Bee/Wasp (venoms)

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Jan Hed, Clin Immunologist, MD, PhD
Karolinska Institutet, IMPI, Div of Clin Immunology
Huddinge University Hospital, Sweden
 
The statements below are based on conclusions from selected publications. Their intention is to highlight recent research and information that could be beneficial in allergy in vitro testing. They can include seemingly contradictory statements due to differences in selecting patient populations as well as in the study design.
  • The most important allergens in hymenoptera venom are different enzymes such as phospholipase A, hyaluronidase and phosphatase. A high degree of cross-reactivity has been shown between different hymenoptera species (1, 2. See ref. 3, 4 for review).
     
  • Venoms from bumblebee and honeybee are highly cross-reactive, which is consistent with the degree of structural similarity found in the enzymes. However, bumblebee contained several minor allergens that were not found in honeybee (5, 6).
     
  • Although a high cross-reactivity occurs between European and American vespid species of the genus Polister, species-specific differences exist (7).
     
  • 30% of patients with clinical history of hymenoptera allergy are double-positive to honey-bee and wasp allergens (8).
     
  • Positive skin-prick tests to any given Hymenoptera venom extract were found in 3.66% of children in an Italian study . There was an association between the presence of positive SPT and atopy-linked IgE response (9).
     
  • Epidemiological studies of Hymenoptera venom allergy in adults show a prevalence of positive venom skin tests and RASTs of 15-25%, but most such individuals have had no systemic reactions to stings (10).
     
  • Specific IgE to Hymenoptera venoms was shown in 27.1% of the sera in a German population, but only 7.1% of these reported systemic reactions to venoms (11).
     
  • In a Swedish population, 9.3% had specific bee or wasp IgE and 1.5% reported systemic reactions. Sensitization correlated positively with atopy but could not be shown for systemic reactions (12).
     
  • Sensitization to hymenoptera venoms is associated with atopy-related humoral IgE hyperresponsiveness (11, 13).
     
  • In a study of a population with anaphylactic reactions, 28 cases (6 bee, 22 wasp) of 172 were due to Hymenoptera venoms compared to 42 due to peanuts, 23 due to tree nuts and 25 due to other foods (14). In another study, 25 of 142 cases with anaphylaxis were due to hymenoptera venom (15).
     
  • In a retrospective study of nine patients with severe anaphylaxis, a possible cause was identified in eight. Three were due to Hymenoptera venom, two to drugs and three to foods (16).
     
  • The relapse rate after discontinuation of venom immunotherapy was higher among patients with high levels of specific IgE before and after immunotherapy. Specific IgE decreased during therapy and no relapses of sting reactions were observed among patients without detectable specific IgE (17).
     
  • In vitro testing of specific IgE to bee and wasp venom in patients with hymenoptera allergy was more sensitive than skin testing in detecting sensitization (8, 18).
     
  • In another study, in vitro testing of specific IgE was the best single predictor of individual diagnostic parameters in predicting clinical reactivity (19).
     
  • High levels of specific IgE to hymenoptera venom were detected in patients experiencing the most severe clinical reactions (20). 
     
  • A significant difference was shown between systemic reactors to Hymenoptera venoms and non-reactors with respect to specific IgE antibodies in beekeepers (21).
     
  • The pre-season presence of serum bee venom-specific IgE at concentrations exceeding 1.0 kU/L increased the risk of systemic reactions 12-fold. The risk was 10-fold if nasal or respiratory symptoms had occurred while working at hives. When less than 8 years had been spent bee-keeping, the risk of systemic sting reaction was 9-fold. Any previous systemic reaction increased the risk 8-fold (22).
     
  • In 61 subjects sensitive to Hymenoptera venoms, those with severe hypotensive response to a sting challenge had higher levels of tryptase at baseline than mild reactors, non-reactors, and controls (23).
     
  • Increased and high levels of tryptase were shown in patients with fatal anaphylaxis (24) and anaphylaxis after sting challenge (25).
     
  • Systemic bee sting reactions were present in 26% and local reactions in 38% of beekeepers. Similar reactions following wasp sting were present in 2% and 13% respectively. A history of atopic symptoms was present in 48% of the systemic reactors compared with 28% of the remaining population (26).
     
  • Sensitization to Hymenoptera venom is higher in beekeepers with less than 5 years working experience and who are sensitized to another allergen (27).
     
  • A short interval between two consecutive stings seems to be a risk factor for the onset of Hymenoptera venom allergy (28).
     
  • Honeybee specific IgG and IgG4 increase in beekeepers either according to their bee-keeping experience or in subjects with local reactions after bee stings (29).
     
  • Patients monosensitive to bee venom had a significantly greater prevalence of specific HLA class II alleles (DRB1*07) compared with polysensitized patients (30).
     
  • Proteins derived from secretions of pharyngeal and salivary glands of honeybee heads as well as pollen proteins (most frequently from Compositae plants), contained in honey cause allergic reactions to honey (31-33).
     
  • In honey allergics, primary sensitization may be due to hymenoptera venom components in 9 of 22 patients (33).

References:

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