Snake venom is a complex, toxic biological substance secreted by specialized glands in certain snakes. This venom consists of a mixture of zootoxins, mostly proteins and polypeptides, alongside enzymes and other compounds that target physiological systems like blood clotting, nerve impulses, and muscle function. When a venomous snake bite causes envenomation, these toxins can quickly lead to severe tissue damage, systemic failure, or death. The only definitive medical treatment capable of counteracting envenomation is the administration of antivenom, a highly specialized biological product.
Producing Antivenom Through Immunization
The process of creating antivenom relies on immunization, which begins with the venom itself. Venom is collected from snakes through “milking,” diluted to a non-lethal concentration, and repeatedly injected into a host animal, typically a horse or a sheep, over several months.
The host animal’s immune system recognizes the venom as foreign and produces large quantities of specific antibodies. These antibodies are the active therapeutic component of the antivenom. Once a high concentration of neutralizing antibodies is developed, a volume of the animal’s blood plasma is collected.
The collected plasma undergoes a series of complex purification steps known as fractionation. Refinement involves enzymatic digestion, often using pepsin or papain, to cleave the whole immunoglobulin G (IgG) molecule into smaller, active fragments.
Manufacturers commonly isolate the F(ab’)2 or Fab fragments. These fragments lack the Fc portion of the antibody molecule, which is most likely to cause severe allergic reactions in humans. Removing the Fc portion reduces the risk of adverse side effects. The resulting concentrated and purified antibody fragments are then prepared for clinical use.
The Mechanism of Venom Neutralization
Once the purified antivenom is injected into a patient, the polyclonal antibodies enter the bloodstream. These antibodies are highly specific, recognizing and binding to the toxins present in the venom. This binding process is the core mechanism of venom neutralization.
When an antibody fragment binds to a venom toxin, it physically blocks the toxin’s active site, preventing it from interacting with the victim’s cells and tissues. This effect, often termed steric hindrance, renders the toxin biologically inert. The antivenom must be administered as soon as possible to neutralize the venom before it can cause irreversible tissue damage.
The antibodies, now complexed with the venom, also facilitate the clearance of the toxins from the body. Specialized cells, such as phagocytes, engulf and remove these neutralized complexes from the circulation. This passive immunity provides the necessary defense, as the patient’s own immune system would take too long to mount an effective response.
Targeting Specific Versus Multiple Snake Species
The effectiveness of antivenom is tied to the specific snake species whose venom was used in its production, leading to two main types: monovalent and polyvalent. Monovalent antivenom is manufactured using the venom from a single snake species, making it highly specific and potent against the toxins of that particular snake.
In contrast, polyvalent antivenom is created by immunizing the host animal with a mixture of venoms from several medically important snake species. This broader approach results in an antivenom that contains antibodies capable of neutralizing the toxins of multiple species. Clinicians often use polyvalent antivenom when the biting snake cannot be definitively identified.
Although monovalent antivenom is more potent against its target, polyvalent types may exhibit paraspecificity, meaning they can sometimes neutralize venoms from related species not specifically included in the manufacturing mixture.
Clinical Use and Managing Treatment Risks
Antivenom must be administered intravenously in a controlled hospital environment. Prompt administration is important to halt the progression of tissue damage and systemic toxicity. Dosing is determined by the severity of the envenomation, not the patient’s body weight, and may require multiple vials to fully neutralize the circulating venom.
Antivenom carries the risk of significant side effects because it is derived from foreign animal proteins. The most common acute hypersensitivity reaction is anaphylaxis, which can occur within minutes to hours of administration. Anaphylaxis can manifest as urticaria, bronchospasm, and hypotension, requiring immediate treatment with medications like epinephrine.
A second, delayed complication is serum sickness, which typically manifests five to fourteen days after the antivenom is given. This reaction is caused by the patient’s immune system reacting to the foreign proteins and forming immune complexes that deposit in various tissues. Symptoms of serum sickness include fever, rash, joint pain (arthralgia), and swelling. Patients receiving antivenom require close monitoring to manage any adverse events.