Adaptation of the electrical stimulation procedure for the collection of vespid venoms.
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Biomedical subjects
Publications and source records attributed to R E Reisman.
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Local nasal immunotherapy (LNIT) of ragweed allergic rhinitis was studied in a double-blind controlled trial. Sixty-seven subjects were divided into three groups. Twenty-one received unmodified ragweed extract (RW), 24 received a glutaraldehyde polymer of ragweed extract (PRW), and 22 received placebo. Mean symptom/medication scores during the season were 2.12, 2.76, and 3.93 for the RW, PRW, and placebo groups, respectively. Both RW- and the PRW-treated group scores were significantly lower than those of the placebo group (p less than 0.01, and p less than 0.025, respectively). The results of the patients' self-evaluations indicated that therapy was effective in 71%, 59%, and 41% for the RW-, PRW-, and placebo-treated groups, respectively. Adverse reactions to treatment were limited to the upper respiratory tract and were noted by all patients. They were significantly more severe in the RW-treated patients than those in the PRW- or placebo-treated groups. We conclude that LNIT is an effective therapy for ragweed allergic rhinitis. The use of a PRW decreased adverse reactions significantly while slightly decreasing the therapeutic benefit.
Local nasal immunotherapy (LNIT) was administered in a double-blind study to 67 subjects. Twenty-three received an unmodified ragweed extract (RW), 24 received a glutaraldehyde polymer of ragweed extract (PRW), and 21 received placebo. Serum ragweed-specific IgE (S-IgE), ragweed-specific nasal secretory (NS-) IgE, secretory IgA (SIgA) and IgG, and NS-albumin were measured. RW therapy caused a significant increase in ragweed-specific S-IgE (p less than 0.005) and NS-SIgA (p less than 0.05). PRW therapy caused a significant rise in ragweed-specific NS-SIgA (p less than 0.001). NS-IgE (p less than 0.05), and NS-IgG (p less than 0.01). Ragweed-specific S-IgG was not affected by any of the treatments. There was no consistent correlation between NS-antibody levels and symptom/medication scores.
This case report demonstrates the lack of correlation between clinical sensitivity to insect venoms and immunologic reactivity as indicated by the presence of venom-specific IgG. A 20-yr-old venom collector was monitored over a 3-yr period with measurements of venom-specific IgE (skin test and RAST) and venom-specific IgG. In the first year of venom collection, multiple stings were tolerated with no reaction. In the second season, she had an anaphylactic reaction after a yellow jacket sting. Subsequently, there was a rising titer of serum yellow jacket and bee venom-specific IgE and positive skin-test reactions. In the third season, yellow jacket, hornet, and bee venom skin tests remained positive and serum IgE antibody titers remained elevated. Stings from all three insects were tolerated with no reaction. Throughout the 3-yr course, serum venom-specific IgG remained low and unchanged. The factors other than IgE-modulating clinical anaphylaxis, perhaps responsible for this clinical and immunologic dichotomy, are unknown. These observations add a further complication to the choice of patients for venom immunotherapy.
During the summer of 1978, 22 patients who had large local reactions following insect stings were evaluated for the development of potential systemic sensitivity. Approximately half the patients had venom IgE antibodies, detected by either the immediate skin test or radioallergosorbent test (RAST). A control group of 26 patients experiencing normal sting reactions had only a 15% incidence of venom-specific IgE. No correlations could be found between the presence of venom-specific IgE and age, sex, sting location, atopic history, or prior stings. IgE antibodies were found in 13 of 17 patients who had experienced local reactions lasting more than 48 hr. Serum venom-specific IgG was detected in only three of 19 patients. These results suggest that following large local reactions from insect stings patients must be individually assessed for the presence of venom-specific IgE and consideration for specific immunotherapy.
Venoms from various yellow jacket species were examined by two-dimensional thin-layer chromatography (TDTLC), double-diffusion gel precipitation (DDGP) using rabbit antisera, and the radioallergosorbent test (RAST). Comparison of representative venoms by the TDTLC showed that the venoms of V. vulgaris and V. maculifrons have a larger number of Ninhydrin (triketohydrindene hydrate)-positive substances than the venom of V. squamosa. The results of the DDGP confirmed the differences; venoms of V. vulgaris, V. maculifrons, V. flavopilosa, and V. germanica have one or more major components with immunogenic identity. The venom of V. squamosa has a species-specific major component and some minor components immunologically identical to the other venoms examined. Sera from 21 patients with a history of anaphylaxis following yellow jacket stings were examined by the RAST. Using the venoms of V. maculifrons, V. vulgaris, V. flavopilosa, and V. germanica as coupling antigens, most sera reacted similarly. The sera did not react with V. squamosa. These results suggest that the major component in venom obtained from the four yellow jacket species has immunogenic identity. Venom of V. squamosa differs from the remaining venoms. As a practical corollary, with the exception of venom from V. squamosa, common sensitivity appears to exist among the yellow jacket venoms examined.
An acute anaphylactic reaction occurred in a patient known to be highly sensitive to penicillin following ingestion of the soft drink Wink. Bacteriologic studies showed the presence of penicillin or a penicillin-like substance in the Wink, suggesting it as the cause of the anaphylaxis. The source of this contaminant could not be identified.
Recent studies have indicated that currently available whole body extracts have little potency and are ineffective for diagnosis and treatment of stinging insect allergy. Pure venom is a potent effective allergen but is difficult to obtain in sufficient quantities from all Hymenoptera species. In these studies, an attempt was made to prepare a potent whole body extract. Whole bee body extracts were prepared with different extraction periods and at cold and room temperatures. Potency was examined biochemically by measurements of phospholipase A (PLA) activity and immunologically by PLA and bee venom radioallergosorbent test (RAST) inhibition experiments and gel diffusion studies with the use of rabbit antisera. All extracts prepared in the laboratory had some potency, indicating that it is possible to make a whole body extract containing small quantities of PLA or bee venom. However, the potency of these extracts was minimal as compared with bee venom. Three commercial extracts were almost devoid of detectable immunologic activity. While further attempts may be made to prepare a potent whole body insect extract, these results suggest that it is necessary to obtain venom in relatively pure form for the diagnosis and treatment of stinging insect allergy.
An individual is described who appeared to be sensitive to nonvenom contaminants in a venom preparation. His IgE antibodies, measured by the immediate direct skin test and the radioallergosorbent test (RAST), reacted with a yellow jacket venom preparation obtained by "washing" of venom sacs. With yellow jacket venom obtained by electriral stimulation, there was a skin test reaction of equivocal significance and no serum antibodies were detected by the RAST. Moderate reactions were also found with yellow jacket body extracts. In contrast, sera obtained from patients with yellow jacket sting anaphylaxis showed strong reactions with the electrically stimulated venom preparation and only a few reacted with the body extract. In additional studies, the patient's serum reacted with yellow jacket extracts devoid of venom and a variety of hornet and wasp extracts. Analyses of the two yellow jacket venoms by gel diffusion using rabbit antisera showed the presence of body proteins in the venom obtained by venom sac "washing." Subsequent history revealed the presence of insect nests in the roof of the patient's bedroom, perhaps the source of inhalant exposure and sensitivity. This case history demonstrates the need for venom extracts that do not contain potentially sensitizing extraneous material.
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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).
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Prostaglandin (PG) E plasma levels, measured by radioimmunoassay using anti-PGB1 antibody, were higher in asthmatic patients than in normal subjects. PGF levels measured with anti-PGF2alpha antibody, were not significantly different between normals and asthmatics. Plasma PGE/F ratios were elevated in the asthmatic patients. The results fail to support the hypothesis of decreased PGE or increased PGF production as an etiological factor in asthma.
Prostaglandin (PG) was extracted from nasal secretions of individuals with hay fever and from nasal washings of normal subjects. The extract was chromatographed in a silicic acid column and the purified PGE fraction was converted to PGB by alkaline dehydration. The PGB was then measured by a competitive radioimmunoassay with tritiated PGB1 and anti-PGB1 antibody, employing the double antibody technique. PGE was detected in the secretions of 6 of 12 hay fever patients and in the pooled normal nasal washings.