234 VENOMOUS SNAKES AND THE PHENOMENA OF THE1B VENOMS 



producing intravascular thrombosis. One group of Crotalinae can cause 

 death by similar toxic principles, while another contains more neurotoxins. 

 The species of Ancistrodon belong to the latter group, and Lachesis to the 

 former. The venom of Crotalus owes its fatal effects to the locally acting 

 principles, the haemorrhagins, which may also be injurious to the vascular 

 system throughout the entire body of the victim. The colubrine snakes 

 inhabiting Australia possess a venom which contains considerable of both 

 neurotoxins and thrombic ferments and can cause death by either of these. 

 Besides, the hsemolytic toxins of Daboia and Notechis appear to play an 

 important part in chronic toxications with these venoms. 



The above brief presentation of the complex nature of the toxic principles 

 of various venoms is introduced here in order to enable one to form a general 

 conception on toxicity before describing how our present knowledge of the 

 specificity of antivenins has gradually developed. 



The first investigator who observed the inefficiency of Calmette's antivenin 

 against the venom of other species was C. J. Martin, who made tests of the 

 neutralizing power of the antivenin against the venom of Pseudechis and 

 found that it had a very feeble protective action. In order to discover the 

 cause of this failure Martin tested the antivenin against the two separate 

 toxic principles which constitute the venom of Pseudechis. 



Martin, 1 some time previously, succeeded in separating these two prin- 

 ciples, either by heating the venom solution to 8o° C. or by filtering through 

 the gelatinized porcelain bougie under 50 atmospheric pressures. The heat- 

 resistant, non-coagulable portion of the venom is filterable through the bougie 

 and has neurotoxic action, while the heat-coagulable, non-filterable component 

 has haemotoxic action and also affects the heart. At that time Martin was 

 unaware of the independent existence of fibrin ferment and failed to allude 

 to this as such, but ascribed this thrombose-production to the extensive 

 destruction of the red corpuscles by haemotoxin. Therefore, as he himself 

 corrected his former view, the principle which he earlier called haemotoxin 

 must be understood as the fibrin ferment. As the result of his experiments on 

 animals Martin 2 pointed out that Calmette's antivenin can protect the animal 

 from the lethal effect of the filterable toxin (neurotoxin), but not at all from 

 that of the unfilterable toxin (haemotoxin, fibrin ferment). This explains 

 why the unmodified venom, which contains both principles in considerable 

 amounts, is not affected by Calmette's serum. 



Meanwhile Kanthack 3 was working on a similar problem and brought out 

 the fact that Calmette's antivenin failed to protect animals from the fatal 

 effects of comparatively small doses of daboia venom, and concluded that the 

 action of antivenin is highly specificifor the|venom which was used for its 

 production. 



1 C. T. Martin. Proc. Roy. Soc. New South Wales, Aug. 5, 1896. 



2 C. J. Martin. Concerning the curative power of antivenomous serum on animals inoculated with 



Australian snake's venom. Intercolon. Med. Jour., 1897, II, 527, 537. 



3 Kanthack. Report on snake venom in its prophylactic relation with poisons of the same and other 



sorts. Rep. Med. Off. Loc. Govern. Bd., 1895-96, London, 1897, 235. 



