The affected fruit have dark spots, about ½ cm diameter, which occur on the skin and/or in the flesh The cells in the spots are dead (necrotic), and turn brown-black.

Bitter pit is a disorder in apple fruits, now believed to be induced by calcium deficiency. It occurs less commonly in pears.

The disease was probably first reported in Germany where it was known as "Stippen". It was also known as "Baldwin spot" and "blotchy cork" in North America. The name "bitter pit" was first used by Cobb in Australia in 1895. The disease has been shown as non-pathological and is now known as a disorder. When it occurs on the tree, it is known as "tree pit"; it may also occur in storage, when it is known as "storage pit".

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.

Calcium (Ca) deficiency is a plant disorder that can be caused by insufficient level of available calcium in the growing medium, but is more frequently a product of low transpiration of the whole plant or more commonly the affected tissue. Plants are susceptible to such localized calcium deficiencies in low or non-transpiring tissues because calcium is not transported in the phloem. This may be due to water shortages, which slow the transportation of calcium to the plant, poor uptake of calcium through the stem, or too much nitrogen in the soil.

The symptoms of Cherry X disease vary greatly depending on the host. On cherry hosts symptoms can usually first be seen on the fruits, causing them to be smaller in size with a leathery skin. Pale fruit is common at harvest time. It is common for symptoms to first be seen in a single branch. The branch may lose its older leaves, and the leaves tend to be smaller with a bronzed complexion.

The rootstock that the cherry is grafted onto can play a significant role in the disease symptoms seen. Rootstocks of Mahaleb cherry exhibit different symptoms from stocks of Colt, Mazzard, or Stockton Morello. When the scion is grafted onto Mahaleb, symptoms consistent with Phytophthora root rot can be seen. To distinguish between root rot and x-disease the wood under the bark at the graft union should be examined. If it is x-disease the wood at the union will have grooves and pits this causes a browning of the phloem and shows the cells in decline. This rapid decline is caused by the rootstock cells near the graft union dying in large quantities. Foliage begins to turn yellow and the curl upward and inward toward the leaf midrib. Trees infected with Mahaleb rootstock die by late summer or early the following year.

When Cherries are grafted onto Colt, Mazzard, or Stockton Morello rootstocks, there is a different range of symptoms. Affected leaves are smaller than normal and the foliage may be sparse. Dieback of shoot tips is common as the disease progresses. Fruit on branches are smaller, lighter, pointed, low sugar content, poor flavor, and a bitter taste.

Peaches are the next most common economic fruit host of the X-disease. Symptoms can be seen after about two months single branches will begin to show symptoms of their individual leaves. These leaves curl up and inward with irregular yellow to reddish-purple spots. These spots can drop out leaving “shotholes”. Leaves that are affected by the disease will fall prematurely. After 2–3 years the entire tree will show symptoms.

Feather-plucking is generally regarded as a multifactorial disorder, although three main aspects of bird keeping may be related to the problem: (1) cage size often restricts the bird’s movements; (2) cage design and barrenness of the environment often do not provide sufficient behavioural opportunities to meet the bird's sensitivity, intelligence and behavioural needs; and (3) solitary housing, which fails to meet the high social needs of the bird.

Feather-plucking, sometimes termed feather-picking, feather damaging behaviour or pterotillomania, is a maladaptive, behavioural disorder commonly seen in captive birds which chew, bite or pluck their own feathers with their beak, resulting in damage to the feathers and occasionally the skin. It is especially common among Psittaciformes, with an estimated 10% of captive parrots exhibiting the disorder. The areas of the body that are mainly pecked or plucked are the more accessible regions such as the neck, chest, flank, inner thigh and ventral wing area. Contour and down feathers are generally identified as the main target, although in some cases, tail and flight feathers are affected. Although feather-plucking shares characteristics with feather pecking commonly seen in commercial poultry, the two behaviours are currently considered to be distinct as in the latter, the birds peck at and pull out the feathers of other individuals.

Feather-plucking has characteristics that are similar to trichotillomania, an impulse control disorder in humans, and hair-pulling which has been reported in mice, guinea pigs, rabbits, sheep and muskox, dogs and cats, leading to suggestions for a comparative psychology approach to alleviating these problems.

Cherry X disease also known as Cherry Buckskin disease is caused by a plant pathogenic phytoplasma. Phytoplasma's are obligate parasites of plants and insects. They are specialized bacteria, characterized by their lack of a cell wall, often transmitted through insects, and are responsible for large losses in crops, fruit trees, and ornamentals. The phytoplasma causing Cherry X disease has a fairly limited host range mostly of stone fruit trees. Hosts of the pathogen include sweet/sour cherries, choke cherry, peaches, nectarines, almonds, clover, and dandelion. Most commonly the pathogen is introduced into economical fruit orchards from wild choke cherry and herbaceous weed hosts. The pathogen is vectored by mountain and cherry leafhoppers. The mountain leafhopper vectors the pathogen from wild hosts to cherry orchards but does not feed on the other hosts. The cherry leafhopper which feeds on the infected cherry trees then becomes the next vector that transmits from cherry orchards to peach, nectarine, and other economic crops. Control of Cherry X disease is limited to controlling the spread, vectors, and weed hosts of the pathogen. Once the pathogen has infected a tree it is fatal and removal is necessary to stop it from becoming a reservoir for vectors.

A person experiencing caries may not be aware of the disease. The earliest sign of a new carious lesion is the appearance of a chalky white spot on the surface of the tooth, indicating an area of demineralization of enamel. This is referred to as a white spot lesion, an incipient carious lesion or a "microcavity". As the lesion continues to demineralize, it can turn brown but will eventually turn into a cavitation ("cavity"). Before the cavity forms, the process is reversible, but once a cavity forms, the lost tooth structure cannot be regenerated.

A lesion that appears dark brown and shiny suggests dental caries were once present but the demineralization process has stopped, leaving a stain. Active decay is lighter in color and dull in appearance.

As the enamel and dentin are destroyed, the cavity becomes more noticeable. The affected areas of the tooth change color and become soft to the touch. Once the decay passes through enamel, the dentinal tubules, which have passages to the nerve of the tooth, become exposed, resulting in pain that can be transient, temporarily worsening with exposure to heat, cold, or sweet foods and drinks. A tooth weakened by extensive internal decay can sometimes suddenly fracture under normal chewing forces. When the decay has progressed enough to allow the bacteria to overwhelm the pulp tissue in the center of the tooth, a toothache can result and the pain will become more constant. Death of the pulp tissue and infection are common consequences. The tooth will no longer be sensitive to hot or cold, but can be very tender to pressure.

Dental caries can also cause bad breath and foul tastes. In highly progressed cases, an infection can spread from the tooth to the surrounding soft tissues. Complications such as cavernous sinus thrombosis and Ludwig angina can be life-threatening.

The alterations in the sense of taste, usually a metallic taste, and sometimes smell are the only symptoms. The duration of the symptoms of dysgeusia depends on the cause. If the alteration in the sense of taste is due to gum disease, dental plaque, a temporary medication, or a short-term condition such as a cold, the dysgeusia should disappear once the cause is removed. In some cases, if lesions are present in the taste pathway and nerves have been damaged, the dysgeusia may be permanent.

Tooth decay, also known as dental caries or cavities, is a breakdown of teeth due to acids made by bacteria. The cavities may be a number of different colors from yellow to black. Symptoms may include pain and difficulty with eating. Complications may include inflammation of the tissue around the tooth, tooth loss, and infection or abscess formation.

The cause of caries is acid from bacteria dissolving the hard tissues of the teeth (enamel, dentin and cementum). The acid is produced from food debris or sugar on the tooth surface. Simple sugars in food are these bacteria's primary energy source and thus a diet high in simple sugar is a risk factor. If mineral breakdown is greater than build up from sources such as saliva, caries results. Risk factors include conditions that result in less saliva such as: diabetes mellitus, Sjogren's syndrome and some medications. Medications that decrease saliva production include antihistamines and antidepressants. Caries is also associated with poverty, poor cleaning of the mouth, and receding gums resulting in exposure of the roots of the teeth.

Prevention of dental caries includes regular cleaning of the teeth, a diet low in sugar, and small amounts of fluoride. Brushing the teeth twice per day and flossing between the teeth once a day is recommended by many. Fluoride may be from water, salt or toothpaste among other sources. Treating a mother's dental caries may decrease the risk in her children by decreasing the numbers of certain bacteria. Screening can result in earlier detection. Depending on the extent of destruction, various treatments can be used to restore the tooth to proper function or the tooth may be removed. There is no known method to grow back large amounts of tooth. The availability of treatment is often poor in the developing world. Paracetamol (acetaminophen) or ibuprofen may be taken for pain.

Worldwide, approximately 2.3 billion people (32% of the population) have dental caries in their permanent teeth. The World Health Organization estimates that nearly all adults have dental caries at some point in time. In baby teeth it affects about 620 million people or 9% of the population. They have become more common in both children and adults in recent years. The disease is most common in the developed world due to greater simple sugar consumption and less common in the developing world. Caries is Latin for "rottenness".

Dysgeusia, also known as parageusia, is a distortion of the sense of taste. Dysgeusia is also often associated with ageusia, which is the complete lack of taste, and hypogeusia, which is a decrease in taste sensitivity. An alteration in taste or smell may be a secondary process in various disease states, or it may be the primary symptom. The distortion in the sense of taste is the only symptom, and diagnosis is usually complicated since the sense of taste is tied together with other sensory systems. Common causes of dysgeusia include chemotherapy, asthma treatment with albuterol, and zinc deficiency. Different drugs could also be responsible for altering taste and resulting in dysgeusia. Due to the variety of causes of dysgeusia, there are many possible treatments that are effective in alleviating or terminating the symptoms of dysgeusia. These include artificial saliva, pilocarpine, zinc supplementation, alterations in drug therapy, and alpha lipoic acid.

Other body-focused repetitive behaviors include excoriation disorder (skin picking), dermatophagia (skin biting), and trichotillomania (the urge to pull out hair), and all of them tend to coexist with nail biting. As an oral parafunctional activity, it is also associated with bruxism (tooth clenching and grinding), and other habits such as pen chewing and cheek biting.

In children nail biting most typically co-occurs with attention deficit hyperactivity disorder (75% of nail biting cases in a study), and other psychiatric disorders including oppositional defiant disorder (36%) and separation anxiety disorder (21%). It is also more common among children and adolescents with obsessive–compulsive disorder. Nail biting appeared in a study to be more common in men with eating disorders than in those without them.

Some fruit juices and fruits can interact with numerous drugs, in many cases causing adverse effects. The effect was first discovered by accident, when a test of drug interactions with alcohol used grapefruit juice to hide the taste of the ethanol.

It is still best-studied with grapefruit and grapefruit juice, but similar effects have more recently been seen with some (not all) other citrus fruits. One medical review advises patients to avoid all citrus juices until further research clarifies the risks. The interacting chemicals are found in many plants, and so many other foods may be affected; effects have been observed with apple juice, but their clinical significance is not yet known.

Normal amounts of food and drink, such as one whole grapefruit or a small glass () of grapefruit juice, can cause drug overdose toxicity. Fruit consumed three days before the medicine can still have an effect. The relative risks of different types of citrus fruit have not been systematically studied. Affected drugs typically have an auxiliary label saying “Do not take with grapefruit” on the container, and the interaction is elaborated on in the package insert. People are also advised to ask their physician or pharmacist about drug interactions.

The effects are caused by furanocoumarins (and, to a lesser extent, flavonoids). These chemicals inhibit key drug metabolizing enzymes, such as cytochrome P450 3A4 (CYP3A4). CYP3A4 is a metabolizing enzyme for almost 50% of drugs, and is found in the liver and small intestinal epithelial cells. As a result, many drugs are affected. Inhibition of enzymes can have two different effects, depending on whether the drug is either

1. metabolized by the enzyme to an inactive metabolite, "or"

2. activated by the enzyme to an active metabolite.

If the active drug is metabolized by the inhibited enzyme, then the fruit will stop the drug being metabolized, leaving elevated concentrations of the medication in the body, which can cause adverse effects. Conversely, if the medication is a prodrug, it needs to be metabolised to be converted to the active drug. Compromising its metabolism lowers concentrations of the active drug, reducing its therapeutic effect, and risking therapeutic failure.

Low drug concentrations can also be caused when the fruit suppresses drug absorption from the intestine.

Nail biting usually leads to deleterious effects in fingers, but also mouth and more generally the digestive system. These consequences are directly derived from the physical damage of biting or from the hands becoming an infection vector. Moreover, it can also have a social impact.

The ten fingernails are usually equally bitten to approximately the same degree. Biting nails can lead to broken skin on the cuticle. When cuticles are improperly removed, they are susceptible to microbial and viral infections such as paronychia. Saliva may then redden and infect the skin. In rare cases, fingernails may become severely deformed after years of nail biting due to the destruction of the nail bed.

Nail biting may have an association with oral problems, such as gingival injury, and malocclusion of the anterior teeth. It can also transfer pinworms or bacteria buried under the surface of the nail from the anus region to the mouth. If the bitten-off nails are swallowed, stomach problems can occasionally develop.

Nail-biting can be a source of guilt and shame feelings in the nail biter, a reduced quality of life, and increased stigmatization in the inner family circles or at a more societal level.

It can be caused by any of the following:

- Nutritional factors.

- Some diseases (such as undiagnosed and untreated celiac disease, chicken pox, congenital syphilis).

- Hypocalcemia.

- Fluoride ingestion (dental fluorosis).

- Birth injury.

- Preterm birth.

- Infection.

- Trauma from a deciduous tooth.

The WHO has recommended three criteria for the diagnosis of konzo:

- a visible symmetric spastic abnormality of gait while walking or running;

- a history of onset of less than one week followed by a non-progressive course in a formerly healthy person;

- bilaterally exaggerated knee or ankle jerk reflexes without signs of disease of the spine.

Depending on its severity, konzo is divided into three categories: mild when individuals are able to walk without support, moderate when individuals need one or two sticks to walk, and severe when the affected person is unable to walk unsupported.

The onset of paralysis (spastic paraparesis) is sudden and symmetrical and affects the legs more than the arms. The resulting disability is permanent but does not progress. Typically, a patient is standing and walking on the balls of the feet with rigid legs and often with ankle clonus.

Initially, most patients experience generalized weakness during the first days and are bedridden for some days or weeks before trying to walk. Occasional blurred vision and/or speech difficulties typically clear during the first month, except in severely affected patients. Spasticity is present from the first day, without any initial phase of flaccidity. After the initial weeks of functional improvement, the spastic paraparesis remains stable for the rest of life. Some patients may suffer an abrupt aggravating episode, e.g. a sudden and permanent worsening of the spastic paraparesis. Such episodes are identical to the initial onset and can therefore be interpreted as a "second onset".

The severity of konzo varies; cases range from only hyperreflexia in the lower limbs to a severely disabled, bedridden patient with spastic paraparesis, associated weakness of the trunk and arms, impaired eye movements, speech and possibly visual impairment. Although the severity varies from patient to patient, the longest upper motor neurons are invariably more affected than the shorter ones. Thus, a konzo patient with speech impairment always shows severe symptoms in the legs and arms.

Recently, neuropsychological effects of konzo have been described from DR Congo.

If Turner's hypoplasia is found on a canine or a premolar, the most likely cause is an infection that was present when the primary (baby) tooth was still in the mouth. Most likely, the primary tooth was heavily decayed and an area of inflamed tissues around the root of the tooth (called a periapical inflammation), affecting the development of the permanent tooth. The tooth most likely affected by this cause is the canine tooth. The appearance of the abnormality will depend on the severity and longevity of the infection.

If Turner's hypoplasia is found in the front (anterior) area of the mouth, the most likely cause is a traumatic injury to a primary tooth. The traumatized tooth, which is usually a maxillary central incisor, is pushed into the developing tooth underneath it and consequently affects the formation of enamel. Because of the location of the permanent tooth's developing tooth bud in relation to the primary tooth, the most likely affected area on the permanent tooth is the facial surface (the side closer to the lips or cheek). White or yellow discoloration may accompany Turner's hypoplasia. Enamel hypoplasia may also be present.

Turner's hypoplasia usually affects the tooth enamel if the trauma occurs prior to the third year of life. Injuries occurring after this time are less likely to cause enamel defects since the enamel is already calcified.

The same type of injury is also associated with the dilaceration of a tooth.

Mulberry molars are a dental condition usually associated with congenital syphilis, characterized by multiple rounded rudimentary enamel cusps on the permanent first molars. Mulberry molars are physically defective permanent molars. The deformity is caused by congenital syphilis. This type of abnormality is characterized by dwarfed molars with cusps covered with globular enamel growths. These teeth are functional but can be cosmetically fixed with crowns, bridges, or implants.

Just above the gum line, the mulberry molar looks normal. A deformity becomes apparent towards the cusp or top grinding surface of the tooth. Here, the size of the mulberry molar is diminished in all aspects, creating a stumpy version of a conventional molar. The cause of the molar atrophy is thought to be enamel hypoplasia, or a deficiency in tooth enamel. The underlying dentin and pulp of the tooth is normal, but the enamel covering or molar sheath is thin and deformed, creating a smaller version of a typical tooth.

The grinding surface of a mulberry molar is also corrupted. Normally, the grinding surface of a molar has a pit and is surrounded by a circular ridge at the top of the tooth, which is used for grinding. The cusp deformity of the mulberry molar is characterized by an extremely shallow or completely absent pit. Instead, the pit area is filled with globular structures bunched together all along the top surface of the cusp. This type of deformity is also thought to be caused by enamel hypoplasia. Mulberry molars are typically functional and do not need treatment. If the deformity is severe or the person is bothered by the teeth, there are several options. The teeth can be covered with a permanent cast crown, stainless steel crown, or the molars can be removed and an implant or bridge can be put in place of the mulberry molar.

A mulberry molar is caused by congenital syphilis, which is passed from the mother to the child in the uterus through the placenta. Since this particular symptom of congenital syphilis manifests later in childhood with the eruption of the permanent molars, it is a late stage marker for the disease. Hutchinson’s teeth, marked by dwarfed teeth and deformed cusps that are spaced abnormally far apart, are another dental deformity caused by congenital syphilis. Mulberry molars and Hutchinson’s teeth will often occur together. Pregnant women with syphilis should tell their doctors about the condition and be treated for it during pregnancy, otherwise the baby should be screened for the disease after birth and treated with penicillin if necessary.

By definition, BMS has no signs. Sometimes affected persons will attribute the symptoms to sores in the mouth, but these are in fact normal anatomic structures (e.g. lingual papillae, varices). Symptoms of BMS are variable, but the typical clinical picture is given below, considered according to the Socrates pain assessment method (see table). If clinical signs are visible, then another explanation for the burning sensation may be present. Erythema (redness) and edema (swelling) of papillae on the tip of the tongue may be a sign that the tongue is being habitually pressed against the teeth. The number and size of filiform papillae may be reduced. If the tongue is very red and smooth, then there is likely a local or systemic cause (e.g. eythematous candidiasis, anemia).

Burning mouth syndrome (BMS) is a burning sensation in the mouth with no underlying dental or medical cause. No related signs of disease are found in the mouth. People with burning mouth syndrome may also have a dry mouth sensation where no cause can be found such as reduced salivary flow, tingling in the mouth, or an altered taste or smell.

A burning sensation in the mouth can be a symptom of another disease when local or systemic factors are found to be implicated, and this is not considered to be burning mouth syndrome, which is a syndrome of medically unexplained symptoms. The International Association for the Study of Pain defines burning mouth syndrome as "a distinctive nosological entity characterized by unremitting oral burning or similar pain in the absence of detectable mucosal changes", and "burning pain in the tongue or other oral mucous membranes", and the International Headache Society defines it as "an intra-oral burning sensation for which no medical or dental cause can be found".

Due to insufficient evidence it is unclear if effective treatments exist.

The most common symptom of all snakebites is overwhelming fear, which contributes to other symptoms, including nausea and vomiting, diarrhea, vertigo, fainting, tachycardia, and cold, clammy skin. Television, literature, and folklore are in part responsible for the hype surrounding snakebites, and people may have unwarranted thoughts of imminent death.

Dry snakebites and those inflicted by a non-venomous species can still cause severe injury. There are several reasons for this: a snakebite may become infected, with the snake's saliva and fangs sometimes harboring pathogenic microbial organisms, including "Clostridium tetani". Infection is often reported with viper bites whose fangs are capable of deep puncture wounds. Bites may cause anaphylaxis in certain people.

Most snakebites, whether by a venomous snake or not, will have some type of local effect. There is minor pain and redness in over 90 percent of cases, although this varies depending on the site. Bites by vipers and some cobras may be extremely painful, with the local tissue sometimes becoming tender and severely swollen within five minutes. This area may also bleed and blister and can eventually lead to tissue necrosis. Other common initial symptoms of pit viper and viper bites include lethargy, bleeding, weakness, nausea, and vomiting. Symptoms may become more life-threatening over time, developing into hypotension, tachypnea, severe tachycardia, severe internal bleeding, altered sensorium, kidney failure, and respiratory failure.

Bites caused by some snakes, such as the kraits, coral snake, Mojave rattlesnake, and the speckled rattlesnake, reportedly cause little or no pain despite being serious potentially life-threatening injuries. Those bitten may also describe a "rubbery", "minty", or "metallic" taste if bitten by certain species of rattlesnake. Spitting cobras and rinkhalses can spit venom in a person's eyes. This results in immediate pain, ophthalmoparesis, and sometimes blindness.

Some Australian elapids and most viper envenomations will cause coagulopathy, sometimes so severe that a person may bleed spontaneously from the mouth, nose, and even old, seemingly healed wounds. Internal organs may bleed, including the brain and intestines and will cause ecchymosis (bruising) of the skin.

Venom emitted from elapids, including sea snakes, kraits, cobras, king cobra, mambas, and many Australian species, contain toxins which attack the nervous system, causing neurotoxicity. The person may present with strange disturbances to their vision, including blurriness. Paresthesia throughout the body, as well as difficulty in speaking and breathing, may be reported. Nervous system problems will cause a huge array of symptoms, and those provided here are not exhaustive. If not treated immediately they may die from respiratory failure.

Venom emitted from some types of cobras, almost all vipers and some sea snakes causes necrosis of muscle tissue. Muscle tissue will begin to die throughout the body, a condition known as rhabdomyolysis. Rhabdomyolysis can result in damage to the kidneys as a result of myoglobin accumulation in the renal tubules. This, coupled with hypotension, can lead to acute renal failure, and, if left untreated, eventually death.

Apitoxin, or honey bee venom, is a bitter colorless liquid containing proteins, which may produce local inflammation. It may have similarities to sea nettle toxin.

Pilonidal cysts are itchy and are often very painful, and typically occur between the ages of 15 and 35. Although usually found near the coccyx, the condition can also affect the navel, armpit or genital region, though these locations are much rarer.

Symptoms include:

- Pain/discomfort or swelling above the anus or near the tailbone that comes and goes

- Opaque yellow (purulent) or bloody discharge from the tailbone area

- Unexpected moisture in the tailbone region

- Discomfort with sitting on the tailbone, doing sit-ups or riding a bike (any activities that roll over the tailbone area)

Some people with a pilonidal cyst will be asymptomatic.