Diseases can have a variety of causes, including bacterial infections from an external source such as "Pseudomonas fluorescens" (causing fin rot and fish dropsy), fungal infections (Saprolegnia), mould infections (Oomycete and "Saprolegnia"), parasitic disorders ("Gyrodactylus salaris", "Ichthyophthirius multifiliis", Cryptocaryon, Oodinium causing velvet disease, "Brooklynella hostilis", head and lateral line erosion, Glugea, "Ceratomyxa shasta", "Kudoa thyrsites", "Tetracapsuloides bryosalmonae", "Ceratomyxa shasta" leeches, nematode, Trematoda, Platyhelminthes and fish louse), viral disorders, metabolic disorders, inappropriate water conditions (insufficient aeration, pH, water hardness, temperature and ammonia poisoning) and malnutrition.

External bacterial infections may cause spots or streaks on the body which appear red or orange Dropsy (bloating) is also a sign of a bacterial infection. "False fungal infections" look like fungus but is actually a bacterial infection known as Columnaris. These symptoms may include a white or gray film on the body.

Ornamental fish kept in aquariums are susceptible to numerous diseases. Due to their generally small size and the low cost of replacing diseased or dead fish, the cost of testing and treating diseases is often seen as more trouble than the value of the fish.

Due to the artificially limited volume of water and high concentration of fish in most aquarium tanks, communicable diseases often affect most or all fish in a tank. An improper nitrogen cycle, inappropriate aquarium plants and potentially harmful freshwater invertebrates can directly harm or add to the stresses on ornamental fish in a tank. Despite this, many diseases in captive fish can be avoided or prevented through proper water conditions and a well-adjusted ecosystem within the tank.

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.

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.

Fish infected with typical BCWD have lesions on the skin and fins. Fins may appear dark, torn, split, ragged, frayed and may even be lost completely. Affected fish are often lethargic and stop feeding. Infection may spread systemically. Salmonid fish can also get a chronic form of BCWD following recovery from typical BCWD. It is characterised by erratic “corkscrew” swimming, blackened tails and spinal deformities.

In rainbow trout fry syndrome, acute disease with high mortality rates occurs. Infected fish may show signs of lethargy, inappetance and exopthalmos before death.

A presumptive diagnosis can be made based on the history, clinical signs, pattern of mortality and water temperature, especially if there is a history of the disease in the area. The organism can be cultured for definitive diagnosis. Alternatively, histology should show periostitis, osteitis, meningitis and ganglioneuritis.

Infection can cause subcutaneous haemorrhage that presents as reddening of the throat, mouth, gill tips, and fins, and eventual erosion of the jaw and palate. Hemorrhaging also occurs on internal organs, and in the later stages of the disease, the abdomen becomes filled with a yellow fluid - giving the fish a "pot-bellied" appearance. The fish often demonstrate abnormal behavior and anorexia. Mortality rates can be high.

A presumptive diagnosis can be made based in the history and clinical signs, but definitive diagnosis requires bacterial culture and serological testing such as ELISA and latex agglutination.

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.

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.

Bacterial cold water disease (BCWD) is a bacterial disease of salmonid fish. It is caused by "Flavobacterium psychrophilum" (previously classified in the genus "Cytophaga"), a gram-negative rod-shaped bacterium of the family Flavobacteriaceae. The disease typically occurs at temperatures below 13⁰C, and it can be seen in any area with water temperatures consistently below 15⁰C. Salmon are the most commonly affected species. This disease is not zoonotic.

Asymptomatic carrier fish and contaminated water provide reservoirs for disease. Transmission is mainly horizontal, but vertical transmission can also occur.

BCWD may be referred to by a number of other names including cold water disease, peduncle disease, fit rot, tail rot and rainbow trout fry mortality syndrome.

An infection will usually first manifest in fish by causing frayed and ragged fins. This is followed by the appearance of ulcerations on the skin, and subsequent epidermal loss, identifiable as white or cloudy, fungus-like patches – particularly on the gill filaments. Mucus often also accumulates on the gills, head and dorsal regions. Gills will change colour, either becoming light or dark brown, and may also manifest necrosis. Fish will breathe rapidly and laboriously as a sign of gill damage. Anorexia and lethargy are common, as are mortalities, especially in young fish.

Some fish species serve as vectors for the disease and have subsequently spread the pathogen to other parts of the world. An example is the fathead minnow ("Pimephales promelas") which is responsible for the spread of redmouth disease to trout in Europe. Other vectors include the goldfish ("Carassius auratus"), Atlantic and Pacific salmon ("Salmo salar"), the emerald shiner ("Notropis atherinoides"), and farmed whitefish ("Coregonus" spp.). Infections have also occurred in farmed turbot ("Scophthalmus maximus"), seabass ("Dicentrarchus labrax"), and seabream ("Sparus auratus"). It can now be found in North and South America, Africa, Asia, and Australia, as well as Europe.

Ulcerations develop within 24 to 48 hours. Fatality occurs between 48 and 72 hours if no treatment is pursued; however, at higher temperatures death may occur within hours. Other symptoms may accompany the disease, including lethargy, color loss, redness around the infection site, loss of appetite and twitching or rubbing the body against objects.

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.

Hallmark symptoms of ciguatera in humans include gastrointestinal, cardiovascular, and neurological effects. Gastrointestinal symptoms include nausea, vomiting, and diarrhea, usually followed by neurological symptoms such as headaches, muscle aches, paresthesia, numbness of extremities, mouth and lips, reversal of hot and cold sensation, ataxia, vertigo, and hallucinations. Severe cases of ciguatera can also result in cold allodynia, which is a burning sensation on contact with cold. Neurological symptoms can persist and ciguatera poisoning is occasionally misdiagnosed as multiple sclerosis. Cardiovascular symptoms include bradycardia, tachycardia, hypotension, hypertension, orthostatic tachycardia, exercise intolerance, and rhythm disorders. Death from the condition can occur, but is extremely rare.

Dyspareunia and other ciguatera symptoms have developed in otherwise healthy males and females following sexual intercourse with partners suffering ciguatera poisoning, signifying that the toxin may be sexually transmitted. Diarrhea and facial rashes have been reported in breastfed infants of poisoned mothers, suggesting that ciguatera toxins migrate into breast milk.

The symptoms can last from weeks to years, and in extreme cases as long as 20 years, often leading to long-term disability. Most people do recover slowly over time. Often patients recover, but symptoms then reappear. Such relapses can be triggered by consumption of nuts, seeds, alcoholic beverages, fish or fish-containing products, chicken or eggs, high histamine foods, temperature extremes, or by exposure to fumes such as those of bleach and other chemicals. Exercise is also a possible trigger.

Fin rot is a symptom of disease or the actual disease in fish. This is a disease which is most often observed in aquaria and aquaculture, but can also occur in natural populations.

Fin rot can be the result of a bacterial infection ("Pseudomonas fluorescens", which causes a ragged rotting of the fin), or as a fungal infection (which rots the fin more evenly and is more likely to produce a white 'edge'). Sometimes, both types of infection are seen together. Infection is commonly brought on by bad water conditions, injury, poor diet, stress, or as a secondary infection in a fish which is already stressed by other disease.

Fin rot starts at the edge of the fins, and destroys more and more tissue until it reaches the fin base. If it does reach the fin base, the fish will never be able to regenerate the lost tissue. At this point, the disease may begin to attack the fish's body; this is called Advanced Fin and Body rot.

Fin rot is common in bettas due to poor water conditions in pet stores.

Initial symptoms include large, angular or blocky, yellow areas visible on the upper surface. As lesions mature, they expand rapidly and turn brown. The under surface of infected leaves appears watersoaked. Upon closer inspection, a purple-brown mold (see arrow) becomes apparent. Small spores shaped like footballs can be observed among the mold with a 10x hand lens. In disease-favorable conditions (cool nights with long dew periods), downy mildew will spread rapidly, destroying leaf tissue without affecting stems or petioles.

At first, fish develop red spots on the skin. These lesions expand to form ulcers and extensive erosions filled with necrotic tissue and mycelium. This is followed by the development of granulomas on the internal organs and death.

A provisional diagnosis can be made by using squash preparations of the skeletal muscle from beneath an ulcer to identify the septate hyphae of the water mould. Definitive diagnosis can be made based on histopathogical findings and isolation of the pathogen.

Downy mildew refers to any of several types of oomycete microbes that are obligate parasites of plants. Downy mildews exclusively belong to Peronosporaceae. In commercial agriculture, they are a particular problem for growers of crucifers, grapes and vegetables that grow on vines. The prime example is "Peronospora farinosa" featured in NCBI-Taxonomy and HYP3. This pathogen does not produce survival structures in the northern states of the United States, and overwinters as live mildew colonies in Gulf Coast states. It progresses northward with cucurbit production each spring. Yield loss associated with downy mildew is most likely related to soft rots that occur after plant canopies collapse and sunburn occurs on fruit. Cucurbit downy mildew only affects leaves of cucurbit plants.

Ciguatera is a foodborne illness caused by eating certain reef fish whose flesh is contaminated with a toxin made by dinoflagellates such as "Gambierdiscus toxicus" which live in tropical and subtropical waters. These dinoflagellates adhere to coral, algae and seaweed, where they are eaten by herbivorous fish which in turn are eaten by larger carnivorous fish like barracudas, shark, and even omnivorous fish like basses and other fish like mullet. This is called biomagnification. Affected fish may show no sign of infection or, in more advanced cases, will be weakened and visibly thin, with yellowish eyes. As well, fish may be pale or a different color than usual.

"Gambierdiscus toxicus" is the primary dinoflagellate responsible for the production of a number of similar polyether toxins, including ciguatoxin, maitotoxin, gambieric acid and scaritoxin, as well as the long-chain alcohol palytoxin. Other dinoflagellates that may cause ciguatera include "Prorocentrum" spp., "Ostreopsis" spp., "Coolia monotis", "Thecadinium" spp. and "Amphidinium carterae". Predator species near the top of the food chain in tropical and subtropical waters are most likely to cause ciguatera poisoning, although many other species cause occasional outbreaks of toxicity.

Ciguatoxin is odourless, tasteless and cannot be removed by conventional cooking.

Researchers such as Ross M. Brown with his "New Religion" theory suggest that ciguatera outbreaks caused by warm climatic conditions in part propelled the migratory voyages of Polynesians between 1000 and 1400AD.

In 2017 an updated review of "Clinical, Epidemiological, Environmental, and Public Health Management" was published and is available at the National Institute of Health website.

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.

Epizootic ulcerative syndrome (EUS), also known as mycotic granulomatosis (MG) or red spot disease (RSD), is a disease caused by the water mould "Aphanomyces invadans". It infects many freshwater and brackish fish species in the Asia-Pacific region and Australia. The disease is most commonly seen when there are low temperature and heavy rainfall in tropical and sub-tropical waters.

The symptoms of little cherry disease in sweet and sour cherries varies greatly depending on cultivar, with respect to both the range and the severity of symptoms; some cultivars show signs of tolerance.

In infected trees of the commercially important cultivar Lambert, the fruit develops normally until about ten days before harvest, when maturation stops. At picking time, the cherries are 1/2–2/3 of the regular size, dull in color, with an angular pointed shape. The sugar and acid levels of the cherries are severely impacted, resulting in tasteless fruits, lacking both sweetness and flavor. Other cultivars show symptoms similar to those in Lambert, but usually less severe and more varied. Typically, dark-fruited cultivars show more severe fruit symptoms than cultivars with red or yellow fruit. The ability to recover is also dependent on cultivar, with some able to return to fruit sizes and coloring comparable to uninfected trees. The taste, however, never recovers.

Some sweet cherry cultivars display foliage symptoms, with the fruit crop less hidden by the canopy, and leaf symptoms, varying from a slight marginal up-curl of the leaves to marked reddening of leaf surfaces. The general vigor of infected trees may be impaired, though this is not always apparent. Diagnosis of the disease can be assisted by RT-PCR assays.

Other "Prunus" species may act as symptomless or tolerant carriers of the disease; especially cultivars of Japanese flowering cherry ("Prunus serrulata") have been implicated as such.

Symptoms typically occur within 10–30 minutes of ingesting the fish and generally are self-limited. People with asthma are more vulnerable to respiratory problems such as wheezing or bronchospasms. However, symptoms may show over two hours after consumption of a spoiled dish. They usually last for about 10 to 14 hours, and rarely exceed one to two days.

Strawberry foliar nematode is a disease common in strawberries and ornamental plants that can greatly affect plant yield and appearance, resulting in a loss of millions of dollars of revenue. Symptoms used to diagnose the disease are angular, water soaked lesions and necrotic blotches. "Aphelenchoides fragariae" is the nematode pathogen that causes the disease. Its biological cycle includes four life stages, three of which are juvenile. The nematode can undergo multiple life cycles in one growing season when favorable conditions are present. They can infect the crowns, runners, foliage, and new buds of the plant via stylet penetration or through the stomata. The best management practices for this disease are sanitation, prevention of induction of the pathogen to the environment, and planting clean seed or starter plants.

The above symptoms can advance to:

- facial rash (intense itching may accompany the rash.)

- torso or body rash: The rash associated with scombroid poisoning is a form of urticaria, but most commonly does not include wheals (patchy areas of skin-swelling also known as hives) that may be seen in true allergies.

- edema (this is generalized if it occurs at all)

- short-term diarrhea

- abdominal cramps