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.

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.

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.

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.

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.

Typically the first symptom of starfish wasting disease is white lesions that appear on the surface of the starfish and spread rapidly, followed by decay of tissue surrounding the lesions. Next the animal becomes limp as the water vascular system fails and it is no longer able to maintain its internal hydrostatic balance. The body structure begins to break down, signs of stretching appear between the arms which may twist and fall off, and the animal dies. The arms may continue to crawl around for a while after being shed. Progression of these events can be rapid, leading to death within a few days.

A deflated appearance can precede other morphological signs of the disease. All of these symptoms are also associated with ordinary attributes of unhealthy stars and can arise when an individual is stranded too high in the intertidal zone (for example) and simply desiccates. "True" wasting disease will be present in individuals that are found in suitable habitat, often in the midst of other individuals that might also be affected.

The final result is a white, mushy blob, which no longer seems to be a sea star.

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.

Symptoms typically begin to appear two months after the fish are transferred from freshwater hatcheries to open net sea cages. Symptoms include mucus build-up on the gills of infected fish and hyper-plastic lesions, causing white spots and eventual deterioration of the gill tissue. Fish will show signs of dyspnoea such as rapid opercular movements and lethargy. Although usually recognised by hyperplastic and proliferative gill lesions, the effects of AGD occur before oxygen transfer across the gill is severely compromised. AGD affected fish show a significant increase in vascular resistance contributing to cardiovascular collapse. Such effects result in compensatory changes in heart shape to improve its efficiency at pumping blood.

Contributing factors are an ambient water temperature above 16 degrees Celsius, crowding and poor water circulation inside the sea pens. Clinical cases are more common in the Summer. The lesions on the gills are highly suggestive of infection. Gill biopsies can be observed under the microscope for amoebas, or tested using fluorescent antibody testing.

Sea star wasting disease or starfish wasting syndrome is a disease of starfish and several other echinoderms that appears sporadically, causing mass mortality of affected starfish. There are around 40 different species of sea stars that have been affected by this disease. The disease seems to be associated with raised water temperatures. It starts with the emergence of lesions, followed by body fragmentation and death. In 2014 it was shown that the disease is associated with a densovirus now known as the sea star-associated densovirus (SSaDV).

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.

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."

Seabather's eruption is a pruritic dermatitis caused by a hypersensitivity reaction to the immature nematocysts of larval-stage Thimble Jellyfish ("Linuche unguiculata"), sea anemones ("Edwardsiella lineata") and other larval cnidarians.

It should not be confused with Swimmer's itch. However, the term "sea lice" is also sometimes used to describe Seabather's eruption.

Symptoms generally arise later after one takes a shower. It is unusual to notice the eruptions immediately. Symptoms can last from a few days up to two weeks, the shorter time being the norm.

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.

Turf necrotic ring spot is known to infect various bluegrass and turfgrass species, especially the cool-season grasses. The fungus also infects fescues and bentgrasses (11). It is common in sodded lawns, rapidly growing lawns, and lawns with layered soil (3). The pathogen produces circular patches of bald spots that are tan or yellow in color (12). These patches are about 5 to 10 cm in diameter, but can grow to be about 1 meter in diameter. Eventually, as the infected turf dies, the spots turn brown. Within the patch, there may be areas of living grass at the center, creating a frog-eye appearance that this pathogen is known for. This is the result of the turf in the center surviving or being recolonized by healthy grass (3).

While the infection happens during cooler seasons, such as fall and spring, the symptoms can carry into summer (7). Should the disease continue through the summer, it may cause the crown and roots to become blackened with visible mycelium (11). As previously mentioned, this disease alters the grass by creating patches of yellow or tan dead grass (1). Another possible symptom is leaf lesions. Leaf lesions are often common among fungal diseases. If there are leaf lesions on the blade, the lesions will be inconsistent in terms of size and shape. The lesions may also be varying colors, such as yellow, tan, or dark brown (11).

Infections on the body may give rise to typical enlarging raised red rings of ringworm. Infection on the skin of the feet may cause athlete's foot and in the groin, jock itch. Involvement of the nails is termed onychomycosis, and they may thicken, discolour, and finally crumble and fall off. They are common in most adult people, with up to 20% of the population having one of these infections at any given moment.

Animals such as dogs and cats can also be affected by ringworm, and the disease can be transmitted between animals and humans, making it a zoonotic disease.

Specific signs can be:

- red, scaly, itchy or raised patches

- patches may be redder on outside edges or resemble a ring

- patches that begin to ooze or develop blister

- bald patches may develop, when the scalp is affected

- nails may thicken, discolour or begin to crack

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.

The most common term for the infection, "ringworm", is a misnomer, since the condition is caused by fungi of several different species and not by parasitic worms.

Areas affected are those the cat can access most easily, including the abdomen, legs, flank, and chest.

- Baldness, usually beginning with the abdomen

- Obvious over-grooming (although some cats may only engage in the behavior in the absence of owners)

- Redness, rashes, pus, scabs on the bald area or areas traumatized by over-grooming

- A highly irritable cat may even cut its face with the claw of its hind foot if over-zealously scratching the back of its head.

So far one agent has been identified, the ciliate protozoan "Halofolliculina corallasia". Skeletal eroding band is the first recorded disease of corals that is caused by a protozoan, and thus the first known to be caused by an eukaryote – most are caused by prokaryotic bacteria. For example, black band disease is caused by microbial mats of variable composition, and White pox disease by the bacterium "Serratia marcescens".

"H. corallasia" is a protozoan that secretes a bottle-like housing called a lorica (Latin for cuirass, flexible body armor), that is anchored to a surface and into which the cells retract when disturbed. When a mature individual cell division divides, it produces a pair of worm-like larvae that settle on undamaged coral just ahead of the black band. There each daughter cell secretes its lorica, at the same spinning to produce the lorica's flask-like shape. This spinning, combined with the chemicals that harden the lorica, crumble the coral skeleton and kill the polyps. The discarded loricae of the "parent" "H. corallasia" cells remain, leaving the distinctive spotted region in the wake of the living black band.

Living fish afflicted with VHS may appear listless or limp, hang just

beneath the surface, or swim very abnormally, such as constant flashing

circling due to the tropism of the virus for the brain.

External signs may include darker coloration, exophthalmia ("pop eye"),

pale or red-dotted gills, sunken eyes, and bleeding around orbits (eye sockets) and

at base of fins.

Genetics researchers at the Lake Erie Research Center at the University of Toledo are developing a test that will speed diagnosis from a month to a matter of hours.

Coral diseases mostly take the form of a narrow band of diseased tissue separating the living tissue from the exposed skeleton. The band moves across the surface of the colony at the rate of a few millimetres a day, leaving behind bare skeletal material that is rapidly colonized by algae.

Many of the diseases that affect corals are known by their most obvious symptoms such as black band disease, white pox and yellow-band disease. However in many instances it has not been possible to identify the pathogens responsible for the disease and culture them in the laboratory; that the coral is sick and the tissue is necrotic is apparent, but whether the fungi or bacteria present caused the disease or merely fed on the already dying tissue is not clear. There is also a minute crab a millimetre or so wide which is often associated with diseased corals, but whether it introduces the disease or just moves in to consume the necrotic tissue is uncertain. Some of the bacteria found on diseased corals are terrestrial species that are not normally considered pathogenic. Further research has shown that viruses may be involved in white plague infections, the coral small circular single-stranded DNA (ssDNA) viruses being present in association with diseased tissue. Viruses in this group are known to cause disease in some plants and animals.

Like humans and other animals, fish suffer from diseases and parasites. Fish defences against disease are specific and non-specific. Non-specific defences include skin and scales, as well as the mucus layer secreted by the epidermis that traps microorganisms and inhibits their growth. If pathogens breach these defences, fish can develop inflammatory responses that increase the flow of blood to infected areas and deliver white blood cells that attempt to destroy the pathogens.

Specific defences are specialised responses to particular pathogens recognised by the fish's body, that is adaptative immune responses. In recent years, vaccines have become widely used in aquaculture and ornamental fish, for example vaccines for furunculosis in farmed salmon and koi herpes virus in koi.

Some commercially important fish diseases are VHS, ich and whirling disease.

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.

VHSV is a hemorrhagic disease, meaning it causes bleeding. Internally,

the virus can cause petechial hemorrhaging (tiny spots of blood) in internal

muscle tissue, and petechial or severe hemorrhaging in internal organs and

other tissues. Internal hemorrhaging can be observed as red spots inside

a dead fish, particularly around the kidney, spleen, and intestines, as

well as the swim bladder, which would normally have a clear membrane.

The liver may be pale, mottled with red hyperemic areas, the kidney

may be swollen and unusually red, the spleen may be swollen, and the digestive

tract may be empty.

External signs are not always present, but if they are, hemorrhaging on the

skin's surface can appear as anywhere from tiny red dots (petechiae) to

large red patches.