Carl Anthony COPPOLINO
Classification: Murderer
Characteristics: Poisoner - Parricide
Number of victims: 1 +
Date of murder: August 28, 1965
Date of birth: 1933
Victim profile: His wife, Dr. Carmela Musetto, 32
Method of murder: Poisoning (anaesthetic succinylcholine chloride)
Location: New Jersey/Florida, USA
Status: Sentenced to life in prison on April 28, 1967. Paroled in 1979
Motive: So that he could marry his lover.
Crime: Coppolino was charged with killing his wife, Carmela at their home on Florida's Gulf of Mexico
coast. He was also tried for murdering Colonel William E. Farber, the husband of his ex-lover Marjorie.
However, he was acquitted from this offence.
Method: Coppolino gave Carmela an overdose in the form of an injection of the anaesthetic
succinylcholine chloride.
Sentence: Coppolino was charged with second degree murder and sentenced to life imprisonment. He
served 12 years, before being let out for good behaviour.
Interesting facts: An overdose of succinylcholine chloride is difficult to detect in the body, as succinic
acid and choline are found naturally in the body. To be able to prove this was the cause of Carmela's
death, toxicologst Dr Joseph Umberger had to devise a test, which in June 1966 he succeeded in doing.
Coppolino was an experienced anaesthetist, who had had to give up work at an early age due to ill
health. So he had the knowledge and the means to kill Carmela in this way.
It was claimed that Coppolino had also killed Farber in the same way. When he was exhumed, it was
discovered that his cricoid cartilage was fractured, which suggested that he had been strangled. In court
it was claimed that this damage could have occurred during exhumation, and that he had sufficient
arteriosclerosis to have died of a heart attack, as was originally supposed.
Succinylcholine
Suxamethonium chloride (INN), also known as suxamethonium or succinylcholine, is a nicotinic acetylcholine
receptor blocker, used to induce muscle relaxation and short-term paralysis, usually to facilitate tracheal
intubation
Suxamethonium is sold under the trade names Anectine, Quelicin, and Scoline. It is colloquially referred to as
"succs" in hospital settings.[1]
Its medical uses are limited to short-term muscle relaxation in anesthesia and intensive care, usually for
facilitation of endotracheal intubation (breathing tube during surgery or breathing tube for life support
measures). Suxamethonium is also commonly used as the sole muscle relaxant during electroconvulsive
therapy, favoured for its short duration of action.
This drug has occasionally been used as a paralyzing agent for executions by lethal injection, although
pancuronium bromide is the preferred agent today because of its longer duration of effect and its absence of
fasciculations as a side effect.
Botulism
Botulinum toxin is a protein and neurotoxin produced by the bacterium Clostridium botulinum.[1][2] It is the most acutely
toxic substance known, with an estimated human median lethal dose of 1.3–2.1 ng/kg intravenously or intramuscularly
and 10–13 ng/kg when inhaled.[3]
Botulinum toxin can cause botulism, a serious and life-threatening illness in humans and animals. Popularly known by
one of its trade names, Botox, it is used for various cosmetic and medical procedures.
History
Justinus Kerner described botulinum toxin as a "sausage poison" and "fatty poison",[4] because the bacterium that
produces the toxin often caused poisoning by growing in improperly handled or prepared meat products. It was Kerner,
a physician, who first conceived a possible therapeutic use of botulinum toxin and coined the name botulism (from Latin
botulus meaning "sausage"). In 1897, Emile van Ermengem found the producer of the botulin toxin was a bacterium,
which he named Clostridium botulinum. [5] In 1928, P. Tessmer Snipe and Hermann Sommer for the first time purified the
toxin.[6] In 1949, Arnold Burgen's group discovered, through an elegant experiment, that botulinum toxin blocks
neuromuscular transmission through decreased acetylcholine release.[7]
The seven serologically distinct toxin types are designated A through G. Additionally, six of the seven toxin types have
subtypes with five subtypes of BoNT A having been described. The toxin is a two-chain polypeptide with a 100-kDa
heavy chain joined by a disulfide bond to a 50-kDa light chain. This light chain is an enzyme (a protease) that attacks one
of the fusion proteins at a neuromuscular junction, preventing vesicles from anchoring to the membrane to release
acetylcholine. By inhibiting acetylcholine release, the toxin interferes with nerve impulses and causes flaccid (sagging)
paralysis of muscles in botulism, as opposed to the spastic paralysis seen in tetanus.
Medical and cosmetic uses
Although botulinum toxin is a lethal, naturally occurring substance, it can be used as an effective and powerful
medication.[34] Researchers discovered in the 1950s that injecting overactive muscles with minute quantities of
botulinum toxin type-A would result in decreased muscle activity by blocking the release of acetylcholine from the
neuron by preventing the vesicle where the acetylcholine is stored from binding to the membrane where the
neurotransmitter can be released. This will effectively weaken the muscle for a period of three to four months.[35]
In cosmetic applications, a Botox injection, consisting of a small dose of botulinum toxin, can be used to prevent
development of wrinkles by paralyzing facial muscles.[36] As of 2007, it is the most common cosmetic operation, with 4.6
million procedures in the United States, according to the American Society of Plastic Surgeons. Qualifications for Botox
injectors vary by county, state and country. Botox cosmetic providers include dermatologists, plastic surgeons, aesthetic
spa physicians, dentists, nurse practitioners, nurses and physician assistants. The wrinkle-preventing effect of Botox
normally lasts about three to four months, but can last up to six months.[36]
In addition to its cosmetic applications, Botox is currently used in the treatment of spasms and dystonias, by weakening
involved muscles, for the 60–70 day effective period of the drug.[37]
March 20, 1995: Poison Gas Wreaks
Tokyo Subway Terror
1995: Religious cultists release the toxic nerve gas sarin at multiple
locations in the Tokyo subway. A dozen people will die, and thousands
suffer injuries ranging from mild to severe.
Aum Shinrikyo was a Japanese cult combining bits of Buddhism, Hinduism,
shamanism and end-of-days Christianity. The name combined the Buddhist
mantra om with the Japanese for "supreme truth."
With a worldwide membership of 20,000 to 40,000, Aum had a net worth
in 1995 of about $1.5 billion. It made money through standard religious
techniques like donations, tithing and paraphernalia sales. It also
employed the New Age technique of high-priced indoctrination seminars.
In addition, it ran some businesses, including a restaurant chain and a
computer factory that assembled Taiwanese electronic components into
computers it sold at its own downtown Tokyo store.
The cult also built a facility to manufacture biological and chemical
weapons by the ton. Aum experimented with botulin toxin, anthrax,
cholera, Q fever and the Ebola virus. Operatives tried to release botulin near the Diet in 1990, and near the imperial
palace in 1993. An anthrax release from its Tokyo office building in 1993 caused foul smells, brown steam, pet deaths
and stains on cars and sidewalks. None of these attacks is known to have caused death or injury.
Things changed on June 27, 1994. Cult members drove a truck to a residential neighborhood in Matsumoto, about 200
miles northwest of Tokyo, then used a computer system to remotely release a cloud of sarin. Their primary targets were
three judges who lived there and were about to rule against the cult in a big real estate case.
Sarin was first created in Nazi Germany. The volatile nerve agent is 500 times more toxic than cyanide: A single pinheadsize drop can kill an adult. The Matsumoto sarin attack killed seven people and injured 500, of whom 200 were admitted
to hospitals at least overnight.
Despite all that, Aum Shinrikyo managed to pull off its most audacious — and deadly — attack just nine months later. In
the Monday morning rush hour of March 20, five cult members boarded different subway trains converging on central
Tokyo.
Four of them each carried two plastic bags loaded with sarin, and the fifth had three bags. At nearly the same moment,
they each dropped the bags to the floor of the jam-packed train and punctured them with a specially sharpened
umbrella tip. The cultists then quickly stepped off the trains as they pulled into the next station. Getaway drivers were
waiting outside the station for each of them.
The liquid began vaporizing, and people began getting sick. Some of them got off the trains at subsequent stations,
stumbling onto the platforms. At each stop, more gas spread, and more liquid was tracked off the trains and into the
stations. The deadly sarin vapor also clung to the clothes and bodies of its victims, sickening those who rushed to their
aid.
Some of the trains continued traveling — one for an hour and 40 minutes — before finally stopping to deal with the
emergency ... and stop spreading it. Emergency and hospital services later got heavily criticized for the uncoordinated
response.
Symptoms included bleeding from the nose and mouth, coma, convulsions, difficulty breathing, extreme sensitivity to
light, flulike symptoms, foaming at the mouth, fevers, loss of consciousness, loss of memory, loss of vision, nausea,
vomiting, paralysis, respiratory problems, seizures and uncontrollable trembling. Some survivors suffered these
problems permanently, along with disturbed sleep, nightmares and post-traumatic stress disorder.
Many victims with initially mild symptoms went to work before sickening later and going to the hospital. Others
probably never sought medical care. Estimates of the injured range from 3,800 up to 6,000. The sarin killed 12 people.
Police began raiding cult buildings and property all over Japan within 48 hours, wearing hazmat equipment that had
been issued to them for this purpose ... the week before the Tokyo attack. The cult had in fact gotten wind of an
impending crackdown and unleashed its subway attack to kill police officers.
The Japanese government revoked Aum Shinrikyo's status a religion and seized as many of the cult's assets as it could
find. Some members later reorganized on a much smaller scale as Aleph (the first letter of the Hebrew alphabet and a
key symbol in mathematical set theory).
About 200 people were arrested. About 20 are either still in Japan's lengthy trial process standing trial or have already
been convicted. At least eight Aum members, including the founder, have received death sentences for their roles in the
attack.
Source: Emerging Infectious Diseases, Japan 101
SARIN GAS
Sarin, or GB, is an organophosphorus compound. It is a colorless, odorless liquid,[4] used as a chemical weapon owing to
its extreme potency as a nerve agent. It has been classified as a weapon of mass destruction in UN Resolution 687.
Production and stockpiling of sarin was outlawed by the Chemical Weapons Convention of 1993 where it is classified as
a Schedule 1 substance.
Its mechanism of action resembles that of some commonly used insecticides, such as malathion. Like other nerve
agents, sarin attacks the nervous system.
Specifically, sarin is a potent inhibitor of the enzyme cholinesterase.[7] With the enzyme inhibited, acetylcholine builds
up in the synapse and continues to act so that any nerve impulses are, in effect, continually transmitted.
Normally, the acetylcholinesterase breaks down the acetylcholine in the synaptic cleft in order to allow the effector
muscle or organ to relax. Death will usually occur as a result of asphyxia due to the inability of the muscles involved in
breathing to function
Sarin is estimated to be over 500 times more toxic than cyanide.[15] The LD50 of subcutaneously injected sarin in mice is
172 μg/kg.[16] Treatment measures have been described.[17]
Initial symptoms following exposure to sarin are a runny nose, tightness in the chest and constriction of the pupils. Soon
after, the victim has difficulty breathing and experiences nausea and drooling. As the victim continues to lose control of
bodily functions, the victim vomits, defecates and urinates. This phase is followed by twitching and jerking. Ultimately,
the victim becomes comatose and suffocates in a series of convulsive spasms.
Copperhead snakes
Agkistrodon contortrix is a species of
venomous snake endemic to North
America, a member of the Crotalinae
(pit viper) subfamily. The common
name for the species is the
"copperhead."
The behavior of Agkistrodon contortrix
may lead to accidental encounters
with humans.
It is found in the United States in the
states of Alabama, Arkansas,
Connecticut, Delaware, Florida,
Georgia, Illinois, Indiana, Iowa, Kansas, Kentucky, Louisiana, Ohio, Oklahoma, Maryland, Massachusetts,
Mississippi, Missouri, New Jersey, New York, North Carolina, Pennsylvania, South Carolina, Tennessee, Texas,
Virginia and West Virginia.
Although venomous, these snakes are generally not aggressive and bites are rarely fatal. Copperhead venom
has an estimated lethal dose of around 100 mg, and tests on mice show its potency is among the lowest of all
pit vipers, and slightly weaker than that of its close relative, the cottonmouth. Copperheads often employ a
"warning bite" when stepped on or agitated and inject a relatively small amount of venom, if any at all. "Dry
bites" involving no venom are particularly common with the copperhead, though all pit vipers are capable of a
dry bite.
Bite symptoms include extreme pain, tingling, throbbing, swelling, and severe nausea. Damage can occur to
muscle and bone tissue, especially when the bite occurs in the outer extremities such as the hands and feet,
areas in which there is not a large muscle mass to absorb the venom. A bite from any venomous snake should
be taken very seriously and immediate medical attention sought, as allergic reaction and secondary infection
are always possible.
Bungarotoxins are a group of closely related neurotoxic proteins derived from the venom of snakes.[1] They
are neurotoxic proteins. α-Bungarotoxin inhibits the binding of acetylcholine (ACh) to nicotinic acetylcholine
receptors.