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At least 19 recordsLinked to original sources

Cancer mortality among beekeepers.

Carcinogenic effects of bee venom were evaluated in a mortality study of 580 occupationally exposed beekeepers. The subjects were identified through obituary notices published between 1949 and 1978 in three journals of the U.S. beekeeping industry. Death certificates of beekeepers were examined for causes of mortality, and proportionate mortality ratios were compared with those for the general U.S. population. Beekeepers had a slightly lower than expected fraction of deaths from cancer. The deficit of lung cancers in male beekeepers was significant (p less than 0.05) and may indicate that fewer beekeepers were cigarette smokers. The frequencies of other cancers did not differ significantly from expectation. Non-Hodgkin lymphoma developed in four persons, and was expected in two. Mortality from diseases other than cancer showed no unusual patterns. At least two persons died from accidents directly related to the care of beehives. Analysis of a subgroup of 377 males with major roles in the beekeeping industry showed no substantial differences in distribution of causes of death. This study of beekeepers reveals neither adverse nor beneficial effects of intense exposure to bee stings.

Bee Venoms

Lack of responsiveness of beekeeper mononuclear cells to in vitro stimulation with pure bee venom.

Lymphocyte proliferation activity after in vitro bee venom (BV) stimulation was examined in a group of patients allergic to bee stings and in a group of beekeepers. Although the allergic patients responded strongly to increasing doses of BV, the beekeepers demonstrated no proliferative activity and an inability to produce interleukin-2 after BV stimulation. Removal of adherent cells or various populations of suppressor cells, including T gamma cells and OKT8 positive cells, did not influence the cellular unresponsiveness of cells of beekeepers after BV stimulation. Furthermore, cells of beekeepers, when they were trypsinized or when they were preincubated for 72 hours, did not proliferate after BV challenge. It is concluded that the lack of proliferation of lymphocytes of beekeepers and the inability to produce interleukin-2 is not due to a suppressor mechanism or to the presence of anti-idiotype antibodies coating the surface of lymphocytes of beekeepers. The mechanism behind the failure of cells of beekeepers to proliferate remains unclear.

Adult

[Epidemiological and clinical study on bee venom allergy among beekeepers].

A randomized population of 222 beekeepers from Lombardy (203 males, 19 females, of mean age 42.5 years) was studied to determine the frequency of allergic reactions to bee sting. The type of reactions, the clinical evolution at the subsequent stings and the risk factors concerning the development of allergy (presence of venom specific IgE, number of stings in a year, atopy, age) were evaluated. It was found that 170 beekeepers never presented reactions to stings while 52 (23.4%) showed allergic reactions consisting in 31 large local reactions and 21 systemic reactions; of these, 3 (5.7%) were life-threatening. In the group of beekeepers with allergic reactions at the subsequent stings, 26 (50%) showed a spontaneous loss of reactivity, 16 (30.8%) presented persistent, but unchanged in severity, reactions and 10 (19.2%) had a worsening of symptoms. Specific honey bee venom IgE levels (measured by means of RAST) were significantly lower in immune beekeepers when compared with the group with allergic reactions (p less than 0.01) and in beekeepers with previous allergy when compared to the ones with persistent reactions (p less than 0.05). We also found significant differences about the number of stings received in a year by beekeepers with persistent allergic reactions (17.5 stings), beekeepers with previous allergy (89.8 stings) and immune subjects (126.9 stings). On the contrary, no significant differences were detected about the age and the presence of atopy. These results suggest that practice of bee-keeping induces a relatively high incidence of allergic reactions but with a trend to the spontaneous improvement of symptoms and a low incidence of severe reactions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent

Clinical and immunological studies of beekeepers.

Thirty-four beekeepers were interviewed and their blood assayed for the presence of antibodies reacting with bee venom, bee venom phospholipase A (PLA), and whole bee body extract. Following a bee sting, most beekeepers experienced only minimal local tissue reaction. Their serum contained high levels of total antibodies (primarily IgG) reacting to bee venom and phospholipase A. These antibody titres correlated with the frequency of bee stings. Bee venom and PLA specific IgE antibodies were present in serum of some beekeepers. Beekeepers who had experienced allergic reactions were characterized by low total antibody and high venom specific IgE antibody titres. Bee body IgE antibodies were found in varying degree and did not correlate with levels of venom IgE antibodies. There was no difference in the titres of bee body IgE in the sera of beekeepers with and without systemic reactions. The data suggest that allergic reactions are mediated by venom specific IgE and immunity is at least in part a function of other antibodies, probably primarily IgG.

Bee Venoms

Bee venom anti-idiotypic antibody is associated with protection in beekeepers and bee sting-sensitive patients receiving immunotherapy against allergic reactions.

Bee venom (BV) anti-idiotypic (anti-Id) antibodies (Abs) were studied in nonreactive beekeepers, patients receiving BV immunotherapy (IT), and in patients with bee-sting hypersensitivity. Detection of serum anti-BV was determined either by the Phadebas RAST test for IgE and IgG concentrations or by isoelectric focusing followed by capillary blotting onto nitrocellulose membranes. Clonotypic analyses of Ab were made with specific probes for BV or BV anti-Id; 13/14 nonreactive multiple-sting beekeepers (93%; p = 0.00006) and 3/3 patients receiving BV IT (100%; p = 0.0026) had detectable amounts of BV anti-Id in serum, whereas five BV-sensitive patients (0%) and four ragweed-sensitive control patients (0%) did not. Beekeeper's serum containing BV anti-Id was found to recognize and bind to IgE anti-BV idiotype from two different patient sources and inhibit their reactions in a Phadebas RAST test in a dose-dependent manner. Nonreactive beekeepers generally had BV-specific IgE levels less than 0.35 PRU/ml in serum with detectable BV anti-Id. BV-allergic patients before IT had elevated BV-specific serum IgE levels, even in the presence of BV-specific IgG greater than 136 U/ml with no BV anti-Id present. These findings provide strong support for a protective role of BV anti-Id against bee sting--allergic reactions.

Adolescent

Histamine release from peripheral blood leukocytes with purified bee venom allergens: effect of hyperimmune beekeeper plasma.

The response of 15 strongly bee-venom-allergic patients to highly purified venom allergens was compared using skin prick test titration, peripheral blood leukocyte (PBL) histamine release and radioallergosorbent test with three highly purified bee venom allergens: phospholipase (PLA2), hyaluronidase (HYAL) and acid phosphatase (ACID P). Sensitivity to the three allergens ranked in the same order for all three tests and in each case PLA2 was found to the most potent allergen. In the presence of hyperimmune beekeeper plasma, maximum histamine release was reduced significantly for all three allergens (p less than 0.001). Furthermore, hyperimmune beekeeper plasma increased the amount of allergen required for a comparable release of histamine (mean shift in dilution curve PLA2 917-fold; HYAL, 492-fold; ACID P, 61-fold). The release of histamine from whole blood was also compared with PBL + 10% normal human serum (NHS). For all three allergens maximum release was much lower from whole blood compared with washed cells + 10% NHS (p less than 0.001). These data confirm PLA2 as the major bee venom allergen by all three tests. Hyperimmune beekeeper plasma reduces maximum histamine release and increases its threshold. Histamine release in response to ACID P appears harder to block with hyperimmune beekeeper plasma than that provoked by PLA2 or HYAL (p less than 0.01). Whole blood releases less histamine and requires more allergen than washed cells, indicating that sensitivity of PBL in vivo is unlikely to be as great as washed PBL in vitro.

Adult

Allergy in beekeepers.

Beekeepers represent a high-risk group for allergic disorders. They are affected by beestings but only a very limited fraction of the population develops severe anaphylactic symptoms. On the other hand several beekeepers have slight anaphylactic symptoms when they start working. Immunologically they are like "spontaneously desensitized subjects". They often have bee-venom specific IgE and all of them have very high titers of bee-venom specific IgG. Beekeepers may present an atopic sensitization to bee-hive dust and develop asthma and rhinitis. Finally, they may present a contact dermatitis to a bee-product: the propolis. This type of allergy is not very frequent.

Anaphylaxis

Comparison of the atopic background between allergic and non-allergic beekeepers.

A study was carried out on beekeepers and their families. 34 subjects with a history of bee sting allergy and also a positive radioallergosorbent test (RAST) to honey bee venom were compared with 47 subjects with neither. 16 subjects in the bee allergy group (47%) had a history of atopic diseases as compared to 6 (13%) in the control group (p less than 0.01). 15 in the bee allergy group (44%) had at least one positive RAST to three common inhalant allergens as compared to 5 (11%) in the control group (p less than 0.01). These results suggest that, although bee sting allergy frequently affects non-atopic subjects, sensitization among beekeepers and their families occurs more readily in atopics. It is notable that a large proportion of patients injected with foreign proteins (the control group) either never develop venom-specific IgE antibodies or have suppressed their production.

Adult

Combined active and passive immunotherapy in honeybee-sting allergy.

Five honeybee sting-allergic patients in whom bee venom immunotherapy (VIT) had previously been stopped because of repeated allergic side effects (SE) were resubmitted to bee VIT after pretreatment with beekeeper gammaglobulin. The tolerated bee venom dose was increased five to 800 times after this passive immunotherapy, and the maintenance dose of 100 micrograms of honeybee venom (BV) was reached in all patients after 6 to 15 days of a rush hyposensitization. The IgG response to BV was not suppressed by the beekeeper-gammaglobulin infusion. After 2 to 9 weeks of continued bee VIT, SE recurred in all patients. Therapy had to be stopped in one patient. The other four patients are currently on a maintenance dose of 60 to 80 micrograms. The possibility of a qualitative inferiority of the patients own IgG response was studied by crossed radioimmunoelectrophoresis and IgG subclass analysis. Lack of an IgG response to particular BV components to which IgE was present was demonstrated in three patients. The IgG subclass antibody pattern to BV at the time of recurrence of SE was similar to that found in beekeepers with a prominent IgG4 response. In contrast to beekeepers, however, there was no IgG2 response in patients.

Adult

A solid-phase radioimmunoassay for detection of human antibodies. I. Measurement of IgG antibody to bee venom antigens.

A solid-phase radioimmunoassay (SPRA) has been developed to measure IgG antibodies to bee venom (BV) and phospholipiase A2 (PLA) in human sera. The principle of the test is similar to that of the radioallergosorbent test (RAST) measuring IgE antibody. Cyanogen-bromide-activated paper discs coupled with BV or PLA followed by supplementary coupling with human serum albumin were incubated with standard or test sera, washed, and incubated with 125I-labeled anti IgG. The serum levels of the IgG antibody have been temporarily expressed in arbitrary units. the reaction between the antigen and antibody was specific and the results were reproducible. Sera from 19 beekeepers, 42 beesting-sensitive patients and 20 blood donors (controls) were assayed by the SPRA. IgG antibodies to BV and PLA could not be detected (less than 4 U/ml) in all control sera, in 25 of the 42 patients and in one beekeeper. The IgG antibodies in 17 patients ranged between 5 to 58 U/ml (mean 7.6 U/ml), and in the 18 beekeepers ranged between 8 to 160 U/ml (mean 59 U/ml).

Animals

Brood indicators are an early warning signal of honey bee colony loss-a simulation-based study.

Honey bees (Apis mellifera) are exposed to multiple stressors such as pesticides, lack of forage, and diseases. It is therefore a long-standing aim to develop robust and meaningful indicators of bee vitality to assist beekeepers While established indicators often focus on expected colony winter mortality based on adult bee abundance and honey reserves at the beginning of the winter, it would be useful to have indicators that allow detection of stress effects earlier in the year to allow for adaptive management. We used the established honey bee simulation model BEEHAVE to explore the potential of different indicators such as population size, number of capped brood cells, flight activity, abundance of Varroa mites, honey stores and a brood-bee ratio. We implemented two types of stressors in our simulations: 1) parasite pressure, i.e. sub-optimal Varroa treatment by the beekeeper (hereafter referred as Biotic stress) and 2) temporal forage gaps in spring and autumn (hereafter referred as Environmental stress). Neither stressor type could be detected by bee abundance or honey reserves at the end of the first year. However, all response variables used in this study did reveal early warning signals during the course of the year. The most reliable and useful measures seem to be related to brood and the abundance of Varroa mites at the end of the year. However, while in the model we have full access to time series of variables from stressed and unstressed colonies, knowledge of these variables in the field is challenging. We discuss how our findings can nevertheless be used to develop practical early warning indicators. As a next step in the interactive development of such indicators we suggest empirical studies on the importance of the number of capped brood cells at certain times of the year on bee population vitality.

Bees

Combination of passive and active immunization in honeybee venom immunotherapy.

Immunotherapy with honeybee venom (HBV) is effective under optimal conditions, but many untoward systemic reactions are observed when venom doses are increased, especially with rush protocols. Although there were large interpatient variations, the levels of serum been venom specific IgG were found to significantly correlate with the protection of the allergic patients. A double-blind, placebo-controlled study was carried out to determine whether passive immunization with fractionated IgG from a beekeeper's serum pool was able to protect patients undergoing a rush immunotherapy program with HBV against untoward systemic reactions, and to observe if the active immunization with HBV could elicit an active IgG immune response toward venom allergens. Hyperimmune IgG was obtained from a pool of sera of beekeepers (Cohn fractions II to III) that was subsequently treated with pepsin for intravenous use. All IgG subclasses were found to be present in the preparation. Twenty-seven patients, highly allergic to HBV, were randomly allocated to two treatment groups. Twenty patients received 10 to 15 gm of fractionated IgG, and seven other patients received saline in a double-blind fashion. The next day, a 3-hour rush protocol attempted to reach a cumulative venom dose of 200 micrograms; 16/20 patients who received the fractionated IgG reached this dose without any systemic reaction, whereas none of the seven subjects who received saline could attain it, and all patients had a systemic reaction. The active immunization with HBV elicited a significant (p less than 0.05; Wilcoxon W Test) increase in venom IgG after 1 week of treatment in the patients who reached the maintenance dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent

An HLA-associated nonresponsiveness to mellitin: a component of bee venom.

Previous work has demonstrated a close association between certain histocompatibility antigens and the gene that controls the IgE response to certain ragweed allergens. For example, there is a 90% association between IgE production to the short ragweed allergen, Amb a V, and an HLA class II allele. To assess whether these HLA linkages are specific for ragweed, we have investigated the association between HLA antigens and the capacity of individuals to mount a specific IgE response to melittin in patients with bee-venom allergy. Twenty-two subjects with bee-venom sensitivity, 22 healthy beekeepers without bee-venom allergy, and a normal population of 149 unselected individuals were studied. With serologic tissue typing and restriction fragment length polymorphism analysis, we have demonstrated a significant decrease in the HLA-DR4 and DQw3 alleles in subjects who are allergic to melittin compared to the control populations. There was also a negative association between the presence of HLA-DR4 and DQw3 alleles with the capacity of the individuals to mount an IgE response to phospholipase A2 (PLA2). The bee-venom sensitive subjects had a slightly lower titer of anti-PLA2 IgG when these subjects were compared to the bee-venom insensitive beekeepers. These results support the view that either HLA-DR or HLA-DQ has a protective role in controlling the IgE immune response. Lack of an IgE response to melittin or PLA2 is unlikely to be due to a failure to recognize allergen.

Adolescent