Patients with ciguatera: request for convalescent sera.
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Biomedical subjects
Publications and source records attributed to S K Sutherland.
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Jumper ant venom was prepared by extraction of venom sacs in distilled water and centrifugation to remove insoluble material. Jumper ant venom (2 micrograms/ml) produced a biphasic response on isolated guinea-pig ileum, i.e. an initial rapid contraction followed by a slower prolonged contraction. The histamine antagonist mepyramine (0.1 microM) inhibited the first phase of this response by greater than 90%. In the isolated rat stomach fundus strip (which is insensitive to histamine), jumper ant venom (6 micrograms/ml) produced only a single contraction. No tachyphylaxis was observed to repeated doses of jumper ant venom in guinea-pig ileum or rat fundus strip. Responses to jumper ant venom of the egg-albumin-sensitised guinea-pig ileum were not significantly different before and after an in vitro anaphylactic response induced by egg albumin (0.5 mg/ml). Fluorometric assay revealed a mean value of 0.9 +/- 0.2% of the dry weight as histamine in jumper ant venom. Both the lipoxygenase/cyclo-oxygenase inhibitor BW755C and the cyclooxygenase inhibitor indomethacin significantly inhibited the second phase response to jumper ant venom of the guinea-pig ileum, and the response of the rat fundus strip. The muscarinic receptor antagonist atropine (0.1 microM), the bradykinin antagonist [Thi5,8,D-Phe7]-bradykinin (10 microM) and the angiotensin converting enzyme inhibitor captopril (20 microM) did not affect either phase of the venom response in guinea-pig ileum. Jumper ant venom caused haemolysis of guinea-pig blood. The degree of haemolysis was significantly reduced when boiled venom was used. These results suggest that jumper ant venom contains histamine and may cause the release of cyclo-oxygenase products. It also contains a heat-sensitive haemolytic factor.
The cardiovascular and haematological effects of purified prothrombin activator derived from the venom of the Australian Common Brown Snake (Pseudonaja textilis) were studied in anaesthetised, mechanically ventilated dogs. Severe depression of systemic blood pressure and cardiac output and a rise in central venous pressure were observed. Thrombocytopenia, prolongation of both prothrombin time and activated partial thromboplastin time and a reduction in serum fibrinogen were also observed. All of these observed effects were prevented by the prior administration of heparin--a naturally occurring anticoagulant. We conclude that the prothrombin activator in Pseudonaja textilis venom may cause cardiovascular depression due to myocardial dysfunction secondary to disseminated intravascular coagulation.
The efficacy of heparin therapy after subcutaneous injection of Common Brown Snake (Pseudonaja textilis) venom was studied in anaesthetised, mechanically ventilated dogs. Intravenous heparin (100 U/kg), administered fifteen minutes after envenomation, neither prevented nor hastened the recovery from cardiovascular depression and coagulopathy observed after venom administration. Heparin therapy is not recommended for the treatment of established human envenomation.
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We report a study of 347 patients with snake bite envenomation in Papua New Guinea. The male: female ratio of the victims was 1.6:1 and their mean age was 24.5 years; 26% were children less than 15 years old. In all cases in which the bite site was known (334) the snake had bitten the extremities of the victim, with 71.3% of these bites being on the ankle or below. The patients came from three regions: urban Papua, rural Papua and (mostly rural) New Guinea. Snake bites occurred more frequently during the daytime in all regions, but this pattern was less obvious in New Guinea (P = 0.004), reflecting the predominance of the death adder (Acanthophis antarcticus) in New Guinea and of the taipan (Oxyuranus scutellatus canni) in Papua. Bites were commoner in the rainy season (November to April) in all groups, but this was less noticeable in rural Papua and New Guinea (P = 0.004). This may relate to seasonal activities of the rural population. The female:male ratio for patients from rural areas was higher for those 30 years of age and over than for those under 30 (P = 0.034), probably reflecting the increased gardening workload of older women. The incidence of envenomation and mortality rates after snake bite in Papua appear to have changed little over 25 years. However, increased relative numbers of taipans seem to be occurring in central Papua possibly related to the cane toad (Bufo marinus) and deforestation. We calculate the annual incidence of envenomation and the mortality rate per 100,000 to be 81.8 and 4.3, respectively, for rural central Papua, 21.8 and 2.1 for urban central Papua, and 3.0 and less than 1.0 for the Madang region of New Guinea. The importance of a standard management protocol and of improved first aid are emphasised.
OBJECTIVE: This case report illustrates the threat to life posed by tiger snake venom-induced coagulopathy, the importance of first-aid, precautions with antivenom administration, the dose of antivenom and the necessity to monitor the coagulation status. CASE SUMMARY: An 11-year-old child was envenomated several times by a tiger snake (Notechis scutatus). Despite administration of three ampoules (9000 units) of tiger snake antivenom, fatal cerebral haemorrhage occurred. Inadequate first-aid had been applied. The bite site was covered with a loose bandage instead of a pressure-immobilisation bandage. In hospital, facilities to monitor coagulation status were unavailable. CONCLUSIONS: More public education is required in first-aid management of snake envenomation. Frequent monitoring of coagulation status is necessary to optimise antivenom and coagulation factor therapy.
The haematological effects of Brown Snake (Pseudonaja) species (textilis, affinis, nuchalis) were studied in anaesthetised, mechanically ventilated dogs. Marked thrombocytopenia, depletion of serum fibrinogen and prolonged prothrombin and activated partial thromboplastin time, were recorded at 5 to 10 and 30 to 40 minutes after intravenous envenomation. Fibrin degradation products were not elevated. Because these haematological effects occurred simultaneously with cardiovascular depression (previously reported), we postulate that hypotension sometimes observed in human envenomation may be due to intravascular coagulation with myocardial ischaemia.
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Most Australian spiders are capable of causing bites that produce some degree of local injury and occasionally systemic effects. To date, only the Sydney funnel-web spider, which is limited to an area with a 160 kilometre radius from the centre of Sydney, and the female red-back spider, which is found in all states, have been documented as causing deaths. The evidence is mounting that various other species must be considered potentially dangerous.
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