Varroa mites:
Varroa destructor
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 visibly deformed wings.
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.
Varroa were first discovered in Southeast Asia in about 1904, but is now present on all continents except Australia. Varroa were discovered in the United States in 1987, in New Zealand in 2000, and in the United Kingdom in 1992 (Devon).
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. Varroa in combination with Deformed Wing Virus and bacteria have been theoretically implicated in Colony Collapse Disorder.
Treatment:
A variety of treatments are currently marketed or practiced to attempt to control Varroa mites. The treatments are generally segregated into chemical controls and “mechanical” controls.
Common chemical controls include “hard” chemicals such as fluvalinate (marketed as Apistan) and coumaphos (marketed as CheckMite) and “soft” chemicals such as thymol (marketed as ApiLife-VAR and Apiguard), sucrose octanoate esters (marketed as Sucrocide), oxalic acid and formic acid (sold in gel packs “Mite-Away” but also used in other formulations).
According to the U.S. Environmental Protection Agency, when used in beehives as directed, these treatments kill a large proportion of the mites while not substantially disrupting bee behavior or life span. Use of chemical controls is generally regulated and varies from country to country. With few exceptions, they are not intended for use during production of marketable honey.
Common “mechanical” controls generally rely on disruption of some aspect of the mites’ lifecycle. These controls are generally intended not to eliminate all mites but merely to maintain the infestation at a level which the colony can tolerate.
Examples of mechanical controls include drone brood sacrifice (varroa mites are preferentially attracted to the drone brood), powdered sugar dusting (which encourages cleaning behaviour and dislodges some mites), screened bottom boards (so that any dislodged mites fall through the bottom and away from the colony), brood interruption and, perhaps, downsizing of the brood cell size. A device called the Varroa Mite Control Entrance (VMCE) is under development as of 2008.
The VMCE works in conjunction with a screened bottom board, by dislodging varroa mites from bees as they enter and exit a hive.
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. Diagnosis for tracheal mites generally involves the dissection and microscopic examination of a sample of bees from the hive.
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.
Treatment:
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:
Nosema apis is a microsporidian that invades the intestinal tracts of adult bees and causes nosema disease, also known as nosemosis. 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. Refined sugar, however, contains fewer nutrients than natural honey which causes some controversy among beekeepers [Nutrient Database(USDA SR-21)]
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 Btfed 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.)”
This study should be interpreted with caution given that there was no repetition of the experiment nor any attempt to find confounding factors. In addition, it is noteworthy that BT toxin and transgenic BT pollen showed no acute toxicity to any of the life stages of the bees examined, even when the BT toxin was fed at concentrations 100 times that found in transgenic BT pollen from maize.
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