Vp envenomation in cats clinical signs outcomes

Retrospective Study Journal of Veterinary Emergency and Critical Care 24(4) 2014, pp 437–443
doi: 10.1111/vec.12207
A retrospective evaluation of Vipera
palaestinae envenomation in 18 cats:
(2006–2011)
Itzik Lenchner, DVM; Itamar Aroch, DVM, DECVIM; Gilad Segev, DVM, DECVIM;
Efrat Kelmer, DVM, DACVECC and Yaron Bruchim, DVM, DACVECC
Abstract
Objective – To describe the clinical signs, clinicopathologic abnormalities, treatment, complications and out-
come, and to identify risk factors for death in cats envenomed by Vipera palaestinae (Vp).
Design – Retrospective study.
Setting – Veterinary teaching hospital.
Animals – Eighteen client-owned cats envenomed by Vp.
Interventions – None.
Measurements and Main Results – All envenomations occurred during the hot season (May to October),
mostly in young (<4 years, 66%) domestic shorthair, outdoor or indoor-outdoor cats. Clinical signs included
tachypnea (>40/min, 100%), lameness (78%), depression (71%), fang penetration marks (55%), hypothermia
(<37.5°C, 43%), hematoma at the envenomation site (27%), tachycardia (>220/min, 20%), and bradycardia
(<140/min, 20%). Hematologic abnormalities included thrombocytopenia (89%), hemoconcentration (33%),
and leukocytosis (33%). The activated partial thromboplastin and prothrombin times were prolonged in 100%
and in 93% of the cats at presentation to a veterinarian, and remained prolonged 12–24 hours later in 92% and in
77% of the cats, respectively. Cats displayed increased serum creatine kinase activity (100%) and hyperglycemia
(89%). Four cats (22%) did not survive. Median hospitalization time was 2 days. Variables associated with death
included lower body weight (P = 0.01), lower initial rectal temperature (P = 0.02), lower initial hematocrit (P <
0.001) and 12–24 hours later (P = 0.001), and lower total plasma protein at 12–24 hours following presentation
(P = 0.001). There was no association between death and administration of antivenom (10 mL/cat), fresh frozen
plasma, or corticosteroids.
Conclusions – Cats are at least as susceptible as dogs to Vp envenomation. Lower body weight, rectal temper-
ature, and hematocrit at presentation were associated with nonsurvival.
(J Vet Emerg Crit Care 2014; 24(4): 437–443) doi: 10.1111/vec.12207
Keywords: antivenom, coagulation, feline, snakebite, viper
Introduction
The Viperidae are a family of venomous snakes with
worldwide distribution. This family is distinguished by
their long, hinged, deep-penetrating fangs, which inject
venom into their prey.1
Viperidae are divided to 4 sub-
families, including adders (viperinae, eg, “true vipers”)
From the Koret School of Veterinary Medicine, Veterinary Teaching Hospital,
The Hebrew University of Jerusalem, Rehovot, Israel.
The authors declare no conflict of interests.
Address correspondence and reprint requests to
Dr. Itzik Lenchner, Koret School of Veterinary Medicine, Veterinary Teaching
Hospital, The Hebrew University of Jerusalem, P.O. Box 12, Rehovot 76100,
Israel. Email: itziklench@walla.com
Submitted September 29, 2012; Accepted May 25, 2014.
Abbreviations
aPTT activated partial thromboplastin time
CK creatine kinase activity
DIC disseminated intravascular coagulation
FFP fresh frozen plasma
PLA2 phospholipases A2
PT prothrombin time
VICC venom-induced consumptive coagulopathy
Vp Vipera palaestinae
and pit-vipers (crotalinae, eg, rattlesnakes).1
Although
all viperidae are venomous, their venom composition is
species-specific.2
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Veterinary Emergency and Critical Care Society 2014 437

I. Lenchner et al.
Viper venom may consist of a mixture of compounds,
including hemorrhagins, thrombins, and cytolysins. Cy-
tolysins are responsible for most clinical signs, which are
generally restricted to the area surrounding the bite, and
include swelling, pain, hemorrhage, acute lameness in
cases of limb envenomations, local lymphadenomegaly,
and rarely, necrosis.3–6
Systemic manifestations of viper
envenomation may include tachypnea, tachycardia,
nausea, and lethargy. Severe complications occur less
frequently, and can include laryngeal edema with
respiratory distress, cardiac arrhythmias, disseminated
intravascular coagulation (DIC), acute kidney injury,
and death.3,5,6
Vipera palaestinae (Vp) is the most common venomous
snake in Israel, and is also present in Jordan, Lebanon,
and Syria.7
It is the only venomous snake in the popu-
lated areas of Central and Northern Israel, and is respon-
sible for most envenomations in people and animals in
the country.4,6,8–15
Its venom contains approximately 30
components, 16 of which have been identified, includ-
ing proteases, hemorrhagins (metalloproteases), amino
acid esterases, phospholipases A2 (PLA2) and B, and
neurotoxins.16–19
The local and systemic signs of enveno-
mation in dogs have been extensively described,4,6,8,14,20
and are similar to those of other Viperidae.5
Clinical
signs of Vp envenomation have been described in 3
cats, and included tachypnea, tachycardia, mental de-
pression, and hemostatic abnormalities.12
Cats have been hypothesized to be more resistant to
snakebites compared to other animal species.21
Survival
rates of cats envenomed by snakes of the Elapidae family
(elapids; eg, tiger and coral snakes) were more favorable
compared to those of dogs, especially when antivenom
was administered.22–24
A more favorable outcome in cats
has been hypothesized in pit-viper envenomation but
has not been objectively studied.25,26
The theory that cats
may have a natural resistance to snakebites is based, at
least partly, on the lethal dose of venom per kilogram
of body mass.21
Others have suggested that snakes are
unable to inject a lethal dose of venom because of dif-
ficulty with restraining the cat and discharging suffi-
cient venom.22
Cats are thought to be bitten less fre-
quently than other domestic animals, especially dogs, be-
cause they are more alert, suspicious, and tend to avoid
snakes.25
It is also possible that some envenomations in
cats are not reported, because cats sometimes hide once
envenomed. The proposed resistance of cats to snakebite
is supported only by brief reports of 2 and 3 cats that
have recovered uneventfully from rattlesnake and Vp
envenomation, respectively.12,26
Feline serum failed to
neutralize Vp venom in vitro, as opposed to hamster
(Mesocricetus auratus) and hedgehog (Erinaceus europeus)
sera,27
and the mortality rates of cats and dogs enven-
omed by Vipera berus, a close relative of Vp, and by neu-
rotoxic rattlesnake venom did not significantly differ.28,29
This study describes the clinical, clinicopathologic signs,
treatment, complications, and outcome in 18 cats enven-
omed by Vp, and analyzes the risk factors for death in
this group.
Materials and Methods
The medical records of cats presented to the Univer-
sity Veterinary Teaching Hospital (UVTH) between 2006
and 2011 and diagnosed with Vp envenomation were
retrospectively reviewed. A definitive diagnosis of the
snakebite was made when the bite was observed by the
owner, and the snake was identified as Vp, or when typ-
ical Vp penetrating fang marks were observed at the en-
venomation site. In other cats, Vp envenomation was
diagnosed based on the history (ie, acute onset of signs
in an outdoor cat), the geographic location (ie, central
Israel, where Vp is the only venomous snake present),
compatible typical clinical signs (ie, acute painful ede-
matous soft tissue swelling), and exclusion of other dif-
ferential diagnoses (eg, trauma, abscess, insect bite, or
tumor).
Data obtained from the medical records included the
signalment, date, history, physical examination, and lab-
oratory findings, disease progression, treatment, hospi-
talization time period, and outcome. Cats discharged
alive were considered survivors, and those that died or
were euthanized during hospitalization were defined as
nonsurvivors.
Statistical Analysis
Continuous measurements are presented as median and
range, because most were not normally distributed based
on the Shapiro-Wilk test. Continuous measurements
were compared between survivors and nonsurvivors us-
ing the Mann-Whitney U-test. Categorical variables were
compared between 2 groups using Fisher’s exact test.
All analyses were performed using a statistical software
package.a
All tests were two-tailed and a P 0.05 was
considered statistically significant.
Results
Twenty-six cats were treated for Vp envenomation be-
tween 2006 and 2011. Five cases were excluded because
other differential diagnoses could not completely be
ruled out, and 3 were excluded due to missing data in
the medical record. The remaining 18 cats were included
in this study. All were domestic shorthair, outdoor or
indoor-outdoor cats, including 9 males (one neutered)
and 9 females (all neutered), with a median age of 24
438 C
Veterinary Emergency and Critical Care Society 2014, doi: 10.1111/vec.12207

Vipera palaestinae envenomation in cats
months (range 6–96). Most (12/18, 66%) were under 4
years of age. Their median body weight (recorded in
13 cats) was 5.0 kg (range 1.9–6.7), and was significantly
(P = 0.001) lower in nonsurvivors compared to survivors
(median 3.5 kg, range 1.8–4.5 versus median 5.5 kg, range
5.0–6.6, respectively). All envenomations occurred dur-
ing the hot, dry season (May to October). The median
lag time from the time the clinical signs were first ob-
served by the owners to presentation was 4 hours (range
0.5–24.0). There was no statistical difference in lag time
(P = 0.09) between nonsurvivors (median 14.3 hours;
range 3.0–24.0) and survivors (median 5.1 hours, range
0.5–12.0).
Bites were localized to the forelimbs (11 cats, 61%),
hind limbs (3 cats, 17%), or in the head and neck area
(4 cats, 22%). Eight cats were anxious or aggressive
at presentation, and required sedation to perform the
physical examination. For these cats, the heart and res-
piratory rates, although recorded, were excluded from
the analysis. Vital sign abnormalities included tachyp-
nea (40/min; 10/10 cats, 100%), hypothermia (37.5°C
[99.5°F]; 7/16, 43%), tachycardia (220/min, 2/10, 20%),
bradycardia (140/min, 2/10, 20%), and hyperther-
mia (39.5°C [103.1°F]; 1/16, 6%). Nonsurvivors had a
significantly (P = 0.021) lower median rectal temper-
ature at presentation compared to survivors (35.9°C;
range 33.7–37.6 versus 38.0°C; range 35.5–40.9, respec-
tively). Other clinical signs included lameness (14/18,
78%), present in 14/14 cats in which the envenoma-
tion had occurred on a limb, hematoma at the en-
venomation site (5/18, 27%), and mental status ab-
normalities (depression, 12/18, 66%; stupor, 1/18, 5%).
Viper fang penetration marks were identified in 10/18
cats (55%).
The most common hematologic abnormalities at pre-
sentation included thrombocytopenia (platelet count
250 × 109
/L [250 × 103
/␮L], 14/18, 77%), hemoconcen-
tration (6/18, 33%), and leukocytosis (WBC count 14
× 109
/L [14 × 103
/␮L], 6/18, 33%) (Table 1). On pre-
sentation, nonsurvivors had a significantly (P 0.001)
lower median RBC count, hematocrit, and hemoglobin
concentration compared to survivors (Table 1). Median
hematocrit was also significantly (P = 0.01) lower in non-
survivors compared to survivors at 12–24 hours follow-
ing presentation (21.7%, range 10–29 versus 32.8%, range
21–42, respectively). Platelet number at presentation was
not lower in nonsurvivors compared to survivors (P =
0.07; Table 1). Thrombocytopenia was present in 4/4 cats
in which a CBC was repeated at 24 hours after presen-
tation. Median PCV at 24 hours from presentation (mea-
sured in 17/18 cats) decreased from 40% at presentation,
to 30%. The activated partial thromboplastin and pro-
thrombin times (aPTT and PT, respectively) were pro-
longed in 16/16 and 15/16 of the cats at presentation,
and remained prolonged 12–24 hours later in 12/13 and
9/13 cats, respectively (Table 1).
The most common serum biochemistry abnormalities
included increased creatine kinase (CK) activity (6/6,
100%), hyperglycemia (8/9, 89%), increased alkaline-
phosphatase activity (4/6, 66%), hypertriglyceridemia
(4/6, 66%), and hypocholesterolemia (3/6, 50%). Me-
dian total plasma protein concentration measured by re-
fractometry, at presentation (n = 17) was 61 g/L (6.1
g/dL; range 45–80 g/L [4.5–8.0 g/dL]) and decreased
to 52 g/L (5.2 g/dL; range 32–78 g/L [3.2–7.8 g/dL])
12–24 hours later. It was not lower in nonsurvivors com-
pared to survivors at presentation (P = 0.07), but was
significantly (P = 0.01) lower in the nonsurvivors at 12–
24 hours after presentation (median 39 g/L [3.9 g/dL],
range 32–50 g/L [3.2–5.0 g/dL] versus 58 g/L [5.8 g/dL],
range 40–78 g/L [4.0–7.8 g/dL], respectively).
All cats received intravenous isotonic crystalloids,
diphenhydramineb
(2 mg/kg SC or IM, q 8 h), ampici-
llinc
(25 mg/kg IV, q8 h), and analgesics such as but-
orphanold
(0.2–0.4 mg/kg IV or SC, q 4–6 h). Hetastarche
was administered to 5 cats (5–10 mL/kg bolus, or as con-
stant rate infusion IV at 1 mL/kg/h). Glucocorticoids
were administered to 5 cats (dose and route unknown).
Vp-specific antivenomf
(9.5 mL in 100 mL of 0.9% saline,
administered IV over 1 hour) was administered to 4 cats
(1 unit to 3 cats, and 2 units to 1 cat) following a nega-
tive response to a hypersensitivity skin test. Fresh frozen
plasma (FFP, 20–30 mL/unit) was administered IV to 10
cats (8 cats, 1 unit; 2 cats, 2 units). No adverse reactions
to the antivenom or FFP were recorded.
The median hospitalization time period was 2 days
(range 1–6), with no significant difference between sur-
vivors and nonsurvivors. The mortality rate was 22%
(4/18 cats). Three cats died, and 1 was euthanized due
to unresponsive distributive shock and severe acute kid-
ney injury. There was no association between death and
administration of antivenom, FFP, or steroids.
Discussion
This is the first large-scale study of Vp envenomation
in cats, and the largest one of viper envenomation in
this species. All envenomations in this study occurred
during the hot, dry season, paralleling the viper’s peak
seasonal activity,30
as also reported in dogs.4,6
However,
this also parallels the increased outdoor activity of cats
in the country. Most envenomed cats were young, with
no gender predilection.4,6,20,23
In contrast to dogs, where
most Vp envenomations are localized to the head and
neck area,4,6
cats were more frequently envenomed in
the forelimbs. These differences can be attributed to dif-
ferences in preying and fighting behavior between cats
and dogs.
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Veterinary Emergency and Critical Care Society 2014, doi: 10.1111/vec.12207 439

I. Lenchner et al.
Table
1:
Selected
hematologic
test
results
at
presentation
and
after
12–24
hours
in
18
cats
envenomed
by
Vipera
palaestinae
All
cats
Survivors
Non
survivors
(n
=
18)
(n
=
14)
(n
=
4)
Analyte
Median
Median
Median
Reference
P
(units)
n
∗
(range)
%
ࣘRI
†
%
RI
†
n
∗
(range)
%
ࣘRI
†
%RI
†
n
∗
(range)
%
ࣘRI
†
%
RI
†
interval
value
‡
Leukocytes
(×10
9
/L
[×10
3
/␮L])
18
11.65
(4.89–38.7)
5.0
33.3
14
11.6
(6.9–22.1)
0
35.7
4
11.2
(4.8–38.7)
25.0
25.0
5.0–14.0
0.48
RBC
(×10
12
/L
[×10
6
/␮L])
18
10.45
(5.34–12.7)
0
72.2
14
11.2
(8.84–12.7)
0
92.8
4
6.4
(5.34–9.42)
0
25.0
5.0–9.0
0.001
Hemoglobin
(g/L
[g/dL])
18
133
(68–161)
[13.3
(6.8–16.1)]
33.3
0
14
145
(117–161)
[14.5
(11.7–16.1)]
14.2
0
4
78
(68–112)
[7.8
(6.8–11.2)]
100
0
120–180
[12–18]
0.001
Hematocrit
(L/L
[%])
18
39.7
(23.6–52.7)
[0.39
(0.23–0.52)]
5.5
33.3
14
44.1
(36.6–52.7)
[0.44
(0.36–0.52)]
0
42.8
4
28.7
(23.6–39.5)
[0.28
(0.23–0.39)]
25.0
0
24-45[0.24–0.45]
0.001
MCHC
¶
(g/L
[g/dL])
18
319
(283–406)
[31.9
(28.3–40.6)]
22.2
5.5
14
319
(294–406)
[31.9
(29.4–40.6)]
14.2
7.1
4
297
(283–320)
[29.7
(28.3–32)]
50.0
0
300–380
[30–38]
0.09
Platelets
(×10
9
/L
[×10
3
/␮L])
18
147.5
(30–356)
77.7
0
14
226.5
(64–356)
71.4
0
4
97.5
(30–126)
100
0
250–700
0.07
TPP-0
a7˜
(g/L
[g/dL])
17
61
(45–80)
[6.1
(4.5–8.0)]
58.8
0
13
62
(48–80)
[6.2
(4.8–8.0)]
61.5
0
4
59
(45–60)
[5.9
(4.5–6.0)]
100
0
66–84
[6.6–8.4]
0.07
TPP-12
∗∗
(g/L
[g/dL])
17
52
(32–78)
[5.2
(3.2–7.8)]
94.1
0
13
58
(40–78)
[5.8
(4.0–7.8)]
93.2
0
4
39
(32–50)
[3.9
(3.2–5.0)]
100
0
66–84
[6.6–8.4]
0.01
PT-0
††
(sec)
16
14.6
(10.5-
100)
0
93.3
13
14.5
(10.5–100)
0
92.3
3
15.1
(12.8–20.2)
0
100
8.7–10.5
0.73
aPTT-0
‡‡
(sec)
16
23.5
(16.8–100)
0
100
13
21.2
(16.8–100)
0
100
3
23.9
(23.1–32.8)
0
100
12.3–16.7
0.45
PT-12
¶¶
(sec)
13
13
(7.6–17.7)
7.6
69.2
12
13.3
(10–17.7)
0
0.75
1
7.6
100
0
8.7–10.5
0.059
aPTT-12
§§
(sec)
13
22.6
(15.5–56)
0
92.3
12
21.8
(15.5–56)
0
91.6
1
42.8
0
100
12.3–16.7
0.14
TPP,
total
plasma
protein
concentration.
∗
Number
of
cats
in
which
the
result
was
recorded.
†
Reference
interval.
‡
P
value
of
comparison
of
medians
of
survivors
and
nonsurvivors.
¶
Mean
corpuscular
hemoglobin
concentration.
§
Total
plasma
protein
at
presentation.
∗∗
Total
plasma
protein
at
12–24
hours
following
presentation.
††
Prothrombin
time
at
presentation.
‡‡
Activated
partial
thromboplastin
time
at
presentation.
¶¶
Prothrombin
time
at
12–24
hours
after
presentation.
§§
Activated
partial
thromboplastin
time
at
12–24
hours
after
presentation.
440 C

The tachypnea and tachycardia observed at presen-
tation probably resulted, at least partially, from pain
and excitement; however, direct systemic venom effects
or compensatory shock might have had a role in their
occurrence. Depression, bradycardia, and hypothermia,
observed at presentation in some cats, were indica-
tive of decompensatory shock.31
Hemodynamic shock
in the envenomed cats may have resulted from hyper-
sensitivity to the venom (ie, anaphylaxis),10
or from
vasodilatation and peripheral blood pooling induced
by the neurotoxins in Vp venom.5,32–34
Venom hemor-
rhagins and phospholipases also contribute to progres-
sion of hypovolemia and shock through local bleeding
and fluid extravasation into the inflamed envenoma-
tion site.5,35
Depression (or coma) was either a direct
manifestation of the venom’s neurotoxic effects or a re-
sult of decreased cerebral perfusion, due to circulatory
shock.28,33,34
Thrombocytopenia was the most common hemato-
logic abnormality at presentation, as previously reported
in dogs and cats envenomed by Vp4,6,12,20,36
and other
closely related vipers.3,29,37
Thrombocytopenia at pre-
sentation has been previously reported as a prognos-
tic factor in a several studies,6,8
but the platelet count
was not significantly different in nonsurvivors in this
study. The vascular injury at the envenomation site
leads to platelet consumption, which may worsen lo-
cal bleeding. Thrombocytopenia may also be induced
by venom factors that promote platelet aggregation (eg,
thromboxane A2 production from increased PLA2 ac-
tivity), and may worsen in the presence of a venom-
induced consumptive coagulopathy (VICC) or more
rarely by DIC.36,38,39
VICC is characterized by multiple
hemostatic abnormalities, similar to DIC; however, evi-
dence of systemic thrombosis and end organ failure are
absent.36
The PT and aPTT at presentation, and 12–24 h later,
were prolonged in most cats. Because additional coag-
ulation tests (eg, antithrombin activity, fibrinogen con-
centration, and D-dimer concentrations) were not per-
formed, it is impossible to definitely diagnose DIC or
VICC in these cats. Nevertheless, the high occurrence of
thrombocytopenia and prolonged clotting times are in-
dicative for the presence of multiple hemostatic abnor-
malities and deranged hemostasis. Such abnormalities
have been reported in dogs envenomed by Vp, and DIC
is a risk factor for nonsurvival in such dogs.8
Viperid ven-
oms contain components with both procoagulant and
anticoagulant properties, capable of inducing thrombo-
sis, bleeding, and VICC.36,39–42
The most common serum biochemistry abnormal-
ity recorded in this study was increased activity of
the CK, likely resulting from skeletal muscle dam-
age at the envenomation site. However, the possibil-
ity that some of this increased CK activity is due to
myocardial damage, which was previously reported in
animals envenomed by Vp,11,14,43
cannot be ruled out,
because specific markers of myocardial injury (e.g., car-
diac troponins) were not measured. Mild-to-moderate
hyperglycemia, observed in 89% of the cats, was likely
due to catecholamine and glucocorticoid release, part
of the physiologic envenomation-associated anxiety and
stress responses. Hypertriglyceridemia and hypocholes-
terolemia, recorded in 4/6 and 3/6 cats, respectively,
were also observed in 62% and 28% of dogs enven-
omed by Vp, respectively.6
Cholesterol concentration
is inversely correlated with the severity of Vp en-
venomations in people, and hypocholesterolemia was
hypothesized to result from capillary lipoprotein ex-
travasation at the envenomation site, and lipoprotein
transport and metabolism changes induced by venom
PLA2 activity.44
There is no standard treatment protocol for Vp en-
venomation in cats, dogs, or people.9
In this study, 4
cats received Vp-specific antivenom, and 10 cats received
FFP. Neither treatment was associated with an impact
on outcome. Similarly, Vp-specific antivenom treatment
was not associated with the outcome in Vp-envenomed
dogs,4,6
although antivenom is considered beneficial in
pit-viper envenomations of dogs.5
The decision to ad-
minister FFP in 10 cats was based on the coagulation
test results (eg, prolonged PT and aPTT) rather than on
clinical signs of active bleeding. After FFP administra-
tion, however, coagulation times were not normalized,
possibly due to continued consumption. VICC is unre-
sponsive to FFP as long as un-neutralized venom is still
circulating.39
FFP may thus only be indicated in animals
with true signs of DIC (eg active bleeding) rather than
VICC alone.
Although some authors favor the use of glucocorti-
coids for treatment of snakebite,25,26,28,39
others claim that
it is contraindicated, because glucocorticoids may slow
and diminish antivenom activity, and increase the risk
for bacterial infection.45
Glucocorticoid administration
was associated with death in dogs envenomed by Vp,6,20
and is therefore not part of our standard treatment pro-
tocol for such envenomations. Only 5 cats in this study
were treated with glucocorticoids, hence, it is difficult to
draw any conclusion regarding their effect in cats enven-
omed by Vp.
The mortality rate for cats in this study was unexpect-
edly high (22%), and higher than previously reported
studies of Vp envenomations in dogs (3.7–15%) and peo-
ple (0.5–1%) in Israel.4,6,8,9
These data are also incon-
sistent with the suggestion that cats are more resistant
to snakebites compared to other animal species.5,25
In
a recent retrospective study, survival rate was not sig-
nificantly different between dogs and cats envenomed
C

I. Lenchner et al.
by neurotoxic rattlesnake venom. In that study, cats
were hospitalized for a significantly longer period than
dogs.29
There are several possible explanations for the high
mortality rate of the cats described herein. First, in out-
door cats, the onset of the envenomation-related clinical
signs may be missed by owners, resulting in delayed pre-
sentation for care.5
Nonsurviving cats also had a signif-
icantly lower body weight compared with survivors, in
agreement with similar previous findings in dogs.3,5,6,37
Because the volume of venom injected by Vp in a single
envenomation does not correlate with the prey size,46
envenomations might have resulted in a higher venom
volume to body weight ratio, leading to more severe en-
venomation. Lastly, the nature of the interaction between
the cat and viper might have antagonized the snake and
provoked a high volume venom injection.5
Several additional risk factors for death were identi-
fied in this study. The significantly lower rectal tempera-
ture of nonsurvivors at presentation suggests that shock
was present in these cats, in agreement with a previous
study of cats envenomed by elapids.22
Nonsurvivors had
significantly lower RBC count, hemoglobin concentra-
tion, and hematocrit at presentation, compared to sur-
vivors. This finding may have been a result of bleeding,
consistent with a more severe envenomation. Nonsur-
vivors also had a significantly lower PCV at 12 to 24
hours following initial examination. The significant to-
tal plasma protein concentration decrease at the 12 to 24
hour blood samples is consistent with hemorrhage, or
may reflect severe local tissue and vascular damage at
the envenomation site causing plasma protein extrava-
sation.
This study has several limitations. First, the number of
cats included is small, thereby limiting the power of the
statistical analyses, mainly the association of variables
with the outcome. Second, it was retrospective, and some
data were missing in the medical records, further limit-
ing the statistical analyses. Third, in 8/18 cats, the diag-
nosis of the envenomation was made by exclusion, since
the event was not witnessed by the owners, and typical
Vp penetrating fang marks were not detected at presen-
tation. We strongly believe that these cases were true Vp
envenomations, because Vp is the only venomous snake
in the region, the presenting clinical signs differed from
those of insect bites common to the country, and other
differential diagnoses were definitively excluded.
In conclusion, Vp envenomations of cats occurred dur-
ing the hot season, and typically affected young outdoor
domestic shorthair cats, with the bite localized to the
forelimbs. Tachypnea, abnormal heart rate, hypother-
mia, and mental depression were common signs. Non-
survivors had significantly lower body weight, rectal
temperature and hematocrit at presentation compared
to survivors. In both groups, abnormally prolonged PT,
aPTT, and thrombocytopenia were common. The mor-
tality rate was 22%, and was higher compared to that of
dogs envenomed by Vp, bringing into question the previ-
ously suggested resistance of cats to viperid snakebites.
Footnotes
a
SPSS 17.0 for Windows, SPSS Inc, Chicago, IL.
b
Diphenhydramine, Fargon, Hamburg, Germany.
c
Ampicillin, Penibrin, Teva, Tel-Aviv, Israel.
d
Butorphanol, Torbugesic, Fort-Dodge Laboratories, Fort Dodge, IA.
e
Hetastarch, Teva Perenteral Industries Inc, Halden, Norway.
f
Antivenom, V. palaestinae antivenom, Rogof Institute, Petach-Tikv, Israel.
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