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.

Host tropism is the infection specificity of certain pathogens to particular hosts and host tissues. This type of tropism explains why most pathogens are only capable of infecting a limited range of host organisms.

Researchers can classify pathogenic organisms by the range of species and cell types that they exhibit host tropism for. For instance, pathogens that are able to infect a wide range of hosts and tissues are said to be amphotropic. Ecotropic pathogens, on the other hand, are only capable of infecting a narrow range of hosts and host tissue. Knowledge of a pathogen's host specificity allows professionals in the research and medical industries to model pathogenesis and develop vaccines, medication, and preventative measures to fight against infection. Methods such as cell engineering, direct engineering and assisted evolution of host-adapted pathogens, and genome-wide genetic screens are currently being used by researchers to better understand the host range of a variety of different pathogenic organisms.

Bacterial wilt of turfgrass is the only known bacterial disease of turf. The causal agent is the Gram negative bacterium Xanthomonas campestris pv. graminis. The first case of bacterial wilt of turf was reported in a cultivar of creeping bentgrass known as Toronto or C-15, which is found throughout the midwestern United States. Until the causal agent was identified in 1984, the disease was referred to simply as C-15 decline. This disease is almost exclusively found on putting greens at golf courses where extensive mowing creates wounds in the grass which the pathogen uses in order to enter the host and cause 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.

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.

The foamy bark canker is a disease affecting oak trees in California caused by the fungus "Geosmithia pallida" and spread by the Western oak bark beetle ("Pseudopityopthorus pubipennis"). This disease is only seen through the symbiosis of the bark beetles and the fungal pathogen. The bark beetles target oak trees and bore holes through the peridermal tissues, making tunnels within the phloem. The fungal spores are brought into these tunnels by the beetles and begin to colonize the damaged cells inside the tunnels. Symptoms of the developing fungus include wet discoloration seeping from the beetle entry holes as the fungus begins to consume phloem and likely other tissues. If bark is removed, necrosis of the phloem can be observed surrounding the entry hole(s). As the disease progresses, a reddish sap and foamy liquid oozes from entry holes, thus giving the disease the name Foamy bark canker. Eventually after the disease has progressed, the tree dies. This disease is important because of its detrimental effects on oak trees and its ability to spread to several new Californian counties in just a couple years.

Creeping bentgrass ("Agrostis stolonifera") and annual bluegrasses ("Poa annua") are the makeup of most putting greens, as well as the preferred hosts of this pathogen. Specifically, Toronto (C-15), Seaside, and Nemisilla are the cultivars of creeping bentgrass most commonly affected. The bacteria enter the plant host and interfere with water and nutrient flow, causing the plant to look drought stressed and to take on a blueish-purple color. Additionally, symptoms of bacterial wilt of turf grass include yellow leaf spots, tan or brown spots, water soaked lesions, elongated yellow leaves and shriveling of aforementioned blue or dark green leaves.Since putting greens are not a pure stand of turf, some grass blades may be resistant to the bacterium and thus remain unharmed while the surrounding turf dies, rendering the putting surface inconsistent and unsightly, especially at high-end golf courses.

Wheat yellow rust ("Puccinia striiformis" f.sp. "tritici"), also known as stripe rust, is one of the three wheat rust diseases principally found in wheat grown in cooler environments. Such locations are generally associated with northern latitudes or cooler seasons.

Hosts associated with "Geosmithia pallida" include a number of tree species, including oak and other hardwoods, pine and spruce trees, depending on the beetle vector. In this case, the western oak bark beetles target live oak trees of western United States. Beetles tend to attack stressed trees that are already weakened from drought or injury. Symptoms causing branch dieback and tree death also include a cinnamon-colored gum seeping from multiple beetle entry holes on the bole, followed by a prolific, cream-colored foamy liquid. These symptoms, as well as signs (entry holes, larvae, beetles) of bark beetles, are key factors in diagnosis. Necrosis of xylem and phloem tissues underneath bark can be observed.

Common Symptoms:

- Wet discoloration on bark

- Phloem necrosis

- Beetle entry holes

- Reddish sap oozing from entry holes

- Foamy liquid from entry holes

"Rabbits, Hares & Lagomorphs"

Usually there do not appear to be any clinical signs. Subcutaneous cysts, warbles, may present upon larval deposition out of the body at maturation.

"Felines & Canines"

There are three forms in which Cuterebriasis may present:

- Myasis

- Cerebrospinal

- Respiratory

Myasis involves subcutaneous cyst formation due to 3rd larval instar maturation, occurring ~30 days post-entry into the body. Cysts are often found on the face, neck and trunk, but location varies with larval migration within the host. Serous discharge may be observed from these cysts, which are typically 3-5mm in diameter and include a central pore through which the larvae respire. This pore also serves as a means of exit for the larvae, which occurs anywhere between 3 and 8 weeks post-entry.

Cerebrospinal cuterebriasis results from larval migration to the brain. This is seen in cats, and is the proposed cause for feline ischemic encephalopathy and a suggestive causative agent of feline idiopathic vestibular disease. Symptoms of this type of presentation include lethargy, seizures, blindness, abnormal vocalization or gait, circling, and abnormal or no reflex responses. When affecting the central nervous system, cats are known to exhibit violent sneezing attacks that can onset weeks prior to manifestation of other clinical signs.

Respiratory disease results when larval migration occurs through the trachea, pharynx, diaphragm, or lungs. Cuterebriasis has been increasingly noted as a cause for dyspnea in felines.

Yersinia pseudotuberculosis is a Gram-negative bacterium that causes Far East scarlet-like fever in humans, who occasionally get infected zoonotically, most often through the food-borne route. Animals are also infected by "Y. pseudotuberculosis". The bacterium is urease positive.

Gaffkaemia (gaffkemia in American English) is a bacterial disease of lobsters, caused by the Gram-positive lactic acid bacterium Aerococcus viridans" var. "homari.

Cuterebriasis is a parasitic disease affecting rodents, lagomorphs (hares, rabbits, pikas), felines and canines. The etiologic agent is the larval development of bot flies within the "Cuterebra" or "Trypoderma" genera, which occurs obligatorily in rodents and lagomorphs, respectively. Felines and canines serve as accidental hosts, but research suggests only by "Trypoderma" spp. Entrance into the body by first instar larva occurs via mucous membranes of natural orifices or open wounds as opposed to direct dermic penetration.

As R.P. Singh, J. Huerta-Espino, and A.P. Roelfs say in their (undated) comprehensive review of literature on the wheat rusts for UN FAO:

"Although Gadd first described stripe rust of wheat in 1777, it was not until 1896 that Eriksson and Henning (1896) showed that stripe rust resulted from a separate pathogen, which they named P. glumarum. In 1953, Hylander et al. (1953) revived the name P. striiformis."

"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.

The effects of gaffkaemia infection include lethargy (typically seen as a drooping tail), anorexia and a pink colour on the ventral side of the abdomen, which gives the disease its alternative common name of red tail disease. When lobsters are moribund, they may lie on their sides, and frequently lose appendages. The effects of gaffkaemia are slowed by low temperatures, such that death can occur within two days of infection at , but can take over 60 days at .

As few as five bacteria can lead to clinical disease. When they enter the host, the bacteria colonise the heart and hepatopancreas. They may be engulfed by phagocytosis into the lobster's blood cells, but continue to survive within the blood cells, feeding on the cytoplasm. The lobster's blood cell count drops, and the infection develops into septicaemia. The stores of glycogen in the hepatopancreas become depleted, concentrations of glucose and lactic acid in the blood drop, and concentrations of adenosine triphosphate in muscles also fall. In a severe infection, the ability of the lobster's blood pigment haemocyanin to carry oxygen may be reduced by up to 50%.

Half of all children and a quarter of previously healthy adults are asymptomatic with "Babesia" infection. When people do develop symptoms, the most common are fever and hemolytic anemia, symptoms that are similar to those of malaria. People with symptoms usually become ill 1 to 4 weeks after the bite, or 1 to 9 weeks after transfusion of contaminated blood products. A person infected with babesiosis gradually develops malaise and fatigue, followed by a fever. Hemolytic anemia, in which red blood cells are destroyed and removed from the blood, also develops. Chills, sweats, and thrombocytopenia are also common symptoms. Symptoms may last from several days to several months.

Less common symptoms and physical exam findings of mild-to-moderate babesiosis:

In more severe cases, symptoms similar to malaria occur, with fevers up to 40.5 °C (105 °F), shaking chills, and severe anemia (hemolytic anemia). Organ failure may follow, including adult respiratory distress syndrome. Severe cases occur mostly in people who have had a splenectomy. Severe cases are also more likely to occur in the very young, very old, and persons with immunodeficiency, such as HIV/AIDS patients.

A reported increase in human babesiosis diagnoses in the 2000s is thought to be caused by more widespread testing and higher numbers of people with immunodeficiencies coming in contact with ticks, the disease vector. Little is known about the occurrence of "Babesia" species in malaria-endemic areas, where "Babesia" can easily be misdiagnosed as "Plasmodium". Human patients with repeat babesiosis infection may exhibit premunity.

Acanthocheilonemiasis is a rare tropical infectious disease caused by a parasite known as "Acanthocheilonema perstans". It can cause skin rashes, abdominal and chest pains, muscle and joint pains, neurological disorders and skin lumps. It is mainly found in Africa. The parasite is transmitted through the bite of small flies. Studies show that there are elevated levels of white blood cells.

Acanthocheilonemiasis belongs to a group of parasitic diseases known as filarial disease (nematode), all of which are classified as Neglected Tropical Diseases. Filarial disease results when microfilariae, which are nematode larvae, reach the lymphatic system; microfilariae reside in the serous cavities of humans. They have a five-stage life cycle that includes birth to thousands of live microfilariae within the host (i.e. human body), and then translocation via blood meal to the dermis layer of the skin. It is here that microfilariae cause major symptoms, which are edema and thickening of the skin and underlying connective tissues. It can also cause skin rashes, abdominal and chest pains, muscle (myalgia) and joint pains, neurological disorders and skin lumps. In addition, it causes spleen and liver enlargement, which is called hepatosplenomegaly. Studies show elevated levels of leukocytes, or white blood cells, which is referred to as eosinophilia. It is mainly found in Africa. The parasite is transmitted through the bite of small flies ("A. coliroides").

Swine brucellosis is a zoonosis affecting pigs, caused by the bacterium "Brucella suis". The disease typically causes chronic inflammatory lesions in the reproductive organs of susceptible animals or orchitis, and may even affect joints and other organs. The most common symptom is abortion in pregnant susceptible sows at any stage of gestation. Other manifestations are temporary or permanent sterility, lameness, posterior paralysis, spondylitis, and abscess formation. It is transmitted mainly by ingestion of infected tissues or fluids, semen during breeding, and suckling infected animals.

Since brucellosis threatens the food supply and causes undulant fever, "Brucella suis" and other "Brucella" species ("B. melitensis, B. abortis, B. ovis, B. canis") are recognized as potential agricultural, civilian, and military bioterrorism agents.

All fish carry pathogens and parasites. Usually this is at some cost to the fish. If the cost is sufficiently high, then the impacts can be characterised as a disease. However disease in fish is not understood well. What is known about fish disease often relates to aquaria fish, and more recently, to farmed fish.

Disease is a prime agent affecting fish mortality, especially when fish are young. Fish can limit the impacts of pathogens and parasites with behavioural or biochemical means, and such fish have reproductive advantages. Interacting factors result in low grade infection becoming fatal diseases. In particular, things that causes stress, such as natural droughts or pollution or predators, can precipitate outbreak of disease.

Disease can also be particularly problematic when pathogens and parasites carried by introduced species affect native species. An introduced species may find invading easier if potential predators and competitors have been decimated by disease.

Pathogens which can cause fish diseases comprise:

- viral infections, such as esocid lymphosarcoma found in "Esox" species.

- bacterial infections, such as "Pseudomonas fluorescens" leading to fin rot and fish dropsy

- fungal infections

- water mould infections, such as "Saprolegnia" sp.

- metazoan parasites, such as copepods

- unicellular parasites, such as "Ichthyophthirius multifiliis" leading to ich

- Certain parasites like Helminths for example "Eustrongylides"

The most frequent clinical sign following "B. suis" infection is abortion in pregnant females, reduced milk production, and infertility. Cattle can also be transiently infected when they share pasture or facilities with infected pigs, and "B. suis" can be transmitted by cow’s milk.

Swine also develop orchitis (swelling of the testicles), lameness (movement disability), hind limb paralysis, or spondylitis (inflammation in joints).

Babesiosis is a malaria-like parasitic disease caused by infection with "Babesia", a genus of Apicomplexa. Human babesiosis is an uncommon but emerging disease in the Northeastern and Midwestern United States and parts of Europe, and sporadic throughout the rest of the world. It occurs in warm weather. Ticks transmit the human strain of babesiosis, so it often presents with other tick-borne illnesses such as Lyme disease. After trypanosomes, "Babesia" is thought to be the second-most common blood parasite of mammals, and they can have a major impact on health of domestic animals in areas without severe winters. In cattle, a major host, the disease is known as Texas cattle fever, redwater, or piroplasmosis.

Although tapeworms in the intestine usually cause no symptoms, some people experience upper abdominal discomfort, diarrhea, and loss of appetite. Anemia may develop in people with the fish tapeworm. Infection is generally recognized when the infected person passes segments of proglottids in the stool (which look like white worms), especially if a segment is moving.

Rarely, worms may cause obstruction of the intestine, and very rarely, T. solium larvae can migrate to the brain causing severe headaches, seizures and other neurological problems. Neurocysticercosis can progress for years before the patient displays symptoms.

In at least one case, cancer cells from a tapeworm spread to the human host in an immunocompromised man, producing swelling, obstructions, and other conventional symptoms of human-originated cancer.

In animals, "Y. pseudotuberculosis" can cause tuberculosis-like symptoms, including localized tissue necrosis and granulomas in the spleen, liver, and lymph nodes.

In humans, symptoms of Far East scarlet-like fever are similar to those of infection with "Yersinia enterocolitica" (fever and right-sided abdominal pain), except that the diarrheal component is often absent, which sometimes makes the resulting condition difficult to diagnose. "Y. pseudotuberculosis" infections can mimic appendicitis, especially in children and younger adults, and, in rare cases, the disease may cause skin complaints (erythema nodosum), joint stiffness and pain (reactive arthritis), or spread of bacteria to the blood (bacteremia).

Far East scarlet-like fever usually becomes apparent five to 10 days after exposure and typically lasts one to three weeks without treatment. In complex cases or those involving immunocompromised patients, antibiotics may be necessary for resolution; ampicillin, aminoglycosides, tetracycline, chloramphenicol, or a cephalosporin may all be effective.

The recently described syndrome "Izumi-fever" has been linked to infection with "Y. pseudotuberculosis".

The symptoms of fever and abdominal pain mimicking appendicitis (actually from mesenteric lymphadenitis) associated with "Y. pseudotuberculosis" infection are not typical of the diarrhea and vomiting from classical food poisoning incidents. Although "Y. pseudotuberculosis" is usually only able to colonize hosts by peripheral routes and cause serious disease in immunocompromised individuals, if this bacterium gains access to the blood stream, it has an LD comparable to "Y. pestis" at only 10 CFU.