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At least 19 recordsLinked to original sources
PubMed1977

Serological investigations in hymenoptera sting allergy: IgE and haemagglutinating antibodies against bee venom in patients with bee sting allergy, bee keepers and non-allergic blood donors.

Specific IgE-antibodies and haemagglutinins to bee venom were determined in fifty-five bee sting allergic patients, fifty-seven bee keepers and fifty-two blood donors without evident allergy to hymenoptera stings. IgE-antibodies were detected by RAST in 70% of allergic patients, 40% of bee keepers and 12% of blood donors. Most bee keepers with detectable IgE-antibodies to bee venom recorded severe local or even general reactions to bee stings. Most blood donors with detectable specific IgE had been stung by hymenoptera in the past. High titres of haemagglutinating antibodies against phospholipase A were found in most bee keepers, occasionally in bee sting allergic patients but only rarely in blood donors. The determination of specific IgE-antibodies to insect venoms by RAST seems to be a valuable method for the diagnosis of hymenoptera sting allergy.

Agglutinins↗
PubMed1980

Immunological studies on bee-keepers: specific IgG and subclass typing IgG against bee venom and bee venom components.

Specific IgE antibodies against bee venom and its components were studied in 23 bee-keepers. The highest IgG serum levels were observed for whole bee venom followed by phospholipase A. The serum levels of specific IgG antibodies against melittin and MCD-peptide were lower, the lowest serum levels being observed for apamin. After a 5 month absence from bee-keeping a fall in the serum levels of IgG antibodies was observed in all the bee-keepers studied. The investigation of the IgG subclass antibodies 1-4 against bee venom and phospholipase A demonstrated the highest serum levels for IgG 4 and IgG 2, the lowest levels were observed for IgG 1. The lowest IgG serum levels were associated with the least effective protection to bee stings. These findings support the concept that specific IgG antibodies prevent the development of allergic symptoms after bee sting.

Adult↗
PubMed2001

Genetic evidence for coinfection of honey bees by acute bee paralysis and Kashmir bee viruses.

Nucleotide sequence analyses were used to identify acute bee paralysis virus (ABPV) and Kashmir bee virus (KBV) isolated from a single honey bee colony. Most of the bees in this colony carried KBV. Some individual bees also carried ABPV, a coexistence not yet seen between these two viruses. Implications of coinfection on viral efficacy are discussed, along with a restriction enzyme assay that can be used to discriminate between these two widespread viruses.

Animals↗
PubMed1983

Honey bee venom specific immunoglobulin G4 in honey bee sting allergic patients and bee keepers.

Honey bee venom (HBV) IgG4 antibody was studied in bee keepers and honey bee sting allergic patients on immunotherapy using mouse monoclonal anti-human IgG4 antibody in a modified microtiter solid phase radioimmunoassay (MSPIRA). The mean HBV IgG4 in bee keepers was 31 units/ml. In patients the mean HBV IgG4 pre- and post-immunotherapy were 2.9 and 11.6 units/ml, respectively, representing a mean rise of 7.3-fold as compared to a rise of 1.6-fold for total HBV IgG. The mean HBV IgG level in bee keepers was 14 micrograms/ml which was not significantly different from the mean level of 17 micrograms/ml in allergic patients at diagnosis. The percentage interference of HBV IgE detection in vitro correlated with HBV IgG but not with HBV IgG4. On the other hand, there was an inverse relationship between serum HBV IgE and HBV IgG4 levels while none was found for HBV IgE and IgG.

Antibodies, Anti-Idiotypic↗
PubMed1983

Antibodies to purified bee venom proteins and peptides. I. Development of a highly specific RAST for bee venom antigens and its application to bee sting allergy.

IgE antibodies to purified proteins and peptides from honeybee venom have been measured by the RAST. Trace amounts (less than 0.1%) of the major venom protein phospholipase A2 (PLA2) grossly distorted the measurement of IgE antibody to the other venom proteins, acid phosphatase (Acid P) and hyaluronidase (HYAL), and overemphasized their importance. Reduction of antigen coupled to the cellulose paper discs, which were used in the assay, diluted out the contaminating PLA2 without apparent loss in sensitivity. The reduction of disc-bound antigen increased the competition between IgE and IgG antibodies but did not affect measurement of IgE antibodies in sera taken from 35 untreated patients who had a history of general allergic reactions to bee stings. In 54% of sera from bee venom--allergic patients, the greatest IgE antibody response was to PLA2. In all, IgE antibodies to PLA2 were present in 91% of these sera. IgE antibodies to Acid P, HYAL, or melittin were present in 60%, 51%, and 31% of sera, respectively, and accounted for the highest level of binding in 17%, 17%, and 6% of these. Only 6% of sera were positive for whole venom but negative for the isolated antigens. A low level of IgE antibody was found to peptide 401 in 6% of sera. No IgE antibodies were found to apamin. While confirming the central role played by PLA2 in bee sting allergy, these results show that other venom components are also important in some patients.

Acid Phosphatase↗
PubMed1986

Sub-class of IgG anti-bee venom antibody produced during bee venom immunotherapy and its relationship to long-term protection from bee stings and following termination of venom immunotherapy.

The IgG sub-class antibody response to bee venom in the four sub-classes was investigated in ten patients during and after venom immunotherapy. All patients tolerated a bee sting challenge 1, 2 and 3 years after the start of treatment as well as 1 and 2 years after treatment was stopped. Anti-phospholipase A2 (PLA2) antibodies were of IgG1 and IgG4 sub-class and rose early in treatment, IgG1 anti-PLA2 fell to pre-treatment levels after 3 years in contrast to IgG4 anti-PLA2 levels, which remained high during maintenance therapy and declined relatively little in the 2 years after the termination of treatment. This data shows that IgG4 antibodies are maintained in the absence of monthly maintenance injections and suggests that they may provide long lasting clinical protection from insect stings.

Adolescent↗
PubMed1983

[Measurement of bee venom specific IgG antibody in bee venom hypersensitivity and the relation between the specific IgE antibody and total IgE].

Bee venom specific IgG antibodies for honeybee and common wasp were measured in normal control group, slightly bee injury group, heavy bee injury group and honeybee keeper's group. Relation among bee venom specific IgG antibody, bee venom specific IgE antibody and total IgE was analyzed. Normal control level of bee venom specific IgG antibody was measured under 60 U/ml. Bee venom specific IgG antibody in slightly bee injury group was higher than that in heavy bee injury group. Bee venom specific IgE antibody in slightly bee injury group was lower than that in heavy bee injury group. Bee venom specific IgE antibody in bee keeper's group was very high but bee venom specific IgG antibody was also high. From this results it seems that bee venom hypersensitivity can be prevented by high titer of bee venom specific IgG antibody even if bee venom specific IgE antibody is high titer.

Adult↗
PubMed1976

Comparison of the allergenic properties of bee venom and whole bee body extract.

The allergenic properties of bee venom and whole bee body extract were compared by in vivo and in vitro tests. The majority of patients with known bee sting sensitivity had positive intracutaneous skin test reactions with bee venom and had bee venom specific IgE in their sera. Of seventeen patients with ppsitive bee venom skin tests, nine had positive tests with whole bee body extract. Of thirty sera containing elevated levels of bee venom specific IgE obtained from untreated patients, fourteen sera contained whole body specific IgE but in much lower titres. In RAST inhibition experiments using both bee venom and whole bee body extract as coupling antigens, bee venom was a more potent inhibiting antigen than whole body extract. From these experiments we conclude that bee venom is a more potent allergen than whole bee body extract.

Animals↗
PubMed1988

Mechanism of biological effects observed in honey bees (Apis mellifera, L.) hived under extra-high-voltage transmission lines: implications derived from bee exposure to simulated intense electric fields and shocks.

This work explores mechanisms for disturbance of honey bee colonies under a 765 kV, 60-Hz transmission line [electric (E) field = 7 kV/m] observed in previous studies. Proposed mechanisms fell into two categories: direct bee perception of enhanced in-hive E fields and perception of shock from induced currents. The adverse biological effects could be reproduced in simulations where only the worker bees were exposed to shock or to E field in elongated hive entranceways (= tunnels). We now report the results of full-scale experiments using the tunnel exposure scheme, which assesses the contribution of shock and intense E field to colony disturbance. Exposure of worker bees (1,400 h) to 60-Hz E fields including 100 kV/m under moisture-free conditions within a nonconductive tunnel causes no deleterious affect on colony behavior. Exposure of bees in conductive (e.g., wet) tunnels produces bee disturbance, increased mortality, abnormal propolization, and possible impairment of colony growth. We propose that this substrate dependence of bee disturbance is the result of perception of shock from coupled body currents and enhanced current densities postulated to exist in the legs and thorax of bees on conductors. Similarly, disturbance occurs when bees are exposed to step-potential-induced currents. At 275-350 nA single bees are disturbed; at 600 nA bees begin abnormal propolization behavior; and stinging occurs at 900 nA. We conclude that biological effects seen in bee colonies under a transmission line are primarily the result of electric shock from induced hive currents. This evaluation is based on the limited effects of E-field exposure in tunnels, the observed disturbance thresholds caused by shocks in tunnels, and the ability of hives exposed under a transmission line to source currents 100-1,000 times the shock thresholds.

Animals↗
PubMed1991

[A new Soviet allergen made from bee venom for the specific diagnosis of allergic reactions to bee stings].

Overall 46 patients with allergic reactions to bee stings were examined. As a result of making skin prick, scarification and intracutaneous tests with an allergen from bee venom, allergy to bee stings was revealed in all the 46 patients, whereas only 37 patients responded to an allergen from the bee body. Specific IgE-antibodies using RAST were detected in 29 out of 31 patients. All the 29 patients had positive skin tests with an allergen from bee venom and only 22 with an allergen from the bee body. Specific histamine release was detected in all 13 patients examined by means of the indicated test. 100% coincidence was recorded with the results of intracutaneous tests with an allergen from bee venom. Only 11 out of the 13 patients had positive intracutaneous tests with an allergen from the bee body. Thus, the new Soviet allergen obtained from bee venom is effective in the diagnosis of allergy in response to bee stings.

Adolescent↗
PubMed1995

Ultra rush bee venom immunotherapy does not reduce cutaneous weal responses to bee venom and codeine phosphate.

BACKGROUND: The rapid administration of bee venom in cumulative doses exceeding the quantity contained in one bee sting is well tolerated by most of the patients during 3.5 h of ultra-rush bee venom immunotherapy (VIT). The mechanism of this tolerance is unknown. OBJECTIVE: The aim of the study was to verify the hypothesis that either slow mediator depletion of mast cells or blockade of their surface receptor mechanisms by increasing doses of allergen might be the major mechanisms of tolerance induced by ultra-rush VIT. METHODS: Nine bee venom allergic patients with a history of severe systemic reactions after a bee sting, positive skin tests and bee venom specific serum IgE antibodies were treated as follows: on the first day a cumulative dose of 111 micrograms was administered over 3.5 h under intensive care conditions. Further injections were given on day 7, day 21 and thereafter at 4 week intervals. Intradermal tests with codeine phosphate (non-specific mast cell degranulation) and bee venom were performed before the initiation of VIT and 30 min after the last injection on the same day as well as before the subsequent bee venom injections. RESULTS: No significant changes of skin reactivity to both codeine phosphate and bee venom were observed on day 1 (before initiation of VIT and after the last injection on the same day). CONCLUSIONS: Ultra-rush VIT does not induce mediator depletion or surface receptor blockade in skin mast cells.

Bee Venoms↗
PubMed1984

Bee keepers' IgG and IgE antibody responses to bee venom studied by means of crossed radioimmunoelectrophoresis.

The immune response to honey bee venom in thirty-seven bee keepers' sera was studied by several methods. Specific IgE antibody levels studied by RAST were generally low, whereas specific IgG antibody levels studied by a Sepharose protein A technique were high. Crossed radioimmunoelectrophoresis was applied for a detailed analysis of the antibody specificities towards the different components of venom in seventeen of the bee keepers' sera. Significant amounts of IgG antibodies were found towards most bee-venom components. The highest IgG response was directed towards phospholipase A. Hyaluronidase, acid phosphatase and two uncharacterized antigens also showed distinct IgG binding. The IgG binding to melittin was low. The IgE binding to the bee venom components was low and primarily directed to the phospholipase. IgE binding to hyaluronidase and acid phosphatase occurred, but was also in very small amounts. One bee-keeper serum caused heavy radiostaining to melittin but the others did not show IgE binding to this component. Thus a low IgE but a high IgG response was demonstrated in bee keepers. The major immunogen was phospholipase A, which is known to be the major allergen in bee venom. Generally, the strongest IgG responses were found to the components capable of inducing the strongest IgE responses.

Adult↗
PubMed1983

Antibodies to purified bee venom proteins and peptides. II. A detailed study of changes in IgE and IgG antibodies to individual bee venom antigens.

Antibodies to individual bee venom antigens were studied in detail in nine bee sting-allergic patients who received venom immunotherapy without side effects, in two patients who failed to reach maintenance, and in two whose sensitivity returned. The study was confined to patients who had IgE antibodies to at least one of four purified bee venom antigens at the start of treatment. IgE and IgG antibodies to phospholipase A2 (PLA2), hyaluronidase (HYAL), and acid phosphatase (ACID P) and IgE antibodies to melittin (MEL) were measured, and changes in the antibody levels were followed during bee venom immunotherapy. Two contrasting patterns of antibody response were seen in the nine successfully treated patients. In five patients there was a rise in serum IgG antibodies to the same antigens as the IgE antibodies. In two patients' serum IgE antibody to HYAL or ACID P fell without a marked IgG antibody response to these antigens, although high levels of IgG antibody to PLA2 were present in both. Although the first pattern is consistent with a "blocking" role for IgG antibody, clearly the second is not. Not all patients can be conveniently divided into these two categories, and two patients did not show any significant change in either IgG or IgE antibody but were nevertheless able to tolerate the maintenance dose of 100 micrograms of venom. Two patients who failed to reach the maintenance dose of 100 micrograms because of their allergic reactions to the injections of venom were distinguished by (1) very high serum IgE antibody and (2) a low ratio of IgG/IgE antibody. Passive immunization with IgG antibody from a hyperimmune beekeeper was, however, protective in these patients, although it did not raise their overall serum IgG antibody level very much. We are unable to explain either the failure of conventional therapy or the beneficial effect of passive immunization in these two patients. Two bee sting--allergic beekeepers lost their sensitivity to stings, but later, when their sera contained IgE antibody to another bee venom antigen, they reacted to stings and inhalation of beehive dander. These data suggest that either falling IgE antibody or IgG- "blocking" antibody could be responsible for providing clinical protection to bee venom--allergic subjects. Renewed clinical sensitivity was observed when the IgE response was modulated, with patients making IgE antibody first to one antigen and then to another.

Acid Phosphatase↗
PubMed1997

Sensitivity to bee and wasp venoms: association with specific IgE responses to the bee and wasp venom and HLA DRB1 and DPB1.

BACKGROUND: Stings from bees and wasps can cause systemic reactions which can be fatal in some individuals. In these venom-sensitive patients, specific IgE to the venom is produced and is considered to participate in the adverse reactions. This immune response requires antigen presentation by human leucocyte antigens (HLA) class II molecules, which includes DR and DP, which are present on antigen presenting cells. OBJECTIVE: To test for associations between HLA class II DRB1 and DPB1 alleles and life-threatening sensitivity to both bee and wasp venoms. To establish further whether any associations are independent of the atopy phenotype. METHODS: A total of 33 bee- and 44 wasp-venom-sensitive patients was studied. DRB1 genotypes were determined by single stranded oligonucleotide (SSO) probing of PCR products, and DPB1 genotypes by amplified fragment length polymorphism (AFLP) analysis. Total and specific IgE were measured using the Pharmacia Immunocap, FEIA. Patients with specific IgE to the venom antigens only were termed monosensitive and those with additional specific IgE to HDM and/or GP were termed polysensitive. RESULTS: Allele frequencies were compared to an unrelated control population. The 33 bee-sensitive patients had a greater prevalence of DRB1*07 alleles than the control subjects, 26% vs 14%, with an odds ratio (OR) of 2.1 (95% CI, 1.2-3.7, P = 0.015, corrected for multiple comparisons, Pc = ns). This association was confined to the 15 monosensitive bee patients, who had a 43% DRB1*07 allele frequency when compared with 11% in the 18 polysensitive bee patients, OR 6.1 (95% CI, 1.73-22, P = 0.004, Pc = 0.05), and when compared with a control group of non-venom subjects, 43% vs 16%, OR 3.9 (95% CI, 1.72-9.0, P = 0.002, Pc = 0.02). The 44 wasp-sensitive patients had an increase in the DRB1*11 allele when compared with the control subjects, 13% vs 6%, with an OR 2.2 (95% CI, 1.0-4.6, P = 0.04, Pc = NS), and a decreased prevalence of DRB1*04 alleles, 10% vs 19%, with an OR 0.33 (95% CI, 0.24-0.99, P = 0.04, Pc = NS), but these were not significant when multiple comparisons were taken into account. The DPB1 alleles were not significantly different between the venom sensitive patients and the controls. CONCLUSION: Patients monosensitive to bee venom had a significantly greater prevalence of DRB1*07 alleles than the non-venom, control population suggesting that IgE responses in these patients may, in part be controlled by immune response HLA class II genes. These results are also suggestive of wasp-sensitive patients having a higher prevalence of DRB1*11 and a lower prevalence of DRB1*04 than the control population.

Adolescent↗
PubMed1979

Enzyme-linked immunosorbent assay of allergen-specific IgG antibodies in bee sting allergic patients hyposensitized with pure bee venom.

An ELISA is presented for detection of IgG antibodies to bee venom. By this method, sera of 11 bee sting allergic patients, who were treated with rapid hyposensitization with pure bee venom, were tested. The highest antibody titers were observed after 30 days of treatment, a maximum rise of 7.4 +/- 1.5 log 2-titer steps. Pure bee venom is shown to be more potent immunologically than whole body bee extract. Prediction of the clinical success, measured by tolerance to a bee sting challenge, is not yet possible using venom specific IgG determinations.

Adolescent↗
PubMed1978

Hymenoptera sting hypersensitivy: IgE, IgG and haemagglutinating antibodies to bee venom constituents in relation to exposure and clinical reaction to bee stings.

High levels of IgE antibodies (Ab) to bee venom constituents were mainly found in patients with bee sting hypersensitivity, whereas the sera of bee keepers usually contained high levels of IgG Ab and haemagglutinins, representing blocking antibody activity. In bee keepers there was a positive correlation between the degree of severity of an adverse reaction to bee stings and IgE Ab, a negative one between the severity of reaction and IgG Ab and haemagglutinins, a positive one between the number of stings per season and IgG Ab and haemagglutinins, and negative one between the number of stings and IgE Ab. This suggests a mutual dependence of the production of IgE Ab and blocking Ab in a regularly exposed population. No such correlation was found in bee sting-allergic patients, indicating that other factors influence the severity of reaction in this only sporadically exposed group. The values of IgG Ab and haemagglutinins correlated well with each other, with IgG Ab giving a better correlation with severity of reaction and number of stings than the haemagglutinins.

Anaphylaxis↗
PubMed1994

Multiplication of Clostridium botulinum in dead honey-bees and bee pupae, a likely source of heavy contamination of honey.

Multiplication of Clostridium botulinum in honey-bees was examined to explain the heavy contamination of honey which may occur with this pathogen. When dead bees were inoculated with C. botulinum spores at levels of 10(2)-10(3) and incubated aerobically for 10 days, the organisms increased to 10(4)-10(5). When botulinum spores were inoculated together with Bacillus alvei, the growth of most strains was significantly enhanced (10(5)-10(7)). Similar results were obtained in bee pupae, but not in bee larvae. The heavy contamination of honey with botulinum spores that we have sometimes encountered may have been caused by contamination from dead bees in which C. botulinum had proliferated.

Animals↗