Johnson Grass / Sorghum (cyanide)

Johnson grass and sorghum poisoning represents one of the most rapidly fatal plant toxicities affecting farm animals, caused by the release of hydrogen cyanide (also known as prussic acid or hydrocyanic acid) from cyanogenic glycosides contained within these plants. This emergency condition occurs when livestock consume plant material from Johnson grass, sorghum, sorghum-sudan hybrids, Sudan grass, or related species under conditions that promote high cyanide concentrations. The toxic compounds are released when plant cells are damaged during chewing and digestion, allowing enzymes to convert cyanogenic glycosides into deadly hydrogen cyanide gas that is rapidly absorbed into the bloodstream.

This toxicity primarily affects ruminant animals including cattle, sheep, and goats, though horses and other livestock species can also be poisoned. Cattle are most commonly affected due to their grazing habits and the widespread use of sorghum-based forages in cattle operations. The condition occurs throughout regions where these warm-season grasses are grown for pasture, hay, or silage, making it a significant concern for livestock producers across temperate and subtropical agricultural areas. Outbreaks frequently occur following environmental stresses such as drought, frost, or rapid regrowth after cutting.

The economic and welfare impact of cyanide poisoning from Johnson grass and sorghum can be devastating to livestock operations. Death can occur within minutes to hours of consumption, often before any treatment can be administered. Multiple animals may be affected simultaneously when a herd grazes toxic pastures, leading to catastrophic losses. Beyond direct mortality, sublethal exposure can cause decreased production, reproductive problems, and neurological damage in surviving animals. The sudden nature of deaths and potential for multiple casualties makes this one of the most economically significant plant toxicities in livestock agriculture.

Despite its severity, cyanide poisoning is treatable when recognized early and when appropriate antidotes are immediately available. The key to successful outcomes lies in rapid recognition of clinical signs, immediate removal of animals from the toxic forage source, and prompt administration of specific antidote therapy. Understanding the conditions that promote cyanide accumulation in plants and implementing preventive management strategies are essential for protecting livestock. Veterinary involvement is critical for both emergency treatment and development of farm-specific prevention protocols to minimize the risk of this devastating toxicity.

The primary cause of Johnson grass and sorghum poisoning is the ingestion of plant material containing high concentrations of cyanogenic glycosides, primarily dhurrin in sorghum species and related compounds in Johnson grass. These glycosides are naturally present in the plants as a defense mechanism against herbivory. Under normal circumstances, the glycosides and the enzymes that break them down are stored in separate cellular compartments. However, when plant tissue is damaged through grazing, cutting, wilting, or frost damage, these compartments rupture and allow the enzymes to contact the glycosides, rapidly producing hydrogen cyanide. The liberated cyanide is then absorbed through the digestive tract and enters the bloodstream, where it exerts its toxic effects on cellular respiration.

Certain environmental and plant growth conditions dramatically increase the cyanide potential of these forages. Young, rapidly growing plants contain the highest concentrations of cyanogenic glycosides, making new growth particularly dangerous. Regrowth following cutting, grazing, or drought-breaking rains is especially hazardous because the young shoots concentrate these compounds. Plants stressed by drought accumulate higher levels of cyanogenic glycosides as growth slows but the compounds continue to be produced. Frost damage is particularly dangerous because it ruptures cell membranes throughout the plant, releasing cyanide even before the animal consumes the forage and creating a highly toxic situation.

Soil fertility and nitrogen availability significantly influence cyanide content in susceptible plants. High nitrogen fertilization increases the concentration of cyanogenic glycosides in plant tissues, making heavily fertilized pastures more dangerous. Soils deficient in phosphorus or potassium may also promote higher cyanide levels. Additionally, certain herbicide applications can stress plants and temporarily increase their toxicity. The interaction between soil conditions, weather patterns, and plant growth stage creates variable and sometimes unpredictable cyanide levels that challenge even experienced producers.

Ruminant animals face particular risk because their digestive physiology enhances cyanide release and absorption. The rumen environment, with its neutral to slightly acidic pH and abundant microbial enzymes, efficiently liberates cyanide from glycosides. The large rumen capacity means that ruminants can consume substantial quantities of toxic material before clinical signs appear. Additionally, the rapid absorption of cyanide from the rumen delivers a concentrated dose of toxin to the bloodstream. Hungry animals that consume large quantities of forage quickly are at greatest risk, as are animals introduced to toxic pastures without gradual adaptation.

The mechanism of cyanide toxicity involves the inhibition of cytochrome c oxidase, a critical enzyme in the mitochondrial electron transport chain. When cyanide binds to this enzyme, it blocks the final step in cellular respiration, preventing cells from utilizing oxygen to produce energy. Despite adequate oxygen in the blood, tissues cannot use it, resulting in cellular hypoxia and rapid death of oxygen-dependent tissues. The brain, heart, and respiratory muscles are particularly sensitive to this form of cellular asphyxiation, explaining the rapid progression of neurological, cardiac, and respiratory signs in affected animals.

The clinical signs of cyanide poisoning from Johnson grass and sorghum develop with alarming rapidity, often progressing from initial symptoms to death within fifteen minutes to several hours depending on the amount of toxin consumed. Early warning signs may be subtle and easily missed, particularly when animals are not under close observation. Initial symptoms include restlessness, increased respiratory rate, and apparent anxiety. Affected animals may separate from the herd and show signs of discomfort or unease. Excessive salivation and lacrimation may be observed, and some animals display muscle tremors or twitching in the early stages. Recognizing these early signs is critical because treatment is most effective when administered before severe clinical deterioration occurs.

As the toxicosis progresses, respiratory signs become prominent and characteristic of the condition. Affected animals exhibit pronounced dyspnea with labored, rapid breathing that reflects the body's futile attempt to obtain more oxygen. Despite these respiratory efforts, the tissues remain hypoxic because cyanide prevents cellular oxygen utilization. A distinctive feature of cyanide poisoning is the bright cherry-red color of mucous membranes, caused by fully oxygenated hemoglobin that cannot release its oxygen to tissues. This finding, when present, is highly suggestive of cyanide toxicity, though it may be difficult to observe in heavily pigmented animals or in poor lighting conditions.

Neurological symptoms develop as the oxygen-dependent brain tissue suffers from the effects of cellular asphyxiation. Animals may appear disoriented, ataxic, and uncoordinated in their movements. Muscle weakness becomes apparent, and animals may stagger or have difficulty standing. Behavioral changes include apparent blindness, head pressing, and aimless wandering. Some animals exhibit hyperexcitability with exaggerated responses to stimuli, while others become progressively more depressed and unresponsive. Seizure activity may occur in some cases, manifesting as paddling movements, opisthotonus, or generalized convulsions.

Cardiovascular signs reflect the heart muscle's sensitivity to cyanide-induced cellular hypoxia. The heart rate typically increases initially as the body attempts to compensate for inadequate oxygen delivery, but cardiac arrhythmias may develop as the myocardium becomes increasingly compromised. Blood pressure becomes unstable, and peripheral perfusion deteriorates. The combination of cardiac dysfunction and cellular inability to utilize oxygen creates a rapidly deteriorating clinical picture that progresses to cardiovascular collapse in severe cases.

The progression of symptoms follows a predictable but rapid course in untreated animals. Within minutes of consuming a lethal dose, animals transition from early signs to severe respiratory distress and neurological dysfunction. Terminal stages are characterized by recumbency, with animals unable to stand and showing decreasing responsiveness to external stimuli. Agonal breathing patterns develop, characterized by gasping respirations that become progressively weaker and more irregular. Coma precedes death, which typically results from respiratory arrest followed by cardiac standstill.

Emergency symptoms requiring immediate veterinary intervention include any combination of acute respiratory distress, bright red or cherry-colored mucous membranes, sudden collapse, or multiple animals showing simultaneous signs of distress while grazing sorghum or Johnson grass pastures. The sudden death of one or more animals in a group that has been grazing these forages should prompt immediate removal of surviving animals from the pasture and emergency veterinary consultation. Finding dead animals with evidence of recent grazing and no signs of struggle or trauma in sorghum or Johnson grass pastures strongly suggests cyanide poisoning. Time is absolutely critical in these situations, as delays of even minutes can mean the difference between survival and death.

Diagnosis of cyanide poisoning from Johnson grass and sorghum typically relies heavily on clinical presentation and history, given the rapid progression of this toxicity that often precludes extensive diagnostic testing in live animals. The combination of acute onset of respiratory distress, characteristic cherry-red mucous membranes, neurological signs, and a history of access to sorghum species or Johnson grass creates a strong presumptive diagnosis. Veterinarians often must initiate treatment based on clinical suspicion alone, as waiting for laboratory confirmation would prove fatal for affected animals. A history of recent environmental stress to the pasture, such as frost, drought breaking, or recent cutting, strengthens the clinical suspicion.

Laboratory confirmation of cyanide poisoning can be achieved through several testing methods, though sample handling is critical due to the volatile nature of hydrogen cyanide. Blood samples should be collected as soon as possible and kept cold to minimize cyanide loss through evaporation. Whole blood cyanide levels above 1 microgram per milliliter are generally considered diagnostic for cyanide toxicosis, though levels in acutely poisoned animals are often substantially higher. Rumen contents can be tested for cyanide using the picric acid paper test, which provides rapid qualitative results at the farm level. This simple test involves suspending a piece of picric acid-impregnated filter paper over a sample of rumen contents in a sealed container; color change from yellow to orange or red indicates the presence of cyanide.

Post-mortem examination in animals that die from cyanide poisoning may reveal characteristic findings, though these changes are not pathognomonic. The blood often appears bright cherry-red due to the high oxygen saturation of hemoglobin that could not release its oxygen to tissues. Internal organs may also appear congested and brighter red than normal. A distinctive bitter almond odor may be detected when the rumen is opened, though the ability to detect this odor is genetically variable and absent in a significant portion of the population. The absence of other obvious pathological findings in an animal with sudden death helps support the diagnosis. Collecting appropriate samples for laboratory testing at the time of necropsy is essential for definitive confirmation.

Differential diagnosis for suspected cyanide poisoning includes other causes of acute respiratory distress and sudden death in livestock. Nitrate-nitrite poisoning produces similar clinical signs but results in brown-colored blood due to methemoglobin formation rather than the cherry-red color of cyanide toxicity. Acute bloat causes respiratory distress but is accompanied by visible ruminal distension. Anaphylactic reactions, lightning strike, clostridial diseases, and acute heart failure may also cause sudden death and should be considered. When multiple animals are affected simultaneously while grazing, plant toxicity becomes more likely. Testing of the pasture forage for cyanide content can confirm the source of poisoning and guide decisions about future use of the affected area. Forage testing is performed by collecting plant samples, particularly young growth, and submitting them to a diagnostic laboratory for cyanogenic glycoside analysis.

Treatment of cyanide poisoning from Johnson grass and sorghum constitutes a true veterinary emergency requiring immediate intervention with specific antidotes. The cornerstone of therapy is the administration of sodium nitrite followed by sodium thiosulfate, a two-step antidote protocol that has been used successfully for decades. Sodium nitrite is administered intravenously at a dose of 10-20 milligrams per kilogram of body weight as a 1-2% solution. This compound works by converting a portion of the hemoglobin to methemoglobin, which has a higher affinity for cyanide than cytochrome oxidase. The cyanide preferentially binds to the methemoglobin, forming cyanmethemoglobin and freeing the cytochrome oxidase to resume cellular respiration.

Sodium thiosulfate is administered immediately following sodium nitrite, typically at a dose of 250-500 milligrams per kilogram intravenously. This compound serves as a sulfur donor for the enzyme rhodanese, which converts cyanide to thiocyanate, a relatively non-toxic compound that is excreted in urine. Because the rhodanese system has limited capacity and cyanide may continue to be absorbed from the digestive tract, sodium thiosulfate may need to be repeated. Some treatment protocols recommend giving sodium thiosulfate alone at higher doses if sodium nitrite is not available, as it can provide some benefit as a sole agent. Commercial cyanide antidote kits containing premeasured doses of both compounds are available and should be part of the emergency supplies on farms where livestock graze potentially toxic forages.

Alternative antidote protocols have been developed for situations where traditional antidotes are unavailable. Hydroxocobalamin (vitamin B12a) has been used effectively as a cyanide antidote in human medicine and can be used in livestock. It binds directly to cyanide to form cyanocobalamin, which is excreted renally. Dicobalt edetate is another alternative that chelates cyanide, though it is less commonly available. Methylene blue has been used historically but is less favored due to its narrower therapeutic margin. Regardless of which antidote is used, speed of administration is the critical factor determining treatment success.

Supportive care measures complement specific antidote therapy and may determine survival in borderline cases. Oxygen supplementation, while not addressing the fundamental problem of cellular oxygen utilization, may provide some benefit by maximizing oxygen availability as antidote effects take hold. Intravenous fluid therapy helps maintain cardiovascular function and supports renal excretion of thiocyanate and other cyanide metabolites. Animals should be kept calm and minimally stimulated, as stress and exertion increase oxygen demand in tissues already compromised by cyanide toxicity. Maintaining body temperature and providing a comfortable environment support recovery.

When multiple animals are affected or at risk, a herd-level treatment approach becomes necessary. Animals showing clinical signs should receive immediate individual antidote treatment. Those with access to the toxic pasture but not yet showing signs should be immediately removed from the forage source. Prophylactic treatment of exposed but asymptomatic animals is controversial; some veterinarians advocate for prophylactic sodium thiosulfate administration while others prefer close monitoring with treatment only if signs develop. All exposed animals should be observed closely for at least 24-48 hours, as continued absorption from rumen contents can cause delayed or recurrent toxicosis.

Treatment decisions in livestock operations must balance individual animal welfare against economic realities and practical constraints. The cost of antidote therapy, veterinary services, and supportive care must be weighed against the value of the animal and prognosis for recovery. Animals that survive the acute episode may have residual neurological damage or organ dysfunction that affects their long-term productivity. In cases where multiple animals are affected and resources are limited, triage decisions may be necessary to direct treatment to those animals most likely to benefit. Post-treatment monitoring and follow-up care require commitment of time and resources that producers must factor into their management decisions.

Recovery from cyanide poisoning due to Johnson grass and sorghum consumption depends heavily on the severity of exposure and the speed with which appropriate treatment was administered. Animals that receive antidote therapy early in the course of poisoning, before significant cellular damage has occurred, may recover remarkably quickly and completely. In these cases, clinical improvement can be observed within minutes of treatment as cellular respiration is restored. Such animals may appear nearly normal within a few hours and can make full recoveries with no lasting effects. However, animals that experienced prolonged hypoxia before treatment may have sustained irreversible damage to oxygen-sensitive organs.

Post-treatment care involves close monitoring for signs of relapse or complications over the first 48-72 hours following the initial episode. Cyanide can continue to be released from plant material remaining in the rumen, potentially causing recurrent toxicosis hours after apparently successful initial treatment. Animals should be observed frequently for any return of clinical signs such as respiratory distress, weakness, or neurological abnormalities. Repeat doses of sodium thiosulfate may be administered if relapse occurs or prophylactically during the monitoring period. Access to fresh, clean water should be ensured to support renal excretion of thiocyanate and maintain hydration.

The prognosis for animals that survive the acute crisis varies based on the duration and severity of cellular hypoxia experienced. Animals treated promptly before severe clinical deterioration generally have good to excellent prognoses for full recovery. Those that experienced prolonged recumbency, seizures, or coma before treatment have more guarded prognoses due to potential neurological damage. Brain damage from hypoxia can result in persistent neurological deficits including vision problems, behavioral changes, and coordination difficulties. Cardiac muscle damage may cause persistent arrhythmias or decreased cardiac function that limits the animal's productive capacity.

Return to production considerations for recovered animals depend on the species, production type, and extent of any residual damage. Meat animals should observe appropriate withdrawal periods for any drugs administered during treatment, though the antidotes themselves do not have established withdrawal times in livestock. Dairy animals should have milk withheld during treatment and recovery until cleared by a veterinarian. Animals showing any persistent neurological signs may be unsuitable for return to the breeding herd or for sale through normal market channels. Individual assessment by a veterinarian can help producers make informed decisions about the future use of recovered animals.

Prevention of cyanide poisoning from Johnson grass and sorghum centers on understanding and managing the conditions that promote cyanogenic glycoside accumulation in these plants. Vaccination is not applicable for toxic plant exposure, so prevention relies entirely on management practices and pasture monitoring. The foundation of prevention is knowledge of which plants contain cyanogenic potential and recognition of the environmental conditions that increase toxicity. All varieties of sorghum, Johnson grass, Sudan grass, and sorghum-sudan hybrids should be considered potentially dangerous under certain conditions. Producers should map their properties to identify areas where these plants grow and implement specific management protocols for those areas.

Biosecurity in the context of plant toxicity prevention involves controlling animal access to dangerous forages and managing grazing timing. Animals should never be turned onto sorghum or Johnson grass pastures that have been recently stressed by drought, frost, or herbicide application. Following a killing frost, these forages should be completely avoided until thoroughly dried or until new growth has reached a safe height of at least 18-24 inches. After drought-breaking rains, new growth should be allowed to mature before grazing resumes. When cutting these forages for hay, allowing adequate drying time before baling reduces but does not eliminate cyanide risk, as some cyanogenic potential may persist in cured hay.

Nutritional management strategies can reduce the risk of cyanide poisoning even when animals must graze potentially toxic forages. Ensuring animals are not hungry when introduced to sorghum or Johnson grass pastures reduces the likelihood of rapid, excessive consumption. Providing supplemental feed before turnout helps moderate intake. Gradually acclimating animals to these forages, starting with limited grazing periods, may allow rumen microorganisms to adapt and improve their capacity to detoxify small amounts of cyanide. Maintaining adequate mineral nutrition, particularly sulfur, supports the enzymatic pathways that convert cyanide to less toxic thiocyanate.

Management practices that reduce cyanide risk include testing forages before grazing or feeding. Simple qualitative tests using picric acid paper can be performed on farm to screen for cyanide presence. Quantitative laboratory testing provides more precise information about cyanide content and safety for grazing. As a general guideline, forages containing less than 500-600 parts per million cyanide potential on a dry matter basis are considered relatively safe for cattle, though lower thresholds may be appropriate for other species. Testing should be repeated after any stress event that might increase toxicity.

Quarantine and monitoring protocols for managing sorghum and Johnson grass pastures should include daily observation of grazing animals during high-risk periods. Producers should be alert for the earliest signs of toxicity and be prepared to remove animals immediately if any problems are suspected. Having cyanide antidote supplies on hand during high-risk grazing periods enables rapid treatment that can save lives. Establishing a working relationship with a veterinarian who is familiar with the farm and its cyanide risk allows for more effective emergency response. Detailed records of pasture management, grazing timing, and any incidents help refine prevention strategies over time.

Daily management of livestock operations where Johnson grass or sorghum forages are used requires ongoing vigilance and systematic monitoring protocols. Animals grazing these pastures should be observed at least twice daily during high-risk periods, with careful attention to any behavioral changes or early signs of distress. Morning checks are particularly important following nights when frost may have occurred. Producers should establish baseline knowledge of normal behavior for their animals so that subtle early changes are more readily detected. Any animal that appears dull, separated from the herd, or exhibits increased respiratory rate should be immediately evaluated and removed from the pasture pending assessment.

Housing and environmental management play important roles in reducing cyanide poisoning risk. When environmental conditions increase the danger of toxic forage, animals should be confined to safe pastures or dry lots with appropriate alternative feed sources. Temporary fencing can be used to exclude animals from areas where dangerous plants grow during high-risk periods. Hay feeding during frost events keeps animals satisfied and reduces the likelihood of their seeking out and consuming frosted forage. Shelter and housing management should account for the stress that extreme weather places on both plants and animals, as both drought stress on forages and heat stress on animals increase the overall risk of toxicity events.

Herd health programs for operations utilizing sorghum-type forages should include specific provisions for cyanide poisoning prevention and response. Written protocols should outline the conditions under which these pastures can be safely grazed, the monitoring requirements during grazing periods, and the emergency response procedures if poisoning is suspected. These protocols should be understood by all farm personnel, not just the primary manager or owner. Regular training sessions help ensure that everyone involved in animal care recognizes the signs of cyanide poisoning and knows how to respond appropriately.

Record keeping is essential for managing cyanide poisoning risk over time and demonstrating due diligence in animal care. Records should document when sorghum and Johnson grass pastures are grazed, what environmental conditions preceded grazing, results of any forage testing, and any incidents of suspected or confirmed toxicity. Tracking weather patterns, particularly frost dates and drought periods, helps predict high-risk times. Production records can reveal subtle impacts of sublethal cyanide exposure, such as decreased weight gain or milk production during certain grazing periods. These records inform future management decisions and can be valuable in insurance claims or legal situations.

Economic considerations in managing cyanide poisoning risk involve balancing the value of sorghum-type forages against the potential costs of toxicity. These warm-season grasses offer significant advantages including high yields, drought tolerance, and good nutritional value during summer months when cool-season grasses may be limited. However, the potential for catastrophic losses from cyanide poisoning represents a significant economic risk. Producers must weigh the forage value against the costs of testing, monitoring, maintaining antidote supplies, and the potential for animal losses. Diversifying forage resources to reduce dependence on cyanogenic species provides a buffer against risk while maintaining overall forage availability.

All breeds of cattle, both beef and dairy, are susceptible to cyanide poisoning from Johnson grass and sorghum, with no breed-specific resistance documented. However, certain production systems and management contexts create higher practical risk for some animals. High-producing dairy cattle face elevated risk because their intense metabolic demands often lead to aggressive grazing behavior, increasing the likelihood of rapid consumption of large quantities of potentially toxic forage. Dairy operations in regions where sorghum-sudan hybrids are commonly used as summer pasture must be particularly vigilant. Feedlot cattle and stocker operations that utilize sorghum stubble or regrowth for grazing similarly face increased exposure risk due to the nature of their forage utilization.

Among small ruminants, both sheep and goats are highly susceptible to cyanide poisoning, with some evidence suggesting that sheep may be somewhat more sensitive than cattle on a body weight basis. Meat goats and dairy goats are at risk when grazing pastures containing Johnson grass or when fed sorghum-type forages. The browsing behavior of goats may offer some protection as they are more likely to select diverse plant species rather than consuming large quantities of a single forage, but this protection is not reliable. Hair sheep breeds raised in regions where these forages predominate require the same careful management as cattle. Lambs and kids are particularly vulnerable due to their smaller body size and lower tolerance for toxic insults.

Production type significantly influences practical risk beyond breed considerations. Animals in intensive grazing systems where pasture rotation is frequent may be exposed to young, regrowth forage more often than those in extensive systems. Conversely, animals in continuous grazing systems may have adapted rumen microbial populations and more selective grazing behavior that offer some protection. Pregnant and lactating animals have increased nutritional demands that may drive more aggressive consumption of available forage, potentially increasing their risk. Young, growing animals similarly tend toward higher intakes relative to body weight. Genetic selection for increased intake efficiency, while valuable for production, may inadvertently increase cyanide poisoning risk by promoting faster, less selective consumption of available forage.

Several conditions commonly co-occur with or complicate cyanide poisoning from Johnson grass and sorghum. Nitrate poisoning frequently affects animals grazing the same types of forages under similar stress conditions, and the two toxicities may occur together in the same animal or herd. Both drought-stressed and heavily fertilized sorghum-type plants can accumulate both cyanogenic glycosides and nitrates, creating a dual toxicity scenario that complicates diagnosis and treatment. Bloat may occur concurrently, particularly when animals consume lush sorghum regrowth rapidly. The presence of multiple toxicities can modify the clinical presentation and affect the response to treatment.

Several other plant toxicities produce clinical signs that may be confused with cyanide poisoning and should be considered in the differential diagnosis. Nitrate-nitrite poisoning causes acute respiratory distress and sudden death similar to cyanide but produces characteristic chocolate-brown blood due to methemoglobin formation. Water hemlock poisoning causes rapid onset of seizures and death but typically occurs near water sources where this plant grows. Yew poisoning results in sudden death but affects the heart primarily. Blue-green algae toxicosis can cause rapid death in animals drinking from contaminated water sources. Distinguishing among these various toxic causes is important for implementing appropriate treatment and preventing additional cases.

Complications and sequelae of cyanide poisoning relate primarily to the hypoxic damage sustained by various organ systems during the acute episode. Neurological sequelae may include persistent vision deficits, behavioral changes, and coordination problems resulting from hypoxic brain injury. Cardiac complications can include arrhythmias and decreased cardiac function from myocardial damage. Kidney and liver dysfunction may occur following severe episodes due to hypoxic injury and the metabolic stress of processing cyanide metabolites. Animals that recover from severe poisoning should be monitored for these potential long-term complications that may affect their productivity and welfare. Sorghum cystitis-ataxia syndrome represents a distinct condition caused by chronic low-level cyanide exposure from sorghum species, characterized by urinary incontinence and posterior ataxia, and should be distinguished from acute cyanide poisoning.