Issue 27 _ october 2020

thewildlifejournal.com ISSUE 27 | OCTOBER 2020

VENOMOUS SPECIES

INTO THE

WILD

Want to learn about
venomous species
and what they can
cause ? Flip through
and you will be
amazed with the
contents.

1. BLACK MAMBA

1.1 INTRODUCTION
1.2 VENOM
1.3 FUNCTION OF VENOM
1.4 SIGN & SYMPTOMS
1.5 PATOGENESIS
1.6 TREATMENT

2. BROWN RECLUSE SPIDER

2.1 INTRODUCTION
2.2 VENOM
2.3 FUNCTION OF VENOM
2.4 SIGN & SYMPTOMS
2.5 PATOGENESIS
2.6 TREATMENT

3. POISON DART FROG

2.1 INTRODUCTION
2.2 VENOM
2.3 FUNCTION OF VENOM
2.4 SIGN & SYMPTOMS
2.5 PATOGENESIS
2.6 TREATMENT

Black mamba is one of the most venomous snakes. It is the second longest venomous

snake after king cobra. Black mamba usually inhabits a wide range in Saharan Africa. It

can live up to 11 years and may live longer than that. It is one of the fastest snakes in the

world. Only two drops of it’s venom is enough to kill a person. The mature specimen can

exceed up to 2 metre. Even though its name is black mamba, it is in grey to dark brown

in colour. It eventually fades off as it grows older.

Fun fact: The black

mamba is born with two COMPOSITION OF BLACK MAMBA VENOM
to three drops of venom
per fang. It is a front- The black mambas venom is composed of three
fanged snake, with fangs substances. Those are dendrotoxins, calciseptine,
up to 6.5 mm in length,
located at the front of the and mambalgins. There are approximately 20
upper jaw. An adult of known enzymes found in snake venom, meaning
the species has between that venom is virtually all protein. No snake has
12 and 20 drops per fang. all of these toxins in their venom. They can have
It takes just two drops of from 6 to 12 of these enzymes in their venom. The
venom to kill an adult
human. This means that black mambas venom consists of proteases,
hyaluronidase, phosphatase, phospholipase, and

neurotoxic peptides.

even young black

mambas are extremely

dangerous.

Just two drops of potent

black mamba venom can

kill a human which attacks

both the nervous system

.and the heart The venom

of a black mamba contains

,neurotoxins much as

cobras and coral snakes

.do The venom is described

" - ."as fast acting The

venom of black mambas is

PATHOGENESIS highly neurotoxic and

A black mamba's bite can cause collapse within 45 minutes or contains a combination of
less in humans. Symptoms usually progress to respiratory
failure without adequate antivenom treatment which leads to neurotoxins that induce
cardiovascular collapse and death. There will be typically
extreme pain and mamba inflictions will cause victims to suffer. neuromuscular junction
Its venom is neuro-toxic. Unlike most poisonous snakes where
the venom slowly moves into the bloodstream, allowing a victim postsynaptic blockade and
to get treatment and remove the poison using a tourniquet, the
poison of the black mamba goes straight to the nerves, dendrotoxins that inhibit
targeting the central nervous system and shutting down major
organs. Twenty minutes after you have been bitten, you will -voltage dependent
lose your ability to speak. You are potentially comatose after ,potassium channels
one hour, and the victim dies by six hours without an antidote.
Within six hours, a person will experience pain, paralysis and increasing the release of
then death.
acetylcholine at the

,neuromuscular junction

creating a neuromuscular

-block similar to a depo

dependent potassium

.channel

SIGN & SYMPTOMS

Nausea, vomiting, abdominal pain, diarrhea,
sweating, salivation, goosebumps and red eyes.
The bite of a black mamba can cause collapse in

humans within 45 minutes or less.

First Aid TREATMENT

In the event of a suspected or confirmed
mamba bite:
(1) Carefully separate the snake from the
victim and others. Killing the snake and
bringing it to the hospital is not necessary,
although positive identification is helpful
to the medical staff.
(2) A lymphatic/venous constriction
bandage (pressure/immobilization)
should be applied immediately.
(3) Transport the victim to a medical
facility as quickly as possible. Rest the
bitten extremity at a level at or below the
victim's heart.(
4) Do not remove the constricting band or
crepe bandage until the victim has
reached the hospital and is receiving
antivenom treatment.

Medical Management

(1) Establish the identity of the offending snake. (8) If there are no symptoms of envenomation
(2) Locate fang marks and areas of swelling and during an I-hour observation period, remove crepe
pain. bandage and observe carefully. If any changes
(3) If a crepe bandage and splint have not been occur, assume envenomation. Otherwise, observe
applied, apply immediately. (4) Secure 16-20 vials the patient carefully for at least 24 h.
of SAIMR polyvalent antiserum regardless of the (9) Begin antivenin therapy if mamba
perceived severity of envenomation, age, or body envenomation is diagnosed. Even if the patient was
weight of the victim. bitten several hours before, antivenin can reverse
(5) Admit the patient to an emergency much of the venom's effects. Reconstitute 6 vials of
department or other intensive care setting. If not SAIMR polyvalent antiserum in lactated Ringer's
already instituted, intubation or respiratory solution at room temperature. Vigorously shake
assistance may be necessary. Begin a peripheral the vials to insure maximum dissolution. Transfer
IV infusion of lactated Ringer's solution at a rate the solution to an IV piggyback set up with a
sufficient to maintain a brisk urine output. volumetric regulator.
(6) Draw blood from an uninvolved extremity (10) A precautionary test dose of antivenin may be
and submit it for the tests. Obtain a urine administered to signal the need for anti
specimen for urinalysis. anaphylaxis therapy. One ml of antiserum solution
(7) Observe the patient. Envenomation is diluted in 9 ml of Ringer's solution slowly
diagnosed by the presence of pain or delivered via IV may be used to elicit an allergic
inflammation or by systemic or neurological response.
signs.

(11) Infuse the diluted antivenin (16) Respiratory obstruction and failure are the
slowly at first, then increase to 1 greatest immediate concerns. Make sure that
vial every 7-10 min (0.7-1.0 adequate suction is available and operative at
ml/min). The crepe bandage the bedside. If any sign of oropharyngeal
should be removed slowly after paralysis or impaired swallowing exists nothing
the second vial of antivenom has should be given orally. The patient should be
been delivered. kept on his side, head down. Intubation may be
(12) Should any manifestations of necessary to protect the airway.
allergy/anaphylaxis present (17) Neostigmine provides an additional
themselves, reduce or discontinue treatment option for neuromuscular junction
antivenin infusion and treat the postsynaptic blockade when used in conjunction
patient with epinephrine, with antivenin or as a second line alternative if
glucocorticoids, or antihistamines. antivenin is not available. Atropine is given to
When the patient has stabilized, prevent overexcitation of the autonomic
resume antivenin administration nervous system.
at a rate tolerated by the patient. (18) Tetanus toxoid vaccination should be
(13) Administer an initial course of current. Prophylactic antibiotics are not
6 vials of SAIMR polyvalent required.
antiserum. Then reassess the (19) Patients who receive antivenin should be
patient's condition observed in an intensive care setting for 12-24h.
(14) The key to subsequent They may be discharged the following day if
therapy lies in the titration of stable.
antivenom against the signs and (20) Patients who receive larger doses of
symptoms of envenomation. antivenin might develop a cutaneous allergic
Symptoms that are not useful in reaction. This usually appears as urticaria 7-21
determining the need for further days after treatment. Oral antihistamines or
(15) Additional antivenin should be corticosteroids may be prescribed to treat the
administered in three vial doses. reaction.
The low neutralizing capacity of a
single vial precludes the
usefulness of more artful titration.
Urine output should be
maintained by aggressive
hydration and the use of diuretics,
as necessary.

Brown Recluse Spider

One of the feared poisonous spiders occurring in Tennessee is the Brown Recluse
Spider. As an angry, bad-tempered monster, this spider is sometimes visualised just
waiting for an opportunity to ambush individuals. The brown recluse spider, in
reality, is a shy, retreating spider that does not target individuals and typically only
bites in response to injury. It is a medium-sized spider belonging to the Family
Loxoscelism (the brown spiders) and the Order Aranea (spiders). The length of the
adult body varies from 7 mm to 12 mm (1/4 inch) and from 3 mm to 5 mm (1/8 inch
to under 1/4 inch). About the size of a quarter to a half-dollar, the legs span an area.
The colour of the brown recluse ranges from a light yellowish brown to a black,
reddish or chocolate brown, but the colour of the recluse ranges from a light
yellowish brown to a dark chocolate brown. They are usually light to medium brown.

Venom ... The major chemical in the
brown recluse venom is the
The brown recluse spider enzyme sphingomyelinase D.
venom is very toxic, but
rarely does a lot of harm Unlike other venoms that
due to the limited amount. invade the nervous system, this
One of the active enzymes
in the venom causes severe enzyme is used to break cell
damage to the blood vessels membranes. All species of the
genus Loxosceles contain this
and cell death at the enzyme in their poison. This
envenom site. enzyme causes extreme necrosis

of the tissue that it infects.
However, this toxin primarily

affects certain mammals,
including humans, guinea pigs
and rabbits but not including

mice and rats. Female brown
recluses have a significantly
higher concentration of venom

than males.

The brown recluse spider HOW DOES THE VENOM
venom is very poisonous WORK
but rarely causes a lot of
damage because of the For those who do have a reaction
small quantity. One of the to the venom, the most common

active enzymes in the response is inflammation that
venom causes significant after one to two days can
damage to blood vessels develop into a dark lesion

and cell death to the surrounding the bite site. The
tissue at the blackening, or necrosis, of the
skin is dead skin cells, evidence
envenomation site. Also, of the immune system's efforts
the venom causes the to prevent spread of the toxin by
preventing blood flow to the
patient's body to release
inflammatory cells like affected area.
interleukins, cytokines to
help deal with the venom
but these cells can cause
harm to the patient once
they activated, this results

in red blood cell
destruction (hemolysis),

platelet destruction
(thrombocytopenia), end-

organ damage (kidney
injury and coma).

PATHOGENESIS

The brown recluse venom can The wound formed from the venom can
destroy human tissue. At first, the quickly and easily allow an infection to
bite site may appear like any other set in, worsening the wound-healing
insect bite - a little red, itchy, and process. The infection as well as the venom
inflamed. Over the course of a few can also spread to the rest of the body
days, the venom destroys the and possibly become life-threatening.
surrounding tissues. The wound gets
larger, more painful, and darker in
colour. Necrosis or tissue death is
identified when the tissue becomes
black in colour and forms a crust
that eventually falls off. The venom
can penetrate deeper in the tissues,
sometimes affecting the fat and
muscles. Often, the bite of a brown
recluse spider leaves a crater-like
scar after it has healed completely.

Brown recluse spider venom is cytotoxic and haemolytic. It has many enzymes that contribute to
the clinical manifestations. Sphingomyelinase D, one of the more well-studied components, has been
shown to direct toxin-mediated haemolysis and complement-mediated erythrocyte destruction. It
does this by activating the complement system. Within the venom, there are additional proteases
that degrade collagen, fibronectin, fibrinogen, gelatine, elastin basement membranes that on their
own may not be able to cause the local reaction seen with brown recluse bites but seem to have a
synergistic effect with sphingomyelinase D leading to many of the cutaneous findings.
Hyaluronidase, alkaline phosphatase, esterase, and ATPase also seem to have effects leading to the
cutaneous manifestations of bites

Sign & Symptoms

INITIAL BITE AFTER 3-5 DAYS

Brown recluses have very small In some people, the brown recluse’s
fangs, and their bite is usually venom is localized to only the area
painless. There would be a red, where the spider bit. If the spider
tender, and inflamed area about injected minimal venom and we are
3 to 8 hours after the spider bite. considered healthy, the discomfort
Over the course of several usually goes away in about 3 to 5
hours, the irritation may cause a days. In others, the venom spreads.
burning sensation. Some people This causes the wound to expand,
will develop a necrotic lesion usually over a period of several days
due to the spider’s bite such as
dry, sinking patch of skin, bluish- to weeks.
appearing patch of skin, redness
around the lesion with a pale AFTER 7-14 DAYS
centre and central blister.
In those with more severe bites, the
3 WEEKS LATER spreading ulcer can grow by inches. It
does not usually break down skin until
Most brown recluse spider bites about 7 to 14 days after the bite occurs.
take about 3 weeks to heal. For
those with more severe bites, the A wound of this nature may last for
site of the wound starts to several months.
develop necrotic (dead) tissue
called eschar. This looks like a 3 MONTHS LATER
big, black, thick scab that covers
the wound. Most brown recluse bites will
heal within 3 months. If the
bite has not healed, it may
not be a brown recluse bite

after all.

Once bitten by the brown recluse spider
should consult a doctor immediately as the

venom can spread all over the body.
However, if the symptoms are mild then
clean the wound with soap and water. Apply
the antibiotic cream and place ice cubes on
it. Keep the hand or leg that is injured raised
to reduce swelling. In some cases a tetanus
shot is needed after the bite. A pain reliever
can be taken such as acetaminophen or
ibuprofen to reduce the discomfort and
pain. It usually takes about 3 weeks to heal.
In severe cases the wound will start to
develop necrotic tissue which is known as

eschar.

PPOOIISSOONN DDAARRTT FFRROOGG

Poison dart frogs, members of the Dendrobatidae
family, wear some of the most brilliant and beautiful

colors on Earth. Poison dart frogs live in the rain
forests of Central and South America. Depending on
individual habitats, which extend from the tropical
forests of Costa Rica to Brazil, their coloring can be
yellow, gold, copper, red, green, blue, or black. Their

elaborate designs and hues are deliberately
ostentatious to ward off potential predators, a tactic
called aposematic coloration, and a few species are

used by South American tribes to coat the tips of
darts and arrows.

VENOM ...

Most of the poison dart frogs
secrete lipophilic alkaloid toxins
such as allopumiliotoxin 267A,

batrachotoxin, epibatidine,
histrionicotoxin, and pumiliotoxin
251D through their skin. Alkaloids
in the skin glands of poison frogs

function as a chemical barrier
against predation and are thus

capable of being present
alongside possible predators
during the day. Approximately 28
structural groups of alkaloids are

identified in poison frogs.
Phyllobates terribilis is the most

toxic of the poison dart frog
species.

HOW DOES THE VENOM WORKS

It contains the poison of an alkaloid toxin called
batrachotoxin within its skin glands. It can kill up to 10
humans. If the poison enters the human bloodstream,
humans can be killed within 10 minutes. This frog will
agitate and start sweating out the poison particularly on
the back which is covered with the white froth. It causes

paralysis and death when it enters the human
bloodstream even in minuscule amounts. Most of the
poison frog species are considered as toxic but it is not
deadly. The poison in their skin can cause nausea and

swelling if touched unnecessarily.

PATHOGENESIS

The toxin is produced in the skin gland and one frog holds enough to kill 10 human beings at
any one time—the toxin kills by reversing the openings of sodium channels in nerves, which
prevents muscles from relaxing. The heart clenches to push blood through the body, but then
cannot unclench, preventing it from working. Batrachotoxin works by irreversibly opening

the sodium channels of nerve cells, which permanently blocks the transmission of nerve
signals to the muscles, while preventing the muscles from being able to relax. Once inside a
victim, the compound embeds itself in certain proteins that are responsible for conducting
electrical impulses through the nerves and muscles, including the heart. By disrupting that

process, it can cause paralysis and a heart attack.

SIGN & SYMPTOMS

It is very potent and specific with doses of less than 0.1 μg
eliciting convulsions, muscle contractions, salivation, and
death. Other symptoms include respiratory paralysis and

muscular paralysis.

TREATMENTS

Antivenoms or direct antidotes for the treatment of this form of
poisoning are not available. However, it is possible to use anti-digitalis
drugs to neutralise circulating toxins for at least some species whose
toxins have a digitalis type activity. It may also be necessary to reduce

the circulating toxin load by hemoperfusion in extreme cases. In
addition to these basic steps, therapy is aimed at encouraging

cardiorespiratory control and, in selected cases, the use of medications
to counteract cardiotoxic activity.

Janaki. (2017). This Frog's Poison Is Among the Deadliest in Nature –
So Why Doesn't It Kill the Frog Itself? Retrieved from

https://thewire.in/science/golden-poison-dart-frogs-epibatidine-
batrachotoxins-mutation-sodium-channels

University of Arizona. (2013, August 29). Spider venom reveals new
secret: Once injected into a bite wound, venom of brown recluse
spider causes unexpected reaction. ScienceDaily. Retrieved
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www.sciencedaily.com/releases/2013/08/130829214742.htm

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