Hymenoptera venom allergy

ie bee/wasp. A common cause of anaphylaxis, and interestingly, not related to atopy.  Reactions can be immunological (IgE or non IgE), or non-immunological (toxic). 

Severe reactions related to allergy but also number of stings, insect type, cardiovascular/respiratory disease and also mastocytosis.

Whether it is bee or wasp or other is sort of important, from the point of view of cross reactivity and risk. Several major allergens eg hyaluronidase, phospholipase A2. Bumblebee PLA2 is 53% identical to honeybee PLA2, so not necessarily cross reactive. Similarly, Apid (bee) hyaluronidase is 50% identical to vespid.  Vespids subdivides into Vespa=hornets (found in UK, biggest, 35mm, reddish brown head). Wasps and hornets not as fuzzy as bees.  Vespula=wasps, Dolichovespula (“short headed wasps”) are harder to distinguish (shorter distance between eyes and upper jaws!). These 3 vespid types cross react strongly, so likely to be allergic to all.

Polistes=”paper wasps”, distinct from other vespids, Southern Europe only (so far) – limited cross reactivity to wasps/hornets, thankfully. 

Ants are also hymenoptera!


  • “Normal” local
  • “large” local = >10cm swelling, plus >24hrs (blisters sometimes present). Mech prob toxic, but sometimes evidence of IgE mediated mechanism,
  • systemic toxic (usually from multiple stings – haemolysis, nephropathy, coagulopathy – rare)
  • systemic +/- anaphylaxis [usually igE, rarely short term IgG, or complement activation by IgG-venom complexes]
  • (plus “unusual”).

Was a barb left behind? Bees not wasps. Multiple stings at the same location? Wasp not bee.

Systemic reactions should be assessed by allergy specialist, including skin prick tests, total IgE and baseline tryptase tests.

  • rapid onset generalized urticaria and/or angio-oedema,
  • bronchospasm
  • laryngeal oedema
  • hypotension (collapse, loss of consciousness).

Hypotension is the dominant feature and may occur alone.

Risk factors for outcome of anaphylactic reaction:

  • age,
  • CVS disease/drugs,
  • insect type,
  • time interval between stings (short interval increases risk of systemic reaction to second sting),
  • number of stings,
  • severity of previous reaction,
  • elevated mast cell tryptase, else known mastocytosis.

Bee allergic at higher risk of systemic reaction than vespid allergic. Hornets risk seems to be esp high.

Frequent stings can induce tolerance (but probably needs more than 200 per year!). 

Venom IgE >1 had 12x risk of anaphylaxis (beekeepers, regardless of previous history). Pos skin test (adults without history of anaphylaxis) had 17% risk, cf 0% of neg skin test [so negative test v reassuring, but risk still low even if you are pos, which would be unusual in most kids]

Majority of fatalities have significant cardioresp co-morbidity. 40-85% of fatal reactions had no documented history of previous anaphylactic reactions.

Mild systemic reaction previously gives 18% risk of subsequent systemic reaction (kids). Compare after large local – 5-15%, so sl higher but not much. Children tend to have mild systemic reactions, cf most adults get resp or CVS symptoms.

Several case reports of severe reactions in mastocytosis; even without mastocytosis, high basal tryptase seems to increase risk of anaphylaxis.


Even when SPT pos, 25-84% of subjects do not react to subsequent sting!
Similarly, up to 22% of those with neg tests will have systemic reaction in future. [Allergy 2005: 60: 1339–1349]

Test all with systemic reaction, not recommended otherwise. If not witnessed? Only really useful to distinguish bees vs wasps (says the Anaphylaxis Campaign)!? Unless you’re a bee keeper, wasps are the one you are most likely to be stung by.

Skin prick testing more sensitive/specific. Probably sensible to leave a month or two between the event and testing else false negative due to “refractory period”. This period can sometimes be longer so consider repeating if good history.  If negative, try IgE; then intradermal ( with 0.001-1mcg/mL solution  -seems to have higher sensitivity).

Stepwise skin testing with 0.01-100mcg/ml solutions incrementally recommended. 

Some people will be persistently negative on testing, probably due to being allergic to an unusual protein. Consider systemic mastocytosis as a differential. 

Family history of venom anaphylaxis is a common cause of concern.  Unfortunately, there is no point testing other family members – you are unlikely to test positive if you have never been stung.

Specific IgE levels (if you do test positive) only vaguely correlate with anaphylaxis risk (not statistically significant) [Allergy 62(8): 884-889, August 2007]. However, having low total IgE (<50kU/l) predicts anaphylaxis (not v sensitive, only explains 25%), whereas high total IgE (>250) protects (very specific)!

Serum IgE appears within a few days of sting, begins to decline at a variable time – wait long enough, and no IgE may be detectable. Double positivity to bee/vespid could be genuine cross sensitivity but might be cross reactivity of IgE to epitopes of unknown clinical significance.

Baseline serum tryptase over 11 has high positive predictive value for anaphylaxis but is not very sensitive. Good for picking up mastocytosis though!

So you may be able to find the occasional person who seems to be at particular risk (high tryptase, low total IgE), or relatively protected (high total IgE) but you will still miss most cases of anaphylaxis.

Immunoblotting, basophil activation tests etc sometimes used if others tests negative. But sens/spec generally not known.  

High basal tryptase may increase risk of reactions with VIT but still indicated.

Give allergy plan and prescribe Adrenaline if severe systemic reaction, consider if moderate. 

If successful VIT, still get adrenaline if further symptoms, continued exposure, high tryptase.

[BSACI guidelines – Clinical & Experimental Allergy. Volume 41, Issue 9, September 2011, Pages: 1201–1220 doi/10.1111/j.1365-2222.2011.03788.x]


See Venom immunotherapy.

Honey allergy

Reported, in most cases appears to be due to pollens contained in the honey, or at least allergens highly cross reacting with pollens. But in a minority, does appear to be due to bee derived components. Type of honey will determine what pollens are contained in it; commercial honey often contains v low amounts due to production techniques.


Risk of sting related to zone, climate, temperature, outdoor activities etc. Some repellents marketed as effective against wasp/bee (IR3535 (Ethyl butylacetylaminopropionate) eg Jungle Formula “outdoor & camping”) but most creams/sprays (DEET, Citronella oils etc) are for biting insects (midges, mosquitoes etc), not stinging. Bees/wasps generally not interested on landing on your skin anyway!  Sting because they are threatened!  

Avoid opening windows, avoid rubbish bins, tidy away food/drink (esp sugary) .  Calmly walk away!

Keep skin covered. Keep surfaces, mouth/face/hands clean of food residues after eating!!!

Raid-type killer sprays for environment.

Patient Support

Anaphylaxis campaign have insect venom leaflet.