The following article appeared in Eric Mussen's July/August newsletter
and is reproduced in full with his permission.
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Honey Bee Sting Allergy

Renewed interest in honey bee sting allergy has surfaced as beekeepers
approach their local agencies with requests to remove prohibitions, or
become more lenient, with beekeeping, especially in urban and suburban
settings. Eventually, the discussions focus on the topics of liability.
Who will be responsible if problems develop and who will intercede in
mitigating the problem?

The most difficult topic is human allergies to honey bee stings. What is
the definition of allergy, for this purpose? What percentage of the
population is allergic to honey bee venom? Can anything be done to
alleviate such allergies?

Dr. David B.K. Golden (MD) has been studying this topic for many years.
He com- bined his results with the results of 51 other studies to write
a summary paper, “Advances in Diagnosis and Management of Insect Sting
Allergy,” published in the Annals of Allergy, Asthma, and Immunology 111
(2013): 84-89. 7 Dr. Golden’s first topic is determining how many people
actually are allergic. As a generality, 5 percent of our population is
aller- gic to honey bee venom. However, how they respond to stings
varies. We think of allergic response as anaphylaxis, leading to
inability to breathe and possible death. The statistics demonstrate 1
percent of children and 3 percent of adults have endured such reactions.
Another 5 percent or more have endured a “large local reaction,” with
abnormally large and often persistent swelling around the sting site.
Skin tests of adults have demonstrated that 20 per- cent will test
positive to honey bee venom, rising to 30-40 percent in the weeks
following a sting. But, if no systemic symptoms develop, most people
lose the positive skin test in a few years. Those who still show a
positive test are about 15 percent likely to have a systemic reaction
with the next sting. However, while having the immunoglobulin E
(antibody IgE) is necessary to have an anaphylactic response to bee
venom, its presence alone is not sufficient to predict an anaphylactic
reaction.

Trying to test for honey bee allergy is fraught with difficulties. In
experiments with challenge stings, 40 percent of folks who al- ready had
suffered severe reactions had a sub- sequent one. Systemic reactions
occurred with 23 percent of those who had moderate systemic reactions
previously. Only 17 percent of those with cutaneous reactions developed
more sev- ere reactions. Although we have been told that wasp venom is
cross-reacting among species, tests suggest that there are two different
types of wasp venom. A negative test to one type does not mean that the
other will test the same.

Skin tests do have a degree of value in predicting reactions to bee
stings. The most sensitive patients are more likely to have stron-ger
reactions. Those barely responding to prick tests are least likely to
have major sting problems. However, there is enough variation in true
responses to stings to suggest that the skin reactions are not truly
reliable indicators of things to come. Up to 30 percent of patients who
already had systemic reactions test negative in prick tests. But, half
of those patients do test positive for venom-specific IgE in their
blood. The remaining 15 percent give no physiologic clues that they
still remain very susceptible, and about six percent of them do have
subsequent anaphylactic responses.

Two newer tests are being studied. Basophil activation tests can be run
on the patient’s blood cells. If the patient is allergic, either the
basophils release a mediator of an allergic response or activation
markers for a number of “clinically significant outcomes.” The second
approach is even more complicated: using recombinant venom allergens to
determine if the reaction is due to bee and/or wasp venom. It is thought
that the cross reaction to both venoms is due to “cross- reacting
carbohydrate determinants,” but that has yet to be proven. The wasp
venom components are predictable. There is considerable variation in the
bee venom component.

The final conclusion is that if someone had a previous severe reaction,
it is likely (70 percent in adults; 30 percent in children) to happen,
again, even 10-20 years later. Interestingly, these patients share
another measure- able trait. Their baseline serum tryptase levels make
them more likely to: 1) have a severe reaction following a sting or from
use of bee venom to try to desensitize them, or 2) not get the expected
results (failure) from venom- immunotherapy (VIT). An elevated tryptase
baseline occurs in about 10 percent of patients who respond severely to
stings. It occurs in 25 percent of those whose blood pressure drops when
stung. Normally, an elevated baseline suggests underlying mast cell
problems, such as mastocytosis.

The paper finishes with an in depth discussion of the use of venom
immune therapy (VIT) to desensitize patients. It discusses screening
patients to determine when the treatment is appropriate. It describes
details of doses and shot regimens: standard (15-20 weeks); modified
rush (6-8 week); rush (2-3 days); and ultrarush (3-6 hours). The
information covers the use of various medications with VIT, how long to
maintain the shot routines, and when to stop getting the shots – can be
up to a lifetime, but more often 5 years or less.

This is likely more information than you would ever need to know for an
interview, but it is nice to have the facts. The paper can be found at:
http://dx.doi.org/10.1016/j.anai.2013.05.026 .
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That link leads to a paywall. I found the following link by searching
the title on Google:
http://www.annallergy.org/article/S1081-1206(13)00360-8/abstract

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