Symptoms may include fever and headache, but the distinguishing characteristic of this disease is attacks of severe pain in the lower chest, often on one side. The slightest movement of the rib cage causes a sharp increase of pain, which makes it very difficult to breathe, and an attack is therefore quite a frightening experience, although it generally passes off before any actual harm occurs. The attacks are unpredictable and strike "out of the blue" with a feeling like an iron grip around the rib cage. The colloquial names for the disease, such as 'The Devil's grip' (see also "other names" below) reflect this symptom.

Inoculation of throat washings taken from people with pleurodynia into the brains of newborn mice revealed that enteroviruses in the Coxsackie B virus group were likely to be the cause of pleurodynia, and those findings were supported by subsequent studies of IgM antibody responses measured in serum from people with pleurodynia. Other viruses in the enterovirus family, including echovirus and Coxsackie A virus, are infrequently associated with pleurodynia.

Barcoo fever is an illness once common in the Australian outback that is now virtually unknown. It was characterised by nausea and vomiting exacerbated by the sight or smell of food and, unlike the usual gastro-intestinal infections, by constipation rather than diarrhoea. Fever and myalgia were also symptoms. Severe cases developed inanition and even death. It was seen in travelers in the outback rather than in cities or towns, but occasionally entire settlements were affected, such as occurred in Toowoomba in 1903. The aboriginal population knew to avoid the ailment by not drinking from certain water sources and by taking water from soaks or pits dug in the dry sandy bed of a stream.

It is postulated that the disease may be due to ingestion of cyanobacterial (blue-green algal) toxins, in particular cylindrospermopsin, a toxin from "Cylindrospermopsis raciborskii" and other cyanobacteria, which is a hepatotoxin. The symptoms of the disease are consistent with a hepatitis or liver disorder, and "Cylindrospermopsis" is known to be widespread in inland Australian water sources. The toxin is not destroyed by boiling and, although it would flavor water, this flavor would be masked by tea, the common beverage in the Australian bush. Provision of safe drinking water sources in Australia, with the development of bores and covered tanks to collect rainwater, explain the demise of a once-common illness.

Listeriosis is a bacterial infection most commonly caused by "Listeria monocytogenes", although "L. ivanovii" and "L. grayi" have been reported in certain cases. "Listeria" primarily causes infections of the central nervous system (meningitis, meningoencephalitis, brain abscess, cerebritis) and bacteremia in those who are immunocompromised, pregnant women, and those at the extremes of age (newborns and the elderly), as well as gastroenteritis in healthy persons who have been severely infected. "Listeria" is ubiquitous and is primarily transmitted via the oral route after ingestion of contaminated food products, after which the organism penetrates the intestinal tract to cause systemic infections. The diagnosis of listeriosis requires the isolation of the organism from the blood and/or the cerebrospinal fluid. Treatment includes prolonged administration of antibiotics, primarily ampicillin and gentamicin, to which the organism is usually susceptible.

The disease primarily affects older adults, persons with weakened immune systems, pregnant women, and newborns. Rarely, people without these risk factors can also be affected. A person with listeriosis usually has fever and muscle aches, often preceded by diarrhea or other gastrointestinal symptoms. Almost everyone who is diagnosed with listeriosis has invasive infection (meaning that the bacteria spread from their intestines to their blood stream or other body sites). Disease may occur as much as two months after eating contaminated food.

The symptoms vary with the infected person:

- High-risk persons other than pregnant women: Symptoms can include fever, muscle aches, headache, stiff neck, confusion, loss of balance, and convulsions.

- Pregnant women: Pregnant women typically experience only a mild, flu-like illness. However, infections during pregnancy can lead to miscarriage, stillbirth, premature delivery, or life-threatening infection of the newborn.

- Previously healthy persons: People who were previously healthy but were exposed to a very large dose of Listeria can develop a non-invasive illness (meaning that the bacteria have not spread into their blood stream or other body sites). Symptoms can include diarrhea and fever.

If an animal has eaten food contaminated with Listeria and does not have any symptoms, most experts believe that no tests or treatment are needed, even for people at high risk for listeriosis.

Necrotising hepatopancreatitis (NHP), is also known as Texas necrotizing hepatopancreatitis (TNHP), Texas Pond Mortality Syndrome (TPMS) and Peru necrotizing hepatopancreatitis (PNHP), is a lethal epizootic disease of farmed shrimp. It is not very well researched yet, but generally assumed to be caused by a bacterial infection.

NHP mainly affects the farmed shrimp species "Litopenaeus vannamei" (Pacific white shrimp) and "Litopenaeus stylirostris" (Western blue shrimp), but has also been reported in three other American species, namely "Farfantepenaeus aztecus", "Farfantepenaeus californiensis", and "Litopenaeus setiferus". The highest mortality rates occur in "L. vannamei", which is one of the two most frequently farmed species of shrimp. Untreated, the disease causes mortality rates of up to 90 percent within 30 days. A first outbreak of NHP had been reported in Texas in 1985; the disease then spread to shrimp aquacultures in South America, in 2009 to China and subsequently Southeast Asia, followed by massive outbreaks in that region in 2012-2013.

NHP is associated with a small, gram-negative, and highly pleomorphic "Rickettsia"-like bacterium that belongs to its own, new genus in the alpha proteobacteria. However, in early-2013 a novel strain of "Vibrio parahaemolyticus" was identified as a more likely causative agent, though involvement of a virus cannot be definitely ruled out yet.

The aetiological agent is the pathogenic agent Candidatus "Hepatobacter penaei", an obligate intracellular bacterium of the Order α-Proteobacteria.

Infected shrimps show gross signs including soft shells and flaccid bodies, black or darkened gills, dark edges of the pleopods, and uropods, and an atrophied hepatopancreas that is whitish instead of orange or tan as is usual.

Whichever of the two bacteria associated with NHP actually causes it, the pathogen seems to prefer high water temperatures (above ) and elevated levels of salinity (more than 20–38 ppt). Avoiding such conditions in shrimp ponds is thus an important disease control measure.

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.

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.

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.

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.

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.

Classically, patients with chronic granulomatous disease will suffer from recurrent bouts of infection due to the decreased capacity of their immune system to fight off disease-causing organisms. The recurrent infections they acquire are specific and are, in decreasing order of frequency:

- pneumonia

- abscesses of the skin, tissues, and organs

- suppurative arthritis

- osteomyelitis

- bacteremia/fungemia

- superficial skin infections such as cellulitis or impetigo

Most people with CGD are diagnosed in childhood, usually before age 5. Early diagnosis is important since these people can be placed on antibiotics to ward off infections before they occur. Small groups of CGD patients may also be affected by McLeod syndrome because of the proximity of the two genes on the same X-chromosome.

Sudden Death Syndrome (SDS) in Soybean plants quickly spread across the southern United States in the 1970s, eventually reaching most agricultural areas of the US. SDS is caused by a Fusarium fungi, more specifically the soil borne root pathogen "Fusarium virguliforme," formerly known as "Fusarium solani" f. sp. "glycines"."." Losses could exceed hundreds of millions of dollars in US soybean markets alone making it one of the most important diseases found in Soybeans across the US

The areas most affected are the toes, fingers, earlobes, nose.

- Blistering of affected area

- Burning and itching sensation in extremities

- Dermatitis in extremities

- Digital ulceration (severe cases only)

- Erythema (blanchable redness of the skin)

- Pain in affected area

- Skin discoloration, red to dark blue

Chilblains usually heal within 7–14 days.

Symptoms of cerebellar abiotrophy include ataxia or lack of balance, an awkward wide-legged stance, a head tremor (intention tremor) (in dogs, body tremors also occur), hyperreactivity, lack of menace reflex, stiff or high-stepping gait, coarse or jerky head bob when in motion (or in very young animals, when attempting to nurse), apparent lack of awareness of where the feet are (sometimes standing or trying to walk with a foot knuckled over), poor depth perception, and a general inability to determine space and distance. The symptoms, when taken as a group, are distinctive and not easily mimicked by other illnesses, though certain types of neurological injury and infection need to be ruled out. Verifying the diagnosis in a laboratory setting is possible only by examining the brain post-mortem to determine if there has been a loss of Purkinje cells.

Most affected animals have normal intelligence and mildly affected animals can, in theory, live out a normal lifespan. However, affected animals are quite accident-prone, and for this reason many animals that develop CA, particularly horses, are euthanized for humane reasons. Horses may experience difficulty stepping up and over objects, run into fences, fall easily, and even if allowed to mature to full growth, are generally considered unsafe to ride. Dogs may need lifetime assistance with tasks such as climbing stairs.

In horses, the symptoms may worsen from the time of onset for six to 12 months, but if not severe enough to mandate euthansia, they stabilize over time. In some dog breeds, symptoms appear to progressively worsen, but research is not consistent on this point. There also is some evidence that affected animals partially compensate for the condition by cognitively learning alternative methods for moving or to determine distance, and thus appear to improve because they become less accident-prone.

Most of the SDS symptoms can be confused with other factors like nutrient deficiencies and some other diseases like brown stem rot and stem canker. Usually the first symptom seen is interveinal chlorosis, which is the yellowing of the plant material between the leaf veins. When leaves begin to die, puckering and mottling can also be observed along with the chlorosis. As severity increases, necrosis (death of cells) occurs and eventually these leaves will fall off, leaving only petioles left on the stem. If the conditions are right (cool and wet), these symptoms can appear suddenly, causing large yield reductions. Normally, this is seen in mid or late July around the time of flowering and pod production.

In addition to foliar symptoms, the stem of the soybean plant can show symptoms as well. If a soybean stem with SDS is split, the pith will be visibly white while the cortical tissue around the pith will be tan to light brown in color. If the pith is brown in color (or if the whole stem looks brown on the inside), it is likely that the plant has brown stem rot, rather than SDS

Along with the above ground foliar and stem symptoms, the roots usually show some kind of rotting and decrease in vigor compared to other healthy soybean roots. If soil conditions are moist, roots are also likely to show blue masses of spores (macroconidia) around the taproot just below the soil surface. Blue fungal masses, found along with the foliar and stem symptoms, are strong diagnostic indicators for SDS

Infants with Krabbe disease are normal at birth. Symptoms begin between the ages of 3 and 6 months with irritability, fevers, limb stiffness, seizures, feeding difficulties, vomiting, and slowing of mental and motor development. In the first stages of the disease, doctors often mistake the symptoms for those of cerebral palsy. Other symptoms include muscle weakness, spasticity, deafness, optic atrophy, optic nerve enlargement, blindness, paralysis, and difficulty when swallowing. Prolonged weight loss may also occur. Juvenile- and adult-onset cases of Krabbe disease also occur, which have similar symptoms but slower progression.

Chilblains — also known as pernio, chill burns and perniosis — is a medical condition that occurs when a predisposed individual is exposed to cold and humidity, causing tissue damage. It is often confused with frostbite and trench foot. Damage to capillary beds in the skin causes redness, itching, inflammation, and sometimes blisters. Chilblains can be reduced by keeping the feet and hands warm in cold weather, and avoiding extreme temperature changes. Chilblains can be idiopathic (spontaneous and unrelated to another disease), but may also be a manifestation of another serious medical condition that must be investigated. A history of chilblains suggests a connective tissue disease (such as lupus). In infants, chilblains together with severe neurologic disease and unexplained fevers occurs in Aicardi–Goutières syndrome, a rare inherited condition.

Krabbe disease (KD) (also known as globoid cell leukodystrophy or galactosylceramide lipidosis) is a rare and often fatal lysosomal storage disease which results in progressive damage to the nervous system. KD involves dysfunctional metabolism of sphingolipids and is inherited in an autosomal recessive pattern. The disease is named after the Danish neurologist Knud Krabbe (1885–1965).

New York, Missouri and Kentucky include Krabbe in the newborn screening panel.

Cerebellar abiotrophy (CA), also referred to as the cerebellar cortical abiotrophy (CCA), is a genetic neurological disease in animals best known to affect certain breeds of horses, dogs and cats. It can also develop in humans. It develops when the neurons known as Purkinje cells, located in the cerebellum of the brain, begin to die off. These cells affect balance and coordination. They have a critical role to play in the brain. The Purkinje layer allows communication between the granular and molecular cortical layers in the cerebellum. Put simply, without Purkinje cells, an animal loses its sense of space and distance, making balance and coordination difficult. People with damage to the cerebellum can experience symptoms like unsteady gait, poor muscle control, and trouble speaking or swallowing.

"Abiotrophy" means the loss of a vital nutritive factor. The exact cause of cerebellar abiotrophy is not known, but it is thought to be due to an intrinsic metabolic defect.

In most cases, the Purkinje neurons begin to die off shortly after the animal is born and the condition is noticeable when the animal is less than six months old, though sometimes the onset of symptoms is gradual and the animal is much older before the owner or caretaker notices a problem.

CA cannot be prevented, other than by selective breeding to avoid the gene, and it cannot be cured. Genetic testing can detect carriers. In addition to dogs and horses, there also have been cases of cerebellar abiotrophy in Siamese and Domestic shorthair cats; in Angus, Polled Hereford, Charolais and Holstein Friesian cattle; Merino and Wiltshire sheep; and Yorkshire pigs.

Chronic granulomatous disease (CGD) (also known as Bridges–Good syndrome, chronic granulomatous disorder, and Quie syndrome) is a diverse group of hereditary diseases in which certain cells of the immune system have difficulty forming the reactive oxygen compounds (most importantly the superoxide radical due to defective phagocyte NADPH oxidase) used to kill certain ingested pathogens. This leads to the formation of granulomata in many organs. CGD affects about 1 in 200,000 people in the United States, with about 20 new cases diagnosed each year.

This condition was first discovered in 1950 in a series of 4 boys from Minnesota, and in 1957 it was named "a fatal granulomatosus of childhood" in a publication describing their disease. The underlying cellular mechanism that causes chronic granulomatous disease was discovered in 1967, and research since that time has further elucidated the molecular mechanisms underlying the disease. Bernard Babior made key contributions in linking the defect of superoxide production of white blood cells, to the cause of the disease. In 1986, the X-linked form of CGD was the first disease for which positional cloning was used to identify the underlying genetic mutation.

Myeloperoxidase deficiency is an autosomal recessive genetic disorder featuring deficiency, either in quantity or of function, of myeloperoxidase, an enzyme found in certain phagocytic immune cells, especially polymorphonuclear leukocytes.

It can appear similar to chronic granulomatous disease on some screening tests.

Although MPO deficiency classically presents with immune deficiency (especially candida albicans infections), the majority of individuals with MPO deficiency show no signs of immunodeficiency.

The lack of severe symptoms suggest that role of myeloperoxidase in the immune response must be redundant to other mechanisms of intracellular killing of phagocytosed bacteria.

Patients with MPO deficiency have a respiratory burst with a normal nitro blue tetrazolium (NBT) test because they still have NADPH oxidase activity, but do not form bleach due to their lack of myeloperoxidase activity. This is in contrast to chronic granulomatous disease, in which the NBT test is 'negative' due to the lack of NADPH oxidase activity (positive test result means neutrophils turn blue, negative means nitroblue tetrazolium remains yellow).

Patients with MPO deficiency are at increased risk for systemic candidiasis.

People with CHS have light skin and silvery hair (albinism) and frequently complain of solar sensitivity and photophobia. Other signs and symptoms vary considerably, but frequent infections and neuropathy are common. The infections involve mucous membranes, skin, and the respiratory tract. Affected children are susceptible to infection by Gram-positive and gram-negative bacteria and fungi, with "Staphylococcus aureus" being the most common infection cause. Infections in CHS patients tend to be very serious and even life-threatening. Neuropathy often begins in the teenage years and becomes the most prominent problem. Few patients with this condition live to adulthood.

Most children with Chédiak–Higashi syndrome ultimately reach a stage known as the "accelerated phase", or the "lymphoma-like syndrome", in which defective white blood cells divide uncontrollably and invade many of the body's organs. The accelerated phase is associated with fever, episodes of abnormal bleeding, overwhelming infections, and organ failure. These medical problems are usually life-threatening in childhood.

Chrysiasis (Gk, "chrysos" – 'gold', "osis" – 'condition of') is a dermatological condition induced by the parenteral administration of gold salts, usually for the treatment of rheumatoid arthritis. Such treatment has been superseded as the best practice for treating the disease because of "numerous side effects and monitoring requirements, their limited efficacy, and very slow onset of action".

Similar to silver, a gold preparation used parenterally for a long period may rarely produce a permanent skin pigmentation – especially if the skin is exposed to sunlight or artificial ultraviolet radiation.

The skin's pigmentation (in this condition) has been described as uniformly gray, grayish purple, slate gray, or grayish blue, and is usually limited to exposed portions of the body. It may involve the conjunctivae over the scleras but usually not the oral mucosa. Location of pigment predominantly in the upper dermis leads to the blue component of skin color through the scattering phenomenon. It is much less likely to be deposited in the nails and hair.

Chrysiasis was said to have been much more common when medicines containing traces of gold were used for treatment of tuberculosis (commonplace forms of treatment nearly fifty years ago). Treatments containing gold traces were also used to treat cases of rheumatoid arthritis – but because the dose used for tuberculosis was higher than for arthritis, it has not afflicted many subscribing to such treatments.

Gold can be identified in the skin chemically by light microscopy, electron microscopy, and spectroscopy.

There is no way to reverse or treat chrysiasis.