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Diseases of the honey bee
Diseases of the honey bee include:
Additional recommended knowledge
Pests and parasites
Varroa destructor and Varroa jacobsoni are parasitic mites that feed off the bodily fluids of adult, pupal and larval bees. Varroa mites can be seen with the naked eye as a small red or brown spot on the bee's thorax. Varroa are carriers for a virus that is particularly damaging to the bees. Bees that are infected with this virus during their development will often have a visible "K-wing" deformity.
Varroa have led to the virtual elimination of feral bee colonies in many areas and is a major problem for kept bees in apiaries. Some feral populations are now recovering — it appears that they have been naturally selected for Varroa resistance (these so-called feral populations may be africanized bees).
Varroa were first discovered in Southeast Asia in about 1904, but has now spread virtually worldwide. Varroa were discovered in the United States in 1987, in New Zealand in 2000.
Varroa are generally not a problem for a hive that is growing strongly. When the hive population growth reduced in preparation for winter or due to poor late summer forage the mite population growth can overtake that of the bees and can then destroy the hive. Often a colony will simply abscond (leave as in a swarm, but leaving no population behind) under such conditions.
Formic acid gel packs are sold as "Mite-Away". According to the U.S. Environmental Protection Agency, when used in beehives as directed, this kills the mites, while not substantially disrupting bee behavior or life span. It is not intended for use during production of marketable honey. 
Acarine (Tracheal) mites
Acarapis woodi is a small parasitic mite that infests the airways of the honey bee. The first known infestation of the mites occurred in the British Isles in the early 20th century. First observed on the Isle of Wight in 1904, the mystery illness known as Isle of Wight Disease was not identified as being caused by a parasite until 1921. It quickly spread to the rest of Great Britain. It was regarded as having wiped out the entire bee population of the British Isles (although later genetic studies have found remnants that did survive) and it dealt a devastating blow to British beekeeping. Brother Adam at the Buckfast Abbey developed a resistant hybrid bee known as the Buckfast bee, which is now available worldwide to combat acarine disease.
Acarine mites, formerly known as tracheal mites are believed to have entered the US in 1984, via Mexico.
Mature female acarine mites leave the bee's airway and climb out on a hair of the bee, where they wait until they can transfer to a young bee. Once on the new bee, they will move into the airways and begin laying eggs.
Acarine mites are commonly controlled with grease patties (typically made from 1 part vegetable shortening mixed with 3-4 parts powdered sugar) placed on the top bars of the hive. The bees come to eat the sugar and pick up traces of shortening, which disrupts the mite's ability to identify a young bee. Some of the mites waiting to transfer to a new host will remain on the original host. Others will transfer to a random bee - a proportion of which will die of other causes before the mite can reproduce.
Menthol, either allowed to vaporize from crystal form or mixed into the grease patties, is also often used to treat acarine mites.
Nosema apis is a spore-forming parasite that invades the intestinal tracts of adult bees and causes nosema disease. Nosema is also associated with Black queen-cell virus. Nosema is normally only a problem when the bees can not leave the hive to eliminate waste (for example, during an extended cold spell in winter or when the hives are enclosed in a wintering barn). When the bees are unable to void (cleansing flights), they can develop dysentery.
Nosema is treated by increasing the ventilation through the hive. Some beekeepers will treat a hive with antibiotics.
Nosema can also be prevented or minimized by removing much of the honey from the beehive then feeding the bees on sugar water in the late fall. Sugar water made from refined sugar has lower ash content than flower nectar, reducing the risk of dysentery, and may have essentially the same nutritional content, although this remains a point of controversy among some beekeepers.
In 1996, a similar type of organism to Nosema apis was discovered on the Asian honey bee Apis cerana and subsequently named Nosema ceranae. This parasite apparently also infects the Western honey bee. 
It has been reported that exposure to corn pollen containing genes for Bacillus thuringiensis (Bt) production may weaken the bees' defense against Nosema. In this study, it is stated that in relation to feeding a group of bees with Bt corn pollen and a control group with non-Bt corn pollen, that: "in the first year the bee colonies happened to be infested with parasites (microsporidia). This infestation led to a reduction in the number of bees and subsequently to reduced broods in the Bt-fed colonies as well as in the colonies fed on Bt-toxin-free pollen. The trial was therefore discontinued at an early stage.This effect was significantly more marked in the Bt-fed colonies. (The significant differences indicate an interaction of toxin and pathogen on the epithelial cells of the honeybee intestine. The underlying mechanism which causes this effect is unknown.)"
Small hive beetle
Aethina tumida is a small, dark-colored beetle that lives in beehives.
Originally from Africa, the first discovery of small hive beetles in the western hemisphere occurred in the US. The first identified specimen was found in St. Lucie, FL in 1998. The earliest specimens confirmed since then were collected from Charleston, SC in 1996. By December 1999, small hive beetle was reported in Iowa, Maine, Massachusetts, Minnesota, New Jersey, Ohio, Pennsylvania, and Wisconsin, and was found in California by 2006.
The life cycle of this beetle includes pupation in the ground outside of the hive. Controls to prevent ants from climbing into the hive are believed to also be effective against the hive beetle. Several beekeepers are experimenting with the use of diatomaceous earth around the hive as a way to disrupt the beetle's lifecycle. The diatoms abrade the insect's surface, causing them to dehydrate and die.
Several pesticides are currently used against the small hive beetle. The chemical is commonly applied inside the corrugations of a piece of cardboard. Standard corrugations are large enough that a small hive beetle will enter the cardboard through the end but small enough that honey bees can not enter (and thus are kept away from the pesticide).
Main article: Waxworm
Galleria mellonella (greater wax moths) will not attack the bees directly, but feed on the wax used by the bees to build their honeycomb. Their full development to adults requires access to used brood comb or brood cell cleanings — these contain protein essential for the larvae's development, in the form of brood coocoons.
The destruction of the comb will spill or contaminate stored honey and may kill bee larvae.
When honey supers are stored for the winter in a mild climate, or in heated storage, the wax moth larvae can destroy portions of the comb, even though they will not fully develop. Damaged comb may be scraped out and will be replaced by the bees. Wax moth larvae and eggs are killed by freezing, so storage in unheated sheds or barns in higher latitudes is the only control necessary.
Because wax moths cannot survive a cold winter, they are usually not a problem for beekeepers in the northern U.S. or Canada, unless they survive winter in heated storage, or are brought from the south by purchase or migration of beekeepers. They thrive and spread most rapidly with temperatures above 30°C (90°F), so some areas with only occasional days that hot, rarely have a problem with wax moths, unless the colony is already weak due to stress from other factors.
Control and Treatment
A strong hive generally needs no treatment to control wax moths; the bees themselves will kill and clean out the moth larvae and webs. Wax moth larvae may fully develop in cell cleanings when such cleanings accumulate thickly where they are not accessible to the bees.
Wax moth development in comb is generally not a problem with top bar hives as unused combs are usually left in the hive during the winter. Since this type of hive is not used in severe wintering conditions, the bees will be able to patrol and inspect the unused comb.
Wax moths can be controlled chemically with paradichlorobenzene (moth crystals or urinal disks). If chemical methods are used, the combs must be well-aired-out for several days before use. The use of naphthalene (mothballs) is discouraged because it accumulates in the wax, which can kill bees or contaminate honey stores. Control of wax moths by other means includes the freezing of the comb for at least twenty-four hours.
American foulbrood (AFB)
American Foul Brood (AFB), caused by the spore- forming Paenibacillus larvae ssp. larvae (formerly classified as Bacillus larvae), is the most widespread and destructive of the bee brood diseases. Paenibacillus larvae is a rod-shaped bacterium, which is visible only under a high power microscope. Larvae up to 3 days old become infected by ingesting spores that are present in their food. Young larvae less than 24 hours old are most susceptible to infection. Spores germinate in the gut of the larva and the vegetative form of the bacteria begins to grow, taking its nourishment from the larva. Spores will not germinate in larvae over 3 days old. Infected larvae normally die after their cell is sealed. The vegetative form of the bacterium will die but not before it produces many millions of spores. Each dead larva may contain as many as 100 million spores. This disease only affects the bee larvae but is highly infectious and deadly to bee brood. Infected larvae darken and die. 
Until 1906 the two foulbrood diseases were not differentiated and the condition was generally referred to as foulbrood. Phillips (1906) used the terms European and American to distinguish the diseases. However the designations did not refer to the geographical distributions but to the areas where they were first investigated scientifically (Shimanuki, 1990). White (1907) demonstrated conclusively that a bacterium that he called Bacillus larvae was the cause of American Foulbrood (AFB) disease by fulfilling Koch's postulates. The geographical origin of AFB is unknown, but it is found almost world-wide (Matheson, 1993,1996)
Lab testing is necessary for definitive diagnosis, but a good field test is to touch a dead larva with a toothpick or twig. It will be sticky and "ropey" (drawn out). Foulbrood also has a characteristic odor, and experienced beekeepers with a good sense of smell can often detect the disease upon opening a hive. In the photo at right, some larvae are healthy while others are diseased. Capped cells with decomposing larvae are sunken, as can be seen at lower right. Some caps may be torn, as well. Compare with healthy brood. The most reliable disease diagnosis is done by sending in some possibly affected brood comb to a laboratory specialized in identifying honey bee diseases. 
When cleaning infected cells, bees distribute spores throughout the entire colony. Disease spreads rapidly throughout the hive as the bees, attempting to remove the spore-laden dead larvae, contaminate brood food. Nectar stored in contaminated cells will contain spores and soon the brood chamber becomes filled with contaminated honey. As this honey is moved up into the supers, the entire hive becomes contaminated with spores. When the colony becomes weak from AFB infection, robber bees may enter and take contaminated honey back to their hives thereby spreading the disease to other colonies and apiaries. Beekeepers also may spread disease by moving equipment (frames or supers) from contaminated hives to healthy ones.
American Foul Brood spores are extremely resistant to desiccation and can remain viable for more than 40 years in honey and beekeeping equipment. Therefore honey from an unknown source should never be used as bee feed, and used beekeeping equipment should be assumed contaminated unless known to be otherwise.
AFB spores are present in virtually every hive. Some brood in weakened colonies can become diseased. If the diseased larva dies within the hive, millions of spores are released. Antibiotics, in non-resistant strains of the pathogen, can prevent the vegetative state of the bacterium to form. Drug treatment to prevent the American foulbrood spores from successfully germinating and proliferating is possible using oxytetracycline hydrochloride (Terramycin). Another drug treatment is tylosin tartrate that was US Food and Drug Administration (FDA) approved in 2005.
Chemical treatment is sometimes used prophylactically, but this is a source of considerable controversy because certain strains of the bacterium seem to be rapidly developing resistance.  In addition, hives that are contaminated with millions of American foulbrood spores have to be prophylactically treated indefinitely. Once the treatment is suspended the American foulbrood spores germinate successfully again leading to a disease outbreak.
Because of the persistence of the spores (which can survive up to 40 years), many State Apiary Inspectors require an AFB diseased hive to be burned completely. A less radical method of containing the spread of disease is burning the frames and comb and thoroughly flame scorching the interior of the hive body, bottom board and covers. Dipping the hive parts in hot paraffin wax or a 3% sodium hypochlorite solution (bleach) also renders the AFB spores innocuous. 
European foulbrood (EFB)
Melissococcus pluton is a bacterium that infests the guts of bee larvae. European foulbrood is less deadly to a colony than is American foulbrood. Melissococcus pluton does not form spores, though it can overwinter on comb.
European foulbrood is often considered a "stress" disease - a disease that is dangerous only if the colony is already under stress for other reasons. An otherwise healthy colony can usually survive European foulbrood. An outbreak of the disease may be controlled chemically with oxytetracycline hydrochloride. Prophylatic treatments are not recommended as it leads to resistant bacteria.
Ascophaera apis is a fungal disease that infests the gut of the larva. The fungus will compete with the larva for food, ultimately causing it to starve. The fungus will then go on to consume the rest of the larva's body, causing it to appear white and 'chalky'.
Chalkbrood is often considered another "stress" disease because the fungal spores are always present but are manageable by an otherwise healthy colony. Chalkbrood is most commonly visible during wet springs. Hives with Chalkbrood can generally be recovered by increasing the ventilation through the hive and/or by requeening the hive.
Stonebrood is a fungal disease caused by Aspergillus fumigatus, Aspergillus flavus and Aspergillus niger. It causes mummification of the brood of a honey bee colony. The fungi are common soil inhabitants and are also pathogenic to other insects, birds and mammals. The disease is difficult to identify in the early stages of infection. The spores of the different species have different colours and can also cause respiratory damage to humans and other animals. When a bee larva takes in spores they may hatch in the gut, growing rapidly to form a collarlike ring near the head. After death the larvae turn black and becomes difficult to crush, hence the name stonebrood. Eventually the fungus erupts from the integument of the larva and forms a false skin. In this stage the larvae are covered with powdery fungal spores. Worker bees clean out the infected brood and the hive may recover depending on factors such as the strength of the colony, the level of infection, and hygienic habits of the strain of bees (there is variation in the trait among different subspecies/races).
Acute bee paralysis virus (ABPV) or (APV)
ABPV (TaxID 92444) is considered to be a common infective agent of bees. It belongs to the family Dicistroviridae, as does the Israel acute paralysis virus, Kashmir bee virus, and the Black queen cell virus. It is frequently detected in apparently healthy colonies. Apparently, this virus plays a role in cases of sudden collapse of honeybee colonies infested with the parasitic mite Varroa destructor.
Israel acute paralysis virus (IAPV)
A related virus described in 2004 is known as the "Israel acute paralysis virus" (TaxID 294365); The virus is named after the place where it was first idenitified - its place of origin is unknown. IAPV has been suggested in September 2007 as a marker associated with Colony Collapse Disorder.
Kashmir bee virus (KBV)
This is another Dicistroviridae, related to the preceding viruses. Recently discovered, KBV (TaxID 68876) is currently only positively identifiable by a laboratory test. Little is known about it yet.
Black Queen Cell Virus (BQCV)
This is another Dicistroviridae, related to the preceding viruses. As its name implies, BQCV (TaxID 92395) causes the queen larva to turn black and die. It is thought to be associated with Nosema. 
Chronic Paralysis Virus [CPV]
Cloudy Wing Virus (CWV)
Deformed Wing Virus (DWV)
Sacbrood virus (SBV)
Morator aetatulas is the virus that causes sacbrood disease. Affected larvae change from pearly white to gray and finally black. Death occurs when the larvae are upright, just before pupation. Consequently, affected larvae are usually found in capped cells. Head development of diseased larvae is typically retarded. The head region is usually darker than the rest of the body and may lean toward the center of the cell. When affected larvae are carefully removed from their cells, they appear to be a sac filled with water. Typically the scales are brittle but easy to remove. Sacbrood-diseased larvae have no characteristic odor. 
Dysentery is a condition resulting from a combination of long periods of inability to make cleansing flights (generally due to cold weather) and food stores which contain a high proportion of indigestible matter. As a bee's gut becomes engorged with feces that cannot be voided in flight as preferred by the bees, the bee voids within the hive. When enough bees do this the hive population rapidly collapses and death of the colony results. Dark honeys and honeydews have greater quantities of indigestible matter.
Occasional warm days in winter are critical for honey bee survival; dysentery problems increase in likelihood if there are periods of more than two or three weeks with temperatures below 50 degrees Fahrenheit. When cleansing flights are few, bees will often be forced out at times when the temperature is barely adequate for their wing muscles to function, and large quantities of bees may be seen dead in the snow around the hives.
Colonies that are found dead in spring from dysentery will have feces smeared over the frames and other hive parts.
In very cold areas of North America and Europe, where honeybees are kept in ventilated buildings during the coldest part of winter, no cleansing flights are possible, and all honey is removed from the hives and replaced with high fructose corn syrup which has nearly no indigestible matter.
Chilled brood is not actually a disease but can be a result of mistreatment of the bees by the beekeeper. It also can be caused by a pesticide hit that primarily kills off the adult population, or by a sudden drop in temperature during rapid spring buildup. The brood must be kept warm at all times; nurse bees will cluster over the brood to keep it at the right temperature. When a beekeeper opens the hive (to inspect, remove honey, check the queen, or just to look) and prevents the nurse bees from clustering on the frame for too long, the brood can become chilled, deforming or even killing some of the bees.
To minimize the risk of chilled brood, open the hive on warm days and at the hottest part of the day (this is also the time when the most field bees will be out foraging and the number of bees in the hive will be at its lowest). Learn to inspect your hive as quickly as possible and put frames with brood back where the bees can cluster on it immediately.
Honey bees are susceptible to many of the chemicals used for agricultural spraying of other insects and pests. Many pesticides are known to be toxic to bees. Because the bees forage up to several miles from the hive, they may fly into areas actively being sprayed by farmers or they may collect pollen from 'contaminated' flowers.
Carbamate pesticides, such as Sevin(R)-Carbaryl (C12H11NO2)can be especially pernicious since toxicity can take as long as two days to become effective; allowing infected pollen to be returned and distributed throughout the colony. Organophosphates and other insecticides are also known to kill honey bee clusters in treated areas.
Pesticide losses may be relatively easy to identify (large and sudden numbers of dead bees in front of the hive) or quite difficult, especially if the loss results from a gradual accumulation of pesticide brought in by the foraging bees. Quick acting pesticides may deprive the hive of its foragers, dropping them in the field before they can return home.
Insecticides that are toxic to bees have label directions that protect the bees from poisoning as they forage. To comply with the label, applicators must know where and when bees forage in the application area, and the length of residual activity of the pesticide.
Some pesticide authorities recommend, and some jurisdictions require, that notice of spraying be sent to all known beekeepers in the area so that they can seal the entrances to their hives and keep the bees inside until the pesticide has had a chance to disperse. This, however, does not solve all problems associated with spraying and the label instructions should be followed regardless of doing this. Sealing honey bees from flight on hot days can kill bees. Beekeeper notification does not offer any protection to bees, if the beekeeper cannot access them, or to wild native or feral honey bees. Thus beekeeper notification as the sole protection procedure does not really protect all the pollinators of the area, and is, in effect, a circumventing of the label requirements. Pesticide losses are a major factor in pollinator decline.
Colony Collapse Disorder
Colony Collapse Disorder (or CCD) is a little-understood phenomenon in which worker bees from a beehive or Western honey bee colony abruptly disappear. CCD was originally found in Western honey bee colonies in North America in late 2006.
European beekeepers observed a similar phenomenon in Belgium, France, the Netherlands, Greece, Italy, Portugal, and Spain, and initial reports have also come in from Switzerland and Germany, albeit to a lesser degree. Possible cases of CCD have also been reported in Taiwan since April 2007.
The cause (or causes) of the syndrome is not yet well understood. Theories include environmental change-related stresses, malnutrition, pathogens (i.e., disease including Israel acute paralysis virus), mites, pesticides such as neonicotinoids or imidacloprid, radiation from cellular phones or other man-made devices, and genetically modified (GM) crops with pest control characteristics such as transgenic maize. Some claim that the disappearances have not been reported from organic beekeepers, suggesting to some that beekeeping practices can be a primary factor.
References and external links
Pages on bee diseases
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Diseases_of_the_honey_bee". A list of authors is available in Wikipedia.|