The exact nature of the poison is still unclear. In the U.S. outbreak, the source of the fish was traced by the Centers for Disease Control and Prevention, and studies of other fish from the same sources showed a hexane-soluble (and hence non-polar lipid) substance that induced similar symptoms in mice; other food-borne poisons commonly found in fish could not be detected. It cannot be inactivated by cooking, as all six CDC cases had consumed cooked or fried fish. Palytoxin has been proposed as a disease model. It has also been suggested that the toxin may have thiaminase activity (i.e. it degrades thiamine, also known as vitamin B1).

Haff disease (German: "Haffkrankheit") is the development of rhabdomyolysis (swelling and breakdown of skeletal muscle, with a risk of acute kidney failure) within 24 hours of ingesting fish.

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 symptoms and signs of Bright's disease were first described in 1827 by the English physician Richard Bright, after whom the disease was named. In his "Reports of Medical Cases", he described 25 cases of dropsy (edema) which he attributed to kidney disease. Symptoms and signs included: inflammation of serous membranes, hemorrhages, apoplexy, convulsions, blindness and coma. Many of these cases were found to have albumin in their urine (detected by the spoon and candle-heat coagulation), and showed striking morbid changes of the kidneys at autopsy. The triad of dropsy, albumin in the urine and kidney disease came to be regarded as characteristic of Bright's disease. Subsequent work by Bright and others indicated an association with cardiac hypertrophy, which was attributed by Bright to stimulation of the heart. Subsequent work by Mahomed showed that a rise in blood pressure could precede the appearance of albumin in the urine, and the rise in blood pressure and increased resistance to flow was believed to explain the cardiac hypertrophy.

It is now known that Bright's disease is due to a wide range of diverse kidney diseases; thus, the term "Bright's disease" is retained strictly for historical application. The disease was diagnosed frequently in patients with diabetes; at least some of these cases would probably correspond to a modern diagnosis of diabetic nephropathy.

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.

Bright's disease is a historical classification of kidney diseases that would be described in modern medicine as acute or chronic nephritis. It was characterized by swelling, the presence of albumin in the urine and was frequently accompanied by high blood pressure and heart disease.

Pacheco's disease is an acute and often lethal infectious disease in psittacine birds. The disease is caused by a group of herpesviruses, "Psittacid herpesvirus 1" (PsHV-1), which consists of four genotypes. Birds which do not succumb to Pacheco's disease after infection with the virus become asymptomatic carriers that act as reservoirs of the infection. These persistently infected birds, often Macaws, Amazon parrots and some species of conures, shed the virus in feces and in respiratory and oral secretions. Outbreaks can occur when stress causes healthy birds who carry the virus to shed it. Birds generally become infected after ingesting the virus in contaminated material, and show signs of the disease within several weeks.

The main sign of Pacheco's disease is sudden death, sometimes preceded by a short, severe illness. If a bird survives Pacheco's disease following infection with PsHV-1 genotypes 1, 2 or 3, it may later develop internal papilloma disease in the gastrointestinal tract.

Susceptible parrot species include the African gray parrot, and cockatoo. Native Australian birds, such as the eclectus parrot, Bourke's parrot, and budgerigar are susceptible to Pacheco's disease, although the disease itself has not been found in Australia.

After an incubation period of up to seven days, the signs associated with swine vesicular disease occur. The first sign is a transient mild fever. Other signs include:

- Vesicles in the mouth and on the snout and feet

- Lameness and an unsteady gait, shivering and jerking–type leg movements

- Ruptured vesicles can cause ulcers on limbs and feet, and foot pads may be loosened.

Young animals are more severely affected. Recovery often occurs within a week. There is no mortality.

Swine vesicular disease has the same clinical signs as foot-and-mouth disease, and can only be diagnosed by laboratory testing.

Swine vesicular disease (SVD) is an acute, contagious viral disease of swine caused by the swine vesicular disease virus, an enterovirus. It is characterized by fever and vesicles with subsequent ulcers in the mouth and on the snout, feet, and teats. The pathogen is relatively resistant to heat, and can persist for a long time in salted, dried, and smoked meat products. Swine vesicular disease does not cause economically-important disease, but is important due to its similarity to foot-and-mouth disease.

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 .

Pogosta disease is a viral disease, established to be identical with other diseases, Karelian fever and Ockelbo disease. The names are derived from the words Pogosta, Karelia and Ockelbo, respectively.

The symptoms of the disease include usually rash, as well as mild fever and other flu-like symptoms; in most cases the symptoms last less than 5 days. However, in some cases, the patients develop a painful arthritis. There are no known chemical agents available to treat the disease.

It has long been suspected that the disease is caused by a Sindbis-like virus, a positive-stranded RNA virus belonging to the Alphavirus genus and family Togaviridae. In 2002 a strain of Sindbis was isolated from patients during an outbreak of the Pogosta disease in Finland, confirming the hypothesis.

This disease is mainly found in the Eastern parts of Finland; a typical Pogosta disease patient is a middle-aged person who has been infected through a mosquito bite while picking berries in the autumn. The prevalence of the disease is about 100 diagnosed cases every year, with larger outbreaks occurring in 7-year intervals.

Feline spongiform encephalopathy is a disease that affects the brains of felines. It is caused by proteins called prions.

The most common symptoms are diarrhea, abdominal pain, weight loss, and joint pains. The joint pains may be due to migratory non-deforming arthritis, which may occur many years before any digestive tract symptoms develop; they tend to involve the large joints but can occur in any pattern and tend not to damage the joint surface to the point that the joint becomes deformed. Fever and chills occur in a small proportion of people.

In its more advanced form, malabsorption (insufficient absorption of nutrients from the diet) leads to wasting and the enlargement of lymph nodes in the abdomen. Neurological symptoms (discussed below) are more common in those with the severe form of the abdominal disease. Chronic malabsorptive diarrhea leads to the poor absorption of fat, causing steatorrhea (fatty, offensive stool), flatulence, and abdominal distension. Protein-losing enteropathy may also occur, causing depletion of albumin, a blood protein, which may lead to peripheral edema caused by the lowered oncotic pressures.

Hyperpigmentation of the skin occurs in almost half; some also have skin nodules. Various eye problems, such as uveitis, may occur; this is typically associated with deteriorating vision and pain in the affected eye. Endocarditis (infection of the heart valve) has been reported in a small number of cases, sometimes in people with no other symptoms of Whipple's disease; this is typically noticed as breathlessness and leg swelling due to fluid accumulation as the heart is unable to pump fluid through the body.

Of those affected by Whipple's disease, 10–40% of people have problems related to the involvement of the brain; the symptoms relate to the part of the brain that is affected. The most common problems are dementia, memory loss, confusion, and decreased level of consciousness. Eye movement disturbances and myorhythmia (rapidly repetitive movements of the muscles) of the face, together referred to as "oculomasticatory myorhythmia", are highly characteristic for Whipple's disease. Weakness and poor coordination of part of the body, headaches, seizures, as well as a number of more uncommon neurological features, are present in some cases.

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

One of the reasons a cat may stop eating is separation anxiety and the emotional stress that results. Moving, gaining or losing housemates or pets, going on vacation, or prolonged boarding are all common situations that pet owners report just prior to the onset of the disease, but it may develop without these conditions existing. Obesity is known to increase the risk of hepatic lipidosis; however, there is no known "official" cause of the disease. Severe anorexia usually precedes the onset of the disease. When the cat has no energy from eating, the liver must metabolize fat deposits in the body into usable energy to sustain life. The cat liver, however, is poor at metabolizing fat, causing a buildup of fat in the cells of the liver, leading to fatty liver. At this point the disease can be diagnosed; however, it will often not be diagnosed, and many animals are euthanized due to improper or no diagnosis.

Whipple's disease is a rare, systemic infectious disease caused by the bacterium "Tropheryma whipplei". First described by George Hoyt Whipple in 1907 and commonly considered a gastrointestinal disorder, Whipple's disease primarily causes malabsorption but may affect any part of the body including the heart, brain, joints, skin, lungs and the eyes. Weight loss, diarrhea, joint pain, and arthritis are common presenting symptoms, but the presentation can be highly variable and approximately 15% of patients do not have these classic signs and symptoms.

Whipple's disease is significantly more common in men, with 87% of the patients being male. When recognized and treated, Whipple's disease can usually be cured with long-term antibiotic therapy; if the disease is left untreated, it is ultimately fatal.

Diagnosis is based on a circular "bull's-eye" rash at the site of infection called erythema chronicum migrans, which is very similar to that seen in Lyme disease. However, the symptoms of STARI are mild, and resemble influenza, with fatigue, muscle pains, and headache. Fever is sometimes seen, but is not characteristic.

Feline spongiform encephalopathy (FSE) is a prion disease thought to be related or identical to Bovine spongiform encephalopathy (BSE).This disease is known to affect domestic and captive feline species. Lezmi S. et al. (2003), suggested that this infectious agent might be spread by both haematogenous and nervous pathways. Like BSE, this disease can take several years to develop. It is probable, but not proven, that the affected animals contract the disease by eating contaminated bovine meat.

Anorexia always precedes liver disease, with the cat refusing to eat enough food for days, or weeks. This may be amplified by frequent vomiting when the cat does choose to eat. A lack of appetite causes the cat to refuse any food, even after it has purged its system of all stomach contents. Severe weight loss proceeds as the liver keeps the cat alive off body fat, causing a yellowing of the skin (jaundice). When the cat runs out of fat to process, severe muscle wasting (cachexia) takes place as the body converts protein into energy. Eventually the body cannot give the brain enough energy to function properly and the cat dies from malnutrition. In addition, an overworked liver can eventually fail causing total system collapse.

The disease appears to be progressive in nature. The Fields twins started having problems when they were four years old. By the time they had reached the age of nine, they were having difficulty walking and needed frames to assist them with walking. Their muscles have been gradually deteriorating over time. The disease affects the twins' nerves, causing them to make involuntary muscle movements such as trembling in the hands.

The extent of the disease is still unknown as the two women are only 21. However, the disease has had no apparent effect on their brains or personalities. Doctors do not know if the disease is fatal and, if so, what the life expectancy of one with this disease is. If the cause of the disease is genetic, there is a chance that the twins could pass it on to their future children.

Southern tick-associated rash illness (STARI) or Masters' disease is an emerging infectious disease related to Lyme disease that occurs in southeastern and south-central United States. It is spread by tick bites, but the organism that causes the infection is unknown.

Fields' disease is considered to be one of the rarest known diseases in the world, with only two diagnosed cases in history. The frequency of this disease is therefore 1 in approximately 3.75 billion (although since the disease manifested in identical twins, the actual frequency is 1 in approximately 7.5 billion). It is named after Welsh twins Catherine and Kirstie Fields, of Llanelli. Fields' disease is a neuromuscular disease, causing muscular degeneration.

The disease was first noticed when the twins were around the age of four. Doctors have been unable to identify it and have not been able to match it to any known diseases. As a result, the Fields sisters have undergone numerous tests, but no treatment has yet been found. No definitive cause has been determined and doctors have generally concluded that they were born with it.

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.

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.