Chalkbrood is common, but overlooking it could be a mistake
Nobody wants to be eaten by a fungus from the inside out. But that’s exactly what happens to honey bee larvae infected with Ascosphaera apis, the pathogen that causes chalkbrood disease. The spores germinate in the larva’s gut, then hyphae (fungal branches) burst from the larva’s backside in just a few days after being consumed.
It sounds like a terrible way to go, and under the wrong conditions it can be terrible for the colony, too. If enough larvae become infected, adult population growth slows down, reducing the colony’s productivity. However, not everyone agrees on what economic impact this disease really has, and data on the subject are sparse.
For example, depending whom you ask, chalkbrood infection may have zero effect on honey production, or it may reduce honey yields by as much as 37%.1 And they would both be correct. Chalkbrood hits some regions harder than others, probably due to differences in climate, innate resistance of the bees, and background prevalence. Other economic metrics, like missed opportunities for nuc production and other knock-on effects are seldom documented.
Because the disease does not always lower honey production, does not usually kill colonies, and tends to clear up in warmer summer temperatures, chalkbrood in North America is typically not taken too seriously. But I think it should be. Though it is certainly not the biggest threat to honey bee health, it is probably one of the most underappreciated.
“I think what is most frustrating for me as a scientist is that I don’t have good advice for controlling this pest when an operation already has an outbreak,” says Elizabeth Walsh, a USDA Agricultural Research Scientist at Baton Rouge, who studies chalkbrood epidemiology. “Advice to “keep strong colonies,” which is what beekeepers have traditionally been advised to do, falls short when they are already doing all that they can.” Developing a treatment for chalkbrood might help, but not everyone agrees that is the answer.
Given how long chalkbrood has afflicted beekeeping and how widespread it is, it is remarkable that there is still no approved treatment for it. The first detailed description of the disease appeared in Europe in 1921,2 but it wasn’t until the 1960s that the disease was discovered in the United States. First came Utah, then California, and quickly beyond — by 1975, it was detected in 34 states, and now it is ubiquitous across all of North America and considered a “moderate” threat by the USDA.3
But in other countries, the disease is taken more seriously. In Australia, chalkbrood is a notifiable pest that must be disclosed to an apiary officer within a week of detection. Jody Gerdst, a honey bee researcher and managing director of Bee Scientifics — an Australian company aimed at improving beekeeping through breeding, education, and training — says that broadly speaking, Australian beekeepers are aware of and troubled by chalkbrood. “The biggest concern is that there doesn’t seem to be a pattern to the outbreak related to conditions or management practices,” Gerdst says.
Almost every chalkbrood resource says that prevalence varies seasonally, with symptoms emerging in the spring, then easing off as temperatures increase in the summer. Conditions in the spring are often cool and wet, the rationale goes, and as the brood area expands, the adult bees need to regulate the nest temperature short-staffed. But as the ambient temperature and the adult bee population increase in the summer, colonies can maintain higher nest temperatures more easily, which may help inhibit fungal growth.
This explanation generally agrees with what has been demonstrated in the lab: that the optimal temperature for A. apis growth is 30 C (86 F), whereas the fungus grows poorly at 35 C (95 F).4 But Gerdst points out that this pattern is not always what happens. Beekeepers in the U.S., too, occasionally see unusual outbreaks in the peak of the summer, which might be linked less to the weather and more to genetic susceptibility of the bees.
When the fungus sporulates, it produces dark cysts which, like little nesting dolls, contain balls containing spores. The spores themselves are around two microns long and shaped a bit like a bean, which makes them easily confused with nosema spores, which are around three microns and shaped like a blunt football. Chalkbrood mummies turn black when the fungus sporulates, and they are full of infectious particles ready to adhere to workers and spread around the colony.
The spores may embed in wax, contaminate honey, or become ingested by adult bees and shared amongst adults and larvae alike. Under the right conditions, the spores can remain viable for up to 15 years,5 and, according to Walsh, they can continue to circulate in the brood even while a colony remains asymptomatic.
This means that nucs or packages which are produced from asymptomatic carrier colonies can become symptomatic once installed in their new home. The increased stress of travel and the difficulty a small colony has at regulating the nest temperature create good conditions for fungal growth, even if the mother colony showed no recent signs.
This can lead to frustrated nuc producers, who think they are making nucs from their best colonies, as well as frustrated consumers, who might have just spent big bucks for a colony that soon became a mummy factory. For this reason, apiary checks for nuc and package producers should probably include spore counts, but such tests are not currently required.
Honey bees do have natural defenses against chalkbrood, the best studied of which is hygienic behavior, but it’s no silver bullet. Heroic efforts have been made to breed highly hygienic bees that are sufficiently good at removing chalkbrood mummies from the colony to curb an infection, but the strategy is difficult to industrialize.
What’s more, although numerous studies show that hygienic behavior effectively mitigates chalkbrood in North America, Gerdst led a large-scale survey which demonstrated no link between the behavior and chalkbrood resistance in eastern Australia.6 It’s not yet clear why, but this means that other traits would need to be identified and targeted for breeding programs there to be successful.
Right now, Gerdst is working on exactly that. This spring (which started in September in Australia), she is identifying sister queens that are either innately resistant or susceptible to see how heritable these characteristics are. “I don’t think treatments are the answer,” Gerdst says. “I think we can get over the chalkbrood hurdle with specific and targeted breeding.”
And that’s a good thing, because no approved chalkbrood treatments yet exist, although some preliminary research has been promising. Over a decade ago, Amanda Van Haga, a then-master’s student at Beaverlodge Research Station, Alberta, showed that a commercially available protein, lysozyme, could be used to control chalkbrood when fed as a syrup supplement.1 Such a treatment could be combined with breeding efforts or used on new packages and nucs, which are most vulnerable, as part of an integrated management plan.
In a field trial, Van Haga inoculated colonies with chalkbrood spores, then tested how well three different doses of lysozyme (an antimicrobial enzyme) could suppress the infection. The highest dose (three treatments of 6 g, dissolved in syrup) was highly effective at ….
