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

The illness lasts about a week and is rarely fatal. Treatment includes the administration of nonsteroidal anti-inflammatory agents or the application of heat to the affected muscles. Relapses during the weeks following the initial episode are a characteristic feature of this disease.

In CNS infection cases, "L. monocytogenes" can often be cultured from the blood or from the CSF (Cerebrospinal fluid).

Bacteremia should be treated for 2 weeks, meningitis for 3 weeks, and brain abscess for at least 6 weeks. Ampicillin generally is considered antibiotic of choice; gentamicin is added frequently for its synergistic effects. Overall mortality rate is 20–30%; of all pregnancy-related cases, 22% resulted in fetal loss or neonatal death, but mothers usually survive.

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.

As "Flavobacterium columnare" is Gram-negative, fish can be treated with a combination of the antibiotics furan-2 and kanamycin administered together. A medicated fish bath (using methylene blue or potassium permanganate and salt), is generally a first step, as well lowering the aquarium temperature to 75 °F (24 °C) is a must, since columnaris is much more virulent at higher temperatures, especially 85–90 °F.

Medicated food containing oxytetracycline is also an effective treatment for internal infections, but resistance is emerging. Potassium permanganate, copper sulfate, and hydrogen peroxide can also be applied externally to adult fish and fry, but can be toxic at high concentrations. Vaccines can also be given in the face of an outbreak or to prevent disease occurrence.

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.

Sodium chloride is believed to mitigate the reproduction of Velvet, however this treatment is not itself sufficient for the complete eradication of an outbreak. Additional, common medications added directly to the fish's environment include copper sulfate, methylene blue, formalin, malachite green and acriflavin, all of which can be found in common fish medications designed specifically to combat this disease. Additionally, because Velvet parasites derive a portion of their energy from photosynthesis, leaving a tank in total darkness for seven days provides a helpful supplement to chemical curatives. Finally, some enthusiasts recommend raising the water temperature of an infected fish's environment, in order to quicken the life cycle (and subsequent death) of Velvet parasites; however this tactic is not practical for all fish, and may induce immunocompromising stress.

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.

The nitroblue-tetrazolium (NBT) test is the original and most widely known test for chronic granulomatous disease. It is negative in CGD, meaning that it does not turn blue. The higher the blue score, the better the cell is at producing reactive oxygen species. This test depends upon the direct reduction of NBT to the insoluble blue compound formazan by NADPH oxidase; NADPH is oxidized in the same reaction. This test is simple to perform and gives rapid results, but only tells whether or not there is a problem with the PHOX enzymes, not how much they are affected.

A similar test uses dihydrorhodamine (DHR), in which whole blood is stained with DHR, incubated, and stimulated to produce superoxide radicals which oxidize DHR to rhodamin in cells with normal function. An advanced test called the "cytochrome C reduction assay" tells physicians how much superoxide a patient's phagocytes can produce. Once the diagnosis of CGD is established, a genetic analysis may be used to determine exactly which mutation is the underlying cause.

Chronic granulomatous disease is the name for a genetically heterogeneous group of immunodeficiencies. The core defect is a failure of phagocytic cells to kill organisms that they have engulfed because of defects in a system of enzymes that produce free radicals and other toxic small molecules. There are several types, including:

- X-linked chronic granulomatous disease (CGD)

- autosomal recessive cytochrome b-negative CGD

- autosomal recessive cytochrome b-positive CGD type I

- autosomal recessive cytochrome b-positive CGD type II

- atypical granulomatous disease

The disease may be diagnosed by its characteristic grouping of certain cells (multinucleated globoid cells), nerve demyelination and degeneration, and destruction of brain cells. Special stains for myelin (e.g.; luxol fast blue) may be used to aid diagnosis.

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.

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.

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 best way to manage SDS is with a resistant variety. One issue is that most resistant varieties are only partially resistant so yield reductions may still occur. Another issue is that the plant needs resistance for SDS and SCN in order to gain true resistance because of their synergistic relationship and most varieties do not have resistance for both. Aside from resistance, the only other ways to control SDS are management practices.

These include:

- Avoid planting in cool, wet conditions

- Plant later when the soil has warmed up

- Try avoiding soil compaction as it creates wet spots in the soil that can increase plant stress and SDS infection rates

- Managing for SCN as this nematode often occurs alongside "F. virguliforme"

- Deep tillage to break up compaction and help the soil warm faster

One common management tactic used in other pathogen management plans is crop rotation. In some cases, disease severity can be reduced but most often it is not effective. This is because of chlamydospores and macroconidia as they can persist in soils for many years.

Fungicides are another common product used to control fungal pathogens. In-furrow applications and seed treatments with fungicides have some effect in decreasing disease instance but in most cases, the timing isn't right and the pathogen can still infect the plants. Foliar applications of fungicides have no effect on disease suppression for SDS because the fungi are found in the soil and mainly the roots of the plants. Most foliar fungicides do not move downward through plants, therefore having no effect on the pathogen.

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 diagnosis is confirmed by bone marrow smears that show "giant inclusion bodies" in the cells that develop into white blood cells (leukocyte precursor cells). CHS can be diagnosed prenatally by examining a sample of hair from a fetal scalp biopsy or testing leukocytes from a fetal blood sample.

Under light microscopy the hairs present evenly distributed, regular melanin granules, larger than those found in normal hairs. Under polarized light microscopy these hairs exhibit a bright and polychromatic refringence pattern.

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.

A skin biopsy can be performed to test for EAC; tests should be performed to rule out other possible diseases such as: pityriasis rosea, tinea corporis, psoriasis, nummular eczema, atopic dermatitis, drug reaction, erythema migrans and other rashes.

The microscopic examination of tissue (histology) gives the definitive diagnosis. The diagnostic histopathologic finding is intravascular cholesterol crystals, which are seen as cholesterol clefts in routinely processed tissue (embedded in paraffin wax). The cholesterol crystals may be associated with macrophages, including giant cells, and eosinophils.

The sensitivity of small core biopsies is modest, due to sampling error, as the process is often patchy. Affected organs show the characteristic histologic changes in 50-75% of the clinically diagnosed cases. Non-specific tissue findings suggestive of a cholesterol embolization include ischemic changes, necrosis and unstable-appearing complex atherosclerotic plaques (that are cholesterol-laden and have a thin fibrous cap). While biopsy findings may not be diagnostic, they have significant value, as they help exclude alternate diagnoses, e.g. vasculitis, that often cannot be made confidently based on clinical criteria.

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.

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.