Allergy to Hymenoptera Venoms

Schmidt, Justin O.

doi:10.1016/b978-0-12-554770-3.50014-0

Cited by 24 publications

(29 citation statements)

References 106 publications

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“…48 In the United States, some 40 deaths per year result from such a reaction and it usually occurs within 1 hr. 47 Such subjects will not benefit from the availability of an antivenom whose use will be limited to those stung by 50 or more bees who often develop features of systemic toxicity many hours later, with the majority of deaths only after ϳ22 hr. 4,11 This suggests that the use of antivenom may still be beneficial even if delayed many hours.…”

Section: Discussionmentioning

confidence: 99%

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A novel Fab-based antivenom for the treatment of mass bee attacks.

Jones

Corteling²,

Bhogal³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

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Abstract. The frequency of mass bee attacks has dramatically increased in the Americas following the introduction and spread of the aggressive Africanized 'killer' bee (Apis mellifera scutellata). As yet no specific therapy is available, which led us to develop an ovine Fab-based antivenom as a potential new treatment. Sera from sheep immunized against the venom contained high levels of specific antibodies, as demonstrated by ELISA and by small-scale affinity chromatography, against both whole (A. m. mellifera) venom and purified melittin. A nerve muscle preparation was used to show the myotoxic effects of the venom and neutralization by the antivenom. Antivenom neutralizing ability was also demonstrated using assays for venom phospholipase A 2 and in vivo activities. Venom from both European and Africanized bees appeared identical when analyzed by acid-urea gel electrophoresis. This antivenom may therefore provide the first specific therapy for the treatment of mass envenomation by either European or Africanized 'killer' bees.The accidental introduction of the native African bee Apis mellifera scutellata into Brazil in 1957 and its subsequent displacement and hybridization of the long-established European bees A. m. mellifera and A. m. ligustica has resulted in the highly aggressive Africanized 'killer' bee. 1,2 It is better adapted to warmer climates than its European counterparts and, as a result, has been highly successful and spread rapidly throughout Latin America. In 1992, the Africanized bee crossed the border into the United States and is now found in Texas, Arizona, New Mexico, and southern California. 3 It is predicted to eventually be distributed as far east as North Carolina. 2 These bees attack much more readily and in greater numbers than the European varieties, 1 and thousands of stings may be inflicted on a single individual. 4,5 About 50 simultaneous stings can cause systemic envenoming and about 500 are probably necessary to cause death by direct toxicity, 4,6-10 although one death in Arizona was due to only ϳ125 stings. 11 By 1985, it was estimated that these bees had caused between 700 and 1,000 deaths, 12 and in Mexico there have been more than 190 such deaths between 1988 and 1993, with future estimates of 60 deaths per year. 13 Clinical features can include rhabdomyolysis, intravascular hemolysis, respiratory distress, hepatic dysfunction, hypertension, myocardial damage, shock, and/or renal failure. 4,5,8,11 Each Africanized bee injects an average of 94 g of venom in less than a minute, compared with 147 g for the slightly larger European bee, and circulating venom levels in patients of up to 3.8 mg/L have been recorded. 4,14,15 The venom contains many biologically active components such as melittin, phospholipase A 2 , apamin, mast cell degranulating peptide, hyaluronidase, histamine, and dopamine. 16 Of these, melittin is predominant (ϳ50% by dry weight) and can disrupt cell membranes and produce pores even at low concentrations. 16,17 Phospholipase A 2 enhances this membrane disruptio...

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Section: Discussionmentioning

confidence: 99%

“…47 These allergic-type individuals are at a high risk of developing life threatening IgE-mediated or anaphylactoid reactions, which must be treated conventionally, (e.g. antihistamines, steroids, alpha/beta agonists, bronchodilators, and adrenaline).…”

Section: Discussionmentioning

confidence: 99%

A novel Fab-based antivenom for the treatment of mass bee attacks.

Jones

Corteling²,

Bhogal³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

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“…Sometimes, a severe reaction may occur-in people with systemic hypersensitivity to hymenoptera venoms. Such persons develop an anaphylactic reaction within 1 h often leading to death (Schmidt 1986;. However, severe or fatal mass attacks of bees have been also reported (Azevedo-Marques et al 2001;Bresolin et al 2002;Deshmukh and Borse 1996;França et al 1994;Vetter et al 1999).…”

Section: Introductionmentioning

confidence: 95%

Electrophysiological and Structural Aspects in the Frontal Cortex After the Bee (Apis mellifera) Venom Experimental Treatment

Florea

Puica²,

Vintan

et al. 2011

Cell Mol Neurobiol

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The aim of this study is to evaluate the bioelectrical and structural-functional changes in frontal cortex after the bee venom (BV) experimental treatments simulating both an acute envenomation and a subchronic BV therapy. Wistar rats were subcutaneously injected once with three different BV doses: 700 μg/kg (T(1) group), 2100 μg/kg (T(3) group), and 62 mg/kg (sublethal dose-in T(SL) group), and repeated for 30 days with the lowest dose (700 μg/kg-in T(S) group). BV effects were assessed by electrophysiological, histological, histochemical, and ultrastructural methods. Single BV doses produced discharges of negative and biphasic sharp waves, and epileptiform spike-wave complexes. The increasing frequency of these elements suggested a dose-dependent neuronal hyperexcitation or irritation. As compared to the lower doses, the sublethal dose was responsible for a pronounced toxic effect, confirmed by ultrastructural data in both neurons and glial cells that underwent extensive, irreversible changes, triggering the cellular death. Subchronic BV treatment in T(S) group resulted in a slower frequency and increased amplitude of cortical activity suggesting neuronal loss. However, neurons were still stimulated by the last BV dose. Structural-functional data showed a reduced cellular density in frontal cortex of animals in this group, while the remaining neurons displayed both specific (stimulation of neuronal activity) and unspecific modifications (moderate alterations to necrotic phenomena). Molecular mechanisms involved in BV interactions with the nervous tissue are also discussed. We consider all these data very important for clinicians who manage patients with multiple bee stings, or who intend to set an appropriate BV therapy.

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“…Less often, the individual knows a bee or wasp is around and starts flailing wildly at it -precisely the action that increases the chances of being stung (Schmidt and Boyer Hassen 1996). Stings can cause local or systemic, hypersensitive reactions that lead to death (Schmidt 1986, Goddard 1996, Levick et al 2000, McGain et al 2000. A survey of about 2000 physicians in the southern USA in 1988 indicated that 22,755 patients had been treated for reactions to fire ant stings; 2% of them suffered anaphylactic shock (Goddard 1996).…”

Section: Stings and Bites Food And Other Productsmentioning

confidence: 99%

Biodiversity of Hymenoptera

Huber

2009

Insect Biodiversity

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Allergy to Hymenoptera Venoms

Cited by 24 publications

References 106 publications

A novel Fab-based antivenom for the treatment of mass bee attacks.

A novel Fab-based antivenom for the treatment of mass bee attacks.

Electrophysiological and Structural Aspects in the Frontal Cortex After the Bee (Apis mellifera) Venom Experimental Treatment

Biodiversity of Hymenoptera

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