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.

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.

Adult walnut twig beetles carry spores of the "Geosmithia morbida" fungus, which grows profusely around the pupal chamber of the beetles. Following emergence from trees the beetles subsequently tunnel into branches and trunks of walnut for production of egg galleries or overwintering shelters. The fungus is introduced into the tree during this wounding where it subsequently germinates and grows.

The fungal mycelium initially colonize tissue immediately surrounding the beetle galleries. However, in less than a month black, oval-shaped, inky cankers extend considerably beyond the galleries and may reach more than 3 cm in length in susceptible hosts (e.g., black walnut). In the beginning these cankers develop in phloem and tissues formed by the cork cambium. The affected area is very shallow and never show the ‘open-faced’, perennial, target-shape typical of many canker diseases of trees (e.g., Nectria canker). Instead in TCD the bark remains firmly attached to the canker face making the necrotic areas very difficult to observe. Branch cankers usually are not visible until the outer bark is shaved to expose the beetle tunnels, although during late stages of the disease a dark amber stain may form on the bark surface in association with the cankers.

Each time a beetle tunnels into a tree a canker is initiated. Cankers also may continue to expand and penetrate into the cambium of the tree. Each such injury destroys the phloem and robs the tree of its ability to store and move nutrients. As TCD progresses cankers coalesce to further girdle branches greatly restricting nutrient movement. As the tree declines, more bark beetles are attracted and more cankers are formed.

Eventually the enormous number of beetle attacks and subsequent canker formation overwhelms and kills the tree. Thousand cankers is a progressive disease and its effects result from the culmination of a large number of relatively small cankers over a period of time. Just as a thousand cuts was once used as a form of human execution in Imperial China, black walnuts are subjected to death by thousands of branch and trunk cankers produced by infection from the "Geosmithia" fungus.

In end stages of the disease external symptoms become visible. Leaf yellowing on the exterior of the crown is often the first symptom and may originally be restricted to a single branch. However, as the cumulative effects of the girdling progress increasingly large areas of the tree are affected. Sudden leaf wilting, ultimately involving large limbs, characterizes end stage thousand cankers disease. In susceptible hosts, trees are almost always killed within 2–3 years after external symptoms of leaf yellowing are first observed.

The progress of thousand cankers will vary due to several factors, notably the susceptibility of the host. There appears to be a considerable range of TCD susceptibility among various "Juglans" species with "Juglans nigra" (black walnut) being particularly susceptible. Conversely, Arizona walnut ("Juglans major") appears to be quite resistant to the disease, with bark beetle attacks largely limited to small diameter branches, the fungus growing to a very limited extent, and effects of the disease rarely, if ever, progressing to involve large areas of the tree. Similarly southern California walnut ("Juglans californica") and little walnut ("Juglans microcarpa") may show fairly high resistance. Northern California walnut ("Juglans hindsii") and the commercial nut-producing Persian (English) walnut ("Juglans regia") apparently show various degrees of intermediate TCD susceptibility.

Thousand cankers disease is a recently recognized disease of certain walnuts ("Juglans" spp.). The disease results from the combined activity of the walnut twig beetle ("Pityophthorus juglandis") and a canker producing fungus, "Geosmithia morbida". Until July 2010 the disease was only known to the western United States where over the past decade it has been involved in several large scale die-offs of walnut, particularly black walnut, "Juglans nigra". However, in late July 2010 a well-established outbreak of the disease was found in the Knoxville, Tennessee area. This new finding is the first locating it within the native range of its susceptible host, black walnut.

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.

It has been observed in spiny lobsters ("Panulirus ornatus") in Vietnam, where it is caused by a species of "Fusarium".

It has been observed in shrimp, where the agent is microscopic protozoan "Hyalophysa chattoni" or a close relative, in Galveston Bay, Texas and other locations.

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.

Blackleg, black quarter, quarter evil, or quarter ill () is an infectious bacterial disease most commonly caused by "Clostridium chauvoei", a Gram-positive bacterial species. It is seen in livestock all over the world, usually affecting cattle, sheep, and goats. It has been seen occasionally in farmed bison and deer. The acute nature of the disease makes successful treatment difficult, but an effective vaccine is available to provide animals with protective immunity.

When infection begins, the animal may develop a fever, and the affected limb can feel hot to the touch. The limb usually swells significantly, and the animal can develop lameness on the affected leg. Crepitation (the sensation of air under the skin) can be noticed in many infections, as the area seems to crackle under pressure.

Once clinical signs develop, the animal may only live a short while, sometimes as few as 12 hours. Occasionally, cattle succumb to the disease without showing any symptoms, and only a necropsy reveals the cause. During a necropsy, a diagnosis is usually made very quickly, as the affected muscle is usually mottled with black patches, which are dead tissue, killed by the toxins the bacteria release when they infect live tissue. If viewed under a microscope, small rod-like bacteria can be seen to confirm the diagnosis.

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.

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.

Columnaris (also referred to as cottonmouth) is a symptom of disease in fish which results from an infection caused by the Gram-negative, aerobic, rod-shaped bacterium "Flavobacterium columnare". It was previously known as "Bacillus columnaris, Chondrococcus columnaris, Cytophaga columnaris" and "Flexibacter columnaris". The bacteria are ubiquitous in fresh water, and cultured fish reared in ponds or raceways are the primary concern – with disease most prevalent in air temperatures above 12–14 °C. It is often mistaken for a fungal infection. The disease is highly contagious and the outcome is often fatal. It is not zoonotic.

There are multiple sources known to cause black gill disease. Poor pond conditions can cause debris to build up in the gills turning them black. Certain kinds of bacteria and the fungus genus Fusarium are also known causes.

Black pod disease is caused by many different "Phytophthora spp." pathogens all expressing the same symptoms in cocoa trees ("Theobroma cacao"). This pathogen if left untreated can destroy all yields; annually the pathogen can cause a yield loss of up to 1/3 and up to 10% of total trees can be lost completely. With the value of the cocoa industry throughout the world being so large there are much research and control efforts that go into these "Phytophthora spp." pathogens.

This pathogen can be located anywhere on the cocoa trees but is most noted for the black mummified look it will give to the fruit of the cocoa tree. Staying ahead of the pathogen is the best means of control, the pathogen can be greatly reduced if leaf litter is not allowed to stay on the ground and if the pathogen gets out of hand chemical control can be used. This pathogen is mostly found in tropical areas where the cocoa trees are located and need rainfall in order to spread its spores.

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.

Apple scab is a disease of "Malus" trees, such as apple trees, caused by the ascomycete fungus "Venturia inaequalis". The disease manifests as dull black or grey-brown lesions on the surface of tree leaves, buds or fruits. Lesions may also appear less frequently on the woody tissues of the tree. Fruits and the undersides of leaves are especially susceptible. The disease rarely kills its host, but can significantly reduce fruit yields and fruit quality. Affected fruits are less marketable due to the presence of the black fungal lesions.

Citrus Black Spot is a fungal disease caused by Guignardia citricarpa. This Ascomycete fungus affects citrus plants throughout subtropical climates, causing a reduction in both fruit quantity and quality. Symptoms include both fruit and leaf lesions, the latter being critical to inter-tree dispersal. Strict regulation and management is necessary to control this disease since there are currently no citrus varieties that are resistant.

The smuts are multicellular fungi characterized by their large numbers of teliospores. The smuts get their name from a Germanic word for dirt because of their dark, thick-walled, and dust-like teliospores. They are mostly Ustilaginomycetes (of the class Teliomycetae, subphylum Basidiomycota) and can cause plant disease. The smuts are grouped with the other basidiomycetes because of their commonalities concerning sexual reproduction.

Smuts are cereal and crop pathogens that most notably affect members of the grass family ("Poaceae"). Economically important hosts include maize, barley, wheat, oats, sugarcane, and forage grasses. They eventually hijack the plants' reproductive systems, forming galls which darken and burst, releasing fungal teliospores which infect other plants nearby. Before infection can occur, the smuts need to undergo a successful mating to form dikaryotic hyphae (two haploid cells fuse to form a dikaryon).

As with other enterotoxemias, the disease leads to sudden death. Nevertheless, sheep with previous vaccination can show a protracted course. The rest of the flock may show loss of appetite and pica.

Human’s clinical signs consisted of swelling and eye infections. There were nodules underneath the skin, abscesses or cysts, and lesions running throughout the body. There were papules, plaques and granulomatous damages on the body. In extreme cases there were deep infections within the eyes, bones, heart and central nervous system.

Grapevine trunk diseases (GTD) are the most destructive diseases of vineyards worldwide. Fungicides (such as sodium arsenite or 8-hydroxyquinoline, used to fight esca) with the potential to control GTD have been banned in Europe and there are no highly effective treatments available. Action to develop new strategies to fight these diseases are needed.

The following fungal species are responsible for grapevine trunk diseases:

- "Botryosphaeria dothidea" and other "Botryosphaeria" species, such as , "B. obtusa", "B. parva" and "B. australis",

- "Cylindrocarpon" spp., "Ilyonectria" spp., "Dactylonectria" spp. and "Campylocarpon" spp.(cause of black foot disease)

- "Diplodia seriata" (cause of bot canker)

- "Diplodia mutila" (cause of Botryosphaeria dieback)

- "Dothiorella iberica"

- "Dothiorella viticola"

- "Eutypa lata" (cause of Eutypa dieback)

- "Fomitiporia mediterranea" (cause of esca)

- "Lasiodiplodia theobromae" (cause of Botryosphaeria dieback)

- "Neofusicoccum australe"

- "Neofusicoccum luteum"

- "Neofusicoccom parvum"

- "Phaeoacremonium minimum" (cause of esca and Petri disease) and other "Phaeoacremonium" species

- "Phaeomoniella chlamydospora" (cause of esca and Petri disease)

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.

Bacterial leaf streak (BLS), also known as black chaff, is a common bacterial disease of wheat. The disease is caused by the bacterial species "Xanthomonas translucens" pv. undulosa. The pathogen is found globally, but is a primary problem in the US in the lower mid-south and can reduce yields by up to 40 percent. BLS is primarily seed-borne (the disease is transmitted by seed) and survives in and on the seed, but may also survive in crop residue in the soil in the off-season. During the growing season, the bacteria may transfer from plant to plant by contact, but it is primarily spread by rain, wind and insect contact. The bacteria thrives in moist environments, and produces a cream to yellow bacterial ooze, which, when dry, appears light colored and scale-like, resulting in a streak on the leaves. The invasion of the head of wheat causes bands of necrotic tissue on the awns, which is called Black Chaff.

The disease is not easily managed, as there are no pesticides on the market for treatment of the infection. There are some resistant cultivars available, but no seed treatment exists. Some integrated pest management (IPM) techniques may be used to assist with preventing infection although, none will completely prevent the disease.

Peritoneal and thoracic cavities contains a great quantity of fluids, as does the pericardial sac.

The liver is sometimes swollen with perihepatitis. There appear a great number of necrotic foci, 3 to 4 mm diameter, which extend deeply in the organ. Hepatic lymph nodes are enlarged. The gallbladder is full.

Subcutaneous tissues are full of cyanotic venous blood. They may darken the hide, hence the name "black disease".

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.