Have you ever had European foulbrood? EFB, or Melissococcus plutonius, is commonly considered the lesser evil of the dreaded foulbroods we either manage for or hope never to catch. But in my day-to-day life as an apiary inspector, I declare EFB to be Public Bee-Enemy Number One. I frequently find it in apiaries far and wide.
EFB is easy to catch and spread. However, diagnosis of this bacterial infection shouldn’t be seen as a doom-and-gloom death sentence for happy-go-lucky hobbyists or commercial-scale apiary managers. Nowadays, I see the appearance of EFB in an apiary as a rite of passage, and I urge beekeepers to resist keeping their EFB secret. EFB is so common, it’s silly to treat it as taboo. The opportunity to manage and/or eradicate this disease is a journey of education, dedication and renewal of one’s own beekeeping experience — a skill builder of the highest caliber.
What is European foulbrood? EFB is a bacterial infection, primarily in the gut of honey bee larvae. The bacteria we credit as the signifier of this disease is Melissococcus plutonius, however, EFB can be present in conjunction with several other forms of bacteria. This creates a disease that can have a host of different symptoms. A “shotgun” brood pattern, or a frame with a disorderly brood pattern of all stages of larvae and capped brood, with several empty cells — this is a key symptom. Other symptoms are twisting, misshapen larvae, dull or discolored larvae, and dried, dead larvae in cells. In some cases, the capped brood can die while pupating. Sometimes a foul smell is associated with EFB (hence the name “foulbrood”). Any beekeeper noticing symptoms like these should call a beekeeping mentor or apiary inspector to identify the disease and recommend treatment — and fast! EFB can spread quickly through single apiaries, nearby apiaries and feral hives. A timely triumph over EFB can save a community.
I myself have had to duke it out in the EFB arena. I first caught it in the summer of 2013. From then through spring of 2014 my bees and I went through quite a trial. At first, my belief in myself was in question: “To continue as a beekeeper, will I have to use antibiotics twice a year? Will that work to keep the European foulbrood away? How long will I have to treat — forever?” This question shook my life.
Back then, I had only been married a year and my husband Raphael was still amenable to helping me with tedious beekeeping tasks. When the going got tough I worried about ending our “honeymoon phase” prematurely as we spent a couple of “date nights” a week in the garage, listening to the radio, scraping stiff old comb and brood and honey into barrels. One week slid into the next. I wondered: “How many more nights of this will he tolerate until he questions our vows?”
A lot of introspection occurs when you try to clean European foulbrood from your apiary. I began hating myself when I remembered my attitude toward two hives: “Hive-zilla” and “Hive-zilla Jr.,” named after their aggressive attitudes and monstrous honey output. Full of surprises, those two just LOVED to sting me in the back! So I retaliated by giving them old comb from deadouts. They were always so strong, they were great at cleaning a little mold, starved bees or wax moths out of comb.
One day, I acquired some old drawn comb from another beekeeper. It was very dry and thin, and looked very clean and safe. I don’t remember where I read this, but I had read that beekeepers with European foulbrood could expect the disease to be eliminated after treating with oxytetracycline (OTC), aka Terramycin, for five years. I thought, “This old comb looks to have hardly been used, and it’s at least five years old. I’ll give this dry old comb to the Hive-zilla twins this spring — they’ll be glad to have it.” O, there began the tempest to my soul! If I could have turned back time! Fast-forward to the next season, comb from 600 frames of my Southern Illinois beekeeping went up in smoke, while my husband and I supped on honey-roasted hotdogs — again!
Soon after I “gifted” the Hive-zillas that “clean, old comb,” I noticed they grew notably weaker, with shotgun brood patterns and wilting, twisting, dying larvae. I caught this change early and took swab samples right away and sent them to the Bee Research Lab in Beltsville, Maryland. “Good news, Honey!” I told Raph, “The tests from Beltsville came back negative for European foulbrood! I’ll treat for mites, because they must have Parasitic Mite Syndrome.” But the populations dwindled quickly and before I knew it, I found my other hives robbing Hive-zilla. Within a week, all six hives in the apiary were showing shotgun brood patterns and dying larvae. I sent another sample to Beltsville, and now it returned positive results. I couldn’t bear to lose my other colonies, so I treated with generic Terramycin according to the label, with little success.
Back in those days, you didn’t need a prescription to buy Terramycin. A versatile, broad-spectrum antibiotic, you could run out to the farm supply store, where it was on hand to treat chickens, pigs, sheep, etc. I meticulously calculated and measured the correct dosage for my colonies, and found not only didn’t the EFB symptoms improve, but some colonies were further weakened. I then switched to a bee-optimized Terramycin powder from a beekeeping supply company and conducted drench treatments which were effective enough to “control” the EFB to get more of my colonies through the winter than not.
Over the winter, I combed the internet and my library for information on EFB. In my experience up to that moment, I believed that treating with Terramycin took care of the problem. But now that my chickens had come home to roost, I was finding that the EFB in my hives was much more stubborn and didn’t automatically “clear up” with the medicine. Brood infections returned, and any equipment associated with EFB-infected hives had the ability to spread the disease. Why was this?
A look at EFB research
I was eager to understand both what I was seeing in my hives, and patterns I was recognizing in the field on my apiary inspections. As an apiary inspector, I traced the movement of EFB outbreaks. For example, in the spring of 2014, I was hot on the trail of an aggressive EFB outbreak in one particular apiary-dense suburban town. Like a bloodhound, I tried to sniff out the source apiary where it started. As it happened, this particular beekeeping community was tightly knit, and happy to talk. I learned of a row of hives in a well-respected apiary that had died out the previous winter.
As I made my way across this town the following spring, finding EFB cases left and right, it appeared that every bee colony within a 2.5-mile radius had visited the deadout apiary to rob it out. While it was a disadvantage to this community of beekeepers that their hives were in such close proximity to the deadouts, and therefore no apiary escaped the outbreak, there was a great advantage in that all of the beekeepers knew each other and were able to band together and help each other with treatment plans. I, of course, was eager to contribute to their efforts with information I had recently learned about EFB treatment options.
One excellent source of information was Eva Forsgren’s scientific review of EFB studies. Dr. Forsgren is a honey bee researcher and manager of the Swedish National Reference Laboratory of Honey Bee Health — a leader in EFB research. Her review, “European foulbrood in Honey Bees” took a comprehensive, up-to-date look at all peer-reviewed research conducted toward understanding European foulbrood between the late 19th century and 2009. Her study recounted an in-depth history of identification, classification, naming, and re-naming of the pathogen. She also examined an interesting factor of EFB — that it so often is accompanied by a “secondary bacterial invasion,” and these piggyback pathogens were identified along with their origins, characteristics, and interactions with M. plutonius in the hive. Transmission of the bacteria was discussed, illustrating how infected larvae release massive amounts of bacteria into brood cells during pupation, and how those bacteria remain viable, surviving long periods of desiccation.
Also interesting was her discovery of surprisingly high levels of M. plutonius in asymptomatic hives (showing no symptoms) in apiaries where EFB occurred, and how adult worker bees acted as carriers of the disease between colonies and apiaries. Finally, she discussed that honey from infected hives was commonly contaminated with M. plutonius, and, while safe for human consumption, could act as a disease vector if fed to colonies or if healthy bees robbed infected hives.
Dr. Forsgren’s study confirmed several “hunches” I had identifying and observing EFB in the field. Bacteria were capable of surviving for years in comb, were present throughout all life stages of honey bees, and could be measured in all hive materials, including honey. Acknowledging how locally prevalent this disease was, I was hungry for more science to help me find a best method of controlling or eradicating local EFB.
I found another study, “A typing scheme for the honey bee pathogen Melissococcus plutonius allows detection of disease transmission events and a study of the distribution of variants.” This study obtained EFB isolates from around the world, but primarily focused on isolates from the U.K. Genetic data was processed from these samples, resulting in an identification of 23 different global “sequencing types,” or variants. These variants showed slight differences in genetic makeup as well as differences in disease virulence (how severe symptoms were), and how fast the disease would progress. They were also able to trace movement and spread of EFB variants though different outbreaks, and referenced an instance where EFB was introduced to an EFB-free apiary with the purchase of infected hive materials from another apiary.
I also found interesting a study conducted by Japanese universities and institutions, led by D. Takamatsu and R. Arai, et al. They found an “atypical strain” of EFB. This study examined M. plutonius-like organisms and showed them to be taxonomically identical to M. plutonius, belonging to a phenotypically and genetically distinguishable strain. Atypical M. plutonius was shown to be a causative agent of EFB. Something that stood out with Atypical M. plutonius was that it maintained virulence even after repeated subculture in laboratory medium — a stronger survivability than typical EFB strains. This and related studies suggested that EFB was an ever-changing pathogen, capable of mutating, like many other pathogens.
Armed with this knowledge, I then searched for a reliable science-backed treatment method to eradicate the disease, should any beekeepers (like myself) so desire. A study performed by the National Bee Unit of the Central Science Laboratory of York had the answer. This study was conducted in Wales, documenting treatment outcomes performed by beekeepers and their apiary inspectors. From 16 EFB-positive apiaries, two infected hives were selected. One hive was treated with an oxytetracycline antibiotic course, and the other was given the same antibiotic course, but then followed with a “shook swarm” treatment, where treated honey bees were shaken from their frames into fresh, clean equipment and virgin foundation. This study found that the OTC-only treatment group had a 21% EFB re-infection rate, while the group that followed OTC with the shook swarm treatment had only a 5% re-infection rate. With such a difference in treatment outcomes, I decided to follow the shook swarm method in hopes of ridding EFB from my yards.
A tale of two treatments (and a nod to one of my local heroes in beekeeping, Julie McKinney)
One truth about my life as an apiary inspector: I got into this job more for my love of beekeepers than my love of bees. I meet the most amazing people, travelling from one apiary to the next, and I make some ….
