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.

White band disease (Acroporid white syndrome) is a coral disease that affects acroporid corals and is distinguishable by the white band of dead coral tissue that it forms. The disease completely destroys the coral tissue of Caribbean acroporid corals, specifically elkhorn coral ("Acropora palmata") and staghorn coral ("A. cervicornis"). The disease exhibits a pronounced division between the remaining coral tissue and the exposed coral skeleton. These symptoms are similar to white plague, except that white band disease is only found on acroporid corals, and white plague has not been found on any acroporid corals. It is part of a class of similar disease known as "white syndromes", many of which may be linked to species of "Vibrio" bacteria. While the pathogen for this disease has not been identified, "Vibrio carchariae" may be one of its factors. The degradation of coral tissue usually begins at the base of the coral, working its way up to the branch tips, but it can begin in the middle of a branch.

Yellow-band disease (similar to Yellow Blotch disease) is a coral disease that attacks colonies of coral at a time when coral is already under stress from pollution, overfishing, and climate change. It is characterized by large blotches or patches of bleached, yellowed tissue on Caribbean scleractinian corals.

Yellow-band disease is a bacterial infection that spreads over coral, causing the discolored bands of pale-yellow or white lesions along the surface of an infected coral colony. The lesions are the locations where the bacteria have killed the coral’s symbiotic photosynthetic algae, called zooxanthellae which are a major energy source for the coral. This cellular damage and the loss of its major energy source cause the coral to starve, and usually cause coral death. There is evidence that climate change could be worsening the disease.

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.

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.

Black band disease is a coral disease in which corals develop a black band. It is characterized by complete tissue degradation due to a pathogenic microbial consortium. The mat is present between apparently healthy coral tissue and freshly exposed coral skeleton.

Black band disease was first observed on reefs in Belize in 1973 by A. Antonius, who described the pathogen he found infecting corals as "Oscillatoria membranacea", one of the cyanobacteria. The band color may be blackish brown to red depending on the vertical position of a cyanobacterial population associated with the band. The vertical position is based on a light intensity-dependent photic response of the cyanobacterial filaments, and the color (due to the cyanobacterial pigment phycoerythrin) is dependent on the thickness of the band. The band is approximately thick and ranges in width from to White specks may be present on surface, at times forming dense white patches. The pathogenic microbial mat moves across coral colonies at rates from to a day. Tissue death is caused by exposure to an hypoxic, sulfide-rich microenvironment associated with the base of the band.

Velvet disease (also called gold-dust, rust and coral disease) is a fish disease caused by dinoflagellate parasites of the genus "Piscinoodinium", specifically "Amyloodinium" in marine fish, and "Oodinium" in freshwater fish. The disease gives infected organisms a dusty, brownish-gold color. The disease occurs most commonly in tropical fish, and to a lesser extent, marine aquaria.

White band disease causes the affected coral tissue to decorticate off the skeleton in a white uniform band for which the disease was given its name. The band, which can range from a few millimeters to 10 centimeters wide, typically works its way from the base of the coral colony up to the coral branch tips. The band progresses up the coral branch at an approximate rate of 5 millimeters per day, causing tissue loss as it works its way to the branch tips. After the tissue is lost, the bare skeleton of the coral may later by colonized by filamentous algae.

There are two variants of white band disease, type I and type II. In Type I of white band disease, the tissue remaining on the coral branch shows no sign of coral bleaching, although the affected colony may appear lighter in color overall. However, a variant of white band disease, known simply as white band disease Type II, which was found on Staghorn colonies near the Bahamas, does produce a margin of bleached tissue before it is lost. Type II of white band disease can be mistaken for coral bleaching. By examining the remaining living coral tissue for bleaching, one can delineate which type of the disease affects a given coral.

Common clinical signs of Tyzzer’s Disease include watery diarrhea, depression, emaciation, and a ruffled coat. Other observed clinical signs include melena, depression, lethargy, and decreased temperature. In muskrats, this disease is characterized by extensive hemorrhaging within the lower intestine and abdomen. Due to the fast-acting nature of this disease, infected individuals often do not live long enough to exhibit symptoms. It is not uncommon for an infected animal to die within 1-10 days of disease contraction.

During necropsy, inflammation of the ileum, cecum, and colon are commonly present. Perhaps the most distinctive trait of this disease, however, is the grayish yellow necrotic lesions found on the liver of diseased animals. The number of these spots present can range from one to countless. Occasionally, lesions are discovered in the lower intestinal tract and heart as well. Even with physical signs and symptoms present, a conclusive diagnosis is dependent upon the presence of "C. piliforme" within the liver of the infected animal.

The single-celled parasite's life cycle can be divided into three major phases. First, as a tomont, the parasite rests at the water's floor and divides into as many as 256 tomites. Second, these juvenile, motile tomites swim about in search of a fish host, meanwhile using photosynthesis to grow, and to fuel their search. Finally, the adolescent tomite finds and enters the slime coat of a host fish, dissolving and consuming the host's cells, and needing only three days to reach full maturity before detaching to become a tomont once more.

Coral has a symbiotic relationship with zooxanthellae that provide the coral glucose, glycerol, and amino acids. Under certain water conditions, like fluctuating temperatures and increased nitrogenous waste, corals will appear stressed. Also, these conditions allow for bacteria to grow inside the coral and compete with zooxanthellae. The bacteria produces the characteristic pale yellow lesions and eventually kills the zooxanthellae by impairing its mitosis and its ability to carry out photosynthesis. Yellow-band disease is found on coral reefs in the Caribbean.

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.

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.

Tyzzer’s disease is an acute epizootic bacterial disease found in rodents, rabbits, dogs, cats, birds, pandas, deer, foals, cattle, and other mammals including gerbils. It is caused by the spore-forming bacterium "Clostridium piliforme", formerly known as "Bacillus piliformis". It is an infectious disease characterized by necrotic lesions on the liver, is usually fatal, and is present worldwide. Animals with the disease become infected through oral ingestion of the bacterial spores and usually die within a matter of days. Animals most commonly affected include young, stressed animals in laboratory environments, such as immature rodents and rabbits. Most commonly affected wild animals include muskrats "(Ondatra zibethicus)" and occasionally cottontail rabbits "(Lepus sylvaticus)". Even today, much remains unknown about Tyzzer’s disease, including how and why it occurs.

Verticillium wilt is a wilt disease of over 350 species of eudicot plants caused by six species of Verticillium genus, "V. dahliae", "V. albo-atrum", "V. longisporum", V. nubilum, V. theobromae and

V. tricorpus. (See, for example, Barbara, D.J. & Clewes, E. (2003). "Plant pathogenic Verticillium species: how many of them are there?" Molecular Plant Pathology 4(4).297-305. Blackwell Publishing.) Many economically important plants are susceptible including cotton, tomatoes, potatoes, oilseed rape, eggplants, peppers and ornamentals, as well as others in natural vegetation communities. Many eudicot species and cultivars are resistant to the disease and all monocots, gymnosperms and ferns are immune.

Symptoms are superficially similar to "Fusarium" wilts. There is no chemical control for the disease but crop rotation, the use of resistant varieties and deep plowing may be useful in reducing the spread and impact of the disease.

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.

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.

"Verticillium" spp. attack a very large host range including more than 350 species of vegetables, fruit trees, flowers, field crops, and shade or forest trees. Most vegetable species have some susceptibility, so it has a very wide host range. A list of known hosts is at the bottom of this page.

The symptoms are similar to most wilts with a few specifics to "Verticillium". Wilt itself is the most common symptom, with wilting of the stem and leaves occurring due to the blockage of the xylem vascular tissues and therefore reduced water and nutrient flow. In small plants and seedlings, "Verticillium" can quickly kill the plant while in larger, more developed plants the severity can vary. Some times only one side of the plant will appear infected because once in the vascular tissues, the disease migrates mostly upward and not as much radially in the stem. Other symptoms include stunting, chlorosis or yellowing of the leaves, necrosis or tissue death, and defoliation. Internal vascular tissue discoloration might be visible when the stem is cut.

In "Verticillium", the symptoms and effects will often only be on the lower or outer parts of plants or will be localized to only a few branches of a tree. In older plants, the infection can cause death, but often, especially with trees, the plant will be able to recover, or at least continue living with the infection. The severity of the infection plays a large role in how severe the symptoms are and how quickly they develop.

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.

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.

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.

Clinical appearance of the disease includes depression, a serous nasal discharge, and sporadically minor facial inflammation in mild form of the disease. In severe form, there is severe inflammation of one or both infraorbital sinuses with edema of the surrounding tissue. The swelling can cause closure of one eye or both of them. Intermandibular space and wattles of corks do swell as a course of the disease .

Infectious coryza is a serious bacterial disease of chickens which affects respiratory system and it is manifested by inflammation of the area below the eye, nasal discharge and sneezing...The disease is found all over the world causing high economic losses. Economic loss is due to stumping off and reduction of egg production in case of laying chickens. The disease was discovered early 1930s by considering clinical signs

In 1977, a disease of scleractinian corals appeared on reefs off the Florida Keys in the United States and was termed white plague. It caused white lesions and was shown to be an infectious disease, being particularly prevalent in "Mycetophyllia ferox". This disease caused little mortality and occurred sporadically, but was still present in the area in 1984. It is now known as white plague type 1.

In 1995, a new coral disease was described as an epizootic disease in the same reefs in the Florida Keys. Many species of coral found in the area were affected and the mortality rate of these was up to 38%. The pathogen involved was found to be a previously unknown species of bacterium in the order Rhizobiales, which was placed in the newly created genus "Aurantimonas" and given the name "Aurantimonas coralicida", and the disease was described as white plague type 2. The pathogen was isolated from a diseased colony of "Dichocoenia stokesi" and cultured in the laboratory, subsequently being used to inoculate two healthy colonies which then developed the disease. In the next few months, it had spread over of reef and was killing seventeen species of coral. Over the next four years, it spread further, but interestingly, was most severe in different regions each year.

However, white plague is an enigmatic disease. Further research cast into doubt the role of "A. coralicida" as a causative agent by finding that bacterium on healthy parts of colonies of "Orbicella annularis" affected by white plague disease but absent from diseased parts. In these diseased colonies, an α-proteobacterium similar to one which causes a disease in juvenile oysters has been implicated, being found on the diseased parts of the coral but not on the sound tissues. These anomalous findings may be caused by the fact that there are two or more diseases with similar symptoms, both known as white plague.

In 1999, a third and still more virulent variant appeared in the northern Florida Keys. White plague type III mostly affected "Colpophyllia natans" and "Orbicella annularis".

A white-plague like disease reported from the Red Sea in 2005 has been shown to be caused by a different bacterial pathogen, "Thalassomonas loyana". Further research has shown that viruses may be involved in white plague infections, the coral small circular ssDNA viruses (SCSDVs) being present in association with diseased tissue. This group of viruses is known to cause disease in plants and animals.