96 



E. KOCHVA 



a ^, 



c ,• 



Jk^3 



. . lmuuuJ ' ' 1 1 — i — i 1 i 1 



M 0.5 1.0 sec. 



of other blood vessels and may be considered as one of the most 

 potent vasoconstrictors. 



In human patients too, cardiotoxic symptoms and a rise in blood 

 pressure were observed, but were considered as secondary develop- 

 ments of some kind of neurotoxic effects. However, neither 

 presynaptic nor postsynaptic neurotoxicity was observed in labora- 

 tory tests with nerve-muscle preparations using whole A. engaddensis 

 venom (Weiser et al, 1984); SRTX does show specific binding to 

 different isolated regions of brain preparations, with the highest 

 binding capacity found in the cerebellum, choroid plexus and hip- 

 pocampus (Ambar et al, 1988), but its function there is not known. 



In human bites by A. engaddensis and A. irregularis, some of 

 which were extremely severe, changes in the ECG were observed 

 (Fig. 11), including S-T elevation or depression, flattening of the T- 

 waves and prolonged P-R intervals pointing to myocardial ischemia 

 and atrioventricular conduction abnormalities (Chajek et ai, 1974; 

 Warrell, 1995; Kurnik, et al, 1999). The transient atrioventricular 

 block that developed in a 17-year old boy bitten on his left foot was 

 considered to be a secondary complication of the bite (Alkan and 

 Sukenik, 1974), rather than a direct influence of the toxins on the 

 heart. 



The other systemic symptoms, which may develop within min- 

 utes, include fever, nausea, general weakness, sweating, pallor, 

 fluctuations in the level of consciousness and a rise in blood pressure 

 (Doucet & Lepesme, 1953; Chajek etai, 1974; Kurnik etal, 1999). 



Most bites were on the fingers and the local effects were demon- 

 strated mainly by gross oedema of the hand that extended up to the 

 forearm and shoulder (A. irregularis - Doucet and Lepesme, 1953; 

 A. corpulenta - Gunders et al., 1960; A. microlepidota - Warrell et 

 al, 1976) and by blistering and serous vesicles that appeared at the 

 site of the bite and underwent hemorrhagic transformation (Fig. 12; 

 Kurnik et al. 1999). In some previously reported cases (Chajek et 

 al, 1974; Chajek & Gunders, 1977), local necrosis developed that 

 required surgical intervention including amputation. In two cases, 

 one by A. bibroni, the other by A. engaddensis, the bitten finger 

 partially or fully recovered within a month, but tenderness of the 

 bitten site remained for a long time (Stewart, 1965; Kurnik et al, 

 1999). 



Although the bites by several species of Atractaspis, such as A. 

 dahomeyensis, A. aterrima, A. corpulenta and A. bibroni were mild 

 (Warrell et al, 1976; Tilbury & Branch, 1989), A. engaddensis, A. 

 irregularis and perhaps other species should be regarded as dangerous 



H 



Fig. 11 ECG recording after Atractaspis engaddensis envenomation. M 

 = mouse: v = venom injection; b - f : 120 - 600 seconds after venom 

 injection. H = human: upper trace - at admission to the hospital: lower 

 trace - 24 hours after the bite (see text). 



toxin; 2) direct effect of the toxin on the cardiac conducting system; 

 and 3) cardiac ischemia, which is caused by constriction of the 

 coronary blood vessels. The latter two cause severe A-V block, 

 which may lead to cardiac arrest. The cardiotoxic effects are mani- 

 fested by marked changes in the ECG, in both human victims and in 

 mice injected with either SRTX-b or whole venom (Fig. 1 1 ). These 

 changes include an increase in amplitude of the R- and T-waves, a 

 prolongation of the P-R interval, 'dropped beats' and complete A- 

 V block and cardiac arrest. In addition. SRTX-b causes contraction 



Fig. 12 Bitten index finger showing hemorrhagic transformation of 

 serous vesicles. 



