Neurotoxic envenoming by South American coral snake (Micrurus lemniscatus helleri): case report from eastern Ecuador and review

Abstract

A man bitten by a large coral snake (Micrurus lemniscatus helleri) in the Amazon basin of Ecuador developed persistent excruciating pain in the bitten arm. On admission to hospital less than 30 min later, he had a polymorphonuclear leucocytosis, thrombocytopenia and mildly prolonged prothrombin time/partial thromboplastin time. Not until 14 h after the bite did he develop the first signs of neurotoxicity. Despite treatment with specific antivenom 50 h after the bite, he required oxygen for respiratory failure 60 h, and 6 h of mechanical ventilation 72 h, after the bite. Over the next 38 h, he required two further intubations and periods of assisted ventilation before being airlifted to a tertiary referral hospital. Complications included bacterial pneumonia, pneumothorax, bronchial obstruction by mucus plugs and mild rhabdomyolysis. He was discharged from hospital 15 days after the bite with persistent limb weakness and urinary incontinence but eventually recovered. The interesting and unusual features of this case (severe local pain, very slow evolution of neurotoxic envenoming, persistent thrombocytopenia and mild coagulopathy) are discussed in the context of what is known of the composition of Micrurus venoms and the small clinical literature on envenoming from their bites.

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Transactions of the Royal Society of Tropical Medicine and Hygiene (2008) 102, 1127—1132
available at www.sciencedirect.com
journal homepage: www.elsevierhealth.com/journals/trst
Neurotoxic envenoming by South American coral
snake (Micrurus lemniscatus helleri): case report
from eastern Ecuador and review
Stephen R. Manocka, German Suareza, David Graham a,
Mar
´
ıa L. Avila-Aguero b, David A. Warrellc,∗
aHospital Vozandes del Oriente, Shell, Pastaza, Ecuador
bHospital Nacional de Ni˜
nos and Minister of Health, San Jos´
e, Costa Rica
cUniversity of Oxford, Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, UK
Received 2 January 2008; received in revised form 27 March 2008; accepted 28 March 2008
Available online 16 May 2008
KEYWORDS
South American coral
snake;
Micrurus lemniscatus
helleri;
Snake bite;
Antivenom;
Anticholinesterase;
Ecuador
Summary A man bitten by a large coral snake (Micrurus lemniscatus helleri) in the Amazon
basin of Ecuador developed persistent excruciating pain in the bitten arm. On admission to
hospital less than 30 min later, he had a polymorphonuclear leucocytosis, thrombocytopenia and
mildly prolonged prothrombin time/partial thromboplastin time. Not until 14 h after the bite did
he develop the first signs of neurotoxicity. Despite treatment with specific antivenom 50 h after
the bite, he required oxygen for respiratory failure 60 h, and 6h of mechanical ventilation 72 h,
after the bite. Over the next 38 h, he required two further intubations and periods of assisted
ventilation before being airlifted to a tertiary referral hospital. Complications included bacterial
pneumonia, pneumothorax, bronchial obstruction by mucus plugs and mild rhabdomyolysis. He
was discharged from hospital 15 days after the bite with persistent limb weakness and urinary
incontinence but eventually recovered. The interesting and unusual features of this case (severe
local pain, very slow evolution of neurotoxic envenoming, persistent thrombocytopenia and mild
coagulopathy) are discussed in the context of what is known of the composition of Micrurus
venoms and the small clinical literature on envenoming from their bites.
© 2008 Royal Society of Tropical Medicine and Hygiene. Published by Elsevier Ltd. All rights
reserved.
∗Corresponding author. Tel.: +44 1865 221332/220968;
fax: +44 1865 220984.
E-mail address: david.warrell@ndm.ox.ac.uk (D.A. Warrell).
1. Introduction
The 70 or more species of coral snakes (genera Leptomi-
crurus,Micrurus and Micruroides) are the sole terrestrial
elapid snakes of the Western Hemisphere. They range in
total length from 40 to 150 cm. Although most coral snakes
are strikingly marked with circumferential bands of red,
0035-9203/$ — see front matter © 2008 Royal Society of Tropical Medicine and Hygiene. Published by Elsevier Ltd. All rights reserved.
doi:10.1016/j.trstmh.2008.03.026

Author's personal copy
1128 S.R. Manock et al.
black, white or yellow they are easily confused with their
many harmless colubrid mimics (Campbell and Lamar, 2004).
Throughout their distribution from the southern United
States south to central Argentina they are responsible for
only a small proportion of snake bites, although the case
fatality, attributable to respiratory paralysis, may be high.
For example, at Hospital Vital Brazil, S˜
ao Paulo, 15 coral
snake bites without any fatalities were admitted between
1902 and 1945; 13 with two fatalities between 1954 and
1965 (Rosenfeld, 1971) and 19 without any fatalities from
1966 to 1979 (Roze, 1996). In the whole of Brazil, only 0.65%
of all snake bites reported from 2001 to 2004 (486 of the
75 312) were attributed to coral snakes, and there were
no fatalities. In the United States and Central America, 3.6
and 2% of snake bites, respectively, were attributed to coral
snakes (Bucaretchi et al., 2006). A variety of local and sys-
temic manifestations of envenoming have been described in
patients bitten by different species of coral snakes (Roze,
1996; Warrell, 2004), but there are few detailed clinical
reports. This is especially true of identified bites by Central
and South American species, such as Micrurus lemniscatus,
which was responsible for the case described here.
2. Case report
A 27-year-old Ecuadorian male biologist employed by a US-
based film company was bitten on the right thumb while
capturing a snake in the eastern jungle of Ecuador near
Shell, Pastaza. He arrived at Hospital Vozandes del Oriente,
a rural mission hospital in Shell, 20 min after being bitten.
The live snake was brought to the hospital. It had alternating
black, red and beige circumferential stripes and was 120 cm
in total length (Figure 1). The patient was extremely anxious
and complained of intense pain and paraesthesiae in the bit-
ten arm. On examination he was a young, well-developed
male who was writhing in pain and sweating profusely. At
the site of the bite there were two small puncture wounds,
approximately 10 mm apart, which were bleeding slightly.
The patient’s vital signs were normal except for tachyp-
noea (temperature 36.8 ◦C, blood pressure 120/78 mmHg,
pulse 70/min, respiratory rate 40/min, oxygen saturation
99% breathing room air). The remainder of the physical
examination was normal except for a small area of non-
erythematous swelling on the upper lip, where he had been
bitten three times by a vampire bat (Desmodus rotundus)on
the previous day. The patient was in the region to make a
documentary about an epidemic of vampire bat rabies in the
Amazon basin (Warner et al., 1999). While handling these
bats for the purpose of filming, he had also been bitten
on the right thumb 2 days previously. Initially, he claimed
to have received pre-exposure vaccination against rabies
(see below) and was given a booster dose of vaccine on the
day before his admission. The admission blood count per-
formed 10 h after the snake bite showed a leucocyte count
of 21 ×109/l with a left shift (4% bands, 93% segmented
cells, 21% lymphocytes, 5% monocytes), haemoglobin of
15.5 g/dl, haematocrit 47% and platelets 86 ×109/l. The
prothrombin time (PT) was 17 (normal range 10—14) s and
partial thromboplastin time (PTT) was 46 (normal range
30—40) s. Plasma sodium concentration was 143 mmol/l,
Figure 1 South American coral snake (Micrurus lemniscatus helleri), 120 cm in total length, responsible for the bite.

Author's personal copy
Neurotoxic envenoming by South American coral snake 1129
Figure 2 The patient 14 h after the bite, showing bilateral
ptosis, facial paralysis, dilated pupils and drooling of saliva.
The patient gave full informed consent for this photograph to
be published exactly as it is, without masking his eyes.
potassium 3.9 mmol/l, calcium 1.9 mmol/l (7.5 mg/dl), ala-
nine aminotransferase 43 U/l, total creatine kinase 256 U/l
and creatinine 79.6 ␮mol/l (0.9mg/dl). Urinalysis was unre-
markable apart from 1+ ketones and 5—10 leucocytes/high
power field.
At this stage, the medical personnel were uncertain
about the identity of the snake and whether the patient was
envenomed. He was admitted to the hospital, but despite
i.v. diazepam 20 mg, ketorolac 60 mg and morphine 3 mg,
his anxiety and pain persisted. Two additional doses of mor-
phine and midazolam were required during the next 7 h, but
by 9 h after the bite the patient was free of pain and anxiety
and had no abnormal neurological signs. He asked to be dis-
charged from hospital but was persuaded to stay. Fourteen
hours after the bite he was found to have bilateral pto-
sis, facial paralysis, horizontal nystagmus, decreased visual
acuity, dysarthria and dysphagia and was drooling saliva
(Figure 2). His pupils were equally dilated to 3—4 mm with
decreased reactivity to light and accommodation. There was
no respiratory distress. His blood clotted within 20 min when
left in a glass tube, making it unlikely that he was severely
envenomed by a pit viper or colubrid snake (Sano-Martins et
al., 1994).
Expert consultation via e-mail confirmed that the snake
involved was Micrurus lemniscatus helleri and so, in
view of unambiguous signs of neurotoxicity, a search was
instigated to obtain an appropriate antivenom. Meanwhile,
i.v. atropine 2 mg and neostigmine 2.5 mg produced no
detectable improvement. The patient’s condition remained
unchanged until 40 h after the bite, when he developed
urinary incontinence. At this time the haematocrit was 46%,
the platelet count was 58 ×109/l and the PT and PTT had
almost returned to normal at 16 and 40 s, respectively. Fifty
hours after the bite, 10 vials of anti-coral antivenom (Costa
Rican Instituto Clodomiro Picado ‘panamerican suero: anti-
coral polyvalente’) were finally obtained and administered
intravenously over 2 h without any reaction. The patient
remained fully alert and had no respiratory difficulty.
At 60 h, the patient began to show progressive weak-
ness of all four limbs and became mildly hypoxic. He was
given oxygen by nasal cannula. A chest radiograph revealed
a small right middle lobe infiltrate, attributed to aspiration,
and a course of i.v. ceftriaxone was begun. A sputum cul-
ture eventually grew fully sensitive Staphylococcus aureus
of uncertain significance. Haematocrit was 52% and platelet
count 90 ×109/l. PT and PTT were within normal limits,
as were the plasma sodium, potassium and creatinine and
serum glutamic oxaloacetic transaminase concentrations.
However, creatine kinase had risen to 749 U/l which, in the
absence of any i.m. injections suggested mild rhabdomy-
olysis. It now emerged that the patient had not received
pre-exposure rabies vaccination. Full post-exposure prophy-
laxis was therefore completed with human rabies immune
globulin and rabies vaccine.
At 72 h, the patient was intubated and mechanically
ventilated because he was requiring more oxygen to main-
tain arterial saturation, had lost the gag reflex and was
exhausted. Six hours later he extubated himself, and was
stable on oxygen 3 l/min by mask for another 7 h. He was now
able to open his eyes to about 70% of normal, could swallow
saliva and make guttural sounds. However, at 85 h sud-
den respiratory distress demanded immediate re-intubation
and resumption of mechanical ventilation. A large left
pneumothorax was confirmed by radiography but the lung
re-expanded after insertion of a chest tube. At 107 h after
the bite the patient was extubated and given supplemen-
tal oxygen by mask. He was fully alert, could open his eyes
completely, was able to speak and swallow and had a gag
reflex. There was increasing strength in his arms, although
his legs remained weak.
At 110 h after the bite, the patient decompensated yet
again. He was re-intubated for a third time and, after the
chest tube had been replaced and pneumothorax excluded
by radiography, he was flown to the capital city in an air-
craft with a pressurized cabin. At Hospital Metropolitano
in Quito, an emergency bronchoscopy was performed to
remove mucus plugs. Two days later he was finally extu-
bated, but weakness in his limbs and urinary incontinence
persisted. He was discharged from hospital 15 days after
the snake bite and went on to make a full and sustained
recovery.
3. Discussion
The South American coral snake M.lemniscatus is widely
distributed in Bolivia, Peru, Ecuador, Colombia, Venezuela,
Trinidad, Guyana, Suriname, French Guinea, Brazil and

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1130 S.R. Manock et al.
perhaps Paraguay. The subspecies M.l.helleri, which was
responsible for biting our patient, occurs on the Amazonian
slopes and Orinocoan watershed of Colombia, south through
eastern Ecuador, northern Bolivia, southern Venezuela and
northwestern Brazil (Campbell and Lamar, 2004).
In the laboratory, M.lemniscatus venom showed post-
synaptic neurotoxic (Jorge da Silva J´
unior and Bucaretchi,
2003), myotoxic (Guti´
errez et al., 1983, 1992), haemor-
rhagic (Barros et al., 1994), oedema-forming and haemolytic
activities (Cecchini et al., 2005).
Literature on envenoming by M.lemniscatus is limited to
a few case reports (Warrell, 2004). In Trinidad, two men bit-
ten on the lip and tongue by a 137 cm-long M.l.diutius died
7 and 8 h later. Two non-fatal cases of M.lemniscatus bites
were admitted to Hospital Vital Brazil, S˜
ao Paulo between
1954 and 1965 (Rosenfeld, 1971). In Pinheiro, Maranh˜
ao,
Brazil, a patient bitten by M.l.lemniscatus developed paral-
ysis, visual disturbances and internal haemorrhage and died
17 h later (Silva-J´
unior, 1956). In Corumbaibo, Goi´
as, Brazil,
a 61-year-old man bitten by M.l.carvalhoi experienced
severe local pain but did not develop systemic envenoming
(Nishioka et al., 1993). In Sert˜
aozinho, northern S˜
ao Paulo
State, Brazil, a child who put one end of a garden hose in
her mouth was fatally envenomed by a small specimen of
M.l.carvalhoi that was hiding there (Laure et al., 2005).
One of a series of eight cases of Micrurus bites in Campinas,
S˜
ao Paulo State, Brazil was proven to be due to M.l.carval-
hoi, but the patient developed no envenoming (Bucaretchi
et al., 2006). In Amazonian Peru, a 21-year-old man bitten
by an adult M.l.helleri developed ptosis and difficulty in
walking 48 h later. His symptoms persisted for several weeks.
The unusual opportunity to observe and treat a patient
severely envenomed by a South American coral snake in a
well-equipped hospital in rural Ecuador has yielded some
unexpected and interesting findings. First aid for snake-
bite victims is a controversial subject (Gold et al., 2002;
Warrell, 2002), but there is some evidence to support the
use of pressure-immobilization in people bitten by coral
snakes, to delay the development of respiratory paraly-
sis (German et al., 2005). The complete lack of any local
swelling or other changes at the site of the bite is not
remarkable for a coral snake bite. Micrurus venoms differ
in their oedema-forming effects, with the Central American
M.nigrocinctus having the greatest effect clinically and
experimentally (Cecchini et al., 2005; Roze, 1996). Our
patient presented with such severe pain and paraesthesiae
in the bitten limb that, despite repeated doses of morphine
and tranquilizers, he was not relieved of his symptoms until
9 h after the bite. This is reminiscent of the 61-year-old man
reported by Nishioka et al. (1993), who, after a bite by M.l.
carvalhoi, experienced intense bursts of pain up the bitten
arm every few minutes, which persisted for 7 h despite com-
mon analgesics, repeated i.v. meperidine, i.m. diclofenac,
lignocaine local block and oral diazepam. Immediate local
pain and paraesthesiae radiating up the bitten limb have
been mentioned in other accounts of coral snake enven-
oming (Morgan et al., 2007; Rosenfeld, 1971; Roze, 1996).
The dermatomal distribution of these symptoms suggests a
direct action of a venom component on the pain-conducting
C fibres.
On admission to hospital less than 30 min after the
bite, our patient had no clinical evidence of systemic
envenoming, but his blood count showed a marked leuco-
cytosis with left shift, suggesting an early inflammatory
response, thrombocytopenia and mild coagulopathy but
no evidence of abnormal bleeding. Platelet-agglutinating
C-type lectins have been found in venoms of several species
of Asian and Australian elapid snakes (Du et al., 2006),
but Micrurus venoms have not been investigated. The
coagulopathy might be attributable to phospholipase A2
(Barros et al., 1994).
According to Rosenfeld (1971): ‘‘Fatal cases [of coral
snake bite] run their course in less than 6 hours’’, and yet
our patient exhibited no neurotoxic signs until 14 h after
the bite. Respiratory muscle paralysis progressed so slowly
that he did not need oxygen until 60 h, and intubation and
mechanical ventilation until 72 h, after the bite. In one of a
series of 39 cases of M.fulvius bites in Florida, neurotoxic
symptoms were delayed for 13 h but then evolved precipi-
tously, resulting in bulbar and respiratory paralysis (Kitchens
and Van Mierop, 1987). Our patient’s recovery was also slow.
By the time he left the hospital 15 days after the bite, he
was still weak and had urinary incontinence, which may have
been the result of neuromuscular blockade of either somatic
or autonomic innervation of the bladder and sphincter. Other
features of autonomic nervous system activity were his pro-
fuse sweating on admission and later drooling of saliva,
both described in other cases of coral snake envenoming
(Warrell, 2004). However, paralysis of bulbar muscles may
have contributed to the impression of increased salivation.
Delays of 3—6 weeks in recovery from paraesthesiae and
weakness have been mentioned in other reports (Kitchens
and Van Mierop, 1987). Because of the well-documented
delay in appearance of neurotoxic signs following coral
snake bites, patients with proof or suspicion of such
accidents must be carefully observed in hospital for at
least 24 h.
There was no detectable response in our patient’s neu-
rotoxic signs to treatment with either anticholinesterase
or specific antivenom. Anticholinesterase is reported to
have ameliorated paralysis in cases of M.frontalis enven-
oming in Brazil and since the venom of M.lemniscatus
is similar in containing only post-synaptic neurotoxins, it
seemed reasonable to try this treatment (Coelho et al.,
1992;Jorge da Silva J´
unior and Bucaretchi, 2003;Vital Brazil
and Vieira, 1996). A generous dose of Costa Rican Instituto
Clodomiro Picado ‘panamerican suero: anticoral polyva-
lente’ was administered 50 h after the bite. This antivenom
has demonstrated pre-clinical efficacy against venoms of
M.lemniscatus as well as eight other species of coral
snakes (M.fulvius,M.alleni,M.carinicaudus dumerilii,
M.corallinus,M.frontalis,M.mipartitus,M.nigrocinctus
and M.spixii)(Bola˜
nos et al., 1978). Early administration of
antivenom is recommended to allow neutralisation of neuro-
toxins before they have become bound, perhaps irreversibly
in the case of pre-synaptic toxins, to their receptor targets
at neuromuscular junctions. This was the basis of the recom-
mendation in the United States that coral snake antivenom
be given immediately in any case of definite coral snake bite,
even before any signs of envenoming have appeared.
Our patient showed a modest increase in serum creatine
kinase activity, from 256 to 749 U/l, during the first 3
days after the bite. Generalised myalgia with evidence
of gross rhabdomyolysis (serum creatine kinase levels

Author's personal copy
Neurotoxic envenoming by South American coral snake 1131
of up to 18 000 U/l) have been described after human
envenoming by M.fulvius (Kitchens and Van Mierop, 1987)
and also in a patient bitten by M.laticollaris (Pettigrew and
Glass, 1985), as well as in mice injected with venoms of
M.nigrocinctus nigrocinctus,M.n.mosquitensis,M.alleni,
M.frontalis,M.carinicauda and M.surinamensis (Guti´
errez
et al., 1983). Haemolysis has been reported in cases of
envenoming by M.corallinus and M.laticollaris (Pettigrew
and Glass, 1985; Warrell, 2004), but in our patient there
was no fall in haemoglobin concentration.
This case exemplifies the difficulties involved in caring for
snake-bite patients in remote areas of the developing world.
The hospital staff in Shell is experienced in the management
of pit viper bites, mainly by Bothrops atrox and B.bilineatus
(Smalligan et al., 2004), but had no experience with coral
snake bites, this being the first such case ever reported in
the province of Pastaza. Uncertain whether or not they were
dealing with a coral snake bite, and despite the absence of
any specific neurological findings, they wisely admitted the
patient for observation and symptomatic treatment. Four-
teen hours later, typical symptoms of neurotoxic Micrurus
envenoming had developed and the snake was identified
by e-mailing digital photographs to international experts.
There was a disconcerting 2 day delay before coral snake
antivenom could be imported from Costa Rica. Because of
the risk of rapid deterioration in respiratory status, and
mechanical ventilation was available at Hospital Vozandes
del Oriente, the staff and patient’s family decided against
an immediate transfer to a tertiary care facility. However,
the intensive management of this patient was very taxing
on the staff of this small hospital. Finally, after respiratory
distress had occurred three times in 38 h, a costly intensive
care medi-vac flight was arranged. This would have been
unaffordable for the vast majority of patients in this region
of rural Ecuador.
In the case we have described, as in 25% of snake bites
in the United States, a young man was struck while handling
a snake injudiciously (Kitchens and Van Mierop, 1987). Coral
snakes are often mistaken for their colubrid mimics. This
accident could have been prevented if the snake had been
recognised as potentially dangerous and had been left alone
or handled using appropriate care and equipment. It is also
incomprehensible that those involved in filmed contact with
vampire bats during a rabies epidemic lacked pre-exposure
rabies vaccination.
Authors’ contributions: SRM, GS, DG, MLA-A and DAW all
contributed to the patient’s clinical care and assessment,
either on site at Shell Hospital or by telephone and/or
e-mail; SRM and DAW drafted the manuscript, which was
reviewed and augmented by all the authors. All authors
read and approved the final manuscript. DAW and SRM are
guarantors of the paper.
Acknowledgements: SRM wishes to thank his wife for her
patience and forbearance during the most taxing 5 days of
their married life.
Funding: None.
Conflicts of interest: None declared.
Ethical approval: Not required; the assessment and treat-
ment of the patient was part of the standard clinical
procedures at Hospital Vozandes del Oriente, Shell, Pastaza,
Ecuador.
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