shaped valley that runs east-west, and is approximately 1 mile wide and 2.5 miles long. It is defined by two steep-sided hills—Mount Pleasant and Snyder Hill—which rise 500 feet above the valley’s floor along its northern and southern sides and on its eastern end; its western end is open (see Figure 1).  The steep slopes and rounded tops of these hills are covered with forests, but the valley bottom is a mixture of fields, more forests, and wetlands along Cascadilla Creek.

Fig. 1. Map of Ellis Hollow near Ithaca, New York. This valley lies between Mount Pleasant and Snyder Hill, with Cascadilla Creek meandering down its middle. Blue cross:  my apiary. Color code for the land cover: light blue, wetland; white: grassy field; tan: brushy area; light green, deciduous forest; dark green, coniferous forest. The land cover data are from the USDA/NRCS 2011 National Land Cover Dataset (NLCD).

Ellis Hollow was settled in the early 1800s and until the 1940s it was home to about twenty small farms whose fields covered the valley’s arable land. These days, though, Ellis Hollow is mainly a rural residential community with some 150 homes, and most of the farms’ fields have grown back into woods and brushy places. Fortunately, many of the plants filling the abandoned fields—such as basswood (Tilia americana) and black locust (Robinia pseudoacacia) trees, pussy willow (Salix discolor) and staghorn sumac (Rhus typhina) shrubs, and patches of milkweed (Asclepias spp.) and goldenrod (Solidago spp.) plants—provide clean and plentiful forage for all sorts of insects, including honey bees.  

There are approximately fifty colonies of honey bees living in Ellis Hollow. About twenty occupy beekeepers’ hives; the rest inhabit trees and buildings. Of the twenty or so colonies in hives, I keep about seventeen in my apiary, and two other beekeepers keep about four more. Regarding colonies in trees, I know that there are approximately 2.5 bee-tree colonies per square mile of forest around Ithaca (see chapter 2 of Seeley 2019), and I know that there are approximately ten square miles of forest on the hills that form the Ellis Hollow valley, so I estimate that there are about twenty-five wild colonies residing in hollow trees in this valley.  As for wild colonies in the walls of buildings, I know of five sites—two in one neighbor’s house, and three in two other neighbors’ barns—where colonies have lived, off and on, for more than twenty years.  I have no doubt that there are many more home sites of wild colonies in the houses and barns within this valley. 

My apiary in Ellis Hollow occupies a clearing in the valley’s northeast corner (Figure 2).  Forty years ago, this spot was the southeast corner of the pasture behind the house, barn, and sawmill of Omar Gleason, one of the old-timers who lived here from the 1910s to the 1970s. I knew Omar in the 1960s, when I was a boy. He and his family moved away in the 1970s and several years later their dilapidated buildings were burned down by our volunteer fire department. In 1986, I moved home to Ithaca to start work as a professor at Cornell. In setting up my laboratory, I needed to find several good apiary sites, so I was delighted to learn that the current owners of the Gleason place had just donated its acreage to the university. (Eventually, it became the Durland Bird Sanctuary, one of several natural areas in Ellis Hollow.)  Wonderful!  Soon I had permission to establish an apiary behind the stone foundation of the Gleason farmhouse, where the cast-iron pitcher pump still stands. I have kept colonies in this lovely spot for the past thirty-four years.  

Fig. 2. My apiary in Ellis Hollow, early one morning after a snowy night.  View is to the southwest.  In the background, we see a wetland nearby and a forested slope of Snyder Hill off in the distance.

I keep my colonies in Langstroth hives, using deep hive bodies for both brood boxes and honey supers. Originally, I used 10-frame hives, but now I use mostly 8-frame equipment.  The hives in my Ellis Hollow apiary are stocked with locally adapted bees. This is something that I have worked to achieve over the past five summers.  My method has been to repopulate the hives in which colonies have died over winter with swarms caught in bait hives that I have set out each spring around the forested hills south of Ithaca (see Chapter 8 in Seeley 2017).  I am confident that most of the swarms that move into my bait hives are from wild colonies living in these woodlands, because when my friends and I have gone bee hunting in the hills south of Ithaca, our beelines have always led us to wild colonies living in trees or buildings (e.g., a hunting cabin), (see, for example, the bee hunts described in Seeley 2017, and in Radcliffe and Seeley 2018).

How have I used the colonies in my apiary in Ellis Hollow? They have served primarily as producers of bees and brood for research projects and only incidentally as producers of honey.  So my management of these colonies has been simple:  in May, I give each colony one or two empty honey supers so it has room to store honey; and in early September, I remove any surplus honey from each colony, making sure that I leave each one with a top box that is stuffed with honey for winter stores.  In most years, the colonies in this apiary will produce—despite the removals of bees and brood for various projects—about 1000 pounds of honey. 

And how have I handled the threat of Varroa destructor to these colonies? Well, I should explain that these mites arrived in the Ithaca area in the mid 1990s. I first spied them on my bees in June 1994, and in August that year I saw a troubling sight in front of my hives:  hundreds of workers crawling feebly through the grass, moving away from the hives.  What I saw the following spring, in April 1995, was even more troubling:  89 percent of my colonies were dead, even though their hives were full of honey. This disaster spurred me to take action against Varroa, so in the summer of 1995 I began treating my colonies with fluvalinate (Apistan). When this miticide became ineffective a few years later, my students and I switched to treating our badly infested colonies (those with high mite counts in early August) with formic acid, oxalic acid, or a thymol-based medication.  

In the spring of 2017, however, I decided to change course with the colonies in my Ellis Hollow apiary:  no more miticide treatments. My students and I would use these colonies as before—as sources of bees and brood for our experiments, and of honey if they produced a surplus—but we would no longer treat them with miticides.  We would, however, continue to make sure that each colony was well stocked with honey (i.e., its top hive body was full of honey) in mid-September, so that none would starve over winter. (Note:  in the future, I may euthanize colonies that have high mite counts—more than 15 mites per 300 bees— in early September. This is because these colonies are apt to collapse in the autumn, and if this happens then their mites can be spread to the healthy colonies nearby through robbing.  For more information on this “mite bomb” phenomenon, see Loftus et al. 2016, and Peck and Seeley 2018.)  

Table 1 shows my records of the fates of the colonies in the Ellis Hollow apiary since 2017. The colony mortality over winter in this apiary has been about 30%, which is much higher than what I experienced here from the mid 1980s to the mid 1990s, i.e., before the arrival of Varroa.  Back then, I had 10-15% colony mortality over winter at this site. (Note: there were, however, two exceptional winters—1990-91 and 1991-92—when I experienced ca. 80% colony mortality across all my apiaries. These were the winters that followed the arrival of the tracheal mite, Acarapis woodi, in the Ithaca area.  Fortunately, this problem subsided quickly.  I suspect that it did so thanks to strong natural selection for bees with resistance to tracheal mites.) 

Table 1.  The number of colonies at end of each summer and winter, and the % colony mortality over each winter.  The losses of colonies over winter have been due mainly to high mite loads in some colonies.  The gains in colony numbers over each summer have occurred by adding colonies caught in bait hives.

I have little doubt that the ca. 30% mortality of colonies shown in Table 1 is a result of high populations of Varroa (and ensuing damage from viruses) in some of the colonies. I say this because I have found that in these untreated colonies, the mite level in a colony in September is a very good predictor of whether this colony will be dead (or alive) the following April. For example, on 18 Sept 2018, I measured the mite loads (mites/300 bees, powdered sugar test) of the 17 colonies in the Ellis Hollow apiary, and on 25 April 2019, I inspected these colonies to see which had died. The results, shown in Table 2, show that there was great variation among the colonies in their mite loads in September 2018, and that this variation was tightly associated with which colonies were dead or alive in April 2019.

Table 2. Mite counts (Varroa mites per 300 bees) for the 17 colonies  in the Ellis Hollow apiary on 18 Sept 2018, grouped according to whether or not the colony was dead or alive the following spring, on 25 April 2019.

In summary, what I have seen so far in my apiary in Ellis Hollow—where I have ceased treating the colonies with miticides, and where each summer I have rebuilt my colony numbers using swarms caught in bait hives—is that 24-31% of the colonies have died over winter. I have also seen that the colonies that have died over winter are the ones with high mite counts in September. This 24-31% level of winter colony mortality is much higher than what I experienced in the 1970s and 1980s (two decades without Varroa), and it is certainly not ideal.  Nevertheless, I will persist with this experiment. I am motivated to do so because I enjoy not dosing the Ellis Hollow colonies with miticides, and because I enjoy catching swarms that, as we shall see next, often produce colonies that are able to control the Varroa mites.  So I remain optimistic that eventually most of the colonies in my Ellis Hollow apiary will possess a satisfactory ability to control Varroa.

My one-year test of three types of queens

As explained above, my program of treatment-free beekeeping is based on capturing swarms in bait hives I have placed in the forested hills south of Ithaca, that is, in locations far from beekeepers’ colonies. I have assumed that these swarms tend to produce colonies that can thrive without treatments to control Varroa destructor. In 2019, I decided to test this assumption by conducting an experiment. I set up twenty colonies that started out as closely matched as possible except with respect to their queens, which were of three types:  Wild Caught by me in New York State; Russians produced by Kirk Webster, a successful commercial beekeeper in Vermont who does not treat for Varroa (see Webster 2015, and Rinderer and Coy 2020); and VSH Italians from a large queen producer in California who does treat for Varroa.  In mid-June 2019, I received five Webster Russian queens and seven VSH Italian queens by mail.  Already, I had eight Wild Caught queens that I had acquired when swarms occupied eight of the bait hives that I had set out (as described above) in mid-April 2019.

Fig. 3. The three clusters of colonies in the Dunlop Meadow.  The seven colonies with VSH Italian queens are in the foreground, the five colonies with Webster Russian queens come next, and the eight colonies with Wild Caught queens sit farthest away.

On 19-20 June, 2019, I introduced these twenty queens (using push-in cages; see Sammataro and Avitabile 2011) into twenty small, queenless colonies that were housed in five-frame hives.  Each colony’s hive contained two frames of comb covered with bees and nearly filled with brood, one frame of comb nearly filled with pollen and honey, and two frames of empty comb.  The forty frames of bees and brood that I used to establish these twenty test colonies came from ten source colonies living in the other two apiaries that I have besides the one in Ellis Hollow. Each source colony provided the bees and brood for two test colonies, and the two test colonies from each source colony were assigned to two different test groups (e.g. Wild Caught and Webster Russian, or Webster Russian and VSH Italian, etc.). I moved all twenty test colonies to a shared site where I arranged them in three clusters (one for each queen type). These clusters were separated by more than 100 feet (Fig. 3).  The shared site was the Dunlop Meadow near Brooktondale, New York (see https://cornellbotanicgardens.org/wp-content/uploads/2018/10/Dunlop-Meadow.pdf), and the three clusters were set up along the 880- foot-long hedgerow that runs east-west along the meadow’s northern boundary (Fig. 4). Every colony’s hive faced south, and every colony’s hive color was unique within its cluster.

Fig. 4.  Aerial view of the Dunlop Meadow, which lies eight miles east of Ithaca, New York, and just north of the village of Brooktondale.  Red letters mark locations of the three clusters of colonies with the three types of queens:  W, Wild Caught; R, Webster Russian; and I, VSH Italian.

On 3 July 2019, I transferred all twenty colonies to ten-frame hives, and I put a dot of white paint on the thorax each colony’s queen.  On 8 July (18 days after the colonies were established), I inspected each colony and measured its brood area (number of frame sides filled with brood).  Here is what I found:  colonies with a Wild Caught queen, 3.9±0.6 frame sides; colonies with a Webster Russian queen, 3.0±0.3 frame sides; and colonies with a VSH Italian queen: 3.5±0.5 frame sides.  I also found that all twenty colonies were queenright.  Seeing this, I decided to not disturb the colonies for the next several weeks.  

On 27 August 2019, I inspected each colony, to see if it was still queenright (and if so, whether or not it contained its original queen) and was thriving, i.e., it had a good brood pattern and good honey stores.  Every colony was queenright, and still had its original queens, except one colony in the VSH Italian group that had replaced its queen.  In this colony, I found an unmarked queen laying eggs and an open queen cell.

On 9 October 2019, I inspected each colony again.  In doing so, I checked (1) whether or not the colony was queenright and (if so) whether or not it had its original queen, (2) whether it was strong or weak (i.e., whether bees filled the hive or covered only some of the frames), and (3) its mite load (i.e., mites per 300 bees, measured using the powdered sugar method).  Table 3 summarises what I found.  We see that two of the eight colonies in the Wild Caught group were queenless and weak (with bees covering just two-four frames), but that all the other colonies were queenright and strong, with bees on all ten frames.  We also see that among the queenright colonies, two out of six in the Wild Caught group, two out of five in the Webster Russian group, and one out of seven in the VSH Italian group had an unmarked queen. These were either supersedure queens or replacement queens reared in colonies that had swarmed in August or September. (In the Ithaca area, about 20% of swarming occurs in late August and early September [Fell et al. 1977]). What is most striking, however, are the differences that we see among the three groups in their mite counts. The mean (± SD) mite counts for the colonies with Wild Caught, Webster Russian, and VSH Italian queens are 4.6 ± 6.7, 1.6 ± 1.2, and 15.3 ± 6.0 mites per 300 bees. The difference between the mean counts for the Wild Caught (WC) and Webster Russian (WR) queen colonies is not significant (p > 0.05), but the differences between the mean counts for these two types of colonies and the mean count for the colonies with VSH Italian queens are both significant (WC vs. VSH Italian, p < 0.01; WR vs. VSH Italian p < 0.001).

Table 3.  Status of each colony in the three groups, with respect to queen status, colony strength, and mite count in October 2019, and with respect to survival to April 2020.

Seven months later, on a warm Spring day in Ithaca (7 April 2020), I again inspected all the colonies.  Table 3 shows what I found:  of the six Wild Caught colonies that went into winter queenright, all but one was alive; of the five Webster Russian colonies (all of which went into winter queenright), all but one was alive; and of the seven VSH Italian colonies (all of which went into winter queenright), only one was alive.  These results are best summarized in terms of the percentages of the queenright colonies that survived winter:  Wild Caught, five out of six colonies (83%); Webster Russian, four out of five colonies (80%), and VSH Italian, one out of seven colonies (14%).

We cannot draw sweeping conclusions from this study, for it involved only twenty colonies and it unfolded over just one year. Nevertheless, I think it is useful to summarise its key findings, for they are least suggestive of where a beekeeper who wishes to pursue treatment-free beekeeping should get his or her queens.  

  1. There was greater heterogeneity—with respect to queen failures over summer and mite counts in October—among the colonies with Wild Caught queens than among those with Webster Russian and VSH Italian queens.  
  2. On average, the mite counts in October were markedly lower in the colonies with Wild Caught queens and Webster Russian queens relative to the colonies with VSH Italian queens.  
  3. Among the colonies that were queenright going into winter, the percentage that survived winter was markedly higher for the colonies with Wild Caught and Webster Russian queens than for the colonies with VSH Italian queens.
  4. Among the seven colonies with VSH Italian queens, there was just one (Colony 4) that had a low mite count in October and that survived winter; this was the colony that changed its queen in August or September. 

I wonder, regarding point 4, did the one colony in the VSH Italian group that survived winter do so because the process of swarming (or supersedure) reduced this colony’s mite load (see Seeley and Smith 2016), or because its new queen acquired genes for mite-resistance when she mated with drones from wild colonies in the area, or both?  I look forward to trying to test the second possibility. Does an abundance of wild colonies in the region where a queen conducts her mating flight(s) help to endow her colony with strong resistance to Varroa destructor, by enabling her to mate primarily with drones from colonies that are thriving without being treated for these mites?  Stay tuned!

References

Fell, R.D., J.T. Ambrose, D.M. Burgett, D. De Jong, R.A. Morse, and T.D. Seeley.  1977.  The seasonal cycle of swarming in honeybees.  Journal of Apicultural Research 16: 170-173.
Loftus, C.L., M.L. Smith, and T.D. Seeley.  2016.  How honey bee colonies survive in the wild: testing the importance of small nests and frequent swarming.  PLoS ONE 11(3):  e0150362. doi:10.1371/journal.pone.0150362.
Peck, D.T. and T.D. Seeley.  2019.  Mite bombs or robber lures? The roles of drifting and robbing in Varroa destructor transmission from collapsing honey bee colonies to their neighbors. PLoS ONE 14(6): e0218392. https://doi.org/10.1371/journal.pone.0218392
Radcliffe, R.R. and T.D. Seeley.  2018.  Deep forest bee hunting: a novel method for finding wild colonies of honey bees in old-growth forests.  American Bee Journal 158(August): 871-877.
Rinderer, T.E. and S.E. Coy.  2020.  Russian Honey Bees.  Salmon Bayou Press.
Sammataro, D. and A. Avitabile.  2011.  The Beekeepers Handbook.  4th Edition.  Cornell University Press, Ithaca, New York.
Seeley. T.D.  2017.  Following the Wild Bees.  Princeton University Press, Princeton, New Jersey.
Seeley, T. D.  2019.  The Lives of Bees.  Princeton University Press, Princeton, New Jersey.
Seeley, T.D. and M.L. Smith.  2015.  Crowding honeybee colonies in apiaries increases their vulnerability to the deadly ectoparasitic mite Varroa destructor.  Apidologie 46:716-727.
Webster, K.  2015a. Commercial beekeeping without treatments of any kind–putting the pieces together.  Part I of Two Parts.  American Bee Journal 145(March): 203-206.
Webster, K.  2015b. Commercial beekeeping without treatments of any kind–putting the pieces together.  Part II of Two Parts.  American Bee Journal 145(April): 312-315.

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