Disease cures are almost always more expensive and less effective than simple prevention measures. Often precautions involve maintaining a stable aquarium that is adjusted for the specific species of fish that are kept and not over-crowding a tank or over-feeding the fish. Common preventive strategies include avoiding the introduction of infected fish, invertebrates or plants by quarantining new additions before adding them to an established tank, and discarding water from external sources rather than mixing it with clean water. Similarly, foods for herbivorous fish such as lettuce or cucumbers should be washed before being placed in the tank. Containers that do not have water filters or pumps to circulate water can also increase stress to fish. Other stresses on fish and tanks can include certain chemicals, soaps and detergents, and impacts to tank walls causing shock waves that can damage fish.

In some cases the causes of an infection or disease will be obvious (such as fin rot), though in other cases it may be due to water conditions, requiring special testing equipment and chemicals to appropriately adjust the water. Isolating diseased fish can help prevent the spread of infection to healthy fish in the tank. This also allows the use of chemicals or drugs which may damage the nitrogen cycle, plants or chemical filtration of a properly-functioning tank. Other alternatives include short baths in a bucket that contains the treated water. Salt baths can be used as an antiseptic and fungicide, and will not damage beneficial bacteria, though ordinary table salt may contain additives which can harm fish. Alternatives include aquarium salt, Kosher salt or rock salt. Gradually raising the temperature of the tank may kill certain parasites, though some diseased fish may be harmed and certain species can not tolerate high temperatures. Aeration is necessary since less oxygen is dissolved in warm water.

There are a number of effective treatments for many stains of bacterial infections. Three of the most common are tetracycline, penicillin and naladixic acid. Salt baths are another effective treatment.

Quaternary ammonium compounds can be added to the water of infected adult fish and fry. Alternatively, the antibiotic oxytetracycline can be given to adults, fry and broodstock. To prevent the disease, it is necessary to ensure water is pathogen-free and that water hardening is completed effectively for eggs.

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.

Several antibiotics are available for the treatment of redmouth disease in fish. Vaccines can also be used in the treatment and prevention of disease. Management factors such as maintaining water quality and a low stocking density are essential for disease prevention.

Sodium chloride is believed to mitigate the reproduction of Velvet, however this treatment is not itself sufficient for the complete eradication of an outbreak. Additional, common medications added directly to the fish's environment include copper sulfate, methylene blue, formalin, malachite green and acriflavin, all of which can be found in common fish medications designed specifically to combat this disease. Additionally, because Velvet parasites derive a portion of their energy from photosynthesis, leaving a tank in total darkness for seven days provides a helpful supplement to chemical curatives. Finally, some enthusiasts recommend raising the water temperature of an infected fish's environment, in order to quicken the life cycle (and subsequent death) of Velvet parasites; however this tactic is not practical for all fish, and may induce immunocompromising stress.

Infected fish should be moved into high quality water, where they may recover if their clinical signs are mild.

If disease occurs eradication is required. Once the disease is eradicated good husbandry, surveillance and biosecurity measures are necessary to prevent recurrence. In countries free of epizootic ulcerative syndrome, quarantine and health certificates are necessary for the movement of all live fish to prevent the introduction of the disease.

As "Flavobacterium columnare" is Gram-negative, fish can be treated with a combination of the antibiotics furan-2 and kanamycin administered together. A medicated fish bath (using methylene blue or potassium permanganate and salt), is generally a first step, as well lowering the aquarium temperature to 75 °F (24 °C) is a must, since columnaris is much more virulent at higher temperatures, especially 85–90 °F.

Medicated food containing oxytetracycline is also an effective treatment for internal infections, but resistance is emerging. Potassium permanganate, copper sulfate, and hydrogen peroxide can also be applied externally to adult fish and fry, but can be toxic at high concentrations. Vaccines can also be given in the face of an outbreak or to prevent disease occurrence.

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.

In Northern Australia, where ciguatera is a common problem, two different folk science methods are widely believed to detect whether fish harbor significant ciguatoxin. The first method is that flies are supposed not to land on contaminated fish. The second is that cats will either refuse to eat or vomit/display symptoms after eating contaminated fish. A third, less common testing method involves putting a silver coin under the scales of the suspect fish. If the coin turns black, according to the theory, it is contaminated.

On Grand Cayman and other islands the locals will test barracuda by placing a piece of the fish on the ground and allowing ants to crawl on it. If the ants do not avoid the flesh and will eat it, then the fish is deemed safe.

In Dominican Republic, another common belief is that during months whose names do not include the letter "R" (May through August), it is not recommended to eat certain kinds of fish, because they are more likely to be infected by the ciguatera toxin.

The validity of many of these tests has been scientifically rejected.

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.

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.

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.

There is no known cure for little cherry disease and tolerance breeding programs have not yielded any cultivars able to withstand the effects of the disease for more than a few seasons. Thus, prevention of spread has been the focal point in combating the disease.

There is no effective treatment or antidote for ciguatera poisoning. The mainstay of treatment is supportive care. There is some evidence that calcium channel blockers like nifedipine and verapamil are effective in treating some of the symptoms that remain after the initial sickness passes, such as poor circulation and shooting pains through the chest. These symptoms are due to the cramping of arterial walls caused by maitotoxin Ciguatoxin lowers the threshold for opening voltage-gated sodium channels in synapses of the nervous system. Opening a sodium channel causes depolarization, which could sequentially cause paralysis, heart contraction, and changing the senses of hot and cold. Some medications such as amitriptyline may reduce some symptoms, such as fatigue and paresthesia, although benefit does not occur in every case.

Mannitol was once used for poisoning after one study reported symptom reversal. Follow-up studies in animals and case reports in humans also found benefit from mannitol. However, a randomized, double-blind clinical trial found no difference between mannitol and normal saline, and based on this result, mannitol is no longer recommended.

Long term management of chronic Ciguatera includes avoiding trigger food and environmental triggers, and managing symptoms with medications and or lifestyle.

Caution may be needed with anesthesia and should be discussed with your healthcare providers.

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.

Metagonimiasis is diagnosed by eggs seen in feces. Only after antihelminthic treatment will adult worms be seen in the feces, and then can be used as part of a diagnostic procedure. A 1993 analysis of the efficacy of ELISA tests to diagnose metagonimiasis implied that simultaneous screening of specific antibodies to several parasite agents are important in serological diagnosis of acute parasitic disease and more research should be done on the efficacy of these methods of diagnosis.

Diagnosis may be difficult because the egg-laying capacity of heterophyids is limited, and therefore sedimentation concentration procedures may be needed to demonstrate eggs in lighter infections. Accurate species identification is also difficult because eggs of most flukes are similar in size and morphology, especially those of "Heterophyes heterophyes", "Clonorchis" and "Opisthorchis". It is important to ask where the person may have contracted the disease, find out if they have been to en endemic area, and check for signs and symptoms that would lead to metagonimiasis.

Strawberry foliar nematodes are difficult to manage due to their robust life cycle. While dormant, they are quite difficult to kill, and they remain viable in dry debris for more than one year. Adult nematodes can survive desiccation and lie dormant for several years. Eggs can stay dormant until survival conditions are optimal for growth. Once eggs or nematodes are present in the soil, they are nearly impossible to eradicate because they can move laterally in the soil to escape non-optimal conditions. They are found in most foliar tissue, including the leaves, stems, buds, and crowns, making it difficult to control the disease on the plant itself once it has been infected

Many plant diseases are managed chemically, but due to a ban of nematicides there are currently no nematicides available for any type of foliar nematode. Some insecticides, pesticides, and plant product extracts from plants such as Ficus and Coffee (of which many pesticides and nematicides are neem-based ) can be used to reduce the numbers of strawberry foliar nematode (a reduction of 67-85%), but none of these chemicals can completely eradicate the nematodes once they are present in the soil. These chemicals affect all stages of the life cycle because they target the nervous system. One chemical, ZeroTol, a broad-spectrum fungicide and algaecide, was shown be to 100% potent against nematodes living in a water suspension, but the study does not show how nematodes are affected in soil or outside of a laboratory environment.

An alternative method of control is a hot water treatment, which affects all stages of the life cycle and can be used on whole plants. This treatment has been used for 60 years with some effect in greenhouse plants, but not on a widespread agricultural level. The difficulty in this treatment is that exposure times to hot water and the temperature of the water must be optimized so that the nematodes are killed, but the cultivar remains undamaged. One study, which researched five California strawberry cultivars including Chandler, Douglas, Fern, Pajaro, and Selva, demonstrated that the minimum-maximum exposure times and temperatures that killed the nematodes but did not harm the cultivars were: 20–30 minutes at 44.4⁰C, 10–15 minutes at 46.1⁰C, and 8–10 minutes at 47.7⁰. The study also found that fruit production was more sensitive to the treatment than mere survival of the plant, so the minimum exposure times are recommended when using plants for fruit production, and the maximum time is recommended when using plants for propagation.

One of the best and most practiced forms of management to reduce the local and geographical spread of the disease is sanitation. Removing the infected leaves of the plant can reduce spread in the individual plant, but because the nematode is found in most foliar tissue the nematodes may already be present in other tissues before the leaf symptoms appear. The nematodes can also move on the outside of the plant surface when water is present, so the nematodes can move around the outside surface of the plant and infect new tissues. Therefore, once plants show any signs of infection, they should be removed and destroyed. Reducing or eliminating overhead irrigation can prevent dispersal of the nematode through water splashing, and keeping the foliage dry prevents the nematodes from moving on the outside of the plant. Plants should be placed further apart to allow water to dry quickly after irrigation. In the greenhouse or nursery, soils, containers, and tools should be sterilized on a regular basis, and the floor and storage areas should be free from plant debris.

The most important form of management is prevention of introduction of the nematode to the environment. One should avoid planting infected plants, and it is recommended that new plants (especially in a personal lawn or greenhouse) be planted in an isolated area to monitor the plant for the development of symptoms before transplanting the plant near established plants. This will prevent the established plants from getting infected from a new, infected plant. All symptomatic plants should be destroyed immediately. Dead plant material should also be handled with caution. Vermiform nematodes can survive and reproduce in compost piles of dead plant material by feeding on fungi that are commonly found in compost. As a result, infected plants should be burned and sterilized to prevent the nematodes from infecting soil (which results directly from burying the material), or other plants (from allowing the plant to remain rooted in the soil near other plants as it dies).

Diagnosis of gnathostomiasis is possible (with microscopy) after removal of the worm.

The primary form of diagnosis of gnathostomiasis is the identification of larva in the tissue. Serological testing such as enzyme-linked immunosorbent assay (ELISA) or the Western blot are also reliable but may not be easily accessible in endemic areas.

CT scanning or MRI can be used to help identify a soft tissue worm and when looking at CNS disease it can be used to reveal the presence of the worm. The presence of haemorrhagic tracks on gradient-echo T2-weighted MRI is characteristic and possibly diagnostic. Urinalysis can also be used to identify the presence of hematuria or the worm, but it is not a very reliable diagnostic tool.

Fungicides applied specifically for downy mildew control may be unnecessary. Broad spectrum protectant fungicides such as chlorothalonil, mancozeb, and fixed copper are at least somewhat effective in protecting against downy mildew infection. Systemic fungicides are labeled for use against cucurbit downy mildew, but are recommended only after diagnosis of this disease has been confirmed. In the United States, the Environmental Protection Agency has approved oxathiapiprolin for use against downy mildew.

Extensive treatments have been used on domestic animals more than on wild animals, probably because infected domestic animals are easier to identify and treat than infected wildlife. Treatment plans and management vary across taxa because this disease tends to affect each species differently. Antifungal drugs are the first line of defense to kill the agents causing phaeohyphomycosis, but despite the significant progress made in the last two decades and a 30% increase in available antifungal drugs since 2000, many drugs are not effective against black fungi. Diseases caused black fungi are hard to treat because the fungi are very difficult to kill. This high resilience may be contributed to the presence of melanin in their cell walls. Current antifungal agents the fungi are not resistant to are posaconazole, voriconazole, and azole isavuconazole.

In 2006, a free-living Eastern box turtle, "Terrapene carolina carolina", was found with a form of phaeohyphomycosis and was brought in the Wildlife Center of Virginia. Its symptom was swelling of the right hindfoot; it was diagnosed as having chromomycosis by histopathology. The center provided a series of antimicrobial treatments and a one-month course of 1 mg itraconazole, administered orally once a day. The eastern box turtle was euthanized due to further complications and the caretakers’ belief that the turtle would not be able to survive if placed back in the wild.

A recent case of a form of phaeohyphomycosis infection was found in a dog in 2011. The Journal of the American Veterinary Medical Association published a case study in which researchers successfully managed an intracranial phaeohyphomycotic fungal granuloma in a one-year-old male Boxer dog. Veterinarians of the Department of Veterinary Clinical Sciences at Tufts University surgically removed the granuloma in the right cerebral hemisphere. The patient was treated with fluconazole for 4 months, and was followed with voriconazole for 10 months. Both are medications used to treat fungal infections. Based on magnetic resonance imaging and cerebrospinal fluid (CSF) analysis 8 months after the surgery, the male Boxer’s outcome was considered excellent.

Emphasis has been placed on how to manage this disease through careful management practices including: proper handling, preventing crowding situation with animals, and transportation. Both the animals and the environment should be treated thoroughly to hinder the spread and control the fungal infection. This is especially important since humans can also contract this disease.

Diagnosis in a live specimen is possible in the field by palpating the abdomen. As with birds, prominence of the keel could be a determinant in diagnosis, but natural history of the species needs to be understood to avoid potential misdiagnoses. However, the best form of diagnosis still remains as necropsy. During the necropsy, the best diagnosis can be determined by the adult nematodes by scanning them with electron microscopy. Different species of Eustrongylidosis nematodes can be differentiated by specific gender characteristics, i.e. “Male specimens of E. ignotus have a caudal sucker that lacks cuticular cleft, while a cuticular cleft is present in the caudal sucker of male specimens of E. excisus”. “Eustrongylidosis can often be misdiagnosed as starvation in nestling because they are often emaciated at the time of death”.

Before necropsy takes place, diagnosis by palpitation can be used to find tubular lesions. Those tubular lesions are firm, firmly attached to organs, and are felt in the subcutaneous tissue. While palpitation is practical and simple, errors can be made in nestlings’ examinations because their ribs have the potential to present as lesions. Diagnosis is also attainable by examining fecal samples, but has the high potential of false negatives. That possibility is increased in fledging feces “where severe disease may precede appearance of eggs in the feces”.

For the worm, humans are a dead-end host. "Anisakis" and "Pseudoterranova" larvae cannot survive in humans, and eventually die. In some cases, the infection resolves with only symptomatic treatment. In other cases, however, infection can lead to small bowel obstruction, which may require surgery, although treatment with albendazole alone (avoiding surgery) has been reported to be successful. Intestinal perforation (an emergency) is also possible.

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.

Even when the fish is thoroughly cooked, "Anisakis" larvae pose a health risk to humans. Anisakids (and related species such as the sealworm, "Pseudoterranova" species, and the codworm "Hysterothylacium aduncum") release a number of biochemicals into the surrounding tissues when they infect a fish. They are also often consumed whole, accidentally, inside a fillet of fish.

Acute allergic manifestations, such as urticaria and anaphylaxis, may occur with or without accompanying gastrointestinal symptoms. The frequency of allergic symptoms in connection with fish ingestion has led to the concept of gastroallergic anisakiasis, an acute IgE-mediated generalized reaction. Occupational allergy, including asthma, conjunctivitis, and contact dermatitis, has been observed in fish processing workers.

Sensitivization and allergy are determined by skin-prick test and detection of specific antibodies against "Anisakis". Hypersensitivity is indicated by a rapid rise in levels of IgE in the first several days following consumption of infected fish.