[Studies on the snake venom enzyme. XIII. On the ribonuclease activity of Formosan snake venoms].
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1. Long neurotoxin S4C6 from Aspidelaps scutatus venom was purified by gel filtration and ion exchange chromatography (Joubert, 1987). 2. It contains 68 amino acids including 10 half-cystines. The toxicity of toxin S4C6 was determined and a LD50 of 0.13 +/- 0.04 micrograms/g mouse was found. 3. The complete primary structure of long neurotoxin S4C6 has been elucidated. In the toxin the 10 structurally invariant amino acids of the neurotoxins and cytoxins and the five functionally invariant amino acids of the neurotoxins are conserved.
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Hemoglobinuria occurs in rats, but not in mice, after i.p. application of Tropidechis carinatus venom. By gel filtration on Sephadex G-75 and G-50 and chromatography on SP-Sephadex C-25 and DEAE-cellulose, a coagulant factor and a phospholipase A were isolated from the venom which in combination only, produced hemoglobinuria.
Pyrularia thionin (P. thionin) is a strongly basic peptide of 47 amino acids which is hemolytic, cytotoxic and neurotoxic. It shows the greatest hemolytic activity toward human erythrocytes. Rabbit, guinea pig and pig erythrocytes show decreasing activity in that order, and little or no activity is shown with sheep, horse, cow or mouse erythrocytes. Crotalus venoms are inactive, but the venoms from Naja naja atra, Naja naja ceylonicus and Naja naja melanoleuca and, more specifically, cardiotoxin from Naja naja kaouthia have significant hemolytic activities toward human erythrocytes. The cardiotoxin preparation used had no phospholipase activity, and was less active than P. thionin (23% compared to 35% hemolysis by P. thionin in 60 min at 10 micrograms/ml toxin). Since iodinated P. thionin is inactive, it was used as an inhibitor of hemolysis catalyzed by native P. thionin, N. ceylonicus venom and by cardiotoxin. Examination of the kinetics of the reactions catalyzed by N. ceylonicus venom and cardiotoxin in the absence and presence of iodinated P. thionin shows that both N. ceylonicus venom and cardiotoxin exhibit Michaelis-Menten kinetics, yielding apparent Km values of 7.4 micrograms/ml and 0.69 microM, respectively. These values compare to an apparent Km for P. thionin of 1.6 microM for erythrocyte hemolysis and a binding constant of 2.1 microM (Osorio e Castro, V. R. Van Kuiken, B. A. and Vernon, L. P. (1989) Action of a thionin isolated from nuts of Pyrularia pubera on human erythrocytes. Toxicon 27, 501). The inhibition constants Ki for iodinated P. thionin in the reactions with N. ceylonicus venom and cardiotoxin are 3.8 and 5.3 microM, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Plasmas from Pseudonaja textilis and Notechis scutatus were tested in vitro for their ability to neutralise the procoagulant activity, in human plasma, of nine elapid venoms. Pseudonaja textilis plasma inhibited the procoagulant activity of all Pseudonaja species and in one taipan (Oxyuranus scutellatus). However there was no inhibitory activity against any from the Notechis species. Plasma from Notechis scutatus exhibited no inhibitory activity against any Notechis species, including self, only weak inhibition against the Pseudonaja species and, again, total inhibition of Oxyuranus scutellatus. Thus, protection of a species from the effects of its own venom does not appear to be universal.
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Groups of four to five, 3-month-old rat snakes (Elaphe obsoleta) were separately gastrically inoculated with 2.0 x 10(6) viable oocysts of Cryptosporidium muris (mice and calves), C. muris-like (Bactrian camels), C. wrairi (guinea pigs), C. baileyi (chickens), C. meleagridis (turkeys), Cryptosporidium sp. (turtles, tortoises, chameleons and lizards) and C. serpentis from clinically (fatal case) and subclinically infected snakes. None of the snakes inoculated with oocysts originating from homothermous vertebrates developed infection as determined by histology and serology, whereas all snakes challenged with reptilian oocyst isolates were infected with Cryptosporidium on weeks 6 and 10 post-inoculation (PI). One week 10 PI, the snakes displayed mild to serve, multifocal to widespread, thinning and disorganization of gastric epithelium and nine out of twelve snakes infected by oocysts originating from reptiles other than snakes displayed severe gastric hyperplasia. Three out of ten snakes infected oocysts originating from snakes had ELISA-detectable Cryptosporidium-specific antibody (Ab) titers on week 6 PI; all snakes were Cryptosporidium-seroconverted on week 10 PI and their serum Ab titer significantly increased. The study demonstrated that Cryptosporidium infections in snakes maintained on the diet of rodents or birds cannot be initiated via ingestion of an infected food item; however, snakes can void ingested oocysts. Lack of host specificity among reptiles to this pathogen, demonstrated for the first time in the present study, indicates that snake-attributed C. serpentis is not distinct from Cryptosporidium sp. infecting reptiles other than snakes, and that clinical manifestations and virulence of Cryptosporidium in snakes in modulated by the species of the host. Housing of snakes with other reptiles can enhance transmission of Cryptosporidium to snakes, and therefore should be avoided.
OBJECTIVE: Studies have noted the relatively common occurrence of positive urine results with the Commonwealth Serum Laboratories Venom Detection Kit (VDK) when testing patients with suspected snakebite who are not envenomed. Possible explanations have been false positive test results or subclinical envenoming. We investigated a third possibility, that there is potential for the venom (or saliva) from mildly venomous and non-venomous snakes to give a positive reading with the VDK. METHODS: Venoms/saliva from three non-venomous and seven mildly venomous snake species were tested in the laboratory with the VDK, along with control venoms from four of the five major snake genera (Brown snake, Tiger snake, Death adder and Black snake). RESULTS: Two of the venom/saliva samples, from Gould's hooded snake (Parasuta gouldii), a mildly venomous snake, and the Black-headed python (Aspidites melanocephalus), a non-venomous snake, caused a positive test for the tiger snake genus. There was also cross-reactivity between black snake venoms and the tiger snake well of the VDK. CONCLUSIONS: This study provides a further possible explanation for 'false positive' VDK results, that is venom/saliva presence or absorption from mildly or non-venomous snakes and cross reactivity with venomous snakes on VDK testing. It has implications for antivenom use should it ever be required for more severe envenoming syndromes from mildly or moderately venomous snakes, and for further research. It reinforces the practice of only using VDK testing in patients who show definite evidence of envenoming.