Cause: Ascosphaera apis, a fungus.
Effect: Chalkbrood disease affects only the brood. The diseased larvae are usually found on the outer edges of the brood nest. Workers, drones, and queens are all susceptible to the disease.
Symptoms: The affected larvae are usually found on the outer fringes of the brood area. Brood cells can either be sealed or unsealed. Diseased larvae are stretched out in their cells in an upright condition. Typically, larvae dead from chalkbrood disease are chalk white, hence the name chalkbrood. Sometimes the diseased larvae can be mottled with brown or black spots, especially on the ventral sides. The color variation is from the brown to black color of the fruiting bodies (spore cysts).
Transmission: The spores of Ascosphaera apis are ingested with the brood food provided by the nurse bees. The germination of the spores and proliferation of the fungus covers the larva with a white mycelium. Spores of Ascosphaera apis remain viable for years. Consequently, the infection source could be present in the cells used to rear brood. Chalkbrood appears to be most prevalent in the spring when the brood area is increasing. Chalkbrood normally does not destroy a colony. However, it can prevent normal population build-up when the disease is serious. No treatment is presently available for the control of chalkbrood. The disease usually disappears or is reduced as the air temperature increases in the summer.
US Dept of Agriculture
Cause: Nosema apis and Nosema ceranae, small microsporidian parasites that live in the digestive tract of honey bees.
Effect: Nosema disease is widespread and causes serious damage to adult honey bees thus reducing the life span of individual bees and weakening or killing colonies. Infected nurse bees do not fully develop and infected queens die off prematurely. The disease may be associated with Colony Collapse Disorder (CCD).
Symptoms: No symptoms are specifically indicative of Nosema disease. Inability of bees to fly, excreta on combs or lighting boards, and dead or dying bees on the ground in front of the hive may be manifestations of Nosema infection, but they may also be caused by other abnormal conditions. N. apis may cause the ventriculus of heavily infected bees to become white, soft and swollen while N. ceranae infections do not. A microscopic examination is the only reliable test for the presence of this disease.
Transmission: The spores of Nosema enter the body of the adult bee through the mouth and germinate in the gut. After germination, the active phase of the organism enters the midgut epithelial cells where it multiplies rapidly and new spores are formed. The cells rupture and shed the new spores into the midgut lumen where they pass down to different tissues or are voided in the excreta of the bee. The cycle begins over again when the spores contaminate the food of other bees. Spores may remain viable for many months in dried spots of excreta on brood combs. Near the end of winter, combs are often soiled with excreta from infected workers. Other bees become infected when they pick up the spores in the excreta as they clean the soiled combs during the spring expansion of the brood nest. Thus, the disease within the colony increases rapidly for a time, and a colony may dwindle in the spring because of the premature death of the overwintered bees. Usually, the colony survives and the proportion of infected bees begins to decline. This decline occurs because the excreta are normally voided away from the hive when regular flights become possible in spring. Nosema apis has been recognized in the U.S. for many years. Recently, it was found that a second species, N. ceranae was also present and that over 90% of Nosema infections in the U.S. are this second species. High infections of N. ceranae are frequently found during the summer months in production colonies.
US Dept. of Agriculture
American Foulbrood (AFB)
Cause: Paenibacillus (=Bacillus) larvae, a spore-forming bacterium.
Effect: American foulbrood is one of the most widespread and the most destructive of the honey bee brood diseases. At first, the population of an infected colony is not noticeably decreased and only a few dead larvae or pupae may be present. The disease may not develop to the critical stage where it seriously weakens the colony until the following year, or it may advance rapidly and seriously weaken or kill the colony the first season.
Symptoms: First the capping of the diseased cell becomes moist and darkens in color. Then as the larva shrinks, the capping is drawn down into the mouth of the cell so the normal convex capping becomes concave. Worker bees may puncture this sunken capping and eventually remove it altogether. Death of an infected larva takes place after the cell has been sealed and the cocoon has been spun. At death, the diseased larva changes from a normal pearly white color to a creamy brown, then gradually darkens. These larval remains can be drawn out into a brown thread or rope. As the larva dries, it becomes dark brown. The final state is a very dark brown scale that lies uniformly on the lower side of the cell and extends from just below the mouth of the cell down to the base. These scales adhere very tightly to the cell and can be removed only with great difficulty. (If death occurs at the pupal stage, the tongue of the pupa may protrude from the scale.) The overall appearance of a comb infected with American foulbrood disease is patchy because of the mixture of diseased and healthy brood cells and also because the remains vary from the ropy moist larvae in cells with dark sunken or perforated cappings to the dry scales lying in open cells whose cappings have been chewed away completely by the bees.
Transmission: The spores are fed to young larvae by the nurse bees. They then germinate in the gut of the larva and multiply rapidly, causing the larva to die soon after it has been sealed in its cell. By the time of death of the larva, the new spores have formed. When the house bees clean out the cell containing the dead larva, these spores are distributed throughout the hive and more and more larvae become infected. The honey in an infected colony can become contaminated with spores and can be a source of infection for any bee that gains access to it. For example, as a colony becomes weak, it cannot defend itself from attacks by robber bees from strong nearby colonies; these robbers take back the contaminated honey to their own colony, continuing the cycle of infection. The beekeeper also may inadvertently spread the disease by exposing contaminated honey to other bees or by the interchange of infected equipment. Moreover, drifting bees or swarms issuing from an infected colony may spread the disease.
Wax moths can be a terrible problem to bee hives if allowed to get out of hand and will destroy brood comb in a very short time if unchecked. There are some simple steps to prevent the damage, but first, it might be simpler to discuss the life cycle to understand where the problem comes from.
A normal healthy hive will keep wax moth under control by ejecting the larvae, but weakened hives with small populations can be overcome by wax moth infestations destroying the brood comb, ultimately destroying the hive.
There are two varieties of moth which take delight in dining on wax the ‘Greater’ and also the ‘Lesser’ Wax Moth the greater wax moth is a mottled grey in colour approx 1 ½ inches in length while the lesser is smaller and slimmer approx a ½ inch in length and white/silver. As all moths, they prefer night time to mate and lay eggs.
Wax moth larvae (pictured above)
Most wax moths are seen in early summer in our area, and we see them under the overhang of hive roofs, out of the daylight, when the hive is disturbed they take off quickly and disappear into the trees.
Preferring to work in the dark the moths enter the hive through top entrances left unscreened and unguarded by the bees, perhaps a sudden cold snap making the bees cluster, and lay eggs in cracks unavailable to the bees. These hatch in due course and the grey larvae begin feeding on wax and hive debris, tunnelling just under the cell caps and feeding on the discarded cocoons left by the bees, leaving behind an extremely sticky white web, similar to spiders web but almost impossible to pull apart. So perhaps they are misnamed and should be called Cocoon moths?
With a little care, the wax moth can be outwitted and the damage they do can be prevented.
First, the practice of top entrances should be examined, provided they have screening then there will be no problem. Leaving a big hole in the inner cover, then a badly fitting roof is just asking for trouble. Or even worse those holes drilled in the top of boxes allowing the bees a second entrance are a real problem. Apart from pollen in the honey, a cold evening and the bees pull down and form a cluster leaving that entrance unguarded, easy pickings for the wax moth, as they will fly in cooler conditions than bees.
They do say that prevention is better than cure. I have already given one way, using screening to prevent wax moth entering the hive top. The second point could be to use a trap to draw the moths away from the hive area. There are, to my knowledge, no commercial wax moth traps, but we use a country cure which works extremely well and I would recommend to all.
Small Hive Beetle
Adults and larvae of the small hive beetle are found in active bee hives and stored bee equipment where they feed on honey and pollen. Adults are broad, flattened beetles about 5.7 mm (¼ inch) long, 3.2 mm wide and dark brown to nearly black in color. Adults are red just after pupation and soon thereafter become blackish. They move rapidly across comb and are difficult to pick up. The larvae are elongate, whitish grubs with rows of small spines along the back. Larvae look superficially like wax moth larvae, but the legs of beetle larvae are larger, more pronounced, and restricted to near the head. Beetle larvae do not spin webs or cocoons in the bee hive but rather pupate in the soil outside the hive. Pupae are whitish brown. The small hive beetle is native to southern Africa where it requires 38-81 days to develop from egg to adult, and five generations per year are possible. The first record of this beetle in the western hemisphere was determined from a commercial apiary in Florida in May 1998. Beetle specimens were found from bee hives near Atlanta, Georgia in June 1998 and confirmed as A. tumida on July 13, 1998.
In Africa the small hive beetle behaves as a scavenger of weakened colonies much like the greater wax moth, and it is relegated to secondary pest status. But that has not been the case for beekeepers in the Southeast in whose apiaries the beetles have caused considerable damage and colony loss. Beetle larvae tunnel through combs, killing bee brood and ruining combs. Larvae can heavily damage delicate, newly drawn-out comb; however, old sturdy brood comb seems to withstand heavy larval infestation without disintegrating. Bees in Florida have been found to abandon combs and entire colonies once they are infested. Beetles defecate in honey and cause it to ferment, producing a frothy mess in supers and honey houses. Honey thus contaminated is no longer salable, and moreover it is unpalatable to bees and cannot even be used as bee feed. Florida observers report that the fermented honey smells like rotting oranges. In heavily-infested operations in Florida larvae by the thousands have been observed crawling out of colony entrances or across honey house floors in an effort to reach soil to dig in and complete their development.
Caron, D.M. 1997. Other insects. In Honey bee pests, predators and diseases 3d ed. (R.A. Morse & K. Flottum eds.). A.I. Root Co., Medina, Ohio
Ellis, J.D., Jr., K.S. Delaplane, & W.M. Hood. A scientific note on small hive beetle (Aethina tumida Murray) weight, gross biometry and sex proportion at three locations in the southeastern United States. Unpublished Data.
Elzen, P.J., J.R. Baxter, D. Westervelt, C. Randall, K.S. Delaplane, F.A. Eischen, L. Cuffs, & W.T. Wilson. 1999. Field control and biology studies of a new pest species, Aethina tumida Murray (Coleoptera: Nitidulidae), attacking European honey bees in the Western Hemisphere. Apidologie 30: 361-366
Lundie, A.E. 1940. The small hive beetle Aethina tumida. South Africa Department of Agriculture & Forestry Entomological Series 3, Science Bulletin 220
Sanford, M.T. 1998. Aethina tumida: a new beehive pest in the western hemisphere. Apis 16(7), University of Florida
Picture courtesy of KeepingBackyardBees.com
The parasitic bee mite, Varroa destructor (=jacobsoni) is one of the most serious pests of the honey bee, Apis mellifera, and its introduction into new countries is causing much concern to beekeepers throughout the world. The first Varroa species, Varroa jacobsoni, was described on Apis indica (= cerana) from Java in 1904. Recent studies by D.L. Anderson and J.W.H. Trueman** show that Varroa jacobsoni is a species complex containing 18 different genetic variants that belong to 2, possibly 5 different species of Varroa. Anderson and Trueman indicated that they were unable to find morphological differences to distinguish the genetic types.
The first report of Varroa attacking Apis mellifera (a new host) was in 1962 on a sample sent to the USDA in Beltsville from Hong Kong, and in 1963 in the Philippines. The mite has since become established on every continent except Australia and will continue to spread due to commercial transport of bees and queens; the migratory activities of beekeepers; swarms that may fly long distances, or be carried by ships or aircraft; and drifting bees.
The adult female Varroa is oval and flat, about 1.1 mm long and 1.5 mm wide, pale to reddish-brown in color, and can be seen easily with the unaided eye. Male mites are considerably smaller and are pale to lightly tanned. Adult bees serve as intermediate hosts when little or no brood is available and as a means of transport. The females attach to the adult bee between the abdominal segments or between body regions (head-thorax-abdomen), making them difficult to detect. These are also places from which they can easily feed on the bees' hemolymph. The adult bee suffers not only the loss of blood but may be subjected to microbial invasion, leading to a reduced life expectancy.
The most severe parasitism occurs on the older larvae and pupae, drone brood being preferred to worker brood. The degree of damage depends on the number of mites parasitizing each bee larva. One or two mites will cause a decrease in vitality of the emerging bee. Higher numbers of Varroa per cell result in malformations like shortened abdomens, misshapen wings, deformed legs or even in the death of the pupa.
The adult female Varroa enter the brood cells shortly before capping and must feed on larval hemolymph before they can lay eggs. Each mite lays 2-6 eggs at approximately 30-hour intervals. The first egg usually develops into a male and the later ones into females. The development proceeds from egg to six-legged larvae, to eight-legged protonymphs, to deutonymphs, to sexually mature adult mites in 6 to 10 days. They mate in the capped cells with the males dying soon afterward. All immature mites will die after the emerging bee opens the cell, while the young adult female mites and the mature (gravid) females move on to passing bees. The mite enters another brood cell in 3 to more than 150 days depending on the season and availability of brood.
**Anderson, D.L. and J.W.H. Trueman, 2000, Varroa jacobsoni (Acari:Varroidae) is more than one species. Exp. Appl. Acarol. 24(3):165-189.
US Dept of Agriculture