Compilation of pathophysiological and medical information

Outpost31Survivor

Arachnoprince
Active Member
Joined
Aug 23, 2019
Messages
1,598
Some of it is repetitive but I felt information is too urgent.

Most of the material within is related to Androctonus, Buthus, Hottentotta, Leiurus, Mesobuthus, Olivierus, and most Tityus envenomations. Especially worthy of note is the following genera: Androctonus, Buthus, Hottentotta, Leiurus, and Tityus which contain species that are potentially lethal.

The autonomic nervous system is a component of the peripheral nervous system that regulates involuntary physiologic processes including heart rate, blood pressure, respiration, digestion, and sexual arousal. It contains three anatomically distinct divisions: sympathetic (adrenergic), parasympathetic (cholinergic), and enteric.

The two divisions of the autonomic nervous system are the sympathetic division and the parasympathetic division. The sympathetic system is associated with the fight-or-flight response, and parasympathetic activity is referred to by the epithet of rest and digest. Homeostasis is the balance between the two systems

The venom of Buthidae family scorpions contains several low-molecular weight proteins (neurotoxins) that act mainly on two classes of ion channels: the sodium (Na +)and potassium (K +)voltage-gated channels.These channels conduct the electrical impulse in most excitable tissues, promoting permeability to ions, which initiates the action potential. Alpha and beta toxins act on Na +channels at two pharmacologically distinct sites: alpha toxins bind to receptor site-4 and inhibit channel inactivation while the beta toxins bind receptor-type 3 and enhance activation of the channel upon subsequent depolarization. Toxins acting on K +channels physically block them, and prevent ionic conduction, thus prolonging the action potential. Therefore, the Na +and K +channel toxins synergize to cause intense and prolonged depolarization, leading to neuronal excitation. This in turn stimulates postganglionary nerve endings of the sympathetic and parasympathetic nervous system and of the adrenal medulla, inducing the release of acetylcholine, adrenaline, and noradrenaline. These mediators act rapidly after the sting to initiate a chain of events that represents scorpion envenoming, triggering the onset of clinical manifestations in practically all systems of the organism.

The initial clinical manifestations are mainly due to venom-induced cholinergic and adrenergic effects. Patient signs and symptoms are variable; the established clinical picture depends on the quantity of mediators released, and on the relative contribution of acetylcholine or adrenaline, which are often antagonistic. Symptoms usually start with more transitory parasympathetic activation. Severity, however, is generally determined by the long-lasting effects of high catecholamine concentrations in the cardiovascular system.

Acetylcholine release (parasympathetic, cholinergic) induces myosis, bradycardia, cardiac arrhythmias, arterial hypotension, increased lachrymal, nasal, salivary, pancreatic, gastric and bronchial secretions, diaphoresis, tremors, piloerection and muscle spasms, and increases blood amylase levels. Cholinergic symptoms from parasympathetic activation, including nausea, vomiting, diarrhea, sweating, salivation, lacrimation, and increase in respiratory secretions, in addition to bradycardia and arterial hypotension, often predominate initially.

Manifestations secondary to catecholamine release (sympathetic, adrenergic) include mydriasis, cardiac arrhythmias, tachycardia, arterial hypertension, acute pulmonary edema (APE), cardiac failure, and shock. Adrenergic firing leads to hyperglycemia and leukocytosis and contributes to hypopotassemia. In severe cases, an increase in sympathetic activity, such as hypertension, arrhythmias, and heart failure, becomes predominant.

Majority of the species of the Buthidae family induce similar reactions, except for Tityus obscurus in Brazil, Centruroides, and Parabuthus which also induce neurological manifestations. Signs and symptoms reported in envenoming caused by T. obscurus in some regions of Pará (Santarém) involve myoclonus (a sensation of an electric shock throughout the body), dysmetria, dysarthria, ataxia, paresthesias and hyperreflexia, compatible with acute cerebellar syndrome with abnormal muscle movements, in addition to rhabdomyolysis and acute renal failure.

Pathophysiologically, the cardiovascular clinical picture depends on the conjunction of three mechanisms: (1) autonomic storm (adrenergic or cholinergic), (2) inflammation, and (3) direct myocardial and endothelial toxicity. Tachycardia and hypertension increase cardiac work, which, in turn, lead to myocardial dysfunction either due to an imbalance between oxygen consumption and demand or due to the presence of factors, such as vasoconstriction or spasm of the coronary arteries, that predispose to myocardial ischemia. Concomitantly, the aforementioned mechanisms favor the appearance of electrocardiographic changes and arrhythmias of various kinds. The different mediators released as a result of the action of the scorpion toxin contribute to myocarditis or stress-induced cardiomyopathy. The vascular endothelium also suffers from envenomation, ranging from mild dysfunction, moderate inflammation (vasculitis), to thrombosis. Cardiac and endothelial dysfunction can cause pulmonary edema or cardiogenic shock, and the resulting hypoxia and hypoperfusion may result in multi-organ failure.

In cases of systemic reactions, the clinical signs and symptoms are highly variable, ranging from mild to life-threatening. Systemic reactions commonly are mild and are not necessarily indicators of a serious problem. Often there is no appreciable swelling or discoloration of the skin at the sting site. An intense aching and burning sensation may spread to adjacent tissues, which in turn often throb, sometimes becoming numb. The acute pain at the sting site turns into a chronic, dull pain accompanied by a feeling of numbness around the edge of the sting site, which may persist for one to several days. Numbness in the face, mouth, and throat is fairly common. Muscles may become spasmodic, resulting in muscular twitching, slurred speech, difficulty swallowing, tightness or cramps in the chest and back, rapid heartbeat, and nausea. Often these systemic responses persist less than an hour after the sting and are not considered serious.

In more severe systemic reactions, neurologic effects can lead to profuse sweating and salivation, restlessness, extreme nervousness, respiratory and cardiovascular problems, mental confusion, and convulsions. As the clinical symptoms indicate, the principal components of the venom of dangerous scorpions are neurotoxins. These toxins act on the autonomic, sympathetic, and neuromuscular systems, causing the wide range of systemic reactions reported in sting victims. They act by disrupting the voltage-sensitive sodium and potassium channels of nerves, which in turn causes neural depolarization, prolonged action potentials, repetitive firing, and uncontrolled release of vasodilators and neurotransmitters, which affect virtually every major organ system. The effect on neurotransmitters results in depletive release of catecholamines (e.g., adrenaline, noradrenaline) that can severely damage the heart and other organs.

The most commonly reported cause of death in scorpion sting cases is cardiac failure and pulmonary edema. In other cases, respiratory failure may be the cause, especially in patients with upper respiratory infections or related problems. Death usually occurs several days after envenomation. If symptoms subside during the first 2–12 h following a sting, the prognosis for recovery is generally good. Mortality rates are quite variable, depending on the species and amount of venom injected. The rates are much higher among children than adults. For further details on the clinical toxicology and symptoms of scorpion stings, see Dehesa-Davila et al. (1995) and Ismail (1995).

Scorpion venom is a very complex mixture of substances that differs significantly among the various taxa, within families, and among genera. Differences also occur in different geographic populations of the same species and even within the same population. The toxins are low-molecular-weight proteins that are among the most powerful toxins known. They are comparable in some species to the neurotoxins of certain deadly snakes. Two recognized types of neurotoxins are α-scorpion toxin, characteristic of the genera Androctonus, Leiurus, and Buthus; and ß-scorpion toxin, characteristic of Centruroides. Tityus spp. appear to have both types. The effects of envenomation by any given scorpion species can differ significantly, owing to a wide range of contributing factors. These include the quantity of venom injected and the age, size, and general health of the victim. Scorpions are generally unable to deliver enough venom to kill healthy adults.

Though adults are most frequently stung, envenomation is more severe among children causing high mortality among them. In adults, scorpion sting is generally harmless and produces local symptoms only, most of the time, excruciating and persistent pain remain the only symptoms. Whereas it is a medical emergency in children, with life-threatening complications such as myocarditis and encephalopathy. Children constitute most of the hospitalized and fatal victims of scorpion stings. Most of the scorpion stings among children occur during playing (50%) and sleeping (33%). High morbidity and lethality rates in children have usually been associated with immune system vulnerability and the ratio of the dose of the venom to the body weight of the patient. Higher concentration of venom per a volume of blood, smaller corporeal body mass, and greater density of the voltage-gated sodium channels that results in a higher sensitivity to the venom’s action on a child's nervous system. These factors contribute to a rapid progression from the mild to the severe phase in young children. The most common reason for high mortality among them is a delay in seeking treatment. A higher mortality rate in some studies is mainly due to late presentation (beyond 6 hours of sting) of cases to the hospital for treatment. Those children who received treatment after 6 hours of being stung are at high risk of complication and death. In addition to patient age and susceptibility, the time-lapsed between the sting and hospital admission, other aspects reported to influence the clinical manifestations or symptoms of scorpion envenomation depend upon the species of scorpion, the region, the site of the sting, the dose of venom, the season of the sting, and the sex of the patient. There is a paucity of epidemiological data on scorpion stings mainly because of the reduced severity of scorpion envenomations among adults and poor organization of health services. Even qualified health providers lack sufficient skills to recognize and manage scorpion envenomation. Lack of standard management guidelines for scorpion envenomation at the hospital level and the absence of a comprehensive national program on animal bites or stings further jeopardize the situation.

For therapeutic and prognostic guidance, envenoming is classified as mild, moderate and serious according to the intensity of the initial symptoms.

Mild

Presence of only local manifestations: mild nausea, agitation, and tachycardia may be present, and are related to pain. These represent the great majority of envenoming episodes.

Moderate

In addition to local symptoms, some of the following low-intensity systemic manifestations may occur: diaphoresis, nauseas, some vomiting episodes, tachycardia, tachypnea, agitation, and arterial hypertension.

Serious

Systemic manifestations are evident and intense: numerous vomiting episodes, excessive salivation, profuse diaphoresis, hypothermia, tachydyspnea, bronchorrhea, tachy or bradyarrythmias, arterial hyper- or hypotension, alternating agitation and prostration, and, rarely, muscle spasms and convulsions. Progression to cardiac failure, APE, shock and death may occur. The local pain is usually masked by the above signs and symptoms, and may later reappear with the improvement of signs and symptoms. Convulsions related to hypoxia or to arterial hypertension and ischemic cerebrovascular accidents have also been described and are quite rare.

The severity of envenoming usually manifests within the first two hours after the sting, i.e., a patient is in a serious condition since the beginning, with the early occurrence of numerous vomiting episodes (a premonitory sign of seriousness) and with progression to systemic manifestations. In the most serious cases, when intense catecholamine release occurs, there is early cardiac aggression.

According to the severity of the signs and symptoms, the following three stages have been established for prognostic and therapeutic purposes:

● Stage I (mild): Agitation, tachycardia, pain, and erythema at the site of the sting.

● Stage II (moderate): Sweating, nausea, vomiting, tachypnea, and hypertension in addition to the above symptoms.

● Stage III (severe): Severe systemic and multi-organ life-threatening involvement.

On admission, detailed clinical history, including the time of sting, symptoms, and details of treatment received before admission and description of the scorpion obtained. All patients are subjected to thorough clinical examination at admission and frequent intervals thereafter. Hourly monitoring of heart rate, respiratory rate, blood pressure, urine output, cardiovascular, and respiratory status is done. Routine investigations such as complete blood counts, peripheral smear, urinalysis, bleeding time, clotting time, blood sugar, chest X-ray, and electrocardiogram are done.

In general, the prognosis is good in stages I and II. In severe cases, the prognosis depends on the age, body surface, type, and size of the scorpion, as well as the time elapsed between the sting and medical assistance.


Screenshot_20240319-234610_Samsung Internet.jpg
Screenshot_20240319-234724_Samsung Internet.jpg
Screenshot_20240319-234859_Samsung Internet.jpg
Screenshot_20240319-234625_Samsung Internet.jpg
Screenshot_20240319-234816_Samsung Internet.jpg
Screenshot_20240319-235223_Samsung Internet.jpg
 

The Snark

Dumpster Fire of the Gods
Old Timer
Joined
Aug 8, 2005
Messages
11,048
@Outpost31Survivor Now if only there was a treatment for the It-Can't-Happen-To-Me! mentality, AKA the Stupidity Syndrome.
Not surprising at all Cardiogenic and Systemic shock has a say in worst case scenarios.
 

Outpost31Survivor

Arachnoprince
Active Member
Joined
Aug 23, 2019
Messages
1,598
@Outpost31Survivor Now if only there was a treatment for the It-Can't-Happen-To-Me! mentality, AKA the Stupidity Syndrome.
Not surprising at all Cardiogenic and Systemic shock has a say in worst case scenarios.
100% agree. Especially, certain individuals that disrespect and irresponsibly push their luck with these potentially lethal mini-beasts. There is a reason why they are armed to the "teeth" with anti-mammalian toxins it is not because they prey upon mammals (though large Buthids e.g. Parabuthus will) but because millions of years ago early mammals first preyed upon scorpions and created a bio weapon arms race.
 

The Snark

Dumpster Fire of the Gods
Old Timer
Joined
Aug 8, 2005
Messages
11,048
millions of years ago early mammals first preyed upon scorpions and created a bio weapon arms race.
What is interesting is much, most or all of the time they keep those traits as venoms on down the time line, often adding to them as environments require adaptation. Ex: Latrodectus with six unique venom molecules.

It can't happen to me duhh. Ambulance, FD and LEO, it's a rare day when they don't have to cope with that thinking.
 

Ultum4Spiderz

Arachnoemperor
Arachnosupporter
Joined
Oct 13, 2011
Messages
4,666
100% agree. Especially, certain individuals that disrespect and irresponsibly push their luck with these potentially lethal mini-beasts. There is a reason why they are armed to the "teeth" with anti-mammalian toxins it is not because they prey upon mammals (though large Buthids e.g. Parabuthus will) but because millions of years ago early mammals first preyed upon scorpions and created a bio weapon arms race.
Why do some scorpions have weak venom then it seems mammals prey upon them still. I even saw a video of a jumping mouse attacking an Australian scorpion.
 

Outpost31Survivor

Arachnoprince
Active Member
Joined
Aug 23, 2019
Messages
1,598
Why do some scorpions have weak venom then it seems mammals prey upon them still. I even saw a video of a jumping mouse attacking an Australian scorpion.
Only scorpions belonging to two families possess toxins dangerous to humans, Buthidae and Hemiscorpiidae. Buthidae have toxins that are mammalian-specific that target the mammalian nervous system.

According to their preference for insect and mammalian Navs, α-ScNaTxs can be divided into three subtypes: 1) Classical α-toxins that are highly toxic on mammals but nontoxic to insects; 2) Anti-insect α-toxins that are especially toxic on insects but weakly toxic on mammals; and 3) α-Like toxins that act on both mammalian and insect Navs (Possani et al. 1999; Zhu et al. 2012).

In accord with their classification into a) anti-mammalian beta-ScTxs, b) anti-insect selective excitatory beta-ScTxs, c) anti-insect selective depressant beta-ScTxs and d) beta-ScTxs active on both insect and mammals Nav channels.

Closer to 70 million years ago, during the dawn of the age of mammals, the Cenozoic era, new animals like shrews — and later bats, rodents, mongooses and badgers — would develop a taste for scorpions. But the scorpions had a few tricks up their curved tails.

“We found that when these toxic scorpions diverge from their relatives, it correlates with the appearance of the mammals that prey on them,” says Santibáñez-López, now a professor at Western Connecticut State University. “It suggests that when the mammals that eat these scorpions appeared, the scorpions started developing these weapons to defend themselves.”


It didn’t hurt that the venom the scorpions used to disable the insects they ate was not that far, chemically speaking, from toxins that would work on their rising predators.

“The toolkit was there,” says Prashant Sharma, study co-author and a UW–Madison professor of integrative biology. “They had an available pool of genes to draw from that were making toxins that could target insect nervous systems. It didn’t take much change to adapt those genes to make toxins that target specific functions in mammal nerve cells.”
 
Last edited:
Top