Anaphylaxis Due to Pachycondyla goeldii Ant: A Case Report

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Effect of non-steroidal anti-inflammatory drugs (NSAID) on the histamine release induced by compound 48/80 and cardiac anaphylaxis in guinea-pig isolated heart

Histamine release from guinea pig heart treated with compound 48/80 was potentiated by the cyclooxygenase inhibitors indomethacin and piroxicam but not by aspirin or phenylbutazone. This differential effect suggests that the potentiation is not merely due to an inhibition of prostaglandin synthesis. Piroxicam potentiated the histamine release induced by cardiac anaphylaxis whereas indomethacin reduced this effect. The SRS-A antagonist FPL 55712 inhibited histamine release induced by cardiac anaphylaxis, but not that evoked by compound 48/80, and also prevented the potentiation due to indomethacin and piroxicam. In total, these data suggest that the potentiation of histamine release by piroxicam and indomethacin is probably due to a diversion of arachidonic acid metabolism from the cyclooxygenase to the lipoxygenase pathways. The resulting lipoxygenase products may then regulate histamine release, with the secretion due to antigen being more sensitive to such modulation than that evoked by compound 48/80.

Suppression by {\it Trypanosoma brucei\/} of anaphylaxis-mediated ion transport in the small intestine of rats

Most tissue-invasive parasitic helminths prime for type 1 hypersensitivity or anaphylaxis during some phase of their life cycles. A prototype in this regard is the nematode Trichinella spiralis. Blood protozoa capable of tissue invasion, such as Trypanosoma brucei, might also be expected to prime for the expression of anaphylaxis. However, this response is usually absent in protozoal infections. The hypothesis tested was that failure of hosts infected with T.brucei to express anaphylaxis is related to this parasite's ability to selectively down-regulate immunoglobulin E (IgE) production, and not to an innate lack of allergenicity on the part of T.brucei-derived antigens. This hypothesis was tested by studying in the intestine of rats, antigen-induced Cl$\sp-$ secretion, which results from a local anaphylactic response mediated by IgE and mucosal mast cells. The Cl$\sp-$ secretory response can be primed either by infection with T.spiralis or by the parenteral administration of antigen. Anaphylaxis-induced Cl$\sp-$ secretion is expressed in vitro, and can be quantified electrophysiologically, as a change in transmural short-circuit current when sensitized intestine is mounted in Ussing chambers and challenged with the sensitizing antigen.^ Rats injected parenterally with trypanosome antigen elicited intestinal anaphylaxis in response to antigenic challenge. In contrast, the intestine of rats infected with T.brucei failed to respond to challenge with trypanosome antigen. Infection with T.brucei also suppressed antigen-induced Cl$\sp-$ secretion in rats sensitized and challenged with various antigens, including T.spiralis antigen. However, T.brucei infection did not inhibit the anaphylactic response in rats concomitantly infected with T.spiralis. Relative to the anaphylactic mediators, T.brucei infection blocked production of IgE in rats parenterally injected with antigen but not in T.spiralis-infected hosts. Also, the mucosal mastocytosis normally associated with trichinosis was unaffected by the trypanosome infection. These results support the conclusion that the failure to express anaphylaxis-mediated Cl$\sp-$ secretion in T.brucei infected rats, is due to this protozoan's ability to inhibit IgE production and not to the lack of allergenicity of trypanosome antigens. ^

MODULATION OF HOST INTESTINAL MYOELECTRIC ACTIVITY BY LOCAL ANAPHYLAXIS: A COMPONENT OF PROTECTIVE IMMUNITY TO AN ENTERIC PARASITE (TRICHINELLA SPIRALIS, EIMERIA NIESCHULZI, BOWEL MOTILITY)

The hypothesis tested was that rapid rejection of Trichinella spiralis infective larvae from immunized rats following a challenge infection is associated with a local anaphylactic reaction, and this response should be reflected in altered small intestinal motility. The objective was to determine if altered gut smooth muscle function accompanies worm rejection based on the assumption that anaphylaxis in vivo could be detected by changes in intestinal smooth muscle contractile activity (ie. an equivalent of the Schultz-Dale reaction or in vitro anaphylaxis). The aims were to (1) characterize motility changes by monitoring intestinal myoelectric activity in conscious rats during the enteric phase of T. spiralis infection in immunized hosts, (2) detect the onset and magnitude of myoelectric changes caused by challenge infection in immunized rats, (3) determine the parasite stimulus causing changes, and (4) determine the specificity of host response to stimulation. Electrical slow wave frequency, spiking activity, normal interdigestive migrating myoelectric complexes and abnormal migrating action potential complexes were measured. Changes in myoelectric parameters induced by larvae inoculated into the duodenum of immune hosts differed from those associated with primary infection with respect to time of onset, magnitude and duration. Myoelectric changes elicited by live larvae could not be reproduced by inoculation of hosts with dead larvae, larval excretory-secretory products, or by challenge with a heterologous parasite, Eimeria nieschulzi. These results indicate that (1) local anaphylaxis is a component of the initial response to T. spiralis in immune hosts, since the rapid onset of altered smooth muscle function parallels in time the expression of rapid rejection of infective larvae, and (2) an active mucosal penetration attempt by the worm is necessary to elicit this host response. These findings provide evidence that worm rejection is a consequence of, or sequel to, an immediate hypersensitivity reaction elicited when parasites attempt to invade the gut mucosa of immunized hosts. ^

Cashew nut allergy is associated with a high risk of anaphylaxis

Cashew allergy is an evolving clinical problem. A retrospective chart review of 213 children with peanut or tree nut allergy was undertaken over a 42 month period. Anaphylaxis to cashew nut was more common than to peanut ( 74.1% v 30.5%). Children with cashew allergy are at risk of anaphylaxis.

Physiological and haematological findings and clinical observations in a model of acute systemic anaphylaxis in Dirofilaria immitis-sensitised cats

Objective This study aims to understand the pathophysiology of anaphylaxis in Dirofflaria immitis-sensitised cats by analysing objective physiological and haematological measurements after challenge. Design Nineteen healthy D immitis-naive cats were sensitised using weekly injections of aluminium hydroxide-adjuvanted D immitis antigen, administered subcutaneously over 6 weeks. After sensitisation, cats (n = 16) were anaesthetised and challenged with intravenous D immitis antigen. A control group (n = 3) was sham-challenged using intravenous sterile 0.9% saline. Systolic blood pressure (measured non-invasively/indirectly), respiratory rate, degree of dyspnoea, blood 0, saturation, expired CO2, and heart rate and were measured immediately before and at 10 to 15 min intervals after challenge until terminal apnoea occurred or euthanasia at 140 mins post-challenge. Blood was collected for complete blood count immediately before and at 10, 20 and 35 mins after challenge. Clinical observations were recorded as they occurred. Results Antigen-challenged cats were divided into two groups: acute (apnoea occurred within 25 mins of challenge) and subacute (breathing at 25 mins after challenge). In both groups, the degree of dyspnoea increased and blood O-2 saturation and blood pressure decreased. Respiratory rate increased in the subacute group. Expired CO2 decreased in both Ag-challenged and control groups. Haematocrit increased in the subacute group. Neutrophil count decreased in the acute group and platelet count decreased in the subacute group. Eosinophil count decreased in the subacute and control groups. Sustained dyspnoea and gastrointestinal signs were the most common clinical manifestations of anaphylaxis in the antigen-challenged cats. Conclusions Intravenous challenge with D immitis antigen in sensitised cats results in dyspnoea, hypoxaemia and systemic hypotension accompanied by haemoconcentration.