Information

Why are bacteria immune to snake poisons?

Why are bacteria immune to snake poisons?


We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

In a test I was asked why bacteria are insensitive to snake toxins.

Is it their membrane that provides a barrier to the toxins? Or do snake poisons have specific targets and thus cannot bind to bacteria?


Short answer
Many snake poisons target specific proteins not present in unicellular organisms.

Background
The question is admittedly broad but the idea behind this question is pretty much what you indicate in your post - many venoms target specific proteins and do not simply destroy their target by, e.g., disrupting gross cellular structure (like alcohol does for example). Instead, they target specific molecules that are essential for the survival of their prey.

Snake toxins can be categorized according to the organ systems they target, namely :

  • the central nervous system
  • the cardiovascular system
  • the muscular system
  • the vascular system

Central nervous system toxins are carried by elapid snakes like cobras, kraits and the taipan. Typical targets are the nicotinic acetylcholine receptor and the muscarinic acetylcholine receptor. Blockade of these receptors at the neuromuscular junctions resulting in death by asphyxiation. Acetylcholine receptors are not present in bacteria.

Cardiovascular toxins are pretty diverse and include things like angiotensin-converting enzyme inhibitors (leading to a drop in blood pressure) and glycosaminoglycans (the sulphated carbohydrate moieties that occur abundantly in cells of cardiovascular tissues) binding proteins that lead to cardiotoxicity. Again, the targets are specific molecules involved in heart function and hormones, stuff not present in bacteria.

Muscular toxins include those that bind specifically to the sarcoplasmic reticulum of muscles or interfere with specific second messenger systems messing up muscular function. Again, quite specific targets not present in bacteria.

Lastly, typical vascular system toxins include anti-coagulants such as protein C activators and inhibitors of prothrombin complex formation. Again, specific targets.

Reference
Koh et al., Cell. Mol. Life Sci (2006); 63: 3030-3041


Venoms from vipers contain high amount of proteolytic enzymes (serine proteases). Many of them act by cleaving fibrinogen and thereby causing blood clot (ref). There is a likelihood that some of these proteases may affect other proteins also. In a study conducted by Bottrall et al. (2010), it was shown that snake venoms do have a general proteolytic activity. The best among tested was the venom of the viper Bitis arietans. However, its activity was significantly lower than the positive control which consisted mainly of trypsin and proteinase-K.

So the venom may have a little effect on the membrane proteins of bacteria. But it might require extended treatment by venom to digest these proteins compared to that by stronger proteases like proteinase-K.

However, there are indeed reports on antibacterial activity of snake venoms (Stiles et al., 1991; Perumal Samy et al., 2007; Charvat et al., 2018). But the enzymes responsible for the antibacterial activity are phospholipase A2 and L-amino acid oxidase, and not the proteases.


Immunity- Immune System and Immunization

Created with BioRender.com

Mechanism of Immunity

  • As much as immunity curtails to the 430 B.C, significantly improved immunity phenomenal were made in the 18th century starting with Edward Jenner in 1798 after he noticed that milkmaids that had contracted the mild-disease of cowpox, were immune to smallpox (a fatally deadly disease).
  • He practically inoculated cowpox pustules into an 8-year old boy and intentionally infected him with smallpox. As he had predicted, the child did not develop smallpox. His work was subsequently followed by Pastuer’s work who developed vaccines for chicken cholera, anthrax, and rabies.
  • To understand the immunity phenomenon, an understanding of the mechanism of immunity was needed, and therefore, the experimental work of Emil von Behring and Shibasaburo Kitasato in 1890 gave the first insight into the mechanism of immunity. They demonstrated that serum contained elements known as antibodies. They functioned to protect against infections thus laying the foundation for the identification of humoral immunity.
  • Emil von Behring received the Nobel Prize in Medicine in 1901 in recognition of his work.
  • Elie Metchnikoff also demonstrated that cells contribute to the immune state of an animal in 1884, earlier before von Bekring’s demonstration of the serum elements. Metchnikoff observed that certain white blood cells, which he termed phagocytes, were able to ingest (phagocytose) microorganisms and other foreign material.
  • He notes that the phagocytic cells were very active in animals that had been immunized, and hypothesized that cells were the major effectors of immunity that the serum components. The active phagocytic cells identified by Metchnikoff were most likely blood monocytes and neutrophils.

Some Mice Have Become Immune to Poison Through Natural but Highly Unusual Evolution

Mice are great (see: high-endurance mice, mice with lab-grown artificial organs, Israeli bomb-sniffing security mice) but sometimes you just don’t want them in your apartment/house/bakery/kitchen/New York subway station, which is why you might buy some warfarin, a common rodent poison. Some mice, however, have developed an immunity to that poison through highly unusual means: horizontal gene transfer, a kind of evolution-through-hybridization that’s only been seen before in microbes.

As reported in the current issue of Current Biology, mice in a German bakery were discovered to have absolutely no reaction to the use of even a particularly nasty form of warfarin, which is usually a kiss of death for our friend the house mouse. A genetic analysis showed that the mice in that kitchen actually had a large chunk of DNA from the Algerian mouse, a separate (though closely related) species from the house mouse that’s usually found around the sandy western coasts of the Mediterranean.

The Algerian mouse, you see, is immune to warfarin–apparently that gene also helps manage a vitamin K deficiency the Algerian mouse’s diet has–and humans, with all of our travel and such, introduced the two species, which would not normally have come into contact with each other. The house mouse bred with the Algerian mouse, and bam: poison-immune super house mice.

This kind of evolution, in which hybridization produces a beneficial genetic makeup, is called horizontal gene transfer. It’s very different from the usual style of evolution, in which beneficial mutations are passed on to the next generation, and has actually never been observed before in any complex animal. Horizontal gene transfer has heretofore only been seen in microbes, so it’s pretty amazing to see it in something as complex and adorable as a mouse. Of course, that may make it more difficult for bakers and MTA employees to rid their businesses and/or subway stations of rodents, but the mice are probably pleased.


Contents

The most common first symptom of all snakebites is an overwhelming fear, which may contribute to other symptoms, and may include nausea and vomiting, diarrhea, vertigo, fainting, tachycardia, and cold, clammy skin. [2] [20] Different snakes cause different types of signs and symptoms depending on the type of snake biting. [ citation needed ]

Dry snakebites and those inflicted by a non-venomous species may still cause severe injury. The bite may become infected from the snake's saliva. The fangs sometimes harbor pathogenic microbial organisms, including Clostridium tetani, and may require an updated tetanus immunization. [21] [22] Infection is often reported from the bites of vipers, whose fangs are capable of deep puncture wounds, which may introduce infectious organisms into the tissue. [ citation needed ]

Most snakebites, from either a venomous or a non-venomous snake, will have some type of local effect. Minor pain and redness occur in over 90 percent of cases, although this varies depending on the site. [2] Bites by vipers and some cobras may be extremely painful, with the local tissue sometimes becoming tender and severely swollen within five minutes. [15] This area may also bleed and blister, and may lead to tissue necrosis. Other common initial symptoms of pit viper and viper bites include lethargy, bleeding, weakness, nausea, and vomiting. [2] [15] Symptoms may become more life-threatening over time, developing into hypotension, tachypnea, severe tachycardia, severe internal bleeding, altered sensorium, kidney failure, and respiratory failure. [2] [15]

Bites by some snakes, such as the kraits, coral snake, Mojave rattlesnake, and the speckled rattlesnake, may cause little or no pain, despite their serious and potentially life-threatening venom. [2] Some people report experiencing a "rubbery", "minty", or "metallic" taste after being bitten by certain species of rattlesnake. [2] Spitting cobras and rinkhalses can spit venom in a person's eyes. This results in immediate pain, ophthalmoparesis, and sometimes blindness. [23] [24]

Some Australian elapids and most viper envenomations will cause coagulopathy, sometimes so severe that a person may bleed spontaneously from the mouth, nose, and even old, seemingly healed wounds. [15] Internal organs may bleed, including the brain and intestines, and ecchymosis (bruising) of the skin is often seen. [ citation needed ]

The venom of elapids, including sea snakes, kraits, cobras, king cobra, mambas, and many Australian species, contains toxins which attack the nervous system, causing neurotoxicity. [2] [15] [26] The person may present with strange disturbances to their vision, including blurriness. Paresthesia throughout the body, as well as difficulty in speaking and breathing, may be reported. [2] Nervous system problems will cause a huge array of symptoms, and those provided here are not exhaustive. If not treated immediately they may die from respiratory failure. [ citation needed ]

Venom emitted from some types of cobras, almost all vipers and some sea snakes causes necrosis of muscle tissue. [15] Muscle tissue will begin to die throughout the body, a condition known as rhabdomyolysis. Rhabdomyolysis can result in damage to the kidneys as a result of myoglobin accumulation in the renal tubules. This, coupled with hypotension, can lead to acute kidney injury, and, if left untreated, eventually death. [15]

Snakebite is also known to cause depression and post-traumatic stress disorder in a high proportion of people who survive. [27]

In the developing world most snakebites occur in those who work outside such as farmers, hunters, and fishermen. They often happen when a person steps on the snake or approaches it too closely. In the United States and Europe snakebites most commonly occur in those who keep them as pets. [28]

The type of snake that most often delivers serious bites depends on the region of the world. In Africa, it is mambas, Egyptian cobras, puff adders, and carpet vipers. In the Middle East, it is carpet vipers and elapids. In Latin America, it is snakes of the Bothrops and Crotalus types, the latter including rattlesnakes. [28] In North America, rattlesnakes are the primary concern, and up to 95% of all snakebite-related deaths in the United States are attributed to the western and eastern diamondback rattlesnakes. [2] In South Asia, it was previously believed that Indian cobras, common kraits, Russell's viper, and carpet vipers were the most dangerous other snakes, however, may also cause significant problems in this area of the world. [28]

Since envenomation is completely voluntary, all venomous snakes are capable of biting without injecting venom into a person. Snakes may deliver such a "dry bite" rather than waste their venom on a creature too large for them to eat, a behaviour called venom metering. [29] However, the percentage of dry bites varies among species: 80 percent of bites inflicted by sea snakes, which are normally timid, do not result in envenomation, [26] whereas only 25 percent of pit viper bites are dry. [2] Furthermore, some snake genera, such as rattlesnakes, significantly increase the amount of venom injected in defensive bites compared to predatory strikes. [30]

Some dry bites may also be the result of imprecise timing on the snake's part, as venom may be prematurely released before the fangs have penetrated the person. [29] Even without venom, some snakes, particularly large constrictors such as those belonging to the Boidae and Pythonidae families, can deliver damaging bites large specimens often cause severe lacerations, or the snake itself pulls away, causing the flesh to be torn by the needle-sharp recurved teeth embedded in the person. While not as life-threatening as a bite from a venomous species, the bite can be at least temporarily debilitating and could lead to dangerous infections if improperly dealt with. [ citation needed ]

While most snakes must open their mouths before biting, African and Middle Eastern snakes belonging to the family Atractaspididae are able to fold their fangs to the side of their head without opening their mouth and jab a person. [31]

Snake venom Edit

It has been suggested that snakes evolved the mechanisms necessary for venom formation and delivery sometime during the Miocene epoch. [32] During the mid-Tertiary, most snakes were large ambush predators belonging to the superfamily Henophidia, which use constriction to kill their prey. As open grasslands replaced forested areas in parts of the world, some snake families evolved to become smaller and thus more agile. However, subduing and killing prey became more difficult for the smaller snakes, leading to the evolution of snake venom. [32] Other research on Toxicofera, a hypothetical clade thought to be ancestral to most living reptiles, suggests an earlier time frame for the evolution of snake venom, possibly to the order of tens of millions of years, during the Late Cretaceous. [33]

Snake venom is produced in modified parotid glands normally responsible for secreting saliva. It is stored in structures called alveoli behind the animal's eyes, and ejected voluntarily through its hollow tubular fangs. Venom is composed of hundreds to thousands of different proteins and enzymes, all serving a variety of purposes, such as interfering with a prey's cardiac system or increasing tissue permeability so that venom is absorbed faster. [ citation needed ]

Venom in many snakes, such as pit vipers, affects virtually every organ system in the human body and can be a combination of many toxins, including cytotoxins, hemotoxins, neurotoxins, and myotoxins, allowing for an enormous variety of symptoms. [2] [34] Earlier, the venom of a particular snake was considered to be one kind only, i.e. either hemotoxic or neurotoxic, and this erroneous belief may still persist wherever the updated literature is hard to access. Although there is much known about the protein compositions of venoms from Asian and American snakes, comparatively little is known of Australian snakes. [ citation needed ]

The strength of venom differs markedly between species and even more so between families, as measured by median lethal dose (LD50) in mice. Subcutaneous LD50 varies by over 140-fold within elapids and by more than 100-fold in vipers. The amount of venom produced also differs among species, with the Gaboon viper able to potentially deliver from 450–600 milligrams of venom in a single bite, the most of any snake. [35] Opisthoglyphous colubrids have venom ranging from life-threatening (in the case of the boomslang) to barely noticeable (as in Tantilla). [ citation needed ]

Snakes are most likely to bite when they feel threatened, are startled, are provoked, or when they have been cornered. Snakes are likely to approach residential areas when attracted by prey, such as rodents. Regular pest control can reduce the threat of snakes considerably. It is beneficial to know the species of snake that are common in local areas, or while travelling or hiking. Africa, Australia, the Neotropics, and southern Asia in particular are populated by many dangerous species of snake. Being aware of—and ultimately avoiding—areas known to be heavily populated by dangerous snakes is strongly recommended. [ citation needed ]

When in the wilderness, treading heavily creates ground vibrations and noise, which will often cause snakes to flee from the area. However, this generally only applies to vipers, as some larger and more aggressive snakes in other parts of the world, such as mambas and cobras, [36] will respond more aggressively. If presented with a direct encounter, it is best to remain silent and motionless. If the snake has not yet fled, it is important to step away slowly and cautiously. [ citation needed ]

The use of a flashlight when engaged in camping activities, such as gathering firewood at night, can be helpful. Snakes may also be unusually active during especially warm nights when ambient temperatures exceed 21 °C (70 °F). It is advised not to reach blindly into hollow logs, flip over large rocks, and enter old cabins or other potential snake hiding-places. When rock climbing, it is not safe to grab ledges or crevices without examining them first, as snakes are cold-blooded and often sunbathe atop rock ledges. [ citation needed ]

In the United States, more than 40 percent of people bitten by snake intentionally put themselves in harm's way by attempting to capture wild snakes or by carelessly handling their dangerous pets—40 percent of that number had a blood alcohol level of 0.1 percent or more. [37]

It is also important to avoid snakes that appear to be dead, as some species will actually roll over on their backs and stick out their tongue to fool potential threats. A snake's detached head can immediately act by reflex and potentially bite. The induced bite can be just as severe as that of a live snake. [2] [38] As a dead snake is incapable of regulating the venom injected, a bite from a dead snake can often contain large amounts of venom. [39]

It may be difficult to determine if a bite by any species of snake is life-threatening. A bite by a North American copperhead on the ankle is usually a moderate injury to a healthy adult, but a bite to a child's abdomen or face by the same snake may be fatal. The outcome of all snakebites depends on a multitude of factors: the type of snake, the size, physical condition, and temperature of the snake, the age and physical condition of the person, the area and tissue bitten (e.g., foot, torso, vein or muscle), the amount of venom injected, the time it takes for the person to find treatment, and finally the quality of that treatment. [2] [40] An overview of systematic reviews on different aspects of snakebite management found that the evidence base from majority of treatment modalities is low quality. [41]

Snake identification Edit

Identification of the snake is important in planning treatment in certain areas of the world, but is not always possible. Ideally the dead snake would be brought in with the person, but in areas where snake bite is more common, local knowledge may be sufficient to recognize the snake. However, in regions where polyvalent antivenoms are available, such as North America, identification of snake is not a high priority item. Attempting to catch or kill the offending snake also puts one at risk for re-envenomation or creating a second person bitten, and generally is not recommended. [ citation needed ]

The three types of venomous snakes that cause the majority of major clinical problems are vipers, kraits, and cobras. Knowledge of what species are present locally can be crucial, as is knowledge of typical signs and symptoms of envenomation by each type of snake. A scoring system can be used to try to determine the biting snake based on clinical features, [42] but these scoring systems are extremely specific to particular geographical areas. [ citation needed ]

First aid Edit

Snakebite first aid recommendations vary, in part because different snakes have different types of venom. Some have little local effect, but life-threatening systemic effects, in which case containing the venom in the region of the bite by pressure immobilization is desirable. Other venoms instigate localized tissue damage around the bitten area, and immobilization may increase the severity of the damage in this area, but also reduce the total area affected whether this trade-off is desirable remains a point of controversy. Because snakes vary from one country to another, first aid methods also vary.

Many organizations, including the American Medical Association and American Red Cross, recommend washing the bite with soap and water. Australian recommendations for snake bite treatment recommend against cleaning the wound. Traces of venom left on the skin/bandages from the strike can be used in combination with a snake bite identification kit to identify the species of snake. This speeds determination of which antivenom to administer in the emergency room. [43]

Pressure immobilization Edit

As of 2008, clinical evidence for pressure immobilization via the use of an elastic bandage is limited. [44] It is recommended for snakebites that have occurred in Australia (due to elapids which are neurotoxic). [45] It is not recommended for bites from non-neurotoxic snakes such as those found in North America and other regions of the world. [45] [46] The British military recommends pressure immobilization in all cases where the type of snake is unknown. [47]

The object of pressure immobilization is to contain venom within a bitten limb and prevent it from moving through the lymphatic system to the vital organs. This therapy has two components: pressure to prevent lymphatic drainage, and immobilization of the bitten limb to prevent the pumping action of the skeletal muscles.

Antivenom Edit

Until the advent of antivenom, bites from some species of snake were almost universally fatal. [48] Despite huge advances in emergency therapy, antivenom is often still the only effective treatment for envenomation. The first antivenom was developed in 1895 by French physician Albert Calmette for the treatment of Indian cobra bites. Antivenom is made by injecting a small amount of venom into an animal (usually a horse or sheep) to initiate an immune system response. The resulting antibodies are then harvested from the animal's blood.

Antivenom is injected into the person intravenously, and works by binding to and neutralizing venom enzymes. It cannot undo damage already caused by venom, so antivenom treatment should be sought as soon as possible. Modern antivenoms are usually polyvalent, making them effective against the venom of numerous snake species. Pharmaceutical companies which produce antivenom target their products against the species native to a particular area. Although some people may develop serious adverse reactions to antivenom, such as anaphylaxis, in emergency situations this is usually treatable and hence the benefit outweighs the potential consequences of not using antivenom. Giving adrenaline (epinephrine) to prevent adverse reactions to antivenom before they occur might be reasonable in cases where they occur commonly. [49] Antihistamines do not appear to provide any benefit in preventing adverse reactions. [49]

Outmoded Edit

The following treatments, while once recommended, are considered of no use or harmful, including tourniquets, incisions, suction, application of cold, and application of electricity. [46] Cases in which these treatments appear to work may be the result of dry bites.

  • Application of a tourniquet to the bitten limb is generally not recommended. There is no convincing evidence that it is an effective first-aid tool as ordinarily applied. [50] Tourniquets have been found to be completely ineffective in the treatment of Crotalus durissus bites, [51] but some positive results have been seen with properly applied tourniquets for cobra venom in the Philippines. [52] Uninformed tourniquet use is dangerous, since reducing or cutting off circulation can lead to gangrene, which can be fatal. [50] The use of a compression bandage is generally as effective, and much safer.
  • Cutting open the bitten area, an action often taken prior to suction, is not recommended since it causes further damage and increases the risk of infection the subsequent cauterization of the area with fire or silver nitrate (also known as infernal stone) is also potentially threatening. [53]
  • Sucking out venom, either by mouth or with a pump, does not work and may harm the affected area directly. [54] Suction started after three minutes removes a clinically insignificant quantity—less than one-thousandth of the venom injected—as shown in a human study. [55] In a study with pigs, suction not only caused no improvement but led to necrosis in the suctioned area. [56] Suctioning by mouth presents a risk of further poisoning through the mouth's mucous tissues. [57] The helper may also release bacteria into the person's wound, leading to infection.
  • Immersion in warm water or sour milk, followed by the application of snake-stones (also known as la Pierre Noire), which are believed to draw off the poison in much the way a sponge soaks up water.
  • Application of a one-percent solution of potassium permanganate or chromic acid to the cut, exposed area. [53] The latter substance is notably toxic and carcinogenic.
  • Drinking abundant quantities of alcohol following the cauterization or disinfection of the wound area. [53]
  • Use of electroshock therapy in animal tests has shown this treatment to be useless and potentially dangerous. [58][59][60][61]

In extreme cases, in remote areas, all of these misguided attempts at treatment have resulted in injuries far worse than an otherwise mild to moderate snakebite. In worst-case scenarios, thoroughly constricting tourniquets have been applied to bitten limbs, completely shutting off blood flow to the area. By the time the person finally reached appropriate medical facilities their limbs had to be amputated.

Estimates vary from 1.2 to 5.5 million snakebites, 421,000 to 2.5 million envenomings, and 20,000 to 125,000 deaths. [3] [10] Since reporting is not mandatory in much of the world, the data on the frequency of snakebites is not precise. [10] Many people who survive bites have permanent tissue damage caused by venom, leading to disability. [15] Most snake envenomings and fatalities occur in South Asia, Southeast Asia, and sub-Saharan Africa, with India reporting the most snakebite deaths of any country. [10]

Most snakebites are caused by non-venomous snakes. Of the roughly 3,000 known species of snake found worldwide, only 15% are considered dangerous to humans. [2] [10] Snakes are found on every continent except Antarctica. [10] The most diverse and widely distributed snake family, the colubrids, has approximately 700 venomous species, [62] but only five genera—boomslangs, twig snakes, keelback snakes, green snakes, and slender snakes—have caused human fatalities. [62]

Worldwide, snakebites occur most frequently in the summer season when snakes are active and humans are outdoors. [10] [63] Agricultural and tropical regions report more snakebites than anywhere else. [10] [64] In the United States, those bitten are typically male and between 17 and 27 years of age. [2] [63] [65] Children and the elderly are the most likely to die. [2] [40]

When venomous snakes bite a target, they secrete venom through their venom delivery system. The venom delivery system generally consists of two venom glands, a compressor muscle, venom ducts, a fang sheath, and fangs. The primary and accessory venom glands store the venom quantities required during envenomation. The compressor muscle contracts during bites to increase the pressure throughout the venom delivery system. The pressurized venom travels through the primary venom duct to the secondary venom duct that leads down through the fang sheath and fang. The venom is then expelled through the exit orifice of the fang. The total volume and flow rate of venom administered into a target varies widely, sometimes as much as an order of magnitude. One of the largest factors is snake species and size, larger snakes have been shown to administer larger quantities of venom. [66]

Predatory vs. defensive bites Edit

Snake bites are classified as either predatory or defensive in nature. During defensive strikes, the rate of venom expulsion and total volume of venom expelled is much greater than during predatory strikes. Defensive strikes can have 10 times as much venom volume expelled at 8.5 times the flow rate. [67] This can be explained by the snake's need to quickly subdue a threat. While employing similar venom expulsion mechanics, predatory strikes are much different than defensive strikes. Snakes usually release the prey shortly after the envenomation allowing the prey to run away and die. Releasing prey prevents retaliatory damage to the snake. The venom scent allows the snake to relocate the prey once it is deceased. [66] The amount of venom injected has been shown to increase with the mass of the prey animal. [68] Larger venom volumes allow snakes to effectively euthanize larger prey while remaining economical during strikes against smaller prey. This is an important skill as venom is a metabolically expensive resource. [ citation needed ]

Venom Metering Edit

Venom metering is the ability of a snake to have neurological control over the amount of venom released into a target during a strike based on situational cues. This ability would prove useful as venom is a limited resource, larger animals are less susceptible to the effects of venom, and various situations require different levels of force. There is a lot of evidence to support the venom metering hypothesis. For example, snakes frequently use more venom during defensive strikes, administer more venom to larger prey, and are capable of dry biting. A dry bite is a bite from a venomous snake that results in very little or no venom expulsion, leaving the target asymptomatic. [69] However, there is debate among many academics about venom metering in snakes. The alternative to venom metering is the pressure balance hypothesis.

The pressure balance hypothesis cites the retraction of the fang sheath as the many mechanism for producing outward venom flow from the venom delivery system. When isolated, fang sheath retraction has experimentally been shown to induce very high pressures in the venom delivery system. [70] A similar method was used to stimulate the compressor musculature, the main muscle responsible for the contraction and squeezing of the venom glad, and then measuring the induced pressures. It was determined that the pressure created from the fang sheath retraction was at times an order of magnitude greater than those created by the compressor musculature. Snakes do not have direct neurological control of the fang sheath, it can only be retracted as the fangs enter a target and the target's skin and body provide substantial resistance to retract the sheath. For these reasons, the pressure balance hypothesis concludes that external factors, mainly the bite and physical mechanics, are responsible for the quantity of venom expelled.

Venom Spitting Edit

Venom spitting is another venom delivery method that is unique to some Asiatic and African cobras. In venom spitting, a stream of venom is propelled at very high pressures outwards up to 3 meters. The venom stream is usually aimed at the eyes and face of the target as a deterrent for predators. There are non-spitting cobras that provide useful information on the unique mechanics behind venom spitting. Unlike the elongated oval shaped exit orifices of non-spitting cobras, spitting cobras have circular exit orifice at their fang tips. [71] This combined with the ability to partially retract their fang sheath by displacing the palato-maxillary arch and contracting the adductor mandibulae, allows the spitting cobras to create large pressures within the venom delivery system. [72] While venom spitting is a less common venom delivery system, the venom can still cause the effects if ingested. [ citation needed ]

Snakes were both revered and worshipped and feared by early civilizations. The ancient Egyptians recorded prescribed treatments for snakebites as early as the Thirteenth Dynasty in the Brooklyn Papyrus, which includes at least seven venomous species common to the region today, such as the horned vipers. [73] In Judaism, the Nehushtan was a pole with a snake made of copper fixed upon it. The object was regarded as a divinely empowered instrument of God that could bring healing to Jews bitten by venomous snakes while they were wandering in the desert after their exodus from Egypt. Healing was said to occur by merely looking at the object as it was held up by Moses.

Historically, snakebites were seen as a means of execution in some cultures. In medieval Europe, a form of capital punishment was to throw people into snake pits, leaving people to die from multiple venomous bites. A similar form of punishment was common in Southern Han during China's Five Dynasties and Ten Kingdoms period and in India. [74] Snakebites were also used as a means of suicide, most notably by Egyptian queen Cleopatra VII, who reportedly died from the bite of an asp—likely an Egyptian cobra [73] [75] —after hearing of Mark Antony's death.

Snakebite as a surreptitious form of murder has been featured in stories such as Sir Arthur Conan Doyle's The Adventure of the Speckled Band, but actual occurrences are virtually unheard of, with only a few documented cases. [74] [76] [77] It has been suggested that Boris III of Bulgaria, who was allied to Nazi Germany during World War II, may have been killed with snake venom, [74] although there is no definitive evidence. At least one attempted suicide by snakebite has been documented in medical literature involving a puff adder bite to the hand. [78]

In 2018, the World Health Organization listed snakebite envenoming as a neglected tropical disease. [79] [80] In 2019, they launched a strategy to prevent and control snakebite envenoming, which involved a program targeting affected communities and their health systems. [81] [82] New monoclonal antibodies, polymer gels and a small molecule inhibitor called Varespladib are in development. [83]

Several animals acquired immunity against venom of snakes that occur in the same habitat. [84] This has been documented in some humans as well. [85]


How does an immune system combat toxins (like snake venom)?

I understand (at least crudely) how our immune system reacts to viruses, bacteria, and mold, but I'm ignorant as to how exactly it fights toxins. The recent TIL about Bill Haast developing a strong resistance to various snake venoms made this thought jump into my head.

Does our immune system simply treat a toxin in whatever way it treats a standard dangerous protein/molecule/peptide (or is any dangerous protein/molecule/peptide automatically considered a toxin by the mere fact that it's dangerous)? How does one actually resist things like specific venoms or poisons? Do we actually keep antibodies around to fight against these chemicals like we would for something like chickenpox? Or do the affected tissues of a specific toxin somehow build up their own resistances to its effects? I feel as though I'm conceptualizing toxins in a way that makes them seem difficult to "fight off", when in truth the methods of stopping them are very similar to the methods of fighting off harmful bacteria or whatnot, and I just can't get over my own mental block.

Your body can't really tell whether a protein is a toxin or not, it just knows that it shouldn't be there in the first place. The immune system will usually recognize and try to neutralize any proteins that it identifies as foreign. That's why organ transplants are problematic your body knows that it's foreign and tries to destroy it.

Protein-based toxins are neutralized by antibodies. The toxins are recognized by our immune systems and antibodies are produced against that specific protein. These antibodies, once made, have the ability to bind to the toxins and prevent it from interacting with the body, thus rendering it harmless and allowing the body to dispose of it. This is true of any foreign proteins, be it snake venom or cholera toxin. It can take up to a week to develop these antibodies, so obviously this won't help you if a snake has injected you with a lethal dose that will kill you in hours. However, if you give yourself small non-lethal doses, it allows the body to produce the antibodies and give you a certain level of immunity over time.

This is actually the basis of antivenom production. Venom is collected and a non-lethal amount injected into a large animal like a horse (or Bill Haast). The horse does the same thing we do and produce copious amounts of antibodies against the venom. All that's left to do is purify the antibody and injected into someone who's been bitten. The antibodies will neutralize the venom in the same way.


Super rats are immune to conventional poisons, UK experts find

A University of Huddersfield scientist has alerted the UK to the mounting problem of destructive "super rats" immune to conventional poison. His research has created nationwide interest, especially in the West of England, where it might be that as many as 75 per cent of rats are the resistant type.

Dr Dougie Clarke, who is Head of Biological Sciences at the University of Huddersfield's School of Applied Sciences, leads the UK Rodenticide Resistance Mapping Project. It takes DNA samples from hundreds of rats around the country in order to establish which regions have the highest prevalence of rats that have genetic mutations that protect them from the most commonly used rat poisons.

The goal is to find which parts of the country have the largest populations of rats with a genetic resistance to the most commonly used rodenticides -- warfarin, bromadiolone and difenacoum. These are anticoagulants that subjects rats to death from internal bleeding and have been widely used since the 1950s but soon after their introduction, it was discovered that some rats were unaffected by these poisons.

After it first became known in the 1950s that some rats could withstand conventional poisons, the Government carried out research. But it had to do this by the laborious method of trapping rats and conducting feeding tests on the whole animal. This research was discontinued in the 1990s but over the past two decades the problem of resistance in rats has increased.

Where the animals thrive they can spread disease, deplete food resources, gnaw electrical cables and even cause structural damage. And because they survived, their descendants have the same resistance. The result, says Dr Clarke, is that while there might have originally been only a few percent of resistant rats in certain urban and rural areas, they now make up a significant proportion of the population.

The highest prevalence has so far been found in certain areas of South of England and West Country where greater than 70 % the animals tested are of the 'super' rat type.

This means that populations of the creatures will grow and there could be a threat to wildlife and even domestic cats that hunt and devour rats whose bodies are carrying the poison to which they have become resistant.

In order to combat the problem there are stronger poisons -- such as brodifacoum and flocoumafen -- that can be used and they have proved to be effective, even against the so-called super rats. But these rodenticides have to be used in strictly controlled conditions, under licence from the Health and Safety Executive. Therefore, local authorities, pest control operators and the chemical giants that manufacture the rat poisons need to know which areas of the country are most heavily infested by resistant rats so that the green light can be given to use the more powerful substances.

"In one area every rat we analysed was resistant and infestation was so bad that the pest control company applied to the Health and Safety Executive for emergency use of the stronger rodenticides and they were eliminated within two weeks."

As a result of the discovery of the genetic mutations that cause the resistance, Dr Clarke and his colleagues have embarked on the major new research project, funded by a roster of leading European pest control industry companies (BASF, Bayer, Bell, Killgerm, PelGar, Syngenta), the British Pest Control Organisation and the National Pest Technicians Association. Instead of using live animals the study analyses the animal's genetic make-up to determine if it is resistant to conventional poisons by using three cms of the tip of a rat's tail.

The aim is to test at least 600 animals and it is hoped that the project will be completed in 2013. The arrival of winter weather, robbing rats of much of their natural food supply, will speed up the numbers of samples dispatched to the University of Huddersfield's labs.

The focus of the research is on a series of hot spots in Britain where it is known or suspected that the resistant rats predominate.

The term "super rat" is quite appropriate, says Dr Clarke. The creatures that are unaffected by routine poisons have not become resistant because of their DNA mutating as a result of their exposure to the rodenticide chemicals. The timescale is too short for that. Instead they have a naturally occuring genetic mutation that protects them from the rodenticide poisons. Over time in an area that is treated with these poisons for rat control with a mixed population of susceptible 'normal' rats and the genetically resistant 'super' rats the population will become exclusively the 'super' rat type that pass the resistance gene to their offspring.

When he has gathered more scientific data, the findings will be published, probably during 2013. But in the interim, news of his research has created nationwide interest, especially in the West of England, where it might be that as many as 75 per cent of rats are the resistant type.


Snake Venom May Help Prevent Stroke

Researchers are studying snake venom in the hope of developing future treatments for stroke, heart disease, and even cancer. Snake venom contains toxins that target a specific receptor protein on blood platelets. The toxins can either prevent blood from clotting or cause clots to develop. Researchers believe that irregular blood clot formation and the spread of cancer can be prevented by inhibiting a specific platelet protein.

Blood clotting occurs naturally in order to stop the bleeding when blood vessels become damaged. Improper platelet clotting, however, can lead to heart attack and stroke. Researchers have identified a specific platelet protein, CLEC-2, that is not only needed for clot formation but also needed for the development for lymphatic vessels, which help to prevent swelling in tissues. They also contain a molecule, podoplanin, that binds to the CLEC-2 receptor protein on platelets similarly to the way snake venom does. Podoplanin promotes blood clot formation and is also secreted by cancer cells as a defense against immune cells. Interactions between CLEC-2 and podoplanin is thought to promote cancer growth and metastasis. Understanding how toxins in snake venom interact with blood may help scientists develop new therapies for those with irregular blood clot formation and cancer.


How bacteria boost the immune system

Scientists have long known that certain types of bacteria boost the immune system. Now, Loyola University Health System researchers have discovered how bacteria perform this essential task.

Senior author Katherine L. Knight, PhD. and colleagues report their discovery in a featured article in the June 15, 2010, issue of the Journal of Immunology, now available online. Knight is professor and chair of the Department of Microbiology and Immunology at Loyola University Chicago Stritch School of Medicine.

The human body is teeming with bacteria. In each person, there are about 10 times as many bacterial cells as human cells. Bacteria live on skin, in the respiratory tract and throughout the digestive tract. The digestive tract alone is home to between 500 and 1,000 bacterial species.

While some bacteria cause infections, most species are harmless or perform beneficial functions, such as aiding digestion. These beneficial bugs are called commensal bacteria. One of the most important functions of commensal bacteria is boosting the immune system. Studies by other researchers have found that mice raised in sterile, germ-free environments have poorly developed immune systems. But until now, scientists have not known the mechanism by which bacteria help the immune system.

Knight's lab studied the spores from rod-shaped bacteria called Bacillus, found in the digestive tract. (A spore consists of the DNA of a bacterium, encased in a shell. Bacteria form spores during times of stress, and re-emerge when conditions improve.) Researchers found that when they exposed immune system cells called B lymphocytes to bacterial spores, the B cells began dividing and reproducing.

Researchers further found that molecules on the surfaces of the spores bound to molecules on the surfaces of B cells. This binding is what activated the B cells to divide and multiply. B cells are one of the key components of the immune system. They produce antibodies that fight harmful viruses and bacteria.

The findings suggest the possibility that some day, bacterial spores could be used to treat people with weakened or undeveloped immune systems, such as newborns, the elderly and patients undergoing bone marrow transplants. In cancer patients, bacterial spores perhaps could boost the immune system to fight tumors. However, Knight cautioned that it would take years of research and clinical trials to prove whether such treatments were safe and effective.

Knight's lab at Loyola is supported by two research grants, totaling $3.3 million, from the National Institute of Allergy and Infectious Diseases. Members of her research group are studying how intestinal microbes interact with the host and promote the development of the immune system. Knight also is principal investigator of a $963,000 NIAID training grant in experimental immunology that supports research stipends, supplies and travel to professional meetings for PhD. students in the basic sciences at Loyola.

Knight's co-authors in the Journal of Immunology study are first author Kari M. Severson, PhD., Adam Driks, PhD. and Michael Mallozzi, PhD.


Acquired Poison Immunity

Here's a typical scenario: The hero has finally appeared at his confrontation with the Big Bad, who's seated at his big table, just about to take his evening meal. "There's no reason to be uncivil," the villain says. Would the hero like some wine? The hero takes a drink and immediately starts choking. The villain laughs - that fool, the hero, should have known that the villain would poison the wine with the dreaded juice of the Ultramurder fruit!

But what's this? The hero's standing back up! "I knew you'd poison the wine with the dreaded juice of the Ultramurder fruit. That's why I've spent years eating small pieces of Ultramurder fruit, to develop an immunity to the poison!" The hero then kicks the villain's tail.

In some cases, the poison builds up and actually turns the poison-proof character into a Poisonous Person.

This can be Truth in Television, or not, depending on the poison in question.

For some (chiefly organic) poisons, the body produces antibodies to clear them from the system so, with repeated exposure to small amounts, you can build up a level of circulating antibody that grants immunity to a typical dose. In the past ages, the few metallic poisons known were rare and expensive therefore most poisons were plant-based alkaloids. However, there are plenty of other poisons (including nearly all heavy metals to which modern civilians and industrial workers are exposed, such as compounds of lead, radium, mercury and cadmium) that don't get cleared from the system and simply build up in your tissues until you reach a lethal dose.

The official term for this is Mithridatism, after a king who made use of the effect. It backfired when he was defeated and tried to commit suicide his immunity to poison worked so well that he ended up needing to hire a mercenary to run him through.

Could be considered a sub-trope of Adaptive Ability. A particularly Crazy-Prepared person may be immune to several &mdash or even all &mdash poisons via this method, though again it's important to note that in real life, not all poisons can be defended from in this manner. This trope is often key to the survival of someone who is pulling a Self-Poisoning Gambit.


Passive Poisons vs. Militant Venoms

Many animals and plants are equipped with potent toxins to deter potential predators like us. The term used for such toxins depends on how they’re used. It’s kind of like how lawyers use the term “murder weapon” to refer to an object used to kill someone — a paperweight, a knife, or a shoe isn’t a murder weapon (or in two of those cases, a weapon at all) until its used to commit the crime. Well, toxins aren’t referred to as poisons or venoms until how they enter someone’s body has been taken into account. Some toxins act when ingested, absorbed through the skin, or inhaled such toxins are referred to as poisons . Others enter our bodies through wounds deliberately inflicted by the toxic species — those are venoms.

Because poisons must be eaten, rubbed on the skin, or breathed in, they’re somewhat “passive” toxins — for the most part, if you’re poisoned, it’s you who did something to cause it. You ate or touched something you really, really shouldn’t have, like an aptly-named poison dart frog, a pufferfish, or certain mushrooms.

The somewhat active role of the intoxicated in poisonings is what sets them apart from envenomations. It essentially boils down to who the aggressor is: the toxic species (venoms) or the one who suffers the effects of the toxins (poisons). Venomous animals and plants by definition are armed with physiological weapons to inflict their terrible chemical cocktails — they bring the toxins to you. It’s entirely possible the only thing someone did to cause an envenomation is unknowingly stray in the general vicinity of a venomous species (though there are certainly times when it’s totally the victim’s fault , and some defensively venomous species just sit and wait for you to impale yourself on them). Though it’s a bit oversimplified, this comic sums up the difference quite nicely:

The difference between poison and venom is why toxinologists cringe every time they see someone referring to a “poisonous snake.” Most snakes are perfectly fine to handle or eat (I hear they taste like chicken with the texture of fish — which, frankly, sounds delicious), presuming you don’t get stuck with the pointy bits in the process . There are even snakes that can kill you with their venomous bites that are considered delicacies in certain cultures’ cuisines … just ask Gordon Ramsay:

That said, there are exceptions to every rule. Yes, there are some poisonous snakes. The most well studied are the species in the genus Rhabdophis , which are both poisonous and venomous. R. tigrinus , for example, is able to sequester and store toxins from the toads it eats and secrete them on its skin to deter would-be predators. But if warning displays and even poison fail to send a message, the snake is also equipped with a potentially deadly venomous bite .

And then there’s even a third subcategory of toxins, for those who appreciate being as accurate as possible: toxungens. Outlined very succinctly by David Nelsen and his colleagues in their 2014 paper , toxungens are poisons that are aggressively wielded, like the squirting of poison by cane toads or spitting of venom by certain cobra species.

Since no wound is inflicted when the toxins are sprayed, they aren’t considered “venoms” in context, but the animals aren’t exactly waiting to be harassed, either. Because the toxic species is actively involved in the delivery of its noxious chemicals, but they aren’t making wounds, we give them a special category all to themselves.

So there you have it. Toxins are substances that cause harm in small amounts. There are three main types of toxins: venoms , poisons and toxungens , which differ based on route of delivery (see the table above). If an animal or plant possesses a toxic chemical cocktail, you can label them with the appropriate adjective(s) — venomous, poisonous and/or toxungenous.

And yes, there are many species which fit into multiple categories, such as poisonous and venomous Rhabdophis snakes or poisonous and toxungenous cane toads. In such cases, you can use whichever terms are most appropriate in context if you’ve just licked a cane toad to try and get high, for example, poison would be most appropriate word for what you’ve ingested. But if you poked it, and it squirted toxins into your eyes, then you get a gold star for calling the beast toxungenous.

Now that you know the right terminology, I encourage you to go forth and correct your friends, family, and coworkers! Though, I would caution you to do your best to be nice about it. You never know what toxins they might have access to …



Comments:

  1. Tejas

    You are wrong. I can defend my position. Write to me in PM, we'll talk.

  2. Thomas

    It is reserve

  3. Kazilkree

    Many thanks for the help in this matter. I did not know this.

  4. Kazranris

    It cannot be said.

  5. Maughold

    I can't take part in the discussion right now - there is no free time. But I'll be free - I will definitely write what I think on this issue.

  6. Yeoman

    I absolutely agree with you. I think this is a good idea. I agree with you.

  7. Birch

    In it something is. Thank you for the help, how can I thank?



Write a message