Calcium deficiency can sometimes be rectified by adding agricultural lime to acid soils, aiming at a pH of 6.5, unless the subject plants specifically prefer acidic soil. Organic matter should be added to the soil to improve its moisture-retaining capacity. However, because of the nature of the disorder (i.e. poor transport of calcium to low transpiring tissues), the problem cannot generally be cured by the addition of calcium to the roots. In some species, the problem can be reduced by prophylactic spraying with calcium chloride of tissues at risk.

Plant damage is difficult to reverse, so corrective action should be taken immediately, supplemental applications of calcium nitrate at 200 ppm nitrogen, for example. Soil pH should be tested, and corrected if needed, because calcium deficiency is often associated with low pH.

Early fruit will generally have the worst systems, with them typically lessening as the season progresses. Preventative measures, such as irrigating prior to especially high temperatures and stable irrigation will minimize the occurrence.

Several decades of research in several countries with many cultivars showed that moderate levels of bitter pit could be controlled with the spraying of the trees with calcium chloride or calcium nitrate during the growing season. However, in the southern hemisphere where highly susceptible fruit had to be harvested early for export to Europe, the problem remained. An attempt to increase the calcium content by applying calcium after harvest had resulted in severe injury to the fruit. Export of susceptible apples from New Zealand was under threat and new methods for controlling bitter pit were investigated. While it was shown that bitter pit was reduced as calcium levels rose, it was not possible to determine a minimum level of calcium that would ensure that the disorder was controlled. The most effective treatment found for closed calyx fruit was to submerge the fruit in the calcium chloride solution and to apply a vacuum and immediately rinsing in water. This overcame the injury problem and gave much better control of the disorder. The vacuum treatment was commercialized in New Zealand for the Cox's Orange Pippin cultivar in 1978 and was used for several years. However the treatment was expensive and could not be used for open calyx cultivars.

A simpler treatment was developed in Western Australia and was adopted in Australia and in New Zealand. This involved dipping the fruit in the calcium solution and rinsing in water after about 36 hours. This treatment has been confirmed by independent workers and has generally been adopted in Australia and New Zealand. Postharvest dipping in a calcium solution has been recommended in some other countries where bitter pit is severe. However the problem of fruit injury does not seem to have been addressed.

It appears that bitter pit can generally be reduced by using good horticultural practices. Usually spraying throughout the growing season with a calcium salt is also necessary for moderately susceptible cultivars. It is more difficult to control storage pit in highly susceptible cultivars as field spraying may not be able to apply sufficient calcium to the fruit. Improved control can be obtained by also dipping the fruit in a 2-3 per cent calcium chloride solution after harvest and rinsing the fruit in water after about 36 hours.

The first approach, which is the best approach at an effective management practice would be to eradicate or severely damage the Mountain and Cherry Leafhopper population because the leafhoppers are the number one vectors for this pathogen. To do this, pesticides (i.e. acephate, bifenthrin, cyfluthrin) could be applied or biological control (predators of the leafhopper) could be used. There should be a pre-season application of control measures as well as a post-season application. This is to maximize the effort at controlling both types of leafhoppers (Cherry and Mountain), thus cutting down the starting inoculum at both stages in the life cycle.

There are numerous steps one has to take to try to manage the disease as best as possible. The aim is at prevention because once the pathogen reaches the cherry trees, disease will surely ensue and there is no cure or remedy to prevent the loss of fruit production as well as the ultimate death of the tree.

Apple juice, especially commercially produced products, interferes with the action of OATPs. This interference can decrease the absorption of a variety of commonly used medications, including beta blockers like atenolol, antibiotics like ciprofloxacin, and antihistamines like montelukast.

Apple juice has been implicated in interfering with etoposide, a chemotherapy drug, and cyclosporine, taken by transplant patients to prevent rejection of their new organs.

The interaction between citrus and medication depends on the individual drug, and not the class of the drug. Drugs that interact usually share three common features: they are taken orally, normally only a small amount enters systemic blood circulation, and they are metabolized by CYP3A4. However, the effects on the CYP3A4 in the liver could in principle cause interactions with non-oral drugs, and non-CYP3A4-meditated effects also exist.

Cytochrome isoforms affected by grapefruit components include CYP3A4, CYP1A2, CYP2C9, and CYP2D6. Drugs that are metabolized by these enzymes may have interactions with components of grapefruit.

An easy way to tell if a medication may be affected by grapefruit juice is by researching whether another known CYP3A4 inhibitor drug is already contraindicated with the active drug of the medication in question. Examples of such known CYP3A4 inhibitors include cisapride (Propulsid), erythromycin, itraconazole (Sporanox), ketoconazole (Nizoral), and mibefradil (Posicor).

In addition to the aforementioned treatments, there are also many management approaches that can alleviate the symptoms of dysgeusia. These include using non-metallic silverware, avoiding metallic or bitter tasting foods, increasing the consumption of foods high in protein, flavoring foods with spices and seasonings, serving foods cold in order to reduce any unpleasant taste or odor, frequently brushing one's teeth and utilizing mouthwash, or using sialogogues such as chewing sugar-free gum or sour-tasting drops that stimulate the productivity of saliva. When taste is impeded, the food experience can be improved through means other than taste, such as texture, aroma, temperature, and color.

The effects of drug-related dysgeusia can often be reversed by stopping the patient's regimen of the taste altering medication. In one case, a forty-eight-year-old woman who was suffering from hypertension was being treated with valsartan. Due to this drug's inability to treat her condition, she began taking a regimen of eprosartan, an angiotensin II receptor antagonist. Within three weeks, she began experiencing a metallic taste and a burning sensation in her mouth that ceased when she stopped taking the medication. When she began taking eprosartan on a second occasion, her dysgeusia returned. In a second case, a fifty-nine-year-old man was prescribed amlodipine in order to treat his hypertension. After eight years of taking the drug, he developed a loss of taste sensation and numbness in his tongue. When he ran out of his medication, he decided not to obtain a refill and stopped taking amlodipine. Following this self-removal, he reported experiencing a return of his taste sensation. Once he refilled his prescription and began taking amlodipine a second time, his taste disturbance reoccurred. These two cases suggest that there is an association between these drugs and taste disorders. This link is supported by the "de-challenge" and "re-challenge" that took place in both instances. It appears that drug-induced dysgeusia can be alleviated by reducing the drug's dose or by substituting a second drug from the same class.

Veterinary treatment or an improved and more stimulating environment may help birds suffering from feather-plucking. Organic bitter sprays are sold in pet stores to discourage plucking, especially of newly grown feathers, although this may make general beak-based grooming difficult for the animal. This is not recommended since it does not address the real reason why the bird is picking feathers.

The most common treatment, which is cheap and widely available, is to apply a clear, bitter-tasting nail polish to the nails. Normally denatonium benzoate is used, the most bitter chemical compound known. The bitter flavor discourages the nail-biting habit.

Behavioral therapy is beneficial when simpler measures are not effective. Habit Reversal Training (HRT), which seeks to unlearn the habit of nail biting and possibly replace it with a more constructive habit, has shown its effectiveness versus placebo in children and adults. A study in children showed that results with HRT were superior to either no treatment at all or the manipulation of objects as an alternative behavior, which is another possible approach to treatment. In addition to HRT, stimulus control therapy is used to both identify and then eliminate the stimulus that frequently triggers biting urges. Other behavioral techniques that have been investigated with preliminary positive results are self-help techniques, and the use of wristbands as non-removable reminders. More recently, technology companies have begun producing wearable devices and smart watch applications that track the position of users' hands.

Another treatment for chronic nail biters is the usage of a dental deterrent device that prevents the front teeth from damaging the nails and the surrounding cuticles. After about two months, the device leads to a full oppression of the nail biting urge.

Evidence on the efficacy of drugs is very limited and they are not routinely used. A small double-blind randomized clinical trial in children and adolescents indicated that N-acetylcysteine, a glutathione and glutamate modulator, could, in the short term only, be more effective than placebo in decreasing the nail-biting behavior.

Nail cosmetics can help to ameliorate nail biting social effects.

Independently of the method used, parental education is useful in the case of young nail biters to maximize the efficacy of the treatment programs, as some behaviors by the parents or other family members may be helping to perpetuate the problem. For example, punishments have been shown to be not better than placebo, and in some cases may even increase the nail biting frequency.

Although no treatment has been found it has been shown that affected individuals benefit considerably from rehabilitation and use of adequate walking aids. In the Central African Republic some children have been operated with an elongation of the Achilles tendon which improved the position of the foot but the long term consequence remains uncertain.

Early reports indicated that the disorder was affected by climate and growing conditions. Dry weather before harvest seemed to increase the condition. Light crops, heavy use of fertilizers, large fruit and early harvesting increased the condition. Fruit that were free of bitter pit at harvest were often severely affected after a short period of storage. Bitter pit has been widely reviewed over many decades.

The disorder became a major problem for exports from the Southern Hemisphere to Europe. The breakthrough in control came with the discovery in North America that the mineral calcium was low in affected fruit. This was confirmed elsewhere.

Most importantly, whether the carious lesion is cavitated or non-cavitated dictates the management. Clinical assessment of whether the lesion is active or arrested is also important. Noncavitated lesions can be arrested and remineralization can occur under the right conditions. However, this may require extensive changes to the diet (reduction in frequency of refined sugars), improved oral hygiene (toothbrushing twice per day with fluoride toothpaste and daily flossing), and regular application of topical fluoride. Such management of a carious lesion is termed "non-operative" since no drilling is carried out on the tooth. Non-operative treatment requires excellent understanding and motivation from the individual, otherwise the decay will continue.

Once a lesion has cavitated, especially if dentin is involved, remineralization is much more difficult and a dental restoration is usually indicated ("operative treatment"). Before a restoration can be placed, all of the decay must be removed otherwise it will continue to progress underneath the filling. Sometimes a small amount of decay can be left if it is entombed and there is a seal which isolates the bacteria from their substrate. This can be likened to placing a glass container over a candle, which burns itself out once the oxygen is used up. Techniques such as stepwise caries removal are designed to avoid exposure of the dental pulp and overall reduction of the amount of tooth substance which requires removal before the final filling is placed. Often enamel which overlies decayed dentin must also be removed as it is unsupported and susceptible to fracture. The modern decision-making process with regards the activity of the lesion, and whether it is cavitated, is summarized in the table.

Destroyed tooth structure does not fully regenerate, although remineralization of very small carious lesions may occur if dental hygiene is kept at optimal level. For the small lesions, topical fluoride is sometimes used to encourage remineralization. For larger lesions, the progression of dental caries can be stopped by treatment. The goal of treatment is to preserve tooth structures and prevent further destruction of the tooth. Aggressive treatment, by filling, of incipient carious lesions, places where there is superficial damage to the enamel, is controversial as they may heal themselves, while once a filling is performed it will eventually have to be redone and the site serves as a vulnerable site for further decay.

In general, early treatment is quicker and less expensive than treatment of extensive decay. Local anesthetics, nitrous oxide ("laughing gas"), or other prescription medications may be required in some cases to relieve pain during or following treatment or to relieve anxiety during treatment. A dental handpiece ("drill") is used to remove large portions of decayed material from a tooth. A spoon, a dental instrument used to carefully remove decay, is sometimes employed when the decay in dentin reaches near the pulp. Some dentists remove dental caries using a laser rather than the traditional dental drill. A Cochrane review of this technique looked at Er:YAG (erbium-doped yttrium aluminium garnet), Er,Cr:YSGG (erbium, chromium: yttrium-scandium-gallium-garnet) and Nd:YAG (neodymium-doped yttrium aluminium garnet) lasers and found that although people treated with lasers (compared to a conventional dental "drill") experienced less pain and had a lesser need for dental anaesthesia, that overall there was little difference in caries removal. Once the caries is removed, the missing tooth structure requires a dental restoration of some sort to return the tooth to function and aesthetic condition.

Restorative materials include dental amalgam, composite resin, porcelain, and gold. Composite resin and porcelain can be made to match the color of a patient's natural teeth and are thus used more frequently when aesthetics are a concern. Composite restorations are not as strong as dental amalgam and gold; some dentists consider the latter as the only advisable restoration for posterior areas where chewing forces are great. When the decay is too extensive, there may not be enough tooth structure remaining to allow a restorative material to be placed within the tooth. Thus, a crown may be needed. This restoration appears similar to a cap and is fitted over the remainder of the natural crown of the tooth. Crowns are often made of gold, porcelain, or porcelain fused to metal.

For children, preformed crowns are available to place over the tooth. These are usually made of metal (usually stainless steel but increasingly there are aesthetic materials). Traditionally teeth are shaved down to make room for the crown but, more recently, stainless steel crowns have been used to seal decay into the tooth and stop it progressing. This is known as the Hall Technique and works by depriving the bacteria in the decay of nutrients and making their environment less favorable for them. It is a minimally invasive method of managing decay in children and does not require local anesthetic injections in the mouth.

In certain cases, endodontic therapy may be necessary for the restoration of a tooth. Endodontic therapy, also known as a "root canal", is recommended if the pulp in a tooth dies from infection by decay-causing bacteria or from trauma. In root canal therapy, the pulp of the tooth, including the nerve and vascular tissues, is removed along with decayed portions of the tooth. The canals are instrumented with endodontic files to clean and shape them, and they are then usually filled with a rubber-like material called gutta percha. The tooth is filled and a crown can be placed. Upon completion of root canal therapy, the tooth is non-vital, as it is devoid of any living tissue.

An extraction can also serve as treatment for dental caries. The removal of the decayed tooth is performed if the tooth is too far destroyed from the decay process to effectively restore the tooth. Extractions are sometimes considered if the tooth lacks an opposing tooth or will probably cause further problems in the future, as may be the case for wisdom teeth. Extractions may also be preferred by people unable or unwilling to undergo the expense or difficulties in restoring the tooth.

Calcium deficiency symptoms appear initially as localized tissue necrosis leading to stunted plant growth, necrotic leaf margins on young leaves or curling of the leaves, and eventual death of terminal buds and root tips. Generally, the new growth and rapidly growing tissues of the plant are affected first. The mature leaves are rarely if ever affected because calcium accumulates to high concentrations in older leaves.

Crop-specific symptoms include:

- Apple : 'Bitter pit' – fruit skins develop pits, brown spots appear on skin and/or in flesh and taste of those areas is bitter. This usually occurs when fruit is in storage, and Bramley apples are particularly susceptible. Related to boron deficiency, "water cored" apples seldom display bitter pit effects.

- Cabbage and Brussels sprouts : Internal browning and "tip burn"

- Carrot : 'Cavity spot' – oval spots develop into craters which may be invaded by other disease-causing organisms.

- Celery : Stunted growth, central leaves stunted.

- Tomatoes and peppers: 'Blossom end rot' – Symptoms start as sunken, dry decaying areas at the blossom end of the fruit, furthest away from the stem, not all fruit on a truss is necessarily affected. Sometimes rapid growth from high-nitrogen fertilizers may exacerbate blossom end rot. Water management and preventing water stress is key to minimizing its occurrence.

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

- Application of a tourniquet to the bitten limb is generally not recommended. There is no convincing evidence that it is an effective first-aid tool as ordinarily applied. Tourniquets have been found to be completely ineffective in the treatment of "Crotalus durissus" bites, but some positive results have been seen with properly applied tourniquets for cobra venom in the Philippines. Uninformed tourniquet use is dangerous, since reducing or cutting off circulation can lead to gangrene, which can be fatal. The use of a compression bandage is generally as effective, and much safer.

- Cutting open the bitten area, an action often taken prior to suction, is not recommended since it causes further damage and increases the risk of infection; the subsequent cauterization of the area with fire or silver nitrate (also known as "infernal stone") is also potentially threatening.

- Sucking out venom, either by mouth or with a pump, does not work and may harm the affected area directly. Suction started after three minutes removes a clinically insignificant quantity—less than one-thousandth of the venom injected—as shown in a human study. In a study with pigs, suction not only caused no improvement but led to necrosis in the suctioned area. Suctioning by mouth presents a risk of further poisoning through the mouth's mucous tissues. The well-meaning family member or friend may also release bacteria into the person's wound, leading to infection.

- Immersion in warm water or sour milk, followed by the application of snake-stones (also known as "la Pierre Noire"), which are believed to draw off the poison in much the way a sponge soaks up water.

- Application of a one-percent solution of potassium permanganate or chromic acid to the cut, exposed area. The latter substance is notably toxic and carcinogenic.

- Drinking abundant quantities of alcohol following the cauterization or disinfection of the wound area.

- Use of electroshock therapy in animal tests has shown this treatment to be useless and potentially dangerous.

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

In addition to antidotes, an important treatment for poisoning is the use of hemodialysis. Hemodialysis is used to enhance the removal of unmetabolized ethylene glycol, as well as its metabolites from the body. It has been shown to be highly effective in the removal of ethylene glycol and its metabolites from the blood. Hemodialysis also has the added benefit of correcting other metabolic derangements or supporting deteriorating kidney function. Hemodialysis is usually indicated in patients with severe metabolic acidosis (blood pH less than 7.3), kidney failure, severe electrolyte imbalance, or if the patient's condition is deteriorating despite treatment. Often both antidotal treatment and hemodialysis are used together in the treatment of poisoning. Because hemodialysis will also remove the antidotes from the blood, doses of antidotes need to be increased to compensate. If hemodialysis is not available, then peritoneal dialysis also removes ethylene glycol, although less efficiently.

The use of dental sealants is a means of prevention. A sealant is a thin plastic-like coating applied to the chewing surfaces of the molars to prevent food from being trapped inside pits and fissures. This deprives resident plaque bacteria of carbohydrate, preventing the formation of pit and fissure caries. Sealants are usually applied on the teeth of children, as soon as the teeth erupt but adults are receiving them if not previously performed. Sealants can wear out and fail to prevent access of food and plaque bacteria inside pits and fissures and need to be replaced so they must be checked regularly by dental professionals.

Calcium, as found in food such as milk and green vegetables, is often recommended to protect against dental caries. Fluoride helps prevent decay of a tooth by binding to the hydroxyapatite crystals in enamel. Streptococcus mutans is the leading cause of tooth decay. Low concentration fluoride ions act as bacteriostatic therapeutic agent and high concentration fluoride ions are bactericidal. The incorporated fluorine makes enamel more resistant to demineralization and, thus, resistant to decay. Topical fluoride is more highly recommended than systemic intake such as by tablets or drops to protect the surface of the teeth. This may include a fluoride toothpaste or mouthwash or varnish. Standard fluoride toothpaste (1,000–1,500 ppm) is more effective than low fluoride toothpaste (< 600ppm) to prevent dental caries. After brushing with fluoride toothpaste, rinsing should be avoided and the excess spat out. Many dental professionals include application of topical fluoride solutions as part of routine visits and recommend the use of xylitol and amorphous calcium phosphate products. Silver diamine fluoride may work better than fluoride varnish to prevent cavities. Water fluoridation also lowers the risk of tooth decay.

An oral health assessment carried out before a child reaches the age of one may help with management of caries. The oral health assessment should include checking the child’s history, a clinical examination, checking the risk of caries in the child including the state of their occlusion and assessing how well equipped the child’s parent or carer is to help the child prevent caries. In order to further increase a child’s cooperation in caries management, good communication by the dentist and the rest of the staff of a dental practice should be used. This communication can be improved by calling the child by their name, using eye contact and including them in any conversation about their treatment.

Vaccines are also under development.

The effect of mercury took some time – the latent period between ingestion and the first symptoms (typically paresthesia – numbness in the extremities) was between 16 and 38 days. Paresthesia was the predominant symptom in less serious cases. Worse cases included ataxia (typically loss of balance), blindness or reduced vision, and death resulting from central nervous system failure. Anywhere between 20 and 40 mg of mercury has been suggested as sufficient for paresthesia (between 0.5 and 0.8 mg/kg of body weight). On average, individuals affected consumed 20 kg or so of bread; the 73,000 tonnes provided would have been sufficient for over 3 million cases.

The hospital in Kirkuk received large numbers of patients with symptoms that doctors recognised from the 1960 outbreak. The first case of alkylmercury poisoning was admitted to hospital on 21 December. By 26 December, the hospital had issued a specific warning to the government. By January 1972, the government had started to strongly warn the populace about eating the grain, although dispatches did not mention the large numbers already ill. The Iraqi Army soon ordered disposal of the grain and eventually declared the death penalty for anyone found selling it. Farmers dumped their supplies wherever possible, and it soon got into the water supply (particularly the River Tigris), causing further problems. The government issued a news blackout and released little information about the outbreak.

The World Health Organization assisted the Iraqi government through the supply of drugs, analytical equipment and expertise. Many new treatments were tried, since existing methods for heavy metal poisoning were not particularly effective. Dimercaprol was administered to several patients, but caused rapid deterioration of their condition. It was ruled out as a treatment for this sort of poisoning following the outbreak. Polythiol resins, penicillamine and dimercaprol sulfonate all helped, but are believed to have been largely insignificant in overall recovery and outcomes. Dialysis was tested on a few patients late in the treatment period, but they showed no clinical improvement. The result of all treatments was varied, with some patients' blood mercury level being dramatically reduced, but a negligible effect in others. All patients received periods of treatment interspersed with lay periods; continuous treatment was suggested in future cases. Later treatment was less effective in reducing blood toxicity.

Following decontamination and the institution of supportive measures, the next priority is inhibition of further ethylene glycol metabolism using antidotes. The antidotes for ethylene glycol poisoning are ethanol and fomepizole. This antidotal treatment forms the mainstay of management of ethylene glycol poisoning. The toxicity of ethylene glycol comes from its metabolism to glycolic acid and oxalic acid. The goal of pharmacotherapy is to prevent the formation of these metabolites. Ethanol acts by competing with ethylene glycol for alcohol dehydrogenase, the first enzyme in the degradation pathway. Because ethanol has a much higher affinity for alcohol dehydrogenase, about a 100-times greater affinity, it successfully blocks the breakdown of ethylene glycol into glycolaldehyde, which prevents the further degradation. Without oxalic acid formation, the nephrotoxic effects can be avoided, but the ethylene glycol is still present in the body. It is eventually excreted in the urine, but supportive therapy for the CNS depression and metabolic acidosis will be required until the ethylene glycol concentrations fall below toxic limits. Pharmaceutical grade ethanol is usually given intravenously as a 5 or 10% solution in 5% dextrose, but it is also sometimes given orally in the form of a strong spirit such as whisky, vodka, or gin.

Fomepizole is a potent inhibitor of alcohol dehydrogenase; similar to ethanol, it acts to block the formation of the toxic metabolites. Fomepizole has been shown to be highly effective as an antidote for ethylene glycol poisoning. It is the only antidote approved by the U.S. Food and Drug Administration for the treatment of ethylene glycol poisoning. Both antidotes have advantages and disadvantages. Ethanol is readily available in most hospitals, is inexpensive, and can be administered orally as well as intravenously. Its adverse effects include intoxication, hypoglycemia in children, and possible liver toxicity. Patients receiving ethanol therapy also require frequent blood ethanol concentration measurements and dosage adjustments to maintain a therapeutic ethanol concentration. Patients therefore must be monitored in an intensive care unit. Alternatively, the adverse side effects of fomepizole are minimal and the approved dosing regimen maintains therapeutic concentrations without the need to monitor blood concentrations of the drug. The disadvantage of fomepizole is that it is expensive. Costing US$1,000 per gram, an average course used in an adult poisoning would cost approximately $3,500 to $4,000. Despite the cost, fomepizole is gradually replacing ethanol as the antidote of choice in ethylene glycol poisoning. Adjunct agents including thiamine and pyridoxine are often given, because they may help prevent the formation of oxalic acid. The use of these agents is based on theoretical observations and there is limited evidence to support their use in treatment; they may be of particular benefit in people who could be deficient in these vitamins such as malnourished or alcoholic patients.

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

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

Konzo can be prevented by use of the “wetting method,” which is used to remove residual cyanogens from cassava flour, as an additional processing method. Cassava flour is placed in a bowl and the level marked on the inside of the bowl. Water is added with mixing until the height of the wet flour comes up to the mark. The wet flour is placed in a thin layer on a mat for 2 hours in the sun or 5 hours in the shade to allow the escape of hydrogen cyanide produced by the breakdown of linamarin by the enzyme linamarase. The damp flour is then cooked in boiling water in the traditional way to produce a thick porridge called “fufu” or “ugali”, which is flavoured by some means such as a sauce. The wetting method is accepted by rural women because it requires little extra work or equipment and produces fufu which is not bitter, because the bitter tasting linamarin has gone.

In 2010 the wetting method was taught to the women in Kay Kalenge village, Popokabaka Health Zone, Bandundu Province, DRC, where there were 34 konzo cases. The women used the method and during the intervention there were no new konzo cases and the urinary thiocyanate content of the school children fell to safe levels. Konzo had been prevented for the first time ever in the same health zone in which it had first been discovered by Dr Trolli in 1938. Fourteen months after the intervention ceased the village was visited again. It was found that there were no new cases of konzo, the school children had low urinary thiocyanate levels, the wetting method was still being used and it had spread by word of mouth to three nearby villages. It is important to teach the women that konzo is due to a poison present in their food, to get them to regularly use the wetting method and posters are available in 13 different languages as a teaching aid as an additional method to remove residual cyanogens.

The wetting method has now been used in 13 villages in DRC with nearly 10000 people. The time of the intervention has been reduced from 18 months in the first intervention, to 12 months in the second intervention, to 9 months in the third and fourth interventions. This has reduced the cost per person of the intervention to prevent konzo by removing cyanogens from cassava flour, to $16 per person. This targeted method to reduce cyanide intake is much cheaper and more effective in preventing konzo than broad based interventions.

Little is currently known on brain dysfunction in feather-plucking. However, it may be hypothesized that abnormal brain function is involved, especially in those cases that appear sensitive to treatment with behavioural intervention and/or environmental changes. Psychotropic therapy for birds has been suggested as treatment for feather-plucking although responses seem variable.

Treatments involve antibiotics that cover for "Pseudomonas aeruginosa". Antipseudomonal penicillins, aminoglycosides, fluoroquinolones, third generation cephalosporins or aztreonam can be given. Usually, the antibiotics are changed according to the culture and sensitivity result. In patients with very low white blood cell counts, Granulocyte-macrophage colony-stimulating factor may be given. Depending on the causal agents, antivirals or antifungals can be added.

Surgery will be needed if there is extensive necrosis not responding to medical treatments.

If a cause can be identified for a burning sensation in the mouth, then treatment of this underlying factor is recommended. If symptom persist despite treatment a diagnosis of BMS is confirmed. BMS has been traditionally treated by reassurance and with antidepressants, anxiolytics or anticonvulsants. A 2016 Cochrane review of treatment for burning mouth syndrome concluded that strong evidence of an effective treatment was not available. Other treatments which have been used include atypical antipsychotics, histamine receptor antagonists, and dopamine agonists.

Localized demodectic mange is considered a common puppyhood ailment, with roughly 90% of cases resolving on their own with no treatment. Minor, localized cases should be left to resolve on their own to prevent masking of the more severe generalized form. If treatment is deemed necessary Goodwinol, a rotenone-based insecticide ointment is often prescribed, but it can be irritating to the skin. Demodectic mange with secondary infection is treated with antibiotics and medicated shampoos.

In more severe generalized cases, Amitraz is a parasiticidal dip that is licensed for use in many countries (the only FDA approved treatment in the USA) for treating canine demodicosis. It is applied weekly or biweekly, for several weeks, until no mites can be detected by skin scrapings. Demodectic mange in dogs can also be managed with avermectins, although there are few countries which license these drugs, which are given by mouth, daily, for this use. Ivermectin is used most frequently; collie-like herding breeds often do not tolerate this drug due to a defect in the blood–brain barrier, though not all of them have this defect. Other avermectin drugs that can be used include doramectin and milbemycin.

Recent results suggest that the isoxazolines afoxolaner and fluralaner, given orally, are effective in treating dogs with generalised demodicosis.

Cats with "Demodex gatoi" must be treated with weekly or bi-weekly sulfurated lime rinses. "Demodex cati" are treated similarly to canine demodicosis. With veterinary guidance, localized demodectic mange can also be treated with a topical keratolytic and antibacterial agent, followed by a lime sulfur drip or a local application of Rotenone. Ivermectin may also be used. Generalized demodectic mange in cats is more difficult to treat. There are shampoos available that can help to clear dead skin, kill mites and treat bacterial infections. Treatment is in most cases prolonged with multiple applications.

Because of the possibility of the immune deficiency being an inherited trait, many veterinarians believe that all puppies with generalized demodex should be spayed or neutered and not reproduce. Females with generalized demodex should be spayed because the stress of the estrus cycle will often bring on a fresh wave of clinical signs.