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.

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 .

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 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.

Zymotic disease was a 19th-century medical term for acute infectious diseases, especially "chief fevers and contagious diseases (e.g. typhus and typhoid fevers, smallpox, scarlet fever, measles, erysipelas, cholera, whooping-cough, diphtheria, &c.)".

Zyme or microzyme was the name of the organism presumed to be the cause of the disease.

As originally employed by Dr W. Farr, of the British Registrar-General's department, the term included the diseases which were "epidemic, endemic and contagious," and were regarded as owing their origin to the presence of a morbific principle in the system, acting in a manner analogous to, although not identical with, the process of fermentation.

In the late 19th century, Antoine Béchamp proposed that tiny organisms he termed "microzymas", and not cells, are the fundamental building block of life. Bechamp claimed these microzymas are present in all things—animal, vegetable, and mineral—whether living or dead . Microzymas are what coalesce to form blood clots and bacteria. Depending upon the condition of the host, microzymas assume various forms. In a diseased body, the microzymas become pathological bacteria and viruses. In a healthy body, microzymas form healthy cells. When a plant or animal dies, the microzymas live on. His ideas did not gain acceptance.

The word "zymotic" comes from the Greek word ζυμοῦν "zumoûn" which means "to ferment". It was in British official use from 1839. This term was used extensively in the English Bills of Mortality as a cause of death from 1842. Robert Newstead (1859–1947) used this term in a 1908 publication in the "Annals of Tropical Medicine and Parasitology", to describe the contribution of house flies ("Musca domestica") towards the spread of infectious diseases. However, by the early 1900s, bacteriology "displaced the old fermentation theory", and so the term became obsolete.

In her "Diagram of the causes of mortality in the army in the East", Florence Nightingale depicts The blue wedges measured from the centre of the circle represent area for area the deaths from Preventible or Mitigable Zymotic diseases ; the red wedges measured from the centre the deaths from wounds, & the black wedges measured from the centre the deaths from all other causes.

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.

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.

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.

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

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.

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.

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.

Six syndromes are known to occur after infection with Marek's disease. These syndromes may overlap.

- Classical Marek's disease or neurolymphomatosis causes asymmetric paralysis of one or more limbs. With vagus nerve involvement, difficulty breathing or dilation of the crop may occur. Besides lesions in the peripheral nerves, there are frequently lymphomatous infiltration/tumours in the skin, skeletal muscle, visceral organs. Organs that are commonly affected include the ovary, spleen, liver, kidneys, lungs, heart, proventriculus and adrenals.

- Acute Marek's disease is an epidemic in a previously uninfected or unvaccinated flock, causing depression, paralysis, and death in a large number of birds (up to 80%). The age of onset is much earlier than the classic form; birds are four to eight weeks old when affected. Infiltration into multiple organs/tissue is observed.

- Ocular lymphomatosis causes lymphocyte infiltration of the iris (making the iris turn grey), unequal size of the pupils, and blindness.

- Cutaneous Marek's disease causes round, firm lesions at the feather follicles.

- Atherosclerosis is induced in experimentally infected chickens.

- Immunosuppression – Impairment of the T-lymphocytes prevents competent immunological response against pathogenic challenge and the affected birds become more susceptible to disease conditions such as coccidiosis and "Escherichia coli" infection . Furthermore, without stimulation by cell-mediated immunity, the humoral immunity conferred by the B-cell lines from the Bursa of Fabricius also shuts down, thus resulting in birds that are totally immunocompromised.

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.

Marek's disease is a highly contagious viral neoplastic disease in chickens. It is named after József Marek, a Hungarian veterinarian. Marek's disease is caused by an alphaherpesvirus known as 'Marek's disease virus' (MDV) or "Gallid alphaherpesvirus 2" (GaHV-2). The disease is characterized by the presence of T cell lymphoma as well as infiltration of nerves and organs by lymphocytes. Viruses "related" to MDV appear to be benign and can be used as vaccine strains to prevent Marek's disease. For example, the related Herpesvirus of Turkeys (HVT), causes no apparent disease in turkeys and continues to be used as a vaccine strain for prevention of Marek's disease (see below). Birds infected with GaHV-2 can be carriers and shedders of the virus for life. Newborn chicks are protected by maternal antibodies for a few weeks. After infection, microscopic lesions are present after one to two weeks, and gross lesions are present after three to four weeks. The virus is spread in dander from feather follicles and transmitted by inhalation.

Kyrle disease symptoms are chronic and have an onset during adulthood between the ages of 30 and 50 years of age. However, there were reported cases of early onset as early as 5 years of age and late onset as late as 75 years of age. The main symptom is the development of small papules into painless lesions that are surrounded by silvery scales. The lesions are painless, however, there is a chance that the patient may experience extreme urges to itch them. In time, these lesions grow up to a radius of 0.75 inch and develop into red-brown nodules with a central plug of keratin. As more lesions develop, they can come together and form larger keratotic plaques. These lesions are usually observed on the lower extremities, however, can also develop on the upper extremities, such as, the arms, the head and the neck. The only parts of the body that Kyrle disease do not form are the palms, soles, and mucous membranes. Lesions may heal spontaneously without treatment, however, new ones will develop in its place.

Other symptoms that may be observed:

- Hyperkeratotic cone-shaped papular plugs

- Hyperkeratotic verrucous plaques

- Diabetes mellitus

- Hepatic insufficiency

- Presence of albumin in the urine

- Excess sugar in the urine

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.

White band disease causes the affected coral tissue to decorticate off the skeleton in a white uniform band for which the disease was given its name. The band, which can range from a few millimeters to 10 centimeters wide, typically works its way from the base of the coral colony up to the coral branch tips. The band progresses up the coral branch at an approximate rate of 5 millimeters per day, causing tissue loss as it works its way to the branch tips. After the tissue is lost, the bare skeleton of the coral may later by colonized by filamentous algae.

There are two variants of white band disease, type I and type II. In Type I of white band disease, the tissue remaining on the coral branch shows no sign of coral bleaching, although the affected colony may appear lighter in color overall. However, a variant of white band disease, known simply as white band disease Type II, which was found on Staghorn colonies near the Bahamas, does produce a margin of bleached tissue before it is lost. Type II of white band disease can be mistaken for coral bleaching. By examining the remaining living coral tissue for bleaching, one can delineate which type of the disease affects a given coral.

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.

Kyrle disease or hyperkeratosis follicularis et parafollicularis in cutem penetrans is identified as a form of an acquired perforating disease. Other major perforating diseases are elastosis perforans serpiginosa and reactive perforating collagenosis. Recently, however, there is a controversy on categorizing Kyrle disease with perforating dermatosis or a subtype of acquired perforating collagenosis.

Kyrle disease was first described by Josef Kyrle in 1916 when a diabetic woman presented generalized hyperkeratotic nodules. The disease is distinguished by large papules with central keratin plus on the skin, usually on the legs of the patient and is often in conjunction with hepatic, renal or diabetic disorders. It can affect both females and males with a 6:1 ratio. The papules usually show up on the patient with an average age of 30 years. Kyrle disease is a rare disease unless there is a high count of patients with chronic renal failure. The disease seems to be more prevalent in African Americans, which can be correlated to the high incidence of diabetes mellitus and renal failure in the population.

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.

The most common presentation of Milroy Disease is bilateral lower extremity lymphedema, and may also be accompanied by hydrocele.

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.

CNS involvement most often occurs as a chronic meningoencephalitis. Lesions tend to occur in the brainstem, the basal ganglia and deep hemispheric white matter and may resemble those of MS. Brainstem atrophy is seen in chronic cases.

Neurological involvements range from aseptic meningitis to vascular thrombosis such as dural sinus thrombosis and organic brain syndrome manifesting with confusion, seizures, and memory loss. Sudden hearing loss (Sensorineural) is often associated with it. They often appear late in the progression of the disease but are associated with a poor prognosis.

Arthralgia is seen in up to half of people, and is usually a non-erosive poly or oligoarthritis primarily of the large joints of the lower extremities.