Coxsackie B virus is spread by contact and epidemics usually occur during warm weather in temperate regions and at any time in the tropics.

As is typical with this virus family, it is shed in large amounts in the feces of infected persons. The disease can be spread by sharing drink containers, and has been contracted by laboratory personnel working with the virus.

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.

Incidence in 2004–2005 was 2.5–3 cases per million population a year in the United States, where pregnant women accounted for 30% of all cases. Of all nonperinatal infections, 70% occur in immunocompromised patients. Incidence in the U.S. has been falling since the 1990s, in contrast to Europe where changes in eating habits have led to an increase during the same time. In the EU, it has stabilized at around 5 cases per annum per million population, although the rate in each country contributing data to EFSA/ECDC varies greatly.

There are four distinct clinical syndromes:

- Infection in pregnancy: "Listeria" can proliferate asymptomatically in the vagina and uterus. If the mother becomes symptomatic, it is usually in the third trimester. Symptoms include fever, myalgias, arthralgias and headache. Miscarriage, stillbirth and preterm labor are complications of this infection. Symptoms last 7–10 days.

- Neonatal infection (granulomatosis infantiseptica): There are two forms. One, an early-onset sepsis, with "Listeria" acquired in utero, results in premature birth. "Listeria" can be isolated in the placenta, blood, meconium, nose, ears, and throat. Another, late-onset meningitis is acquired through vaginal transmission, although it also has been reported with caesarean deliveries.

- Central nervous system (CNS) infection: "Listeria" has a predilection for the brain parenchyma, especially the brain stem, and the meninges. It can cause cranial nerve palsies, encephalitis, meningitis, meningoencephalitis and abscesses. Mental status changes are common. Seizures occur in at least 25% of patients.

- Gastroenteritis: "L. monocytogenes" can produce food-borne diarrheal disease, which typically is noninvasive. The median incubation period is 21 days, with diarrhea lasting anywhere from 1–3 days. Patients present with fever, muscle aches, gastrointestinal nausea or diarrhea, headache, stiff neck, confusion, loss of balance, or convulsions.

"Listeria" has also been reported to colonize the hearts of some patients. The overall incidence of cardiac infections caused by "Listeria" is relatively low, with 7-10% of case reports indicating some form of heart involvement. There is some evidence that small subpopulations of clinical isolates are more capable of colonizing the heart throughout the course of infection, but cardiac manifestations are usually sporadic and may rely on a combination of bacterial factors and host predispositions, as they do with other strains of cardiotropic bacteria.

"Listeria monocytogenes" is ubiquitous in the environment. The main route of acquisition of "Listeria" is through the ingestion of contaminated food products. "Listeria" has been isolated from raw meat, dairy products, vegetables, fruit and seafood. Soft cheeses, unpasteurized milk and unpasteurised pâté are potential dangers; however, some outbreaks involving post-pasteurized milk have been reported.

Rarely listeriosis may present as cutaneous listeriosis. This infection occurs after direct exposure to "L. monocytogenes" by intact skin and is largely confined to veterinarians who are handling diseased animals, most often after a listerial abortion.

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.

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.

Ulcerations develop within 24 to 48 hours. Fatality occurs between 48 and 72 hours if no treatment is pursued; however, at higher temperatures death may occur within hours. Other symptoms may accompany the disease, including lethargy, color loss, redness around the infection site, loss of appetite and twitching or rubbing the body against objects.

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.

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.

Velvet (in an aquarium environment) is usually spread by contaminated tanks, fish, and tools (such as nets or testing supplies). There are also rare reports of frozen live foods (such as bloodworms) containing dormant forms of the species. Frequently, however, the parasite is endemic to a fish, and only causes a noticeable "outbreak" after the fish's immune system is compromised for some other reason. The disease is highly contagious and can prove fatal to fish.

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

In infantile Krabbe disease, death usually occurs in early childhood. A 2011 study found 1, 2, 3 year survival rates of 60%, 26%, and 14%, respectively. A few survived for longer and one was still alive at age 13. Patients with late-onset Krabbe disease tend to have a slower progression of the disease and live significantly longer.

There are currently no studies detailing the long term outcome of chronic granulomatous disease with modern treatment. Without treatment, children often die in the first decade of life. The increased severity of X-linked CGD results in a decreased survival rate of patients, as 20% of X-linked patients die of CGD-related causes by the age of 10, whereas 20% of autosomal recessive patients die by the age of 35.

Recent experience from centers specializing in the care of patients with CGD suggests that the current mortality has fallen to under 3% and 1% respectively.

CGD was initially termed "fatal granulomatous disease of childhood" because patients rarely survived past their first decade in the time before routine use of prophylactic antimicrobial agents. The average patient now survives at least 40 years.

Krabbe disease occurs in about one in 100,000 births. A higher incidence, about six in 1,000, has been reported in certain communities in Israel. Scandinavian countries have comparatively high rates of the disease, reported to be one in 50,000 births.

People with CGD are sometimes infected with organisms that usually do not cause disease in people with normal immune systems. Among the most common organisms that cause disease in CGD patients are:

- bacteria (particularly those that are catalase-positive)

- "Staphylococcus aureus".

- "Serratia marcescens".

- "Listeria" species.

- "E. coli".

- "Klebsiella" species.

- "Pseudomonas cepacia, a.k.a. Burkholderia cepacia.

- "Nocardia".

- fungi

- "Aspergillus" species. Aspergillus has a propensity to cause infection in people with CGD and of the Aspergillus species, "Aspergillus fumigatus" seems to be most common in CGD.

- "Candida" species.

Patients with CGD can usually resist infections of catalase-negative bacteria but are susceptible to catalase-positive bacteria. Catalase is an enzyme that catalyzes the breakdown of hydrogen peroxide in many organisms. In infections caused by organisms that lack catalase (catalase-negative), the host with CGD is successfully able to "borrow" hydrogen peroxide being made by the organism and use it to fight off the infection. In infections by organisms that have catalase (catalase-positive), this "borrowing mechanism" is unsuccessful because the catalase enzyme first breaks down any hydrogen peroxide that would be borrowed from the organism. Therefore in the CGD patient, hydrogen peroxide cannot be used to make oxygen radicals to fight infection, leaving the patient vulnerable to infection by catalase-positive bacteria.

Cerebellar abiotrophy (CA) is best known as a condition affecting Arabian horses. It has also been observed in the Curly horse, Miniature horse, the Gotland Pony, one Eriskay Pony, and possibly the Oldenburg. Most foals appear normal at birth, with symptoms noticeable at an average age of four months, though there have been cases where the condition is first seen shortly after birth and other cases where symptoms are first recognized in horses over one year of age.

Breeds DNA tested that reveal some carrier lines, but to date no affected animals, include the Welsh pony and the Trakehner. However, other breeds heavily influenced by Arabian breeding, such as the Thoroughbred and the American Saddlebred, do not appear to carry the mutation.

In horses, CA is believed to be linked to an autosomal recessive gene. This means it is not sex-linked, and the allele has to be carried and passed on by both parents in order for an affected animal to be born. Horses that only carry one copy of the gene may pass it on to their offspring, but themselves are perfectly healthy—without symptoms of the disease. Because it is recessive, the allele for CA may pass through multiple generations before it is expressed.

CA is sometimes misdiagnosed. Though the symptoms are quite distinguishable from other neurological conditions, it has been confused with Wobbler's syndrome, Equine Protozoal Myeloencephalitis (EPM), and injury-related problems such as a concussion.

A DNA test which identifies markers associated with cerebellar abiotrophy became available in 2008. The test was refined to identify the most likely mutations, and retesting of earlier samples based on an earlier indirect marker test developed by UCD, indicated a 97% accuracy rate for the old test relative to the newer version, with no false negatives. The causative mutation was identified in 2011. Research on CA and the DNA test was led by the Veterinary Genetics Laboratory at the UC Davis School of Veterinary Medicine. Researchers working on this problem include Dr. Cecilia Penedo, PhD, and Leah Brault, PhD. The late Dr. Ann T. Bowling made significant early contributions to the genetics research on CA.

The medieval "Bald's Leechbook" recommended treating chilblains with a mix of eggs, wine, and fennel root.

A common tradition of Hispanic America recommends warm garlic on the chilblains.

In the US, SDS was first found in 1971 in Arkansas and in other southern states within a few years. In 1993, a SDS epidemic broke out in Illinois and some locations in Iowa, where 100% infection rates were found, causing large reductions is yields. Currently, SDS is the most important disease in soybeans across the US, affecting soybeans in almost all states where soybeans are grown. Nationally, yield losses have ranged from 20-30 million bushels across the past 10 years, with local variation due to the large range factors that determine the severity of the disease. Though, if conditions are conductive to this pathogen, yield losses can be devastating. In 2010, SDS ran wild throughout the Midwest because of the cool and wet conditions. In 2013 alone, studies showed a loss of 25 million bushels across the US. These yield losses are primarily from root deterioration causing a reduction in nutrient uptake, loss of photosynthetic area, and flower or pod abortion, causing reduction in seed numbers.

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.

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.

Buerger's is not immediately fatal. Amputation is common and major amputations (of limbs rather than fingers/toes) are almost twice as common in patients who continue to smoke. Prognosis markedly improves if a person quits smoking. Female patients tend to show much higher longevity rates than men. The only known way to slow the progression of the disease is to abstain from all tobacco products.

Often no specific cause for the eruptions is found. However, it is sometimes linked to underlying diseases and conditions such as:

- Food (including blue cheese or tomatoes).

- Contact Dermatitis (i.e. cleaning agents, fabric softeners, etc.)

- Fungal, Bacterial and Viral infections such as sinusitis, tuberculosis, candidiasis or tinea.

- Drugs including finasteride, etizolam (and benzodiazepines), chloroquine, hydroxychloroquine, oestrogen, penicillin and amitriptyline.

- Cancer (especially the type known as erythema gyratum perstans, in which there are concentric and whirling rings).

- Primary biliary cirrhosis.

- Graves disease.

- Appendicitis.

- Lupus

- Pregnancy (EAC usually disappears/stops soon after delivery of baby).

- Hormone (Contraceptive Pill, Stress, Hormone Drugs)

- Lyme Disease

The cause of the disease is thought to be autoimmune in nature and heavily linked to tobacco use in patients with Buerger's as primary disease.

Parasitic infestations, stings, and bites in humans are caused by several groups of organisms belonging to the following phyla: Annelida, Arthropoda, Bryozoa, Chordata, Cnidaria, Cyanobacteria, Echinodermata, Nemathelminthes, Platyhelminthes, and Protozoa.

- "Acanthamoeba" infection

- Amebiasis cutis

- Ant sting

- Arachnidism

- Baker's itch

- "Balamuthia" infection

- Bedbug infestation (bedbug bite, cimicosis)

- Bee and wasp stings

- Blister beetle dermatitis

- Bombardier beetle burn

- Bristleworm sting

- Centipede bite

- Cheyletiella dermatitis

- Chigger bite

- Coolie itch

- Copra itch

- Coral dermatitis

- Creeping eruption (cutaneous larva migrans)

- Cutaneous leishmaniasis (Aleppo boil, Baghdad boil, bay sore, Biskra button, Chiclero ulcer, Delhi boil, Kandahar sore, Lahore sore, leishmaniasis tropica, oriental sore, "pian bois, uta")

- "Cysticercosis" cutis

- Demodex mite bite

- Dogger Bank itch

- Dracunculiasis (dracontiasis, guinea worm disease, Medina worm)

- Echinococcosis (hydatid disease)

- Elephantiasis tropica (elephantiasis arabum)

- Elephant skin

- Enterobiasis (oxyuriasis, pinworm infection, seatworm infection)

- "Erisipela de la costa"

- Feather pillow dermatitis

- Funnel web spider bite

- Gamasoidosis

- Gnathostomiasis (larva migrans profundus)

- Grain itch (barley itch, mattress itch, prairie itch, straw itch)

- Grocer's itch

- Head lice infestation (cooties, pediculosis capitis)

- Hookworm disease (ancylostomiasis, ground itch, necatoriasis, uncinariasis)

- Human trypanosomiasis

- Hydroid dermatitis

- Irukandji syndrome

- Jellyfish dermatitis

- Ked itch

- Larva currens

- Latrodectism (widow spider bite)

- Leech bite

- Leopard skin

- Lepidopterism (Caripito itch, caterpillar dermatitis, moth dermatitis)

- Lizard bite

- Lizard skin

- Loaiasis (Calabar swelling, fugitive swelling, "loa loa", tropical swelling)

- Loxoscelism (brown recluse spider bite, necrotic cutaneous loxoscelism)

- "Mal morando"

- Millipede burn

- Mosquito bite

- Mucocutaneous leishmaniasis (espundia, leishmaniasis americana)

- Myiasis

- Nairobi fly dermatitis (Kenya fly dermatitis, Nairobi eye)

- Nematode dermatitis

- Norwegian scabies (crusted scabies)

- Onchocerciasis

- Ophthalmia nodosa

- Paederus dermatitis

- Pediculosis corporis (pediculosis vestimenti, Vagabond's disease)

- Pediculosis pubis (crabs, phthirus pubis, pthirus pubis, pubic lice)

- Pneumocystosis (often classified as fungal)

- Portuguese man-of-war dermatitis

- Post-kala-azar dermal leishmaniasis (post-kala-azar dermatosis)

- Protothecosis

- Pulicosis (flea bites)

- Reduviid bite

- Scabies (itch mite infestation, seven-year itch)

- Scorpion sting

- Sea anemone dermatitis

- Seabather's eruption (sea lice)

- Sea urchin injury

- Seaweed dermatitis

- Snake bite

- Sowda

- Sparganosis

- Spider bite

- Stingray injury

- Swimmer's itch (cercarial dermatitis, schistosome cercarial dermatitis)

- Tarantula bite

- Tick bite

- Toxoplasmosis

- Trichinosis

- Trichomoniasis

- Tungiasis ("bicho de pie", chigoe flea bite, jigger bite, "nigua, pique")

- Visceral leishmaniasis (dumdum fever, "kala-azar")

- Visceral schistosomiasis (bilharziasis)

- Viscerotropic leishmaniasis

- Wheat warehouse itch