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TRANSACTIONS OP THE ROYAL SOCIETY OF TROPICAL MEDICINE AND HYGIENE, VOL. 75, No. 5, 1981

Envenoming by Cerastes vipera-a report of two cases

JOSEPH ZIMMERMAN~, GIDEON MANNA, HAIM Y. KAPLAN? AND URI SAGHER~

IDept. of Medicine B, Hadassah University Hospital 2Dept. of Orthopaedic Surgery, Mt. Scopus, Hadassah University Hospital 3Dept. of Plastic Surgery, Hadassah University Hospital 4Department of Plastic and Maxillofacial Surgery, Shaare-Zedek Hospital, Jerusalem, Israel

Summary Two cases of envenoming by Cerastes vipera

are described Both were in snake collectors who were accidentally bitten on the finger while handling the snake. In both cases, local signs included a haemorrhagic bulla with fang marks, swelling and tenderness. These signs were mild in one case and moderately severe in the other, necessitating fasc- iotomy. No systemic signs were observed. Some coagulation abnormalities were found in both cases. In one, prolonged bleeding from the wound and a shortened euglobulin lysis time may suggest acti- vation of the fibrinolytic mechanism. In the other, prolongation of prothrombin time occurred with no haemorrhagic diathesis. Treatment included fas- ciotomy in one case and elevation of the affected part and antibiotics in the other. It appears that the clinical course of this snakebite is relatively benign.

Introduction Cerastes vipera, a poisonous snake of the Viperidae,

is found in the dune areas of North Africa and the Sinai and Negev deserts. Although the effect of its bite has been studied in laboratory animals (Mo- HAMED et al., 1977), no human victims have hitherto

been reported. We here describe the clinical course of its bite in two patients.

Case 1 T.E., a 17 year-old snake-collector, was admitted

to hosnital on 26 Seutember 1979, about six hours after he had been accidentally bitten on his right middle finger while handling the snake. The dura- tion of the bite was estimated by the victim to be about 30 seconds, as he avoided undue force while removing the snake from his finger. Immediately following the bite, marked swelling developed in the affected finger, and extended proximally. It was accompanied by sharp pain that radiated up to the right axilla. A haematoma appeared at the site of the bite and there was a tendency for blood to ooze from the wound for about 12 hours.

On admission the patient was found to be in good general condition. Blood pressure was 130/60, pulse 6O/min and regular, and the oral temperature 37 -4°C. Physical examination was negative apart from the local signs which included a haemorrhagic bulla with only one fang mark and marked swelling that extended from the bitten finger to the ante- cubital fossa (Figs. 1 and 2). Small and very tender

Fig. 1. The hand of patient 1,lO hours after he was bitten showing a haemorrhagic bulla with marked swelling of the finger.

J. ZIMlMERMAN et al.

Fig. 2. Close-up view of the affected finger, case 1.

Table I-Laboratory findings in patient T.E. following bite by C. vipera

Date 26 Nov. 27 Nov. 28 Nov.

1979 1979 1979

WBC/mm3 Haemoglobin (gr/dl) Platelets ( x 103/mm3) Prothrombin time (%) Partial thromboplastin time (sec., normal:

45-55) Clot retraction (%, normal : O-25) Euglobulin lysis time (hr., normal start after

1.5 hours) Fibrinogen (mg/dl., normal: 150-350) Thrombin time (sec., normal: 11-15) Fibrin degradation products-FDP (pg/ml.

control-2 * 5)

13,000

2:: 85 45

02

n.d. 164 13’5 n.d. n.d. 2.5

8,900 14.3 230 68 47

8,400 14.7

156

ii

21 1.75

187

2.2

n.d. - not done

Table II-Some laboratory findings in Patient S.I. following bite by C. vipera

22 Dec. 23 Dec. 24 Dec. 25 Dec. Date 1979 1979 1979 1979

WBC count (mn~-~) 7,900 7,000 4,400 5,500 Haemoglobin (gr/dl) 14.1 13.8 14.2 14.5 Prothrombin time (%) 58

40596 53 100

Partial thromboplastin time* (set) 24 n.d. 31’4 Fibrinogen (mg/dl)* n.d. 210 n.d. 220 Serum LDH (units/ml. normal-up to 225 252 n.d. 250 235

units/ml)

*For normal values see Table I. n.d. - not done

704 ENVENOMING BY c. vipera-CASE REPORTS

axillary lymph node was palpated on the affected side.

Laboratory Examinations: The urine contained traces of acetone on admission which disappeared by the following day. No formed elements were found in the urinary sediment on repeated examin- ations and no proteinuria was detected. Normal urine output was maintained throughout the course. The blood urea was transiently elevated to 8.4 mmol/l with a normal creatinine of 45 pmol/l. Serum glucose, electrolytes, proteins, bilirubin, calcium, phosphorous and uric acid were all normal, as were the levels of aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase. Serum alkaline phosphatase was 94 mu/ml (normal up to 85 mU/ml). - Results of blood ‘counts and coagulation studies are summarized in Table I. WI% differential count and serum complement levels were normal. Repeated ECG tracings were normal.

Several hours after admission, and 11 hours after being bitten, blanching of the affected finger was noted and therefore fasciotomy was performed. The subsequent hospital course was uneventful. Treatment included O-5 ml tetanus toxoid I.M., elevation of affected arm and analgesics. The swelling of the affected limb was maximal two to three days after the bite and thereafter gradually receded. Hypoesthesia developed and persisted at the site of the bite. The only residue that was found in a follow-up after six months, aside from the fasciotomy scars, is a 0.5 x 0.5 cm area of hypoesthesia at the site of the snakebite.

Case 2 S.I., a 13-year-old snake collector was accident-

ally bitten on his right index finger while feeding an adult specimen of Cerastes vipera. on 22 December 1979. On-admission the patient was in a good gener- al condition, blood pressure was 140/90, pulse 75, regular, and the oral temperature was 37.4%. The bitten finger was swollen to the level of the metacarpophalangeal joint. A small haemorrhagic vesicle with two fang marks were noted at site of the bite. The rest of the physical examination was negative.

Laboratory Examinations: The urine was normal. Results of blood counts and coagulation studies are summarized in Table II. Serum electrolytes, urea, glucose, bilirubin, SGOT, SGPT were normal. The lactate dehydrogenase was 252 units/ml (normal up to 225 units/ml).

The hospital course was uneventful. No systemic manifestations were noted. Treatment included elevation of the affected arm, tetanus hyperimmune globulin 250 units I.M. (owing to lack of previous tetanus immunization) tetanus toxoid 0 * 5 ml I.M., and I.V. ampicillin (10 gr/day) and cloxacillin (10 gr/day). Antibiotic treatment was continued orally for a total of eight days. Follow-up examin- ations after three months disclosed no residual im- pairment.

Cerastes vipera, formerly called Aspis vipera, is an ovoviviparous snake that inhabits the sandy dunes of the western Negev, Sinai and North

Fig. 3. Cerasres vipera, an adult specimen that caused the envenoming in case 1.

African deserts. It lives mainly on lizards and its salient physical characteristics are: length about 30 cm including a short tail of about 3 cm, and weight of 50 g (Fig. 3). For detailed description see THEODOR, 1955.

The venom of C. vipera has a total protein con- tent of about 4 gr/dl, and can be fractionated by electrophoresis and immunodiffusion techniques to 13 distinct fractions, of which only three retain lethal properties. The venom of C. vipera is note- worthy in its high phospholipase A activity (Mo- HAMED et al., 1969). In addition, it has significant phospholipase B activity, as well as proteinase and glutamate-pyruvate transaminase activities. It lacks any cholinesterase or amylase activity (MO- HAMED et al., 1974).

The marked phospholipase activity of this venom accounts for many of its biological properties such as haemolysis (both in vitro and in vivo), disruption of white clood cells, and inhibition of oxygen uptake in brain tissue (MOHAMED et al., 1969).

The two cases of envenoming by C. vipera described here have several aspects in common. Both were snake-collectors who were accidentally bitten on the hand while handling the snake. As the natural habitat of this reptile is remote sandy deserts, man will rarely be bitten and we were unable to find a previously documented’ case, although bites by the related species Aspis cerastes and Vipera aspis have been quoted by EFRATI (1979) and KNOEPFFLER (1965).

J. zmhmhxm et al. 705

The clinical course in the two cases was similar, and had a benign andself-limited character. The local signs observed included haemorrhagic bullae with the fang marks (one in the iirst case and two in the second). In the first case, blood oozed from the wound for several hours, marked swelling of the affected fmgers developed, reaching a peak in the third day after envenoming and the local signs necessitated the performance of fasciotomy.

The difference in the severity of the local signs in the two cases can be attributed to the prolonged bite in the first case, which nrobablv resulted in injection of a larger quantity of venom. No clin- ically significant systemic signs were observed.

The laboratory features observed in the two ca es were inconsistent. Abnormalities in the coagulati & studies were observed in both cases. In the first, shortening of the euglobulin lysis time occurred. This finding, combined with the haemorrhagic diathesis, might suggest activation of the fibrinolytic system, The normal values of platelet counts, prothrombin and partial thromboplastin time, thrombin time and fibrin degradation products exclude disseminated intravascular coagulation in this case. In the second case mild prolongation of the prothrombin time occurred. This non-specific abnormality resolved spontaneously after three days.

Signs of haemoconcentration, including haemo- globin concentration, white blood cell count and serum urea levels, were observed in Case 1. These were corrected after rehydration with intravenous fluids.

No sequelae were observed in the second case but in the first, a small area ofhypoesthesia persisted. However, this may result from the fasciotomy performed and not from the bite itself.

From this limited experience we conclude that the clinical course of envenoming by C. vipera is benign and self limited. The treatment is essen- tially supportive and includes elevation of the affected part, tetanus immunization and analgesics. Wound infection should be treated with antibiotics and fasciotomy should be performed if local swelling prevents adequate blood supply to the affected part. Antivenin against C. viperu venom is not currently available. It has been reported that C. cerastes antivenin, as well as Echis carinatus antivenin can

effectively neutralize the action of C. vipera venom (MOHAMED et al.. 1974; SCHWICK & DICKGIESSER

Acknowledgements The authors thank Dr. M. Fainaru and Prof.

R. N. Melmed for review of the manuscript.

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Accepted for publication 26th January, 1981.