Bee Venom

Bee venom is a secretion from the venom glands of the worker or queen of a species of honey bee (Apis); it is not produced by stingless bees (Meliponinae). The main components of commercial freeze-dried venom from A. mellifera worker bees include 15 to 17% enzymes, including phospholipase and hyaluronidase; 48 to 58% small proteins, including especially mellitin; 3% physiologically active amines, including histamine; 0.8 to 1.0% amino acids, and numerous minor components. Queen venom differs somewhat from worker venom in its composition and its pattern of change with the age of the bee. A few studies have been made on the venom of other Apis species; for instance, toxicity has been reported to be similar in venoms from A. mellifera and A. dorsata, less in A. florea venom but twice as high in A. cerana venom.

Bee venom is by far the most pharmacologically active product from honey bees. The general mechanism of its action on humans who are not hypersensitive is as follows. Hyaluronidase breaks down hyaluronic acid polymers that serve as intercellular cement, and the venom spreads through the tissue. (Protective antibodies that develop in the serum of most beekeepers can effectively neutralize hyaluronidase, preventing the spread of the venom.) A protease inhibitor prevents enzymatic destruction of the hyaluronidase. Simultaneously, the mast cell degranulating peptide penetrates the membrane of the mast cells, creating pores. This releases histamine, which (in combination with some small molecules of the venom) contributes to the swelling and flare, and the local itching and burning sensation. As venom penetrates blood vessels and enters the circulatory system, phospholipase A and mellitin (as a micelle, a colloidal-sized aggregate of molecules) act synergistically to rupture blood cells.

When only a few stings are received, the action just described is mostly localized, and actual toxic effects are insignificant. After massive stinging (or injection of venom directly into the circulatory system), the action may become widespread and toxic effects severe, particularly when significant amounts of venom enter the circulatory system. Apamine acts as a poison to the central nervous system, and both mellitin and phospholipase A are highly toxic. Large concentrations of histamine are produced and contribute to overall toxicity. The role of other components is unknown.

Only a very small number of people are allergic (hypersensitive) to insect venom, between 0.35 and 0.40% of the total population in one U.S. survey. In a person allergic to bee venom, the hyaluronidase may participate immediately in an antigen—antibody reaction, triggering an allergic response; both mellitin and phospholipase A can also produce allergic reactions. There may be antigen—antibody reactions to any or all of the components mentioned. Severe reactions can result in death from anaphylactic shock.

Antihistamines can give some protection to a moderately hypersensitive person if taken before exposure to stings. Systemic reactions following a sting should be treated immediately with adrenaline; extremely prompt medical treatment is essential for acute anaphylaxis.

Some allergy clinics provide carefully regulated courses of venom injection, which can decrease sensitivity to the venom; various types of immunotherapy (desensitization) have been used, involving the application of a series of graded doses of pure venom, and these can be effective in 95% of cases. If a beekeeper or another member of the household develops serious hypersensitivity to bee stings, an allergy specialist may be able to recommend a course of desensitization that will allow the beekeeper to continue.

Germany was probably the first country to produce bee venom commercially. Between 1930 and 1937, girls stationed in front of hives would pick up one worker bee at a time and press it so that it stung into a fabric tissue that absorbed the venom; the venom was extracted from the fabric with a solvent (distilled water), which later was removed by freeze-drying, leaving the venom as a crystalline powder.

A more recent method is to use a bare wire stretched to and fro across a thin membrane mounted on a horizontal frame placed directly in front of a hive entrance. When a low voltage is applied to the ends of the wire, a few "guard" bees are shocked; they sting into the membrane and also release alarm pheromone that quickly alerts other bees to sting into the membrane as well. The bees can withdraw their stings and are unharmed, and the drops of venom released are removed from the underside of the membrane; in hot weather they dry and can be scraped off.

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