Black band disease is a coral disease in which corals develop a black band. It is characterized by complete tissue degradation due to a pathogenic microbial consortium. The mat is present between apparently healthy coral tissue and freshly exposed coral skeleton.

Peach scab, also known as peach freckles, is a disease of stone fruits caused by the fungi "Cladosporium carpophilum". The disease is most prevalent in wet and warm areas especially southern part of the U.S. as the fungi require rain and wind for dispersal. The fungus causes scabbing, lesions, and defoliating on twig, fruit, and leaf resulting in downgrade of peach quality or loss of fruits due to rotting in severe cases.

Black band disease was first observed on reefs in Belize in 1973 by A. Antonius, who described the pathogen he found infecting corals as "Oscillatoria membranacea", one of the cyanobacteria. The band color may be blackish brown to red depending on the vertical position of a cyanobacterial population associated with the band. The vertical position is based on a light intensity-dependent photic response of the cyanobacterial filaments, and the color (due to the cyanobacterial pigment phycoerythrin) is dependent on the thickness of the band. The band is approximately thick and ranges in width from to White specks may be present on surface, at times forming dense white patches. The pathogenic microbial mat moves across coral colonies at rates from to a day. Tissue death is caused by exposure to an hypoxic, sulfide-rich microenvironment associated with the base of the band.

Life expectancy with Fabry disease for males was 58.2 years, compared with 74.7 years in the general population, and for females 75.4 years compared with 80.0 years in the general population, according to registry data from 2001 to 2008. The most common cause of death was cardiovascular disease, and most of those had received kidney replacements.

Pythiosis occurs in areas with mild winters because the organism survives in standing water that does not reach freezing temperatures. In the United States, it is most commonly found in the Southern Gulf states, especially Louisiana, Florida, and Texas, but has also been reported as far away as California and Wisconsin. It is also found in southeast Asia, eastern Australia, New Zealand, and South America.

Due to the effectiveness of fungicide application and it’s relatively minor damage to crops, there are few cultural controls and no resistant peach variants that have been developed for the current market. For prevention of peach scab, proper pruning of leaves to allow adequate sunlight will drastically reduce the risk of infection and propagation. The primary form of regulation for peach scab requires frequent applications of commercial fungicides. There are three main types of fungicides that are effective against peach scab: captan, chlorothalonil, and demethylation inhibitors. Proper use of chlorothalonil requires application starting from shuck split and reapplication every two weeks. Increased temperature and wet weather will necessitate more frequent applications. Applications are necessary until 4–6 weeks until harvest.

In humans, it can cause arteritis, keratitis, and periorbital cellulitis. This has previously been thought to be a rare disease with only 28 cases reported in the literature up to 1996. However, keratitis due to Pythium may be more common than previously thought, accounting for a proportion of cases that were due to unidentified pathogens. Although this disease was first reported in 1884 the species infecting humans - "Pythium insidiosum" - was only formally recognised in 1987. Diagnosis can be difficult in part because of a lack of awareness of the disease. It does not appear to be transmissible either animal to animal or animal to human. There appear to be three clades of this organism: one in the Americas, a second from Asia and Australia and a third with isolates from Thailand and the USA. The most probable origin of the organism seems to be in Asia.

Most human cases have been reported in Thailand, although cases have been reported elsewhere. In humans, the four forms of the disease are: subcutaneous, disseminated, ocular, and vascular. The ocular form of the disease is the only one known to infect otherwise healthy humans, and has been associated with contact lens use while swimming in infected water. This is also the rarest form with most cases requiring enucleation of the eye. The other forms of the disease require a pre-existing medical condition, usually associated with thalassemic hemoglobinopathy. Prognosis is poor to guarded and treatments include aggressive surgical resection of infected tissue, with amputation suggested if the infection is limited to a distal limb followed by immunotherapy and chemotherapy. A recently published review lists nine cases of vascular pythiosis with five survivors receiving surgery with free margins and all except one requiring amputation. The same review lists nine cases of ocular pythiosis with five patients requiring enucnleation of the infected eye and four patients requiring a corneal transplant.

There is currently no specific treatment for the virus. A vaccine is available, but only experimentally. It has not been released to the public due to the risk it poses to already exposed birds.

Therapeutic intervention is limited to treating secondary infections. The individual bird can sometimes recover, but this is rare. If only the feathers are affected and the bird suffers no other symptoms, it can usually experience an acceptable quality of life. But if the bird's beak or nails are affected, veterinarians will recommend euthanasia.

The management of the disease lies thus mostly in prevention. Every new bird that enters a pen with other birds should be quarantined first and be tested for BFDV. Birds which are known carriers should not be introduced into new pens, especially not if those contain young birds.

PBFD has the potential to become a major threat to all species of wild parrots and to modern aviculture, due to international legal and illegal bird trade. Cases of PBFD have now been reported in at least 78 psittacine species. At least 38 of 50 Australian native species are affected by PBFD, both captive and in the wild. In 2004, PBFD was listed as a key threatening process by the Australian Commonwealth Government for the survival of five endangered species, including one of the few remaining species of migratory parrots, the orange-bellied parrot, of which only an estimated 60 mating pairs remained in 2006.

Left untreated, Wilson's disease tends to become progressively worse and is eventually fatal. With early detection and treatment, most of those affected can live relatively normal lives. Liver and neurologic damage that occurs prior to treatment may improve, but it is often permanent.

The National Gaucher Foundation (United States) states the incidence of Gaucher's disease is about one in 20,000 live births. Around one in 100 people in the general US population is a carrier for type I Gaucher's disease, giving a prevalence of one in 40,000. Among Ashkenazi Jews, the rate of carriers is considerably higher, at roughly one in 15.

Type II Gaucher's disease shows no particular preference for any ethnic group.

Type III Gaucher's disease is especially common in the population of the northern Swedish region of Norrbotten, where the incidence of the disease is one in 50,000.

Fabry disease is estimated to occur in one in 40,000 to one in 120,000 live births.

Carrion's disease is caused by "Bartonella bacilliformis".

Recent investigations show that "Candidatus Bartonella ancashi" may cause verruga peruana, although it may not meet all of Koch's postulates. There has been no experimental reproduction of the Peruvian wart in animals and there is little research on the disease's natural spread or impact in native animals.

GSS is one of a small number of diseases that are caused by prions, a class of pathogenic proteins highly resistant to proteases.

A change in codon 102 from proline to leucine has been found in the prion protein gene ("PRNP", on chromosome 20) of most affected individuals. Therefore, it appears this genetic change is usually required for the development of the disease.

There is no cure or treatment for GSS. It can, however, be identified through genetic testing. GSS is the slowest to progress among human prion diseases. Duration of illness can range from 3 months to 13 years, with an average duration of 5 or 6 years.

In general, a diet low in copper-containing foods is recommended with the avoidance of mushrooms, nuts, chocolate, dried fruit, liver, and shellfish.

It is prevalent in parts of Africa and Asia where eating snake meat is common. In Africa it has also been associated with groups who use the snake as a totem. Unlike linguatuliasis, humans are only ever an accidental intermediate host for "Armillifer", i.e. the larvae establish themselves in the visceral organs causing human visceral pentastomiasis, but adults do not occur in the human respiratory system. After a while the larvae die within the host and sometimes calcify, leaving characteristic crescent-shaped structures seen in X-ray. In extreme cases a heavy parasite burden can have serious medical consequences and can even be fatal.

The clinical symptoms of bartonellosis are pleomorphic and some patients from endemic areas may be asymptomatic. The two classical clinical presentations are the acute phase and the chronic phase, corresponding to the two different host cell types invaded by the bacterium (red blood cells and endothelial cells). An individual can be affected by either or both phases.

Urbach–Wiethe disease is very rare; there are fewer than 300 reported cases in medical literature. Although Urbach–Wiethe disease can be found worldwide, almost a quarter of reported diagnoses are in South Africa. Many of these are in patients of Dutch, German, and Khoisan ancestry. This high frequency is thought to be due to the founder effect. Due to its recessive genetic cause and the ability to be a carrier of the disease without symptoms, Urbach–Wiethe disease often runs in families. In some regions of South Africa, up to one in 12 individuals may be carriers of the disease. Most of the case studies involving Urbach–Wiethe disease patients involve only one to three cases and these cases are often in the same family. Due to its low incidence, it is difficult to find a large enough number of cases to adequately study the disease.

Porocephaliasis is a condition associated with species in the closely related genera "Porocephalus" and "Armillifer". (The term "pentastomiasis" encompasses all diseases of Pentastomida, which includes Porocephaliasis and Linguatulosis.)

Porocephaliasis is associated with contact with snakes. (This is in contrast with Linguatulosis, which is associated with contact with dogs or wolves.)

It has been reported from Africa, Malaysia and the Middle East. Its occurrence has been rare in Europe and North America where it has been found in immigrants and travelers.

Gaucher's disease or Gaucher disease () (GD) is a genetic disorder in which glucocerebroside (a sphingolipid, also known as glucosylceramide) accumulates in cells and certain organs. The disorder is characterized by bruising, fatigue, anemia, low blood platelet count and enlargement of the liver and spleen, and is caused by a hereditary deficiency of the enzyme glucocerebrosidase (also known as glucosylceramidase), which acts on glucocerebroside. When the enzyme is defective, glucocerebroside accumulates, particularly in white blood cells and especially in macrophages (mononuclear leukocytes). Glucocerebroside can collect in the spleen, liver, kidneys, lungs, brain, and bone marrow.

Manifestations may include enlarged spleen and liver, liver malfunction, skeletal disorders or bone lesions that may be painful, severe neurological complications, swelling of lymph nodes and (occasionally) adjacent joints, distended abdomen, a brownish tint to the skin, anemia, low blood platelet count, and yellow fatty deposits on the white of the eye (sclera). Persons seriously affected may also be more susceptible to infection. Some forms of Gaucher's disease may be treated with enzyme replacement therapy.

The disease is caused by a recessive mutation in the GBA gene located on chromosome 1 and affects both males and females. About one in 100 people in the United States are carriers of the most common type of Gaucher disease. The carrier rate among Ashkenazi Jews is 8.9% while the birth incidence is one in 450.

Gaucher's disease is the most common of the lysosomal storage diseases. It is a form of sphingolipidosis (a subgroup of lysosomal storage diseases), as it involves dysfunctional metabolism of sphingolipids.

The disease is named after the French physician Philippe Gaucher, who originally described it in 1882.

Urbach–Wiethe disease is typically not a life-threatening condition. The life expectancy of these patients is normal as long as the potential side effects of thickening mucosa, such as respiratory obstruction, are properly addressed. Although this may require a tracheostomy or carbon dioxide laser surgery, such steps can help ensure that individuals with Urbach–Wiethe disease are able to live a full life. Oral dimethyl sulfoxide (DMSO) has been shown to reduce skin lesions, helping to minimize discomfort for these individuals.

Ehrlichiosis (; also known as canine rickettsiosis, canine hemorrhagic fever, canine typhus, tracker dog disease, and tropical canine pancytopenia is a tick-borne disease of dogs usually caused by the organism "Ehrlichia canis". "Ehrlichia canis" is the pathogen of animals. Humans can become infected by "E. canis" and other species after tick exposure. German Shepherd Dogs are thought to be susceptible to a particularly severe form of the disease, other breeds generally have milder clinical signs. Cats can also be infected.

Progressive disease or progressive illness is a disease or physical ailment whose course in most cases is the worsening, growth, or spread of the disease. This may happen until death, serious debility, or organ failure occurs. Some progressive diseases can be halted and reversed by treatment. Many can be slowed by medical therapy. Some cannot be altered by current treatments.

Though the time distinctions are imprecise, diseases can be "rapidly progressive" (typically days to weeks) or "slowly progressive" (months to years). Virtually all slowly progressive diseases are also chronic diseases in terms of time course; many of these are also referred to as degenerative diseases. Not all chronic diseases are progressive: a chronic, non-progressive disease may be referred to as a "static" condition.

"Progressive disease" can also be a clinical endpoint i.e. an endpoint in a clinical trial.

There are examples of slowly and rapidly progressive diseases affecting all organ systems and parts of the body. The following are some examples of rapidly and slowly progressive diseases affecting various organ systems:

- Brain: Creutzfeldt–Jakob disease progresses rapidly compared to Alzheimer's disease.

- Eyes: Cataracts can be static or slowly progressive. Macular degeneration is slowly progressive, while retinal detachment is rapidly progressive.

- Lungs: Emphysema due to alpha-1 antitrypsin deficiency is a slowly progressive pulmonary disease.

- Kidneys: Goodpasture's syndrome is a rapidly progressive glomerulonephritis, while diabetic glomerulosclerosis is slowly progressive.

- Pancreas: Type 1 diabetes mellitus involves rapidly progressive loss of insulin secretory capacity compared to type 2 diabetes mellitus, in which the loss of insulin secretion is slowly progressive over many years. MODY 2, due to "GCK" mutation, is a relatively static form of reduced insulin secretion.

- Joints: Both osteoarthritis and rheumatoid arthritis are slowly progressive forms of arthritis.

- Nerves: Essential tremor is a slowly progressive neurological disorder which is usually genetically passed down.