Chalkbrood, Stonebrood, and Sacbrood Explained

December 31, 2025

The hierarchy of honey bee diseases works like this: Varroa destructor gets the most attention because it kills the most colonies. American foulbrood gets the second most because it's regulated, reportable, and the treatment protocol involves burning equipment. Nosema gets the third most because it's invisible, widespread, and the only approved treatment might make it worse.

Below those big three sits a group of diseases that rarely makes the front page of any beekeeping journal but shows up in hives with reliable regularity - particularly in spring, particularly in cold or damp climates, and particularly in colonies that are already stressed by something else. These are the diseases that don't destroy colonies outright but weaken them, confuse beekeepers who haven't seen them before, and resist the instinct to solve problems by adding chemicals.

Chalkbrood

Chalkbrood is caused by Ascosphaera apis, a fungus that infects larvae through ingestion of spores mixed into their food. The spores germinate in the larval gut. The fungal mycelium grows through the larva's body, consuming it from the inside. The larva dies - typically in the late larval or early pupal stage, after the cell has been capped - and the fungal growth replaces the body's contents with a dense mycelial mass.

The result is a "mummy" - a hard, shrunken, chalky white larva-shaped object that rattles loosely in the cell. If the fungus produces spores on the mummy's surface (which happens when reproductive structures of opposite mating types are present), the mummy turns grey or black. The white and grey-black mummies are diagnostic: no other bee disease produces them.

Hygienic workers detect the dead brood, uncap the cells, and remove the mummies. Dropped mummies accumulate on the bottom board and on the ground in front of the hive entrance. A beekeeper who finds small, hard, white pellets scattered in front of the hive has chalkbrood.

The disease is ubiquitous. Spores are present in essentially every hive in every apiary. Whether those spores cause clinical disease depends on conditions. Chalkbrood is overwhelmingly a disease of stress: cold springs that chill the brood nest below the optimal 35 degrees Celsius, nutritional stress from poor pollen availability, genetic susceptibility, and any disruption that causes the colony to fail to maintain brood nest temperature.

The spores can survive for 15 years in stored equipment. The fungus survives freezing. It survives desiccation. The only reliable "treatment" is improving colony conditions - requeening with hygienic stock, ensuring adequate nutrition, reducing excess space that the colony can't thermoregulate effectively, and waiting. Strong colonies in good conditions suppress chalkbrood through hygienic behavior and brood nest temperature maintenance. Weak colonies in bad conditions get overrun.

There is no registered chemical treatment for chalkbrood in the United States. Antifungal compounds exist. None are approved for use in bee hives. Some beekeepers have experimented with essential oil treatments (thymol, tea tree oil) with anecdotal reports of improvement. The peer-reviewed evidence for these approaches is thin.

European Foulbrood

European foulbrood (EFB) is often described as the "lesser" foulbrood, which is like describing influenza as the lesser pneumonia. It's less destructive than American foulbrood - it doesn't produce persistent spores, it doesn't require burning equipment, and colonies can recover from it without treatment. But EFB can kill colonies, especially in combination with other stressors, and it has a nasty habit of recurring.

The causative agent is Melissococcus plutonius, a gram-positive bacterium that colonizes the larval gut. Unlike AFB, which kills larvae after capping, EFB typically kills larvae before they're capped - in the 4 to 5-day-old larval stage. The dead larvae twist into unnatural positions in their cells, often described as "coiled" or "melted." They turn yellow, then brown, then dry into a dark scale that, unlike AFB scales, can usually be removed from the cell by hygienic workers.

The smell is distinctive but different from AFB. EFB produces a sour, vinegary odor - sometimes described as rotting meat, sometimes as fermented fruit. It doesn't have the pungent, ropy quality of AFB. The "ropiness test" - pulling a matchstick from a dead larva and seeing if the remains stretch into a rope - is one of the field diagnostic differences: EFB remains don't rope. AFB remains rope to 2 centimeters or more.

Treatment: oxytetracycline (Terramycin) or tylosin (Tylan), both of which require a veterinary prescription as of 2017. But many EFB cases resolve without antibiotics when the colony is strong enough. Requeening - replacing the queen to create a brood break and introduce potentially more hygienic genetics - is often the most effective intervention. A colony that recovers from EFB may harbor the bacteria indefinitely, with clinical disease recurring during stress events. The analogy to human cold sores (dormant virus that reactivates under stress) isn't perfect but captures the pattern.

EFB is notifiable in most states - beekeepers are legally required to report it - though enforcement varies. Some states treat it the same as AFB: mandatory destruction. Others allow treatment and management. The regulatory patchwork mirrors the broader inconsistency of US beekeeping regulation.

Sacbrood

Sacbrood is caused by Sacbrood virus (SBV), an RNA virus in the family Iflaviridae. It's one of the most common honey bee viruses, detected in colonies worldwide. Most of the time, it causes no visible disease - the virus is present at low levels, managed by the colony's collective immune response, and undetectable without laboratory testing.

When clinical sacbrood occurs, it's distinctive. Infected larvae die in the prepupal stage, fail to shed their larval skin, and the space between the dead prepupa and the unshed skin fills with fluid. The result is a "sac" - a dead, fluid-filled prepupa enclosed in a tough, transparent skin. The fluid is initially clear and turns yellow-brown as the prepupa decomposes. If a beekeeper uncaps a sacbrood cell and lifts the dead prepupa with tweezers, it comes out intact, like a small water balloon.

The head end of the dead prepupa darkens first, giving it a characteristic "Chinese slipper" or "gondola" shape - curved, with a darkened, upturned anterior end. This shape is nearly pathognomonic for sacbrood.

Like chalkbrood, sacbrood has no approved treatment. Like chalkbrood, it's overwhelmingly a disease of stress and colony condition. Strong colonies clear sacbrood quickly through hygienic behavior. Weak colonies - especially colonies stressed by Varroa, which vectors the virus - can suffer significant brood losses.

The Varroa connection is important. SBV is one of several viruses that Varroa transmits directly when feeding on bee pupae. The mite acts as both a vector (mechanically transmitting the virus between bees) and an immunosuppressant (its feeding weakens the bee's antiviral defenses). Colonies with high Varroa loads are more likely to show clinical sacbrood. Treating the Varroa treats the sacbrood, indirectly but effectively.

Stonebrood

Stonebrood is the rarest of the common brood diseases - a contradiction in terms that accurately reflects its status. It's caused by Aspergillus flavus or Aspergillus fumigatus, the same fungal species responsible for aspergillosis in birds and immunocompromised humans. The spores are ubiquitous in soil and air. Healthy colonies don't develop stonebrood. Weakened colonies occasionally do.

The disease gets its name from the result: larvae and pupae killed by Aspergillus become petrified - hard, stone-like, covered in a powdery layer of fungal spores that can be green (A. flavus) or grey-green (A. fumigatus). The mummies are harder than chalkbrood mummies and more difficult for hygienic bees to remove from cells.

Stonebrood is also the only common bee disease that poses a direct human health risk. Aspergillus spores are a respiratory hazard. Beekeepers working with stonebrood-affected hives - particularly when scraping combs or cleaning equipment - can inhale spores. For most healthy adults, this is not a significant risk. For immunocompromised individuals, Aspergillus inhalation can cause serious pulmonary aspergillosis.

There is no treatment for stonebrood in honey bees. The disease is almost always self-limiting in otherwise healthy colonies - the bees remove the infected brood, conditions improve, and the fungus doesn't gain a foothold. In severely weakened colonies, stonebrood may accelerate the decline. But by the time a colony develops clinical stonebrood, it usually has other problems that are more urgent.

The Virus Alphabet

Beyond sacbrood, honey bees carry a roster of viruses that reads like a catalog of creative naming: deformed wing virus (DWV), black queen cell virus (BQCV), chronic bee paralysis virus (CBPV), acute bee paralysis virus (ABPV), Israeli acute paralysis virus (IAPV), Kashmir bee virus (KBV), and several others.

DWV is the most significant. It's the virus most commonly vectored by Varroa - the mite feeds on the pupa and injects viral particles directly into the bee's hemolymph. Bees emerging with high DWV loads have crumpled, deformed wings, shortened abdomens, and lifespans measured in days. They can't fly. They can't forage. They crawl on the front of the hive and die. Deformed wing virus is, in practical terms, the mechanism by which Varroa kills colonies. The mite is the vector; the virus is the weapon.

CBPV causes trembling, darkened, hairless bees that are often attacked by their nestmates - the diseased bees' altered pheromone profile marks them as foreign. Clusters of trembling, black bees on the front of the hive or on the landing board are suggestive of CBPV. The virus can spread rapidly through colonies via direct contact and fecal contamination. It's been increasing in prevalence in Europe and North America, possibly due to increased colony density and migratory beekeeping practices.

IAPV gained notoriety in 2007 when it was initially implicated as a possible cause of Colony Collapse Disorder. A study led by Diana Cox-Foster at Penn State found IAPV in CCD colonies but not in healthy controls. Subsequent research showed the correlation was less clean than the initial findings suggested - IAPV was found in many healthy colonies too, and CCD colonies carried multiple pathogens. IAPV joined the long list of factors that contribute to colony losses without being solely responsible for any of them.

No antiviral treatments are available for honey bees. The management approach for all bee viruses is the same: reduce Varroa (because Varroa vectors and amplifies most of them), maintain strong colonies with good nutrition, and select for genetics that show resistance or tolerance.

The Common Thread

The striking pattern across all these diseases - chalkbrood, EFB, sacbrood, stonebrood, the viruses - is that the causative agents are everywhere. The spores are in every hive. The viruses are in every colony. The bacteria are in every apiary. The difference between a healthy colony and a sick one isn't the presence or absence of pathogens. It's the colony's ability to manage them.

A strong colony with adequate nutrition, good genetics, a productive queen, a healthy gut microbiome, manageable Varroa levels, and stable brood nest temperature doesn't develop clinical chalkbrood, even though the spores are there. A weak colony with nutritional stress, high mite loads, a failing queen, and fluctuating brood nest temperature develops chalkbrood, sacbrood, and possibly EFB simultaneously - not because it encountered new pathogens but because it lost the capacity to suppress the ones it was already carrying.

This is why the "minor" diseases aren't really minor. They're indicators. A hive full of chalkbrood mummies isn't just a hive with a fungal problem. It's a hive that has failed - through size, nutrition, genetics, management, or some combination - to maintain the conditions under which the resident pathogen stays dormant. The mummies on the bottom board are a symptom. The disease is the weakness.

And that weakness is the space where everything else walks in. Varroa vectors the viruses. The viruses suppress immunity. The suppressed immunity allows the fungi. The fungi compromise brood production. The compromised brood production weakens the colony. The weakened colony can't thermoregulate the brood nest. The cold brood nest lets in more chalkbrood.

The spiral is the same one that operates in every complex biological system: stress creates vulnerability, vulnerability creates disease, disease creates more stress. The "minor" diseases are the middle of the spiral - the point where things are going wrong but haven't yet gone completely wrong. The mummies are a message. The message is: something else is the real problem. Find it.