Substances & Homeopatic Remedies

Naja tripudians

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POISONOUS SNAKES.
Venoms can be divided into the following categories: neurotoxic, cardiotoxic, cytotoxic.
A fourth, rarer type of hemolytic toxin is produced by some species. Toxins in the this category activate complement via the alternative pathway (C3-C9 sequence).
The snake may have a mixture of the 4 types, but generally has a preponderance of 1 type.
 With most species, excluding some of the African spitting cobras, the most clinically significant toxins are postsynaptic neurotoxins that competitively bind to nicotinic acetylcholine receptors to produce depolarizing neuromuscular blockade. One group in this category has 60-62 amino acids and 4 disulfide bridges. Another has 71-74 amino acids and 5 disulfide bridges.
(coral snake, cobra, naja naja, mamba, etc.)
The second venom category comprises so-called cardiotoxins, which are actually generalized cell-membrane poisons that produce irreversible cell depolarization. Such depolarization may cause dysrhythmia, hypotension, and death.
The third category is composed of enzyme toxins, such as phospholipase A2 (variable toxicity), hyaluronidase (facilitates tissue dispersion of other toxins), L-amino acid oxidase (gives many venoms a characteristic yellow coloration), and acetylcholine acetylhydrolase (unknown toxicity). Other proteolytic enzymes are found in the venom of the king cobra.This cytotoxic variety causes severe local tissue destruction, due to enzyme action on the tissues (rattlesnake, puffadder, etc.).  

Naja philippinensis (Philippine cobra) venom is the most toxic, with a subcutaneous median lethal dose (LD50) of 0.14 mg/kg in mice. In comparison, the corresponding LD50 for Naja naja (Indian cobra) venom is 0.29 mg/kg, for Naja haje (Egyptian cobra) venom is 1.75 mg/kg, for king cobra venom is 1.73 mg/kg, and for Naja nigricollis (black-necked spitting cobra) venom is 3.05 mg/kg.

 Cobra envenomation is an extremely variable process. The envenomations of some species cause profound neurological abnormalities (eg, cranial nerve dysfunction, abnormal mental status, muscle weakness, paralysis, and respiratory arrest) as is the case in naja naja.

With other snakes, local tissue damage is of primary concern: Necrosis is typical of bites by the African spitting cobras (Naja nigricollis, Naja mossambica, Naja pallida, and Naja katiensis), Naja atra (the Chinese cobra), Naja kaouthia (monocellate cobra), and Naja sumatrana (Sumatran spitting cobra). Although the venoms of these cobras contain neurotoxins, necrosis often is the chief or only manifestation of envenoming in humans. Occasionally, a combination of neurologic dysfunction and tissue necrosis is observed.
Cobra venoms have been studied extensively. As with all snake venoms, they are multicomponent systems whose toxins are mostly proteins and polypeptides.

 To many people, the cobra is the quintessential venomous snake. Cobras discussed in this chapter include species in the genus Naja and other similar venomous snakes, such as Ophiophagus hannah (king cobra), Hemachatus haemachatus (ringhals), Walterinnesia aegyptia (desert black snake), Boulengerina species (water cobras), and Pseudohaje species (tree cobras).
Most cobras are large snakes, 1.2-2.5 m in length. The king cobra, which may reach 5.2 m, is the largest venomous snake in the world. Cobras live throughout most of Africa and southern Asia. Their habitats vary. Some species adapt readily to life in cultivated areas and around villages.
When encountered, cobras usually try to escape but occasionally defend themselves boldly and may appear aggressive. Most of these snakes elevate the head and spread the neck as a threat gesture. However, a number of other snakes, venomous and nonvenomous, employ this defense as well.
Most snakebites are inflicted on body extremities. Because cobras are popular as show snakes, bites on the hands and fingers are common.
By far, rural agricultural workers and other people in Asia and Africa receive most bites while working outdoors without protective footwear. In North America and Europe, captive snakes usually cause bites, zookeepers and amateur collectors being at greatest risk.
Not all snakebites result in envenomation. In the case of cobras, the percentage of blank bites may be quite high, 45% in one series of 47 cases from Malaysia. In another series, 1 of 3 snake charmers bitten by large king cobras showed no signs of envenomation.
In addition to biting, some cobra species have a unique defense; they eject jets of venom toward an enemy, usually at the eyes. The fangs of these species are specially modified with the discharge orifice on the anterior face rather than at the tip. The effective discharge range of a large snake is at least 3 m. The ringhals and certain African species of Naja are the most effective spitters, but the spitting behavior also is observed among some Asian Naja species.

The onset of symptoms and signs following a cobra bite can be extremely variable:
Immediate, local pain (almost always present)
Soft tissue swelling (may be progressive)
Neurologic findings, which may begin early and be rapidly progressive (in anecdotal cases, victims have suffered respiratory arrest in a matter of minutes), or may be delayed in onset as long as 24 hours
Alteration of mental status (eg, drowsiness, occasionally with euphoria)
Complaints related to cranial nerve dysfunction, such as ptosis (often one of the earliest neurotoxic findings), ophthalmoplegia, dysphagia, and dysphasia
Profuse salivation, nausea, vomiting, and abdominal pain
Paresis of neck and jaw muscles and generalized muscular weakness followed by flaccid paralysis
Shortness of breath, respiratory failure (muscular paresis and accumulated secretions)
Chest pain or tightness
Eye pain, tearing, blurred vision (with eye exposure to venom from spitting cobras)
Physical:
Impending respiratory failure
Respiratory distress or weakness
Cyanosis
Neurologic dysfunction
Altered mental status
Ptosis (may be the earliest sign of systemic toxicity)
Generalized weakness or paralysis
Cardiovascular collapse
Hypotension
Tachycardia or bradycardia
Soft tissue edema
Signs of necrosis usually appear within 48 hours of the bite.
The area around the fang punctures darkens.
Blistering may follow.
Necrosis usually is confined to the skin and subcutaneous tissue but may be quite extensive.
A putrid smell is characteristic.
Acute inflammation of the eye follows venom-spitting exposure and is characterized by ocular congestion, edema of the conjunctiva and cornea, and a whitish discharge.
                 



THE MEDICINAL USE OF SNAKES IN CHINA

Snake bile has long been valued as a tonic, characterized as such by its sweet aftertaste.  It is used to make a special health drink at snake restaurants (which are today still found in southern China, Hong Kong, and Taiwan).  The bile of a snake to be eaten is mixed with some rice wine and consumed before the meal as an invigorating beverage and appetite stimulant.  In the treatment of diseases, snake bile is used for whooping cough, rheumatic pain, high fever, infantile convulsion, hemiplegia, hemorrhoids, gum bleeding, and skin infections.  
One of the best known remedies using snake bile is San She Dan Chuan Bei Mu, or the mixture of three snake gallbladders plus the herb fritillaria (F. thunbergii).  It is made as a powder or a liquid; only the powder is imported to the West.  The three snake gallbladders are usually derived from agkistrodon and zaocys species, but there are numerous substitute species used in the marketplace.  In fact, a major active component-the bile acid known as taurocholic acid-was analyzed in the 16 species of snakes now traded commonly and in 8 samples of snake bile and fritillaria liquids.  The highest level of this component was in the bile from a species of Naja snake (a cobra).
The bile from two snakes, Naja naja (Indian cobra) and Ophiophagus hannah (king cobra) show 11 bands in thin layer chromatography (TLC), while the bile from most other snakes show only 8 of those bands, indicating unique medicinal ingredients in the cobra.  All the snakes contain cholic acid but not deoxycholic acid or lithocholic acid.  

Indicazioni cliniche

Laringiti
Asma
Bronchiti
Insufficienza valvolare
Ovariti-metriti
Tosse cardiaca
Iriti
Cecità
Paralisi da intossicazioni
Emorragie
Depressioni

L'azione del veleno è quella di dare dopo un breve tempo come una certa depressione del sensorio che dal punto d'inoculo interesserà tutto l'organismo conducendolo a morte per sincope.
Il soggetto è stanco e lentamente, dopo aver manifestato dei sintomi gastro intestinali, che si possono riassumere in vomito e diarrea, muore. La morte in genere avviene per paralisi respiratoria e cardiaca. Quindi come veleno rispetto agli altri dei serpenti presenta un'azione più a carico del sistema nervoscentrale, con risentimento sia sul cuore che sul circolo. Azione neuritossica
Naja può colpire anche le mucose dell'apparato respiratorio provocandone una flogosi produttiva con senso di costrizione faringea e tosse, sempre accompagnato da una certa depressione.

This person has received a bite and probable envenomation from an Indian or Common Cobra (Naja naja naja). This is a very venomous and dangerous snake. In this particular species, envenomation usually presents predominately with local necrosis and systemic manifestations. Drowsiness, Neurological and Neuromuscular symptoms may develop early; paralysis, ventilatory failure or death could ensue rapidly.

Signs and Symptoms of Envenomation:

A.    Neurological and Neuromuscular:

These signs and symptoms will usually manifest earliest. Not all of these will necessarily develop, even with severe envenomation.
Drowsiness     (>90%)
Eyelid drooping (Ptosis)     (75-85%)
Respiratory paralysis or Dyspnea     (70-80%)
Ophthalmoplegia     (35-45%)
Palatal paralysis     (30-40%)
Glossopharyngeal paralysis     (30-40%)
Limb paralysis     (20-30%)
Convulsions     (10-20%)
Head drooping (Cervical muscle paresis or paralysis)     
Headache     
Sudden loss of consciousness     
Stumbling gait (Ataxia)     

B.    General:

These symptoms typically manifest within one to four hours following the bite if envenomation occurred.
Nausea and Vomiting
Hypotension
Flushing of the face
Warm skin
Pain around bite site
Abdominal Pain

C.    Cardiotoxicity:

Increased Blood Pressure and increased Cardiac Output followed by Myocardial Depression and Asystole. Mortality approaches 100% if cardiotoxic complications occur.

D.    Local Symptoms:

In some Cobra bites, local tissue destruction and necrosis can dominate the clinical presentation. Gangrene requiring amputation can occur. Local tissue damage appears to be less frequent and less severe in most cases of Indian Cobra (Naja naja naja) envenomation, but may include:
Localized discoloration of skin
Vesiculation (usually small and localized)
Necrosis (can be extensive, but is characteristically localized to the bite site)
Local edema (usually minimal)

E.    Fang Marks:

Fang marks may be present as one or more well defined punctures, as a series of small lacerations or scratches, or there may not be any noticeable or obvious markings where the bite occurred. The absence of fang marks does not preclude the possibility of a bite (especially if a juvenile snake is involved). In general, the fang marks from an Indian Cobra tend to be small, but deep. The snake in delivering the bite may hold on and chew savagely, and may inject up to 60% of its venom. Multiple bites inflicted by a single snake or by more than one snake are also possible, and should be noted if present (See Special Considerations below). The presence of fang marks does not always imply that the injection or deposition of venom into the bite wound (envenomation) actually occurred.

Neurotoxins

Neurotoxins are classic venom components, particularly those affecting the neuromuscular junction and causing flaccid paralysis. However, not all neurotoxins have the same target site, nor the same mode of action or clinical effects.

Neurotoxins affecting the neuromuscular junction:

The neuromuscular junction NMJ in skeletal muscle involves all voluntary and respiratory muscles. At the junction, a signal transmitted through the nervous system finally results in an action potential at the terminal axon, with activation of ion channels, resulting in release of packets of the neurotransmitter, acetylcholine (Ach). Ach is produced in the terminal axon, and stored in synaptic vesicles. Once released, it crosses the minute extracellular space to bind with the acetylcholine receptor proteins on the surface of the muscle end plate. Once sufficient binding has occurred, an action potential of the muscle cell will cause specific membrane ion channel changes, resulting in muscle cell contraction. Following this the Ach will be released and metabolised by cholinesterases in the extracellular space, these metabolites being recycled back into the terminal axon for reprocessing into further Ach.

Presynaptic NMJ neurotoxins affect the terminal axon through incompletely understood mechanisms, resulting in disruption of synaptic vesicles, damage to the terminal axon and cessation of release of Ach, thus completely blocking neuromuscular transmission. This causes flaccid paralysis of affected muscles. However, the process is not instantaneous. On reaching the NMJ the presynaptic neurotoxin must bind to the terminal axon membrane, damage the membrane, and then exert its toxin effects. Initially this may cause release of Ach, with some muscle twitching, rarely noticed clinically, before destroying vesicles and blocking further Ach release. This whole process takes up to an hour experimentally. Clinically, because of the extra time taken for the neurotoxin to be absorbed, reach the circulation, exit again to the extravascular compartment, then reach the NMJ, a process that may take from half an hour to several hours, presynaptic paralysis is unlikely to manifest in less than 1-2 hours post bite. The clinical features of early paralysis are usually first seen in the cranial nerves, with ptosis (drooping of the upper eyelids) the most obvious first sign. This will be described more completely in the next chapter (clinical effects). Because presynapticneurotoxins cause damage to the terminal axon, they are poorly responsive to antivenom therapy. Thus, once severe flaccid paralysis is established, with respiratory involvement, antivenom is unlikely to reverse paralysis. It is therefore crucial to recognise the early signs of paralysis and give antivenom early, before more major and irreversible paralysis occurs. Presynaptic neurotoxins are found principally in some snake venoms, such as kraits (b-bungarotoxin), some Australian elapids (notexin, taipoxin, textilotoxin) and a few vipers (crotoxin). They also occur in paralysis tick saliva and probably in a few other arthropod venoms. They are mostly based on phospholipase A2, though often highly evolved and sometimes muticomponent.(See the photo in the section of the pictures)

Postsynaptic NMJ neurotoxins are more common than presynaptic toxins, less potent, but more rapid in action, and are certainly lethal in potential. They bind to or adjacent to the acetylcholine receptor protein on the muscle end plate, thus blocking signal arival at the muscle, resulting in flaccid paralysis. Because they can act as soon as they reach the NMJ, they can cause paralysis earlier than presynaptic toxins, but clinically the first signs of flaccid paralysis, such as ptosis, is still rarely seen in less than one hour post bite, and often may be delayed for several hours. As these toxins remain exposed on the cell surface, in the extravascular extracellular compartment, they are accessible to antivenom. Thus postsynaptic paralysis may be reversible with antivenom therapy. As an alternative, if increased amounts of Ach are released they may overwhealm the postsynaptic neurotoxin, thus overcomming the blockade and re-establishing NMJ transmission. One technique to achieve this is to effectively increase Ach concentration by blocking its removal. This can be done by giving an anticholinesterase such as neostigmine. Postsynaptic NMJ neurotoxins are widely distributed in snake venoms, especially elapid venoms, the classic component being a-bungarotoxin, from krait venom. Often a snake venom may have both presynaptic and postsynaptic neurotoxins, but there are a number of species, notably some of the Asian cobras, where only postsynaptic neurotoxins are present. These toxins are moderately uniform in structure and size. They mostly have a complex folded structure resulting in a classic "three finger" configuration, the active site placed on the second or middle "finger". They are subdivided into two major groups, based on size; the short chain toxins and the long chain toxins. The short chain toxins contain 60-62 amino acid residues, crosslinked by 4 disulphide bonds. The long chain toxins have 70-74 amino acid residues cross linked with 5 disulphide bonds. All bind with high affinity to the a-subunit of the nicotinic cholinergic (acetylcholine) receptor.

Toxicity of Selected Snake Venoms

Species : Spectacled cobra (Naja naja) Mouse LD50 (mg/kg) : 0.28 Venom yield per snake (mg) : 150.0-600.0