Snakebite envenoming

Injury MONDO:0018669 Pathograph 17 Show in embeddings browser Neglected tropical disease

Snakebite envenoming is an acute, life-threatening toxic injury and neglected tropical disease caused by the parenteral injection of complex proteinaceous snake venoms comprising neurotoxins, hemotoxins, cytotoxins, myotoxins, and metalloproteases. Depending on snake species and venom composition, envenoming produces a clinical spectrum ranging from severe local swelling and cutaneous/soft-tissue necrosis to systemic venom-induced consumption coagulopathy with spontaneous hemorrhage, presynaptic or postsynaptic neuromuscular paralysis, systemic rhabdomyolysis, and acute kidney injury.

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🏷

Classifications

Harrison's Part
POISONING ENVENOMATION
🔗

Mappings

MONDO
MONDO:0018669 snakebite envenomation
skos:exactMatch MONDO
Exact MONDO concept for snakebite envenomation.
◆

Subtypes

2
Neurotoxic snakebite envenoming
Envenoming dominated by presynaptic beta-neurotoxins (such as phospholipase A2 complexes) or postsynaptic alpha-neurotoxins that block neuromuscular transmission, producing cranial nerve palsy, descending flaccid paralysis, and respiratory failure.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"In cases of neurotoxic envenoming, patients with neurological manifestations are monitored by serial general physical and neurological examination with special attention to cranial nerve function, airway, respiration, and bedside measures, such as Peak Expiratory Flow Rate (PEFR) and blood..."
Recognizes neurotoxic snakebite envenoming as a distinct clinical syndrome characterized by cranial nerve and respiratory muscle paralysis.
Hemotoxic and cytotoxic snakebite envenoming
Envenoming dominated by venom metalloproteases, serine proteases, and cytotoxins that degrade extracellular matrix and consume coagulation factors, resulting in local edema and necrosis, venom-induced consumption coagulopathy, systemic hemorrhage, rhabdomyolysis, and acute kidney injury.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury. These clinical manifestations result from complex biochemical venom constituents comprising of..."
Supports the clinical and biochemical distinction of hemotoxic, cytotoxic, and myotoxic snakebite syndromes.
⚙

Pathophysiology

6
Presynaptic phospholipase A2 neurotoxin blockade
Presynaptic phospholipase A2 beta-neurotoxins (such as Mojave toxin) trigger intracellular Ca2+ and arachidonic acid cascades, endoplasmic reticulum stress, and neurotransmitter overload in excitatory synapses, leading to presynaptic blockade of nerve signals that is relatively refractory to antivenom and anticholinesterase reversal once established.
motor neuron CL:0000100 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves motor neuron (CL:0000100). CL:0000100 is a cell type from the Cell Ontology.
neuromuscular synaptic transmission GO:0007274 ↓ DECREASED Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves decreased neuromuscular synaptic transmission (GO:0007274). GO:0007274 is a biological process from the Gene Ontology.
skeletal muscle tissue UBERON:0001134 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in skeletal muscle tissue (UBERON:0001134). UBERON:0001134 is an anatomical location from the Uberon multi-species anatomy ontology.
Downstream
Paralysis Presynaptic blockade of motor nerve signal transmission causes descending flaccid neuromuscular paralysis.
Respiratory failure Presynaptic neuromuscular blockade of bulbar and respiratory musculature leads to ventilatory failure.
Show evidence (2 references)
PMID:40149917 SUPPORT In vitro / ex vivo
"The MTX, which is composed of heterodimers of basic and acidic phospholipase-A2, co-opts the host arachidonic acid and Ca2+ second messenger mechanisms and triggers multiple signaling cascades, such as the activation of MAPKs and NF-κB-regulated proinflammatory genes; the neurotransmitter..."
Demonstrates the molecular mechanism by which snake venom phospholipase A2 neurotoxins induce presynaptic blockade of nerve signals and cellular stress.
PMID:34430847 SUPPORT Human clinical
"However, while antivenoms save countless lives, they are associated with adverse reactions, limited potency, and are relatively inefficacious against presynaptic neurotoxicity and in preventing necrosis."
Highlights presynaptic neurotoxicity as a distinct mechanism in snakebite envenoming that responds poorly to established antivenom reversal.
Postsynaptic alpha-neurotoxin neuromuscular blockade
Postsynaptic neurotoxins competitively block nicotinic acetylcholine receptors at the skeletal muscle motor endplate, impairing neuromuscular synaptic transmission in a manner responsive to anticholinesterase ancillary therapy.
muscle cell CL:0000187 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves muscle cell (CL:0000187). CL:0000187 is a cell type from the Cell Ontology.
neuromuscular synaptic transmission GO:0007274 ↓ DECREASED Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves decreased neuromuscular synaptic transmission (GO:0007274). GO:0007274 is a biological process from the Gene Ontology.
skeletal muscle tissue UBERON:0001134 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in skeletal muscle tissue (UBERON:0001134). UBERON:0001134 is an anatomical location from the Uberon multi-species anatomy ontology.
Downstream
Paralysis Postsynaptic blockade at the neuromuscular junction produces flaccid paralysis.
Respiratory failure Postsynaptic neuromuscular blockade of respiratory muscles impairs ventilation and causes respiratory failure.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"Anticholinesterase inhibitors (e.g. edrophonium or tensilon) have been used to assess and provide immediate ancillary treatment, especially following envenomings by snakes causing post-synaptic neurotoxic envenoming"
Establishes postsynaptic neurotoxic envenoming as a distinct neuromuscular blockade mechanism responsive to anticholinesterase inhibition.
Venom-induced consumption coagulopathy
Procoagulant and hemotoxic venom components activate and consume host coagulation factors, causing severe hypofibrinogenemia (venom-induced consumption coagulopathy) with incoagulable blood and spontaneous systemic hemorrhage.
blood coagulation GO:0007596 ⚠ ABNORMAL Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves abnormal blood coagulation (GO:0007596). GO:0007596 is a biological process from the Gene Ontology.
blood vessel UBERON:0001981 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in blood vessel (UBERON:0001981). UBERON:0001981 is an anatomical location from the Uberon multi-species anatomy ontology.
Downstream
Abnormal bleeding Depletion of fibrinogen and clotting factors in venom-induced consumption coagulopathy results in incoagulable blood and spontaneous systemic hemorrhage.
Hypotension Severe systemic hemorrhage and intravascular volume depletion contribute to circulatory shock and hypotension.
Venom-associated renal injury Microvascular coagulopathy and hemorrhagic shock contribute to downstream renal injury.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"If the blood is still liquid (unclotted) and runs out, the patient has incoagulable blood (hypofibrinogenaemia) as a result of venom-induced consumption coagulopathy and is in need of antivenom treatment."
Establishes venom-induced consumption coagulopathy and hypofibrinogenemia as the mechanism of incoagulable blood in hemotoxic snakebite envenoming.
Venom metalloprotease and cytotoxin-mediated extracellular matrix degradation and local tissue necrosis
Snake venom metalloproteases (SVMPs) and cytotoxins digest the extracellular matrix to facilitate venom spread and induce severe local tissue swelling and necrosis at the bite site.
extracellular matrix organization GO:0030198 ⚠ ABNORMAL Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves abnormal extracellular matrix organization (GO:0030198). GO:0030198 is a biological process from the Gene Ontology. proteolysis GO:0006508 ↑ INCREASED Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves increased proteolysis (GO:0006508). GO:0006508 is a biological process from the Gene Ontology.
extracellular matrix GO:0031012 Gene Ontology (GO) Relation: this pathophysiological event involves this cellular component This pathophysiological event involves extracellular matrix (GO:0031012). GO:0031012 is a cellular component from the Gene Ontology.
skeletal muscle tissue UBERON:0001134 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in skeletal muscle tissue (UBERON:0001134). UBERON:0001134 is an anatomical location from the Uberon multi-species anatomy ontology.
Downstream
Edema Extracellular matrix digestion and local tissue injury produce rapid swelling at the bite site.
Cutaneous necrosis Cytotoxins and metalloproteases cause direct local soft-tissue and cutaneous necrosis of the bitten body part.
Show evidence (2 references)
PMID:40149917 SUPPORT In vitro / ex vivo
"Our results suggest that snake venom metalloproteases, although having a limited repertoire in Type A venom, facilitate venom spread by digesting the tissue's extracellular matrix."
Demonstrates that snake venom metalloproteases digest extracellular matrix components to promote tissue damage and venom spread.
PMID:34430847 SUPPORT Human clinical
"The resulting clinical features following bites may include swelling and necrosis of the bitten body part, rhabdomyolysis, local bleeding, systemic hemorrhage, incoagulable blood, anaemia, shock, and paralysis."
Documents local swelling and necrosis of the bitten body part following cytotoxic and proteolytic snakebite envenoming.
Venom myotoxin-mediated skeletal muscle damage
Venom myotoxins disrupt sodium channels in skeletal muscle cells and induce myonecrosis, causing muscle paralysis and systemic rhabdomyolysis.
muscle cell CL:0000187 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves muscle cell (CL:0000187). CL:0000187 is a cell type from the Cell Ontology.
proteolysis GO:0006508 ↑ INCREASED Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves increased proteolysis (GO:0006508). GO:0006508 is a biological process from the Gene Ontology.
skeletal muscle tissue UBERON:0001134 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in skeletal muscle tissue (UBERON:0001134). UBERON:0001134 is an anatomical location from the Uberon multi-species anatomy ontology.
Downstream
Paralysis Disruption of skeletal muscle sodium channels by venom myotoxins causes muscle paralysis.
Rhabdomyolysis Venom myotoxins damage skeletal muscle fibers, causing systemic rhabdomyolysis.
Venom-associated renal injury Systemic release of myoglobin and cellular breakdown products from rhabdomyolysis contributes to renal injury.
Show evidence (2 references)
PMID:40149917 SUPPORT BACKGROUND In vitro / ex vivo
"The myotoxins disrupt sodium channels in muscle cells causing muscle paralysis and lowered median lethal dose (LD50) when present."
Explains how venom myotoxins disrupt muscle sodium channels to cause muscle paralysis.
PMID:34430847 SUPPORT Human clinical
"These clinical manifestations result from complex biochemical venom constituents comprising of cytotoxins, hemotoxins, neurotoxins, myotoxins, and other substances."
Identifies myotoxins as a core biochemical class of snake venom constituents driving skeletal muscle injury.
Venom-associated renal injury
Systemic envenoming causes renal tubular and filtration injury through the combined effects of rhabdomyolysis, hemodynamic shock, consumption coagulopathy, and direct nephrotoxic venom components.
renal filtration GO:0097205 ↓ DECREASED Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves decreased renal filtration (GO:0097205). GO:0097205 is a biological process from the Gene Ontology.
kidney UBERON:0002113 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in kidney (UBERON:0002113). UBERON:0002113 is an anatomical location from the Uberon multi-species anatomy ontology. nephron tubule UBERON:0001231 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in nephron tubule (UBERON:0001231). UBERON:0001231 is an anatomical location from the Uberon multi-species anatomy ontology.
Downstream
Acute kidney injury Renal tubular and microvascular injury from systemic envenoming results in clinical acute kidney injury.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury. These clinical manifestations result from complex biochemical venom constituents comprising of..."
Supports systemic venom-induced renal injury as a major life-threatening manifestation of snakebite envenoming.
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Pathograph

Use Group by to collapse related nodes into one box. Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Snakebite envenoming Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.
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Phenotypes

8
Blood 1
Abnormal bleeding HP:0001892 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Abnormal bleeding (HP:0001892). HP:0001892 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury."
The abstract lists systemic hemorrhage and incoagulable blood.
Cardiovascular 1
Hypotension HP:0002615 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Hypotension (HP:0002615). HP:0002615 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury."
Shock is listed among the main systemic clinical features of snakebite envenoming.
Genitourinary 1
Acute kidney injury HP:0001919 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Acute kidney injury (HP:0001919). HP:0001919 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury."
The abstract lists acute kidney injury among clinical features.
Integument 1
Cutaneous necrosis HP:0033126 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Cutaneous necrosis (HP:0033126). HP:0033126 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury."
Tissue necrosis is a cardinal local feature of cytotoxic snakebite envenoming.
Metabolism 1
Edema HP:0000969 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Edema (HP:0000969). HP:0000969 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury."
The abstract lists local swelling among clinical features.
Musculoskeletal 1
Rhabdomyolysis HP:0003201 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Rhabdomyolysis (HP:0003201). HP:0003201 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury."
The abstract lists rhabdomyolysis among the main clinical manifestations of snakebite envenoming.
Nervous System 1
Paralysis HP:0003470 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Paralysis (HP:0003470). HP:0003470 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury."
The abstract lists paralysis among clinical features.
Respiratory 1
Respiratory failure HP:0002878 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Respiratory failure (HP:0002878). HP:0002878 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"In cases of neurotoxic envenoming, patients with neurological manifestations are monitored by serial general physical and neurological examination with special attention to cranial nerve function, airway, respiration, and bedside measures, such as Peak Expiratory Flow Rate (PEFR) and blood..."
Highlights airway and respiratory compromise requiring PEFR and SpO2 monitoring in neurotoxic snakebite envenoming.
💊

Medical Actions

3
Intravenous antivenom administration
Action: PharmacotherapyNCI Thesaurus (NCIT) Relation: this treatment is this clinical intervention This treatment is Pharmacotherapy (NCIT:C15986). NCIT:C15986 is a clinical intervention from the NCI Thesaurus. NCIT:C15986
Platform: Other
Intravenous administration of specific or polyvalent immunoglobulin antivenom is the only specific therapy to neutralize circulating snake venom toxins and reverse venom-induced consumption coagulopathy, though its clinical efficacy is limited against established presynaptic neurotoxicity and local tissue necrosis.
Mechanism Target:
INHIBITS Postsynaptic alpha-neurotoxin neuromuscular blockade — Neutralizes circulating postsynaptic neurotoxins to halt or reverse neuromuscular junction blockade.
INHIBITS Presynaptic phospholipase A2 neurotoxin blockade — Neutralizes circulating presynaptic neurotoxins prior to irreversible nerve terminal injury, although efficacy is limited once presynaptic neurotoxicity is established.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"However, while antivenoms save countless lives, they are associated with adverse reactions, limited potency, and are relatively inefficacious against presynaptic neurotoxicity and in preventing necrosis."
Notes that antivenom neutralizes systemic envenoming but has limited efficacy against established presynaptic neurotoxicity.
INHIBITS Venom-induced consumption coagulopathy — Neutralizes procoagulant and hemorrhagic venom toxins in patients with incoagulable blood from venom-induced consumption coagulopathy.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"If the blood is still liquid (unclotted) and runs out, the patient has incoagulable blood (hypofibrinogenaemia) as a result of venom-induced consumption coagulopathy and is in need of antivenom treatment."
Directly links venom-induced consumption coagulopathy to the indication for antivenom therapy.
INHIBITS Venom metalloprotease and cytotoxin-mediated extracellular matrix degradation and local tissue necrosis — Neutralizes circulating cytotoxic and proteolytic venom toxins, although efficacy in preventing local necrosis is limited.
INHIBITS Venom myotoxin-mediated skeletal muscle damage — Neutralizes circulating venom myotoxins to limit systemic muscle injury.
Show evidence (1 reference)
PMID:28905944 SUPPORT Human clinical
"Intravenous administration of antivenom is the only specific treatment to counteract envenoming."
The abstract states antivenom is the only specific treatment.
Organ supportive care (ventilator support, fluid therapy, and hemodialysis)
Action: supportive careNCI Thesaurus (NCIT) Relation: this treatment is this clinical intervention This treatment is supportive care (NCIT:C15747). NCIT:C15747 is a clinical intervention from the NCI Thesaurus. Ontology label: Supportive Care NCIT:C15747
Platform: Other
Critical supportive interventions including mechanical ventilation for neurotoxic respiratory paralysis, intravenous fluid resuscitation for shock, hemodialysis for acute kidney injury, analgesia, and antibiotic therapy for secondary wound infection.
Mechanism Target:
BYPASSES Presynaptic phospholipase A2 neurotoxin blockade — Mechanical ventilation maintains oxygenation and ventilation while presynaptic neuromuscular transmission recovers.
BYPASSES Postsynaptic alpha-neurotoxin neuromuscular blockade — Mechanical ventilation supports respiration during postsynaptic neuromuscular paralysis.
BYPASSES Venom-associated renal injury — Fluid resuscitation and hemodialysis support renal clearance and fluid-electrolyte homeostasis during acute kidney injury.
Show evidence (1 reference)
PMID:28905944 SUPPORT Human clinical
"Intravenous administration of antivenom is the only specific treatment to counteract envenoming. Analgesics, ventilator support, fluid therapy, haemodialysis and antibiotic therapy are also used."
Supports ventilator support, fluid therapy, hemodialysis, analgesics, and antibiotics as essential adjunctive treatments for snakebite envenoming.
Anticholinesterase ancillary therapy
Action: PharmacotherapyNCI Thesaurus (NCIT) Relation: this treatment is this clinical intervention This treatment is Pharmacotherapy (NCIT:C15986). NCIT:C15986 is a clinical intervention from the NCI Thesaurus. NCIT:C15986
Platform: Small molecule
Anticholinesterase inhibitors such as edrophonium (Tensilon) are used to assess and provide immediate ancillary treatment following envenomings by snakes causing postsynaptic neurotoxic envenoming, whereas they are generally not useful for presynaptic neurotoxicity.
Mechanism Target:
RESTORES Postsynaptic alpha-neurotoxin neuromuscular blockade — Inhibits acetylcholinesterase at the neuromuscular junction to provide immediate ancillary reversal in postsynaptic neurotoxic envenoming.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"Anticholinesterase inhibitors (e.g. edrophonium or tensilon) have been used to assess and provide immediate ancillary treatment, especially following envenomings by snakes causing post-synaptic neurotoxic envenoming"
Directly supports anticholinesterase inhibitors as an ancillary therapy targeting postsynaptic neurotoxic envenoming.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"Anticholinesterase inhibitors (e.g. edrophonium or tensilon) have been used to assess and provide immediate ancillary treatment, especially following envenomings by snakes causing post-synaptic neurotoxic envenoming"
Supports anticholinesterase therapy as an ancillary treatment for postsynaptic neurotoxic snakebite envenoming.
🌍

Environmental Factors

1
Snake venom exposure
exposure to toxin ECTO:0000537 Environmental Conditions, Treatments and Exposures Ontology (ECTO) Relation: this environmental factor is this exposure This environmental factor is exposure to toxin (ECTO:0000537). ECTO:0000537 is an exposure from the Environmental Conditions, Treatments and Exposures Ontology.
Parenteral injection of venomous snake toxins (metalloproteases, phospholipase A2 neurotoxins, three-finger toxins, myotoxins, and procoagulant/hemorrhagic enzymes) via a snakebite.
Show evidence (1 reference)
PMID:28905944 SUPPORT Human clinical
"Snake venoms are complex mixtures of proteins that exert a wide range of toxic actions."
Confirms exposure to proteinaceous snake venom toxins as the direct environmental cause of snakebite envenoming.
🔬

Diagnosis

2
Blood coagulation testing and 20-minute whole blood clotting test
Bedside 20-minute whole blood clotting test (20WBCT) and laboratory coagulation assays (prothrombin time, INR, aPTT, fibrinogen, and fibrin degradation products/D-dimer) detect venom-induced consumption coagulopathy and guide antivenom indication.
coagulation study NCIT:C62662 NCI Thesaurus (NCIT)
Results: Incoagulable blood on 20WBCT, prolonged PT/INR and aPTT, hypofibrinogenemia, and elevated D-dimer/fibrin degradation products.
Show evidence (2 references)
PMID:34430847 SUPPORT Human clinical
"Tests of blood coagulation, such as prothrombin time (PT), the International Normalized Ratio (INR), or activated partial thromboplastin time (aPTT), measurement of fibrin(ogen) related proteins also known as fibrin degradation products (FDP), or D-dimer, can also be used to diagnose snakebite..."
Supports coagulation testing (PT, INR, aPTT, FDP, D-dimer) for diagnosing hemotoxic snakebite envenoming.
PMID:34430847 SUPPORT Human clinical
"If the blood is still liquid (unclotted) and runs out, the patient has incoagulable blood (hypofibrinogenaemia) as a result of venom-induced consumption coagulopathy and is in need of antivenom treatment."
Supports bedside whole blood clotting assessment showing unclotted liquid blood as diagnostic of venom-induced consumption coagulopathy.
Serial neurological and respiratory monitoring
Serial physical and neurological examination assessing cranial nerve function (ptosis, ophthalmoplegia, bulbar function), airway patency, Peak Expiratory Flow Rate (PEFR), and pulse oximetry (SpO2) to detect neurotoxic envenoming and impending respiratory failure.
neurologic examination NCIT:C81313 NCI Thesaurus (NCIT)
Results: Progressive cranial nerve palsy, declining PEFR, and desaturation indicating neurotoxic neuromuscular blockade.
Show evidence (1 reference)
PMID:34430847 SUPPORT Human clinical
"In cases of neurotoxic envenoming, patients with neurological manifestations are monitored by serial general physical and neurological examination with special attention to cranial nerve function, airway, respiration, and bedside measures, such as Peak Expiratory Flow Rate (PEFR) and blood..."
Establishes serial neurological examination and respiratory monitoring as essential diagnostic assessments in neurotoxic snakebite envenoming.
📊

Prevalence

1
Global annual burden
Unknown
Snakebite envenoming causes more than 100,000 deaths and more than 400,000 permanent disabilities annually worldwide, predominantly in tropical and subtropical agricultural populations.
Show evidence (1 reference)
PMID:28905944 SUPPORT Human clinical
"Snakebite envenoming is a neglected tropical disease that kills >100,000 people and maims >400,000 people every year."
Documents the global annual mortality and disability burden of snakebite envenoming.
📊

Related Datasets

1
Neurocellular stress response to Mojave Type A Rattlesnake venom: A study of molecular mechanisms using a human iPSC-derived neural stem cell model geo:GSE287744
The Mojave rattlesnake (Crotalus scutulatus scutulatus) is classified as the “highest medically important” snake in the risk categories in the United States. Although responsible for fewer snakebite envenomations and deaths compared to other species, Mojave rattlesnake venom is poorly characterized and shows significant geographical variability. The venom of Type A animals primarily contains the β-neurotoxin referred to as Mojave Toxin (MTX), which is responsible for the neurotoxic effects that make bites from this snake particularly feared.
human BULK RNA SEQ n=24
PMID:40149917
Identified by GEO DataSets index search for Snakebite envenoming (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-08-01. Title, sample count, and organism are GEO's own values.
{ }

Source YAML

click to show 
name: Snakebite envenoming
creation_date: "2026-01-26T16:06:17Z"
category: Injury
description: >-
  Snakebite envenoming is an acute, life-threatening toxic injury and neglected
  tropical disease caused by the parenteral injection of complex proteinaceous
  snake venoms comprising neurotoxins, hemotoxins, cytotoxins, myotoxins, and
  metalloproteases. Depending on snake species and venom composition,
  envenoming produces a clinical spectrum ranging from severe local swelling and
  cutaneous/soft-tissue necrosis to systemic venom-induced consumption
  coagulopathy with spontaneous hemorrhage, presynaptic or postsynaptic
  neuromuscular paralysis, systemic rhabdomyolysis, and acute kidney injury.
disease_term:
  term:
    id: MONDO:0018669
    label: snakebite envenomation
  preferred_term: Snakebite envenoming
parents:
- Neglected tropical disease
synonyms:
- Snakebite envenomation
- Venomous snakebite
- Ophidism
classifications:
  harrisons_chapter:
  - classification_value: POISONING_ENVENOMATION
    evidence:
    - reference: PMID:28905944
      reference_title: "Snakebite envenoming."
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: "Snake venoms are complex mixtures of proteins that exert a wide range of toxic actions."
      explanation: Establishes snakebite envenoming as an acute toxic envenomation disorder.
mappings:
  mondo_mappings:
  - term:
      id: MONDO:0018669
      label: snakebite envenomation
    mapping_predicate: skos:exactMatch
    mapping_source: MONDO
    mapping_justification: Exact MONDO concept for snakebite envenomation.
has_subtypes:
- name: Neurotoxic snakebite envenoming
  description: >-
    Envenoming dominated by presynaptic beta-neurotoxins (such as phospholipase
    A2 complexes) or postsynaptic alpha-neurotoxins that block neuromuscular
    transmission, producing cranial nerve palsy, descending flaccid paralysis,
    and respiratory failure.
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "In cases of neurotoxic envenoming, patients with neurological manifestations are monitored by serial general physical and neurological examination with special attention to cranial nerve function, airway, respiration, and bedside measures, such as Peak Expiratory Flow Rate (PEFR) and blood oxygen saturation (SpO2)."
    explanation: Recognizes neurotoxic snakebite envenoming as a distinct clinical syndrome characterized by cranial nerve and respiratory muscle paralysis.
- name: Hemotoxic and cytotoxic snakebite envenoming
  description: >-
    Envenoming dominated by venom metalloproteases, serine proteases, and
    cytotoxins that degrade extracellular matrix and consume coagulation
    factors, resulting in local edema and necrosis, venom-induced consumption
    coagulopathy, systemic hemorrhage, rhabdomyolysis, and acute kidney injury.
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury. These clinical manifestations result from complex biochemical venom constituents comprising of cytotoxins, hemotoxins, neurotoxins, myotoxins, and other substances."
    explanation: Supports the clinical and biochemical distinction of hemotoxic, cytotoxic, and myotoxic snakebite syndromes.
prevalence:
- population: Global annual burden
  measure_type: UNKNOWN
  notes: >-
    Snakebite envenoming causes more than 100,000 deaths and more than 400,000
    permanent disabilities annually worldwide, predominantly in tropical and
    subtropical agricultural populations.
  evidence:
  - reference: PMID:28905944
    reference_title: "Snakebite envenoming."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Snakebite envenoming is a neglected tropical disease that kills >100,000 people and maims >400,000 people every year."
    explanation: Documents the global annual mortality and disability burden of snakebite envenoming.
environmental:
- name: Snake venom exposure
  exposure_term:
    preferred_term: exposure to toxin
    term:
      id: ECTO:0000537
      label: exposure to toxin
  description: >-
    Parenteral injection of venomous snake toxins (metalloproteases,
    phospholipase A2 neurotoxins, three-finger toxins, myotoxins, and
    procoagulant/hemorrhagic enzymes) via a snakebite.
  evidence:
  - reference: PMID:28905944
    reference_title: "Snakebite envenoming."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Snake venoms are complex mixtures of proteins that exert a wide range of toxic actions."
    explanation: Confirms exposure to proteinaceous snake venom toxins as the direct environmental cause of snakebite envenoming.
pathophysiology:
- name: Presynaptic phospholipase A2 neurotoxin blockade
  description: >-
    Presynaptic phospholipase A2 beta-neurotoxins (such as Mojave toxin) trigger
    intracellular Ca2+ and arachidonic acid cascades, endoplasmic reticulum
    stress, and neurotransmitter overload in excitatory synapses, leading to
    presynaptic blockade of nerve signals that is relatively refractory to
    antivenom and anticholinesterase reversal once established.
  cell_types:
  - preferred_term: motor neuron
    term:
      id: CL:0000100
      label: motor neuron
  locations:
  - preferred_term: skeletal muscle tissue
    term:
      id: UBERON:0001134
      label: skeletal muscle tissue
  biological_processes:
  - preferred_term: neuromuscular synaptic transmission
    term:
      id: GO:0007274
      label: neuromuscular synaptic transmission
    modifier: DECREASED
  evidence:
  - reference: PMID:40149917
    reference_title: "Neurocellular Stress Response to Mojave Type A Rattlesnake Venom: Study of Molecular Mechanisms Using Human iPSC-Derived Neural Stem Cell Model."
    supports: SUPPORT
    evidence_source: IN_VITRO
    snippet: "The MTX, which is composed of heterodimers of basic and acidic phospholipase-A2, co-opts the host arachidonic acid and Ca2+ second messenger mechanisms and triggers multiple signaling cascades, such as the activation of MAPKs and NF-κB-regulated proinflammatory genes; the neurotransmitter overload in excitatory synapses leading to a presynaptic blockade of nerve signals; and the upregulation of unfolded protein response (UPR) due to the depletion of Ca2+ from the endoplasmic reticulum."
    explanation: Demonstrates the molecular mechanism by which snake venom phospholipase A2 neurotoxins induce presynaptic blockade of nerve signals and cellular stress.
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "However, while antivenoms save countless lives, they are associated with adverse reactions, limited potency, and are relatively inefficacious against presynaptic neurotoxicity and in preventing necrosis."
    explanation: Highlights presynaptic neurotoxicity as a distinct mechanism in snakebite envenoming that responds poorly to established antivenom reversal.
  downstream:
  - target: Paralysis
    description: Presynaptic blockade of motor nerve signal transmission causes descending flaccid neuromuscular paralysis.
  - target: Respiratory failure
    description: Presynaptic neuromuscular blockade of bulbar and respiratory musculature leads to ventilatory failure.
- name: Postsynaptic alpha-neurotoxin neuromuscular blockade
  description: >-
    Postsynaptic neurotoxins competitively block nicotinic acetylcholine
    receptors at the skeletal muscle motor endplate, impairing neuromuscular
    synaptic transmission in a manner responsive to anticholinesterase ancillary
    therapy.
  cell_types:
  - preferred_term: muscle cell
    term:
      id: CL:0000187
      label: muscle cell
  locations:
  - preferred_term: skeletal muscle tissue
    term:
      id: UBERON:0001134
      label: skeletal muscle tissue
  biological_processes:
  - preferred_term: neuromuscular synaptic transmission
    term:
      id: GO:0007274
      label: neuromuscular synaptic transmission
    modifier: DECREASED
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Anticholinesterase inhibitors (e.g. edrophonium or tensilon) have been used to assess and provide immediate ancillary treatment, especially following envenomings by snakes causing post-synaptic neurotoxic envenoming"
    explanation: Establishes postsynaptic neurotoxic envenoming as a distinct neuromuscular blockade mechanism responsive to anticholinesterase inhibition.
  downstream:
  - target: Paralysis
    description: Postsynaptic blockade at the neuromuscular junction produces flaccid paralysis.
  - target: Respiratory failure
    description: Postsynaptic neuromuscular blockade of respiratory muscles impairs ventilation and causes respiratory failure.
- name: Venom-induced consumption coagulopathy
  description: >-
    Procoagulant and hemotoxic venom components activate and consume host
    coagulation factors, causing severe hypofibrinogenemia (venom-induced
    consumption coagulopathy) with incoagulable blood and spontaneous systemic
    hemorrhage.
  locations:
  - preferred_term: blood vessel
    term:
      id: UBERON:0001981
      label: blood vessel
  biological_processes:
  - preferred_term: blood coagulation
    term:
      id: GO:0007596
      label: blood coagulation
    modifier: ABNORMAL
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "If the blood is still liquid (unclotted) and runs out, the patient has incoagulable blood (hypofibrinogenaemia) as a result of venom-induced consumption coagulopathy and is in need of antivenom treatment."
    explanation: Establishes venom-induced consumption coagulopathy and hypofibrinogenemia as the mechanism of incoagulable blood in hemotoxic snakebite envenoming.
  downstream:
  - target: Abnormal bleeding
    description: Depletion of fibrinogen and clotting factors in venom-induced consumption coagulopathy results in incoagulable blood and spontaneous systemic hemorrhage.
    evidence:
    - reference: PMID:34430847
      reference_title: "Clinical management of snakebite envenoming: Future perspectives."
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: "If the blood is still liquid (unclotted) and runs out, the patient has incoagulable blood (hypofibrinogenaemia) as a result of venom-induced consumption coagulopathy and is in need of antivenom treatment."
      explanation: Directly links venom-induced consumption coagulopathy and hypofibrinogenemia to incoagulable blood.
  - target: Hypotension
    description: Severe systemic hemorrhage and intravascular volume depletion contribute to circulatory shock and hypotension.
  - target: Venom-associated renal injury
    description: Microvascular coagulopathy and hemorrhagic shock contribute to downstream renal injury.
- name: Venom metalloprotease and cytotoxin-mediated extracellular matrix degradation and local tissue necrosis
  description: >-
    Snake venom metalloproteases (SVMPs) and cytotoxins digest the extracellular
    matrix to facilitate venom spread and induce severe local tissue swelling
    and necrosis at the bite site.
  locations:
  - preferred_term: skeletal muscle tissue
    term:
      id: UBERON:0001134
      label: skeletal muscle tissue
  cellular_components:
  - preferred_term: extracellular matrix
    term:
      id: GO:0031012
      label: extracellular matrix
  biological_processes:
  - preferred_term: extracellular matrix organization
    term:
      id: GO:0030198
      label: extracellular matrix organization
    modifier: ABNORMAL
  - preferred_term: proteolysis
    term:
      id: GO:0006508
      label: proteolysis
    modifier: INCREASED
  evidence:
  - reference: PMID:40149917
    reference_title: "Neurocellular Stress Response to Mojave Type A Rattlesnake Venom: Study of Molecular Mechanisms Using Human iPSC-Derived Neural Stem Cell Model."
    supports: SUPPORT
    evidence_source: IN_VITRO
    snippet: "Our results suggest that snake venom metalloproteases, although having a limited repertoire in Type A venom, facilitate venom spread by digesting the tissue's extracellular matrix."
    explanation: Demonstrates that snake venom metalloproteases digest extracellular matrix components to promote tissue damage and venom spread.
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "The resulting clinical features following bites may include swelling and necrosis of the bitten body part, rhabdomyolysis, local bleeding, systemic hemorrhage, incoagulable blood, anaemia, shock, and paralysis."
    explanation: Documents local swelling and necrosis of the bitten body part following cytotoxic and proteolytic snakebite envenoming.
  downstream:
  - target: Edema
    description: Extracellular matrix digestion and local tissue injury produce rapid swelling at the bite site.
  - target: Cutaneous necrosis
    description: Cytotoxins and metalloproteases cause direct local soft-tissue and cutaneous necrosis of the bitten body part.
- name: Venom myotoxin-mediated skeletal muscle damage
  description: >-
    Venom myotoxins disrupt sodium channels in skeletal muscle cells and induce
    myonecrosis, causing muscle paralysis and systemic rhabdomyolysis.
  cell_types:
  - preferred_term: muscle cell
    term:
      id: CL:0000187
      label: muscle cell
  locations:
  - preferred_term: skeletal muscle tissue
    term:
      id: UBERON:0001134
      label: skeletal muscle tissue
  biological_processes:
  - preferred_term: proteolysis
    term:
      id: GO:0006508
      label: proteolysis
    modifier: INCREASED
  evidence:
  - reference: PMID:40149917
    reference_title: "Neurocellular Stress Response to Mojave Type A Rattlesnake Venom: Study of Molecular Mechanisms Using Human iPSC-Derived Neural Stem Cell Model."
    supports: SUPPORT
    evidence_source: IN_VITRO
    quote_role: BACKGROUND
    snippet: "The myotoxins disrupt sodium channels in muscle cells causing muscle paralysis and lowered median lethal dose (LD50) when present."
    explanation: Explains how venom myotoxins disrupt muscle sodium channels to cause muscle paralysis.
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "These clinical manifestations result from complex biochemical venom constituents comprising of cytotoxins, hemotoxins, neurotoxins, myotoxins, and other substances."
    explanation: Identifies myotoxins as a core biochemical class of snake venom constituents driving skeletal muscle injury.
  downstream:
  - target: Paralysis
    description: Disruption of skeletal muscle sodium channels by venom myotoxins causes muscle paralysis.
    evidence:
    - reference: PMID:40149917
      reference_title: "Neurocellular Stress Response to Mojave Type A Rattlesnake Venom: Study of Molecular Mechanisms Using Human iPSC-Derived Neural Stem Cell Model."
      supports: SUPPORT
      evidence_source: IN_VITRO
      quote_role: BACKGROUND
      snippet: "The myotoxins disrupt sodium channels in muscle cells causing muscle paralysis and lowered median lethal dose (LD50) when present."
      explanation: Directly links venom myotoxin action on muscle cell sodium channels to muscle paralysis.
  - target: Rhabdomyolysis
    description: Venom myotoxins damage skeletal muscle fibers, causing systemic rhabdomyolysis.
  - target: Venom-associated renal injury
    description: Systemic release of myoglobin and cellular breakdown products from rhabdomyolysis contributes to renal injury.
- name: Venom-associated renal injury
  description: >-
    Systemic envenoming causes renal tubular and filtration injury through the
    combined effects of rhabdomyolysis, hemodynamic shock, consumption
    coagulopathy, and direct nephrotoxic venom components.
  locations:
  - preferred_term: kidney
    term:
      id: UBERON:0002113
      label: kidney
  - preferred_term: nephron tubule
    term:
      id: UBERON:0001231
      label: nephron tubule
  biological_processes:
  - preferred_term: renal filtration
    term:
      id: GO:0097205
      label: renal filtration
    modifier: DECREASED
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury. These clinical manifestations result from complex biochemical venom constituents comprising of cytotoxins, hemotoxins, neurotoxins, myotoxins, and other substances."
    explanation: Supports systemic venom-induced renal injury as a major life-threatening manifestation of snakebite envenoming.
  downstream:
  - target: Acute kidney injury
    description: Renal tubular and microvascular injury from systemic envenoming results in clinical acute kidney injury.
phenotypes:
- name: Edema
  category: Dermatologic
  description: Rapidly progressive local swelling at and extending from the bite site due to venom metalloprotease- and cytotoxin-mediated tissue injury.
  phenotype_term:
    preferred_term: Edema
    term:
      id: HP:0000969
      label: Edema
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury."
    explanation: The abstract lists local swelling among clinical features.
- name: Cutaneous necrosis
  category: Dermatologic
  description: Local soft-tissue and skin necrosis at the bite site caused by venom cytotoxins, phospholipases, and metalloproteases.
  phenotype_term:
    preferred_term: Cutaneous necrosis
    term:
      id: HP:0033126
      label: Cutaneous necrosis
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury."
    explanation: Tissue necrosis is a cardinal local feature of cytotoxic snakebite envenoming.
- name: Abnormal bleeding
  category: Hematologic
  description: Spontaneous systemic hemorrhage and incoagulable blood resulting from venom-induced consumption coagulopathy.
  phenotype_term:
    preferred_term: Abnormal bleeding
    term:
      id: HP:0001892
      label: Abnormal bleeding
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury."
    explanation: The abstract lists systemic hemorrhage and incoagulable blood.
- name: Hypotension
  category: Cardiovascular
  description: Circulatory shock and hypotension complicating systemic snakebite envenoming.
  phenotype_term:
    preferred_term: Hypotension
    term:
      id: HP:0002615
      label: Hypotension
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury."
    explanation: Shock is listed among the main systemic clinical features of snakebite envenoming.
- name: Paralysis
  category: Neurologic
  description: Descending flaccid neuromuscular paralysis, including ptosis, bulbar palsy, and respiratory muscle paralysis, caused by presynaptic or postsynaptic venom neurotoxins and myotoxins.
  phenotype_term:
    preferred_term: Paralysis
    term:
      id: HP:0003470
      label: Paralysis
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury."
    explanation: The abstract lists paralysis among clinical features.
- name: Respiratory failure
  category: Respiratory
  description: Ventilatory impairment and respiratory failure resulting from neurotoxic paralysis of bulbar and respiratory muscles.
  phenotype_term:
    preferred_term: Respiratory failure
    term:
      id: HP:0002878
      label: Respiratory failure
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "In cases of neurotoxic envenoming, patients with neurological manifestations are monitored by serial general physical and neurological examination with special attention to cranial nerve function, airway, respiration, and bedside measures, such as Peak Expiratory Flow Rate (PEFR) and blood oxygen saturation (SpO2)."
    explanation: Highlights airway and respiratory compromise requiring PEFR and SpO2 monitoring in neurotoxic snakebite envenoming.
- name: Rhabdomyolysis
  category: Musculoskeletal
  description: Generalized or local skeletal muscle breakdown caused by venom myotoxins and phospholipases.
  phenotype_term:
    preferred_term: Rhabdomyolysis
    term:
      id: HP:0003201
      label: Rhabdomyolysis
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury."
    explanation: The abstract lists rhabdomyolysis among the main clinical manifestations of snakebite envenoming.
- name: Acute kidney injury
  category: Renal
  description: Acute renal failure secondary to venom-induced rhabdomyolysis, hypotension, consumption coagulopathy, and direct nephrotoxicity.
  phenotype_term:
    preferred_term: Acute kidney injury
    term:
      id: HP:0001919
      label: Acute kidney injury
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Generally, the main clinical features of snakebites are local swelling, tissue necrosis, shock, spontaneous systemic hemorrhage, incoagulable blood, paralysis, rhabdomyolysis, and acute kidney injury."
    explanation: The abstract lists acute kidney injury among clinical features.
diagnosis:
- name: Blood coagulation testing and 20-minute whole blood clotting test
  diagnosis_term:
    preferred_term: coagulation study
    term:
      id: NCIT:C62662
      label: Coagulation Study
  description: >-
    Bedside 20-minute whole blood clotting test (20WBCT) and laboratory
    coagulation assays (prothrombin time, INR, aPTT, fibrinogen, and fibrin
    degradation products/D-dimer) detect venom-induced consumption
    coagulopathy and guide antivenom indication.
  results: Incoagulable blood on 20WBCT, prolonged PT/INR and aPTT, hypofibrinogenemia, and elevated D-dimer/fibrin degradation products.
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Tests of blood coagulation, such as prothrombin time (PT), the International Normalized Ratio (INR), or activated partial thromboplastin time (aPTT), measurement of fibrin(ogen) related proteins also known as fibrin degradation products (FDP), or D-dimer, can also be used to diagnose snakebite envenoming."
    explanation: Supports coagulation testing (PT, INR, aPTT, FDP, D-dimer) for diagnosing hemotoxic snakebite envenoming.
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "If the blood is still liquid (unclotted) and runs out, the patient has incoagulable blood (hypofibrinogenaemia) as a result of venom-induced consumption coagulopathy and is in need of antivenom treatment."
    explanation: Supports bedside whole blood clotting assessment showing unclotted liquid blood as diagnostic of venom-induced consumption coagulopathy.
- name: Serial neurological and respiratory monitoring
  diagnosis_term:
    preferred_term: neurologic examination
    term:
      id: NCIT:C81313
      label: Neurologic Examination
  description: >-
    Serial physical and neurological examination assessing cranial nerve
    function (ptosis, ophthalmoplegia, bulbar function), airway patency, Peak
    Expiratory Flow Rate (PEFR), and pulse oximetry (SpO2) to detect
    neurotoxic envenoming and impending respiratory failure.
  results: Progressive cranial nerve palsy, declining PEFR, and desaturation indicating neurotoxic neuromuscular blockade.
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "In cases of neurotoxic envenoming, patients with neurological manifestations are monitored by serial general physical and neurological examination with special attention to cranial nerve function, airway, respiration, and bedside measures, such as Peak Expiratory Flow Rate (PEFR) and blood oxygen saturation (SpO2)."
    explanation: Establishes serial neurological examination and respiratory monitoring as essential diagnostic assessments in neurotoxic snakebite envenoming.
treatments:
- name: Intravenous antivenom administration
  description: >-
    Intravenous administration of specific or polyvalent immunoglobulin
    antivenom is the only specific therapy to neutralize circulating snake
    venom toxins and reverse venom-induced consumption coagulopathy, though its
    clinical efficacy is limited against established presynaptic neurotoxicity
    and local tissue necrosis.
  therapeutic_modality: OTHER
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
  target_mechanisms:
  - target: Postsynaptic alpha-neurotoxin neuromuscular blockade
    treatment_effect: INHIBITS
    description: Neutralizes circulating postsynaptic neurotoxins to halt or reverse neuromuscular junction blockade.
  - target: Presynaptic phospholipase A2 neurotoxin blockade
    treatment_effect: INHIBITS
    description: Neutralizes circulating presynaptic neurotoxins prior to irreversible nerve terminal injury, although efficacy is limited once presynaptic neurotoxicity is established.
    evidence:
    - reference: PMID:34430847
      reference_title: "Clinical management of snakebite envenoming: Future perspectives."
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: "However, while antivenoms save countless lives, they are associated with adverse reactions, limited potency, and are relatively inefficacious against presynaptic neurotoxicity and in preventing necrosis."
      explanation: Notes that antivenom neutralizes systemic envenoming but has limited efficacy against established presynaptic neurotoxicity.
  - target: Venom-induced consumption coagulopathy
    treatment_effect: INHIBITS
    description: Neutralizes procoagulant and hemorrhagic venom toxins in patients with incoagulable blood from venom-induced consumption coagulopathy.
    evidence:
    - reference: PMID:34430847
      reference_title: "Clinical management of snakebite envenoming: Future perspectives."
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: "If the blood is still liquid (unclotted) and runs out, the patient has incoagulable blood (hypofibrinogenaemia) as a result of venom-induced consumption coagulopathy and is in need of antivenom treatment."
      explanation: Directly links venom-induced consumption coagulopathy to the indication for antivenom therapy.
  - target: Venom metalloprotease and cytotoxin-mediated extracellular matrix degradation and local tissue necrosis
    treatment_effect: INHIBITS
    description: Neutralizes circulating cytotoxic and proteolytic venom toxins, although efficacy in preventing local necrosis is limited.
  - target: Venom myotoxin-mediated skeletal muscle damage
    treatment_effect: INHIBITS
    description: Neutralizes circulating venom myotoxins to limit systemic muscle injury.
  evidence:
  - reference: PMID:28905944
    reference_title: "Snakebite envenoming."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Intravenous administration of antivenom is the only specific treatment to counteract envenoming."
    explanation: The abstract states antivenom is the only specific treatment.
- name: Organ supportive care (ventilator support, fluid therapy, and hemodialysis)
  description: >-
    Critical supportive interventions including mechanical ventilation for
    neurotoxic respiratory paralysis, intravenous fluid resuscitation for shock,
    hemodialysis for acute kidney injury, analgesia, and antibiotic therapy for
    secondary wound infection.
  therapeutic_modality: OTHER
  treatment_term:
    preferred_term: supportive care
    term:
      id: NCIT:C15747
      label: Supportive Care
  target_mechanisms:
  - target: Presynaptic phospholipase A2 neurotoxin blockade
    treatment_effect: BYPASSES
    description: Mechanical ventilation maintains oxygenation and ventilation while presynaptic neuromuscular transmission recovers.
  - target: Postsynaptic alpha-neurotoxin neuromuscular blockade
    treatment_effect: BYPASSES
    description: Mechanical ventilation supports respiration during postsynaptic neuromuscular paralysis.
  - target: Venom-associated renal injury
    treatment_effect: BYPASSES
    description: Fluid resuscitation and hemodialysis support renal clearance and fluid-electrolyte homeostasis during acute kidney injury.
  evidence:
  - reference: PMID:28905944
    reference_title: "Snakebite envenoming."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Intravenous administration of antivenom is the only specific treatment to counteract envenoming. Analgesics, ventilator support, fluid therapy, haemodialysis and antibiotic therapy are also used."
    explanation: Supports ventilator support, fluid therapy, hemodialysis, analgesics, and antibiotics as essential adjunctive treatments for snakebite envenoming.
- name: Anticholinesterase ancillary therapy
  description: >-
    Anticholinesterase inhibitors such as edrophonium (Tensilon) are used to
    assess and provide immediate ancillary treatment following envenomings by
    snakes causing postsynaptic neurotoxic envenoming, whereas they are
    generally not useful for presynaptic neurotoxicity.
  therapeutic_modality: SMALL_MOLECULE
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
  target_mechanisms:
  - target: Postsynaptic alpha-neurotoxin neuromuscular blockade
    treatment_effect: RESTORES
    description: Inhibits acetylcholinesterase at the neuromuscular junction to provide immediate ancillary reversal in postsynaptic neurotoxic envenoming.
    evidence:
    - reference: PMID:34430847
      reference_title: "Clinical management of snakebite envenoming: Future perspectives."
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: "Anticholinesterase inhibitors (e.g. edrophonium or tensilon) have been used to assess and provide immediate ancillary treatment, especially following envenomings by snakes causing post-synaptic neurotoxic envenoming"
      explanation: Directly supports anticholinesterase inhibitors as an ancillary therapy targeting postsynaptic neurotoxic envenoming.
  evidence:
  - reference: PMID:34430847
    reference_title: "Clinical management of snakebite envenoming: Future perspectives."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Anticholinesterase inhibitors (e.g. edrophonium or tensilon) have been used to assess and provide immediate ancillary treatment, especially following envenomings by snakes causing post-synaptic neurotoxic envenoming"
    explanation: Supports anticholinesterase therapy as an ancillary treatment for postsynaptic neurotoxic snakebite envenoming.
datasets:
- accession: geo:GSE287744
  title: 'Neurocellular stress response to Mojave Type A Rattlesnake venom: A study of molecular mechanisms using a human iPSC-derived neural stem cell model'
  description: The Mojave rattlesnake (Crotalus scutulatus scutulatus) is classified as the “highest medically important” snake in the risk categories in the United States. Although responsible for fewer snakebite envenomations and deaths compared to other species, Mojave rattlesnake venom is poorly characterized and shows significant geographical variability. The venom of Type A animals primarily contains the β-neurotoxin referred to as Mojave Toxin (MTX), which is responsible for the neurotoxic effects that make bites from this snake particularly feared.
  organism:
    preferred_term: human
    term:
      id: NCBITaxon:9606
      label: Homo sapiens
  data_type: BULK_RNA_SEQ
  sample_count: 24
  publication: PMID:40149917
  notes: Identified by GEO DataSets index search for Snakebite envenoming (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-08-01. Title, sample count, and organism are GEO's own values.
references:
- reference: PMID:28905944
  title: "Snakebite envenoming."
- reference: PMID:34430847
  title: "Clinical management of snakebite envenoming: Future perspectives."
- reference: PMID:40149917
  title: "Neurocellular Stress Response to Mojave Type A Rattlesnake Venom: Study of Molecular Mechanisms Using Human iPSC-Derived Neural Stem Cell Model."
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References & Deep Research

References

3
PMID:28905944
Snakebite envenoming.
No top-level findings curated for this source.
PMID:34430847
Clinical management of snakebite envenoming: Future perspectives.
No top-level findings curated for this source.
PMID:40149917
Neurocellular Stress Response to Mojave Type A Rattlesnake Venom: Study of Molecular Mechanisms Using Human iPSC-Derived Neural Stem Cell Model.
No top-level findings curated for this source.