Stings and Reactions
There’s a lot been written about sting reactions, and whether we should take antihistamines before beekeeping, carry adrenalin-injecting epipens or undertake desensitization treatment. This all looks frightening and bothersome, so I’ve been thinking about what causes reactions, and what the risks are.
Bee venom has lots of different things in it, but there are three main components of interest. The first is mellitin, a little protein that can burst open cells, especially red blood cells, and trigger our deep pain receptors. Then there’s phospholipase A2, which breaks down cell walls and interferes with communication. And a third is histamine, which makes blood vessels leaky and triggers inflammation. These things are mainly why the normal reaction to a sting is pain, swelling, redness and inflammation.
But not all reactions are normal. Sometimes the reactions are different, and away from the sting site – rashes, trouble breathing, high pulse rate, for example. And sometimes we won’t react at all. So, what’s going on, and can we be ‘immune’ or ‘allergic’?
Any puncture of the skin will provoke an response from our immune system which produces inflammation. Inflammation isn’t a bad thing – it draws blood to the area and, with it, defensive cells and chemicals that attack any strange substance they find. Some of these defensive cells will try to produce antibodies against the substance.
Antibodies are large molecules that ‘recognise’ other molecules. One type of antibodies, called IgG, work to smother anything strange found in our blood or tissues. For example, when we catch a cold, we start to produce IgG antibodies that match up with molecules on the coat of the virus that causes it. These antibodies then stick to the side of the virus, smothering it and stopping it from being nasty, until the whole bundle can be broken down in our liver. The same thing happens with any strange substance, so we also produce antibodies to some of the components of of bee venom.
However, it takes about five days to produce enough IgG to smother a cold, and that’s a long time to wait. Moreover, IgG gets broken down quite quickly, so if we relied on IgG alone, it wouldn’t stop us catching the same cold, ever five days, over and over again.
Happily, there’s another sort of antibody, called IgE, that works a bit differently. IgE, instead of floating around in the blood on its own, sticks to a type of cell called a ‘mast cell’. Mast cells are little packets of histamine that move around the body, waiting for a strange molecule to lock on to the IgE they’re carrying. If that happens, then the histamine gets released, the blood vessels nearby become leaky and white blood cells flood out to eat up the nasties. This is a much quicker way to deal with problems and because mast cells don’t get broken down very quickly, once we’ve made some IgE against a strange molecule, we’re virtually immune.
IgE, however, doesn’t seem to be very well tuned. We can produce more of it than necessary, which can make us hypersensitive or allergic, which results in a much greater reaction. And, given that both mellitin and phospholipase are very similar to compounds we make naturally, it might recognise the wrong targets. At present, we don’t really understand this part of the immune system, so there’s no way to tell who will become hypersensitive, when or for how long. And there are degrees of hypersensitivity, from slightly greater local responses to severe systemic reactions, including anaphylaxis. The picture is even less clear as many of the symptoms of anaphylaxis can be caused by other things, including ‘normal’ shock.
But it does mean we’re all at risk of becoming hypersensitive. The risk isn’t very great, but it’s probably higher than you’d think.
A recent research paper  describes a study of 4141 cases of anaphylaxis events across Austria, Germany and Switzerland reported (a population of about 98m) over a seven-year period. About 10% (412) of cases were caused by bee stings, none of which were fatal (wasps caused over three times as many cases and three fatalities). The chance of anaphylactic shock in response to a bee sting is, on average, about two in three million.
Rare events do happen, though, so is there anything that might indicate we’re at particular risk? According to a study on German beekeepers:
“[Risk factors] were, in descending order of importance, symptoms of upper respiratory allergy while working on the hive, presence of other allergies, time spent as a beekeeper, and more severe nonallergic reactions to bee stings in springtime. These factors identified beekeepers at risk of allergic reactions to bee venom in 85.2% of cases. Our results also showed an association between allergy and emotional instability.” 
Another, slightly more tactful, study on British beekeepers  found additional risk factors included being female, having a relative with an allergy to bee venom, and taking antihistamines before attending the hives.
So, it looks like we’re all potentially at risk and, though the risks are small, they might not stay small. If we have other allergies, or notice symptoms (runny noses, wheezing) when working the hives, it might be advisable to ask a GP about desensitisation treatment. Desensitisation treatment does seem to work, by lowering the IgE levels, and though it’s not free of risk itself , it seems to work, as another paper happily reports:
“It appears that [venom immunotheraphy] not only decreases the risk of anaphylaxis and death, but also improves quality of life by reduction of anxiety and depression, especially in female subjects.” 
As for carrying epipens, that’s up to you. It may come in useful one day, perhaps, especially if you have allergies already, or work on your own away from other people. You’re perhaps 200 times more likely to be run over than to ever have to use it, but never mind that. If we worried about everything we’d never get anything done.
 Dtsch Arztebl Int. May 2014; 111(21): 367–375. “Triggers and Treatment of Anaphylaxis – An Analysis of 4000 Cases From Germany, Austria and Switzerland” Worm M, Eckermann O, Dölle S et al.
 Annals of Allergy, Asthma & Immunology Feb 2011; 106 (2): 159–163 “Risk factors for systemic reactions to bee venom in British beekeepers”, Richter AG, Nightingale P, Huissoon AP, Krishna MT
 J Investig Allergol Clin Immunol. 2008;18(2):100-5. “Allergy to bee venom in beekeepers in Germany.” Münstedt K1, Hellner M, Winter D, von Georgi R.
 Ann Allergy Asthma Immunol. 2014 Jun;112(6):559-60. “Human albumin causes anaphylaxis during bee venom immunotherapy.” Nakonechna A, Abuzakouk M.
 Allergy Asthma Proc. 2014 May-Jun;35(3):260-4. “The relationship between insect sting allergy treatment and patient anxiety and depression.” Findeis S, Craig T.