As of November 2013, no identifiable cause for the disease had been found. Pathogenic bacteria did not seem to be present, and though the plague might be caused by a viral or fungal pathogen, no causal agent had been found. Each episode of plague might have a different cause.

Other possible causes of the condition that have been suggested include high sea temperatures, oxygen depletion and low salinity due to freshwater runoff. Research suggests that high water temperatures are indeed linked to the disease, increasing its incidence and virulence. The disease also seems more prevalent in sheltered waters than in open seas with much wave movement. One result of global warming is higher sea temperatures. There is a wave of unusually warm water along the west coast of the United States, which is where all of the sea stars are dying off. These may impact both on starfish and on echinoderm populations in general, and a ciliate protozoan parasite ("Orchitophrya stellarum") of starfish, which eats sperm and effectively emasculates male starfish, thrives at higher temperatures.

Research in 2014 showed that the cause of the disease is transmissible from one starfish to another and that the disease-causing agent is a microorganism in the virus-size range. The most likely candidate causal agent was found to be the sea star-associated densovirus (SSaDV), which was found to be in greater abundance in diseased starfish than in healthy ones.

In 2014, Point Defiance Zoo and Aquarium lost more than half of its 369 sea stars, and by September 2015 they numbered fewer than 100. The aquarium treated its affected sea stars with antibiotics in 2014, which proved effective. Although a mechanism is still unknown, evidence suggests that a single mutation in the elongation factor 1-alpha locus in "Pisaster ochraceus" may be associated with reduced mortality.

Skeletal eroding band (SEB) is a disease of corals that appears as a black or dark gray band that slowly advances over corals, leaving a spotted region of dead coral in its wake. It is the most common disease of corals in the Indian and Pacific Oceans, and is also found in the Red Sea.

So far one agent has been clearly identified, the ciliate "Halofolliculina corallasia". This makes SEB the first coral disease known to be caused by a protozoan. When "H. corallasia" divides, the daughter cells move to the leading edge of the dark band and produce a protective shell called a lorica. To do this, they drill into the coral's limestone skeleton, killing coral polyps in the process.

A disease with very similar symptoms has been found in the Caribbean Sea, but has been given a different name as it is caused by a different species in the genus "Halofolliculina" and occurs in a different type of environment.

Coral diseases, comprising the diseases that affect corals, injure the living tissues and often result in the death of part or the whole of the colony. These diseases have been occurring more frequently in the twenty-first century as conditions become more stressful for many shallow-water corals. The pathogens causing the diseases include bacteria, fungi and protozoa, but it is not always possible to identify the pathogen involved.

This reaction occurs mainly in the tropics and in Florida, due to the proximity of the Gulf Stream to the U.S. state. It has been identified in other locations as well.

Bald sea urchin disease is a bacterial disease known to affect several species of sea urchins on Mediterranean Sea, North Atlantic and California coastlines. Research suggests two pathogens are responsible for the disease, "Listonella anguillarum" and "Aeromonas salmonicida".

Infection generally occurs at the site of an existing physical injury. The affected area turns green and spines and other appendages are lost. If the lesion remains shallow and covers less than 30% of the animal's surface area, the animal tends to survive and eventually regenerates any lost tissue. However if the damage is more extensive or so deep that the hard inner test is perforated, the disease is fatal.

Cases have been found in Bermuda in 2011, 2014 and 2015 with Paradise Lakes proving particularly bad. In 2015 many felt the effects after swimming in Mangrove Bay and Harrington Sound.

Corals growing in the Caribbean Sea are particularly affected by disease, perhaps because of the limited water circulation and the density of the human population on the surrounding land masses. Disease is also present in the tropical Indo-Pacific, but it is not so widespread, perhaps because of the more dispersed locations of the reefs.

Necrotic ring spot is a common disease of turf caused by soil borne fungi (Ophiosphaerella korrae) that mainly infects roots (4). It is an important disease as it destroys the appearance of turfgrasses on park, playing fields and golf courses. Necrotic Ring Spot is caused by a fungal pathogen that is an ascomycete that produces ascospores in an ascocarp (6). They survive over winter, or any unfavorable condition as sclerotia. Most infection occurs in spring and fall when the temperature is about 13 to 28°C (5). The primary hosts of this disease are cool-season grasses such as Kentucky bluegrass and annual bluegrass (6). Once turf is infected with "O. korrae", it kills turf roots and crowns. Symptoms of the disease are quite noticeable since they appear as large yellow ring-shaped patches of dead turf. Management of the disease is often uneasy and requires application of multiple controls. The disease can be controlled by many different kind of controls including chemicals and cultural.

Bletting is a process of softening that certain fleshy fruits undergo, beyond ripening. There are some fruits that are either sweeter after some bletting, such as sea buckthorn, or for which most varieties can be eaten raw only after bletting, such as medlars, persimmons, quince, service tree fruit, and wild service tree fruit ("chequers"). The rowan or mountain ash fruit must be bletted and cooked to be edible, to break down the toxic parasorbic acid (hexenollactone) into sorbic acid.

Necrotic ring spot can be managed through chemical and cultural controls. Cultural control includes the use of ammonium sulfate or other acidifying fertilizers to suppress the pathogen by lowering the pH of the soil to between 6.0 and 6.2. The more acidic soil discourages the activity of "O. korrae" (9) When reducing pH to these levels, additional manganese applications should be undertaken to compensate for lower pH. As of now, there are only two resistant cultivars of bluegrass, which are ‘Riviera’, and ‘Patriot’ (9). One component of their resistance could be that they are tolerant to low temperature, because the grass is more susceptible to the pathogen under colder temperatures(8). In addition, reducing watering inputs and growing turf on well drained soils can lessen disease symptoms.

Many different fungicides are used to control the pathogen, Fenarimol, Propiconazole, Myclobutanil, and Azoxystrobin (8). Historically, Fenarimol and Myclobutanil were predominantly used (14). In a study where diluted pesticides were sprayed throughout infested test plots, Fenarimol was found to be the most effective with a 94.6% reduction of the disease. Myclobutanil also decreased the amount of disease, but only by 37.7% (8). Myclobutanil is generally recognized as a very weakly acting demethylation inhibitor (DMI) fungicide and fenarimol is no longer registered for turf so a number of other DMI fungicides have been employed successfully, including Propiconazole, Tebuconazole, Metconazole and others. Pyraclostrobin and Fluoxastrobin have also been used to control the pathogen.

Skeletal eroding band is visible as a black or dark gray band that slowly advances over corals, leaving a spotted region of dead coral in its wake. The spotted area distinguishes skeletal eroding band from black band disease, which also forms an advancing black band but leaves a completely white dead area behind it.

Skeletal eroding band was first noticed in 1988 near Papua New Guinea and then near Lizard Island in Australia's Great Barrier Reef, but was regarded as a gray variant of black band disease, as were instances off Mauritius in 1990. Surveys in 1994 in and around the Red Sea first identified the condition as a unique disease. It is now considered the commonest disease of corals in the Indian and Pacific Oceans, especially in warmer or more polluted waters.

The spread of the disease across an infected coral has been measured at in the Red Sea and around the Great Barrier Reef. Corals of the families Acroporidae and Pocilloporidae are the most vulnerable to infection. A study in 2008 found that the infection spread at about per day in colonies of "Acropora muricata", eventually wiping out 95% of its victims. However, experiments showed that the disease easily spread to already dead and dying areas of corals but did not attack undamaged corals.

Currently, the most effective treatment is transferring the affected fish to a freshwater bath for a period of 2 to 3 hours. This is achieved by towing the sea cages into fresh water, or pumping the fish from the sea cage to a tarp filled with fresh water. Mortality rates have been lowered by adding Levamisole to the water until the saturation is above 10ppm. Due to the difficulty and expense of treatment, the productivity of salmon aquaculture is limited by access to a source of fresh water. Chloramine and chlorine dioxide have also been used. Other potential in-feed treatments such as immunosupportive-based feeds, mucolytic compounds such as L-cysteine ethyl ester and the parasticide bithionol have been tested with some success although not developed for commercial use.

Chemically speaking, bletting brings about an increase in sugars and a decrease in the acids and tannins that cause the unripe fruit to be astringent.

Ripe medlars, for example, are taken from the tree, placed somewhere cool, and allowed to ripen for several weeks. In "Trees and Shrubs", horticulturist F. A. Bush wrote about medlars that "if the fruit is wanted it should be left on the tree until late October and stored until it appears in the first stages of decay; then it is ready for eating. More often the fruit is used for making jelly." Ideally, the fruit should be harvested from the tree immediately following a hard frost, which starts the bletting process by breaking down cell walls and speeding softening.

Once the process is complete, the medlar flesh will have broken down enough that it can be spooned out of the skin. The taste of the sticky, mushy substance has been compared to sweet dates and dry applesauce, with a hint of cinnamon. In "Notes on a Cellar-Book", the great English oenophile George Saintsbury called bletted medlars the "ideal fruit to accompany wine."

Ulcerative dermal necrosis (UDN) is a chronic dermatological disease of cold water salmonid fish that had a severe impact on north Atlantic Salmon and sea trout stocks in the late 1960s, the 1970s and 1980.

Affected fish developed severe skin lesions over large parts of their body which penetrated into skeletal muscle. The onset of symptoms only occurred after migration into freshwater. Lesions became quickly infected with overgrowths of "Saprolegnia" fungus giving the affected fish an appearance of being covered in slimy white pustules. The most severely affected fish frequently die before spawning.

Although the worst effects of the disease were seen in the 1970s and 1980, even now large numbers of salmon will succumb to the disease after spawning. This is thought be due in part to their weak post-spawning condition, and lack of food for several months whilst in the river.

Those fish that do make it back to the sea are thought to make a good recovery.

Amoebic gill disease (AGD) is a potentially fatal disease of some marine fish. It is caused by "Neoparamoeba perurans", the most important amoeba in cultured fish. It primarily affects farm raised fish of the Salmonidae family, most notably affecting the Tasmanian Atlantic Salmon (Salmo salar) industry, costing the A$20 million a year in treatments and lost productivity. Turbot, bass, bream, sea urchins and crabs have also been infected.

The disease has also been reported affecting the commercial salmon fisheries of the United States, Australia, New Zealand, France, Spain, Ireland and Chile. It was first diagnosed in the summer of 1984/1985 in populations of Atlantic Salmon off the east coast of Tasmania and was found to be caused by the "Neoparamoeba perurans" n.sp.

White plague is a suite of coral diseases of which three types have been identified, initially in the Florida Keys. They are infectious diseases but it has proved difficult to identify the pathogens involved. White plague type II may be caused by the gram negative bacterium "Aurantimonas coralicida" in the order Rhizobiales but other bacteria have also been associated with diseased corals and viruses may also be implicated.

Advice often given includes:

- Avoid sharing clothing, sports equipment, towels, or sheets.

- Wash clothes in hot water with fungicidal soap after suspected exposure to ringworm.

- Avoid walking barefoot; instead wear appropriate protective shoes in locker rooms and sandals at the beach.

- Avoid touching pets with bald spots, as they are often carriers of the fungus.

PSP has been implicated as a possible cause of sea otter mortality and morbidity in Alaska, as one of its primary prey items, the butter clam "(Saxidonus giganteus)" bioaccumulates saxitoxin as a chemical defense mechanism. In addition, ingestion of saxitoxin-containing mackerel has been implicated in the death of humpback whales

Additional cases where PSP was suspected as the cause of death in Mediterranean monk seals ("Monachus monachus") in the Mediterranean Sea have been questioned due to lack of additional testing to rule out other causes of mortality.

As first described by Dunstan in 1977, white plague type 1 produces lesions on any part of the colony. These increase gradually in size, advancing at the rate of a few millimetres per day. The advancing edge exhibits a sharp boundary between the apparently healthy tissue and the bare skeleton. Type II, first appearing in 1995 is similar, but it usually starts at the base of the colony, and the edge advances at a faster rate, up to per day. White plague type III advances at a rate in excess of two centimetres per day.

A number of different species of fungi are involved in dermatophytosis. Dermatophytes of the genera "Trichophyton" and "Microsporum" are the most common causative agents. These fungi attack various parts of the body and lead to the conditions listed below. The Latin names are for the conditions (disease patterns), not the agents that cause them. The disease patterns below identify the type of fungus that causes them only in the cases listed:

- Dermatophytosis

- Tinea pedis (athlete's foot) – fungal infection of the feet

- Tinea unguium – fungal infection of the fingernails and toenails, and the nail bed

- Tinea corporis – fungal infection of the arms, legs, and trunk

- Tinea cruris (jock itch) – fungal infection of the groin area

- Tinea manuum – fungal infection of the hands and palm area

- Tinea capitis – fungal infection of the scalp and hair

- Tinea barbae – fungal infestation of facial hair

- Tinea faciei (face fungus) – fungal infection of the face

- Other superficial mycoses (not classic ringworm, since not caused by dermatophytes)

- Tinea versicolor – caused by "Malassezia furfur"

- Tinea nigra – caused by "Hortaea werneckii"

Psychogenic alopecia, also called "over-grooming" or "psychological baldness," is a compulsive behavior that affects domestic cats. Generally, psychogenic alopecia does not lead to serious health consequences or a decreased lifespan.

Grooming is a natural behavior for cats. Cats spend 5%-25% of their waking hours grooming. Grooming becomes excessive when it takes precedence over other activities or no longer seems functional. Excessive grooming, which can lead to hair loss, skin wounds, and ulceration, can result from chronic stress or develop in cats who already exhibit nervous temperaments. Even when the source of stress is resolved or removed, excessive grooming may continue. There may be some genetic basis for the behavior, and it predominantly affects purebred cats of oriental breeds, but can develop in any feline. Female cats appear more susceptible. Environmental factors suspected of causing over grooming include flea allergy, boredom, food allergy, dust or pollen causing an allergic reaction, constipation and/or urinary tract infection caused by avoidance of a dirty litter tray, dermatitis, anxiety caused by inconsistent meal times. Deprivation of sunlight could be the part of the problem for indoors only cats.

Tinea capitis caused by species of "Microsporum" and "Trichophyton" is a contagious disease that is endemic in many countries. Affecting primarily pre-pubertal children between 6 and 10 years, it is more common in males than females; rarely does the disease persist past age sixteen. Because spread is thought to occur through direct contact with afflicted individuals, large outbreaks have been known to occur in schools and other places where children are in close quarters; however, indirect spread through contamination with infected objects ("fomites") may also be a factor in the spread of infection. In the USA, tinea capitis is thought to occur in 3-8% of the pediatric population; up to one-third of households with contact with an infected person may harbor the disease without showing any symptoms.

The fungal species responsible for causing tinea capitis vary according to the geographical region, and may also change over time. For example, "Microsporum audouinii" was the predominant etiological agent in North America and Europe until the 1950s, but now "Trichophyton tonsurans" is more common in the USA, and becoming more common in Europe and the United Kingdom. This shift is thought to be due to the widespread use of griseofulvin, which is more effective against "M. audounii" than "T. tonsurans"; also, changes in immigration patterns and increases in international travel have likely spread "T. tonsurans" to new areas. Another fungal species that has increased in prevalence is "Trichophyton violaceum", especially in urban populations of the United Kingdom and Europe.

The toxins responsible for most shellfish poisonings are water-insoluble, heat and acid-stable, and ordinary cooking methods do not eliminate the toxins. The principal toxin responsible for PSP is saxitoxin. Some shellfish can store this toxin for several weeks after a harmful algal bloom passes, but others, such as butter clams, are known to store the toxin for up to two years. Additional toxins are found, such as neosaxiton and gonyautoxins I to IV. All of them act primarily on the nervous system.

PSP can be fatal in extreme cases, particularly in immunocompromised individuals. Children are more susceptible. PSP affects those who come into contact with the affected shellfish by ingestion. Symptoms can appear ten to 30 minutes after ingestion, and include nausea, vomiting, diarrhea, abdominal pain, tingling or burning lips, gums, tongue, face, neck, arms, legs, and toes. Shortness of breath, dry mouth, a choking feeling, confused or slurred speech, and loss of coordination are also possible.