Covering sickness, or dourine (French, from the Arabic "darina", meaning mangy (said of a female camel), feminine of "darin", meaning dirty), is a disease of horses and other members of the family Equidae. The disease is caused by "Trypanosoma equiperdum", which belongs to an important genus of parasitic protozoa, and is the only member of the genus that is spread through sexual intercourse. The occurrence of dourine is notifiable in the European Union under legislation from the OIE. There currently is no vaccine and although clinical signs can be treated, there is no cure.

"Trypanosoma equiperdum" is one of three known strains from the "Trypanosoma" family; along with "Trypanosoma evansi" and "Trypanosoma brucei". "Trypanosoma equiperdum" has been discovered to be most closely linked to "Trypanosoma evansi", so much so that even observation under microscope is not sufficient to differentiate between the two as their structure is very similar.

Dourine is a unique disease in the sense that it has no known vectors or fomites existing in the natural world, other than members of the equine family, including donkeys, mules, and horses. In a laboratory setting, "Trypanosoma equiperdum" has been manipulated to adapt to and proliferate in other species, such as dogs, rabbits, mice and rats, but this has never been observed to occur naturally and without scientific manipulation. Although this limits spread of the disease because it is restricted to the equine population alone, the organism has developed complex mechanisms over time to better equip itself for prolonged survival in the equine species. This parasite efficiently evades the host animal's immune system through the use of variable surface glycoproteins or VSGs. These VSGs allow the organism to constantly manipulate and change the surface structure of its proteins, which means it is constantly being presented to the immune system as a new foreign organism and this prevents the body from mounting a large enough immune response to eradicate the disease. In this sense, "Trypanosoma equiperdum" is a very efficient organism; it may infect less species than other diseases, but it infects and survives very efficiently within its specified hosts.

This disease affects the external genitalia, and is caused by equine herpesvirus 3. This disease remains with the horse for all its life. Equine coital exanthema is believed to only be transmitted during the acute phase of the disease through serous fluid from the blisters during sexual intercourse, and via breeding tools, handlers, etc.

Clinical signs include cute small lesions, no bigger than 2 mm in diameter around the vulva in mares, and on the sheath in stallions. The small bumps blister and then rupture, leaving raw, ulcerated, painful sores. While the majority of the symptoms are external, the presence of the virus can cause small and large plaque variants in tissues.

Affected animals normally have generalised signs such as depression, dullness, weakness and lethargy, pyrexia and weight loss and decreased production. They will also have respiratory signs including bilateral nasal discharge, dyspnoea, tachypnoea and coughing. Occasionally the only sign seen is sudden death.

Typical pathological lesions are very suggestive of the disease - they are localised exclusively to the lung and pleura. Lungs are normally a port wine colour and abundant pleural exudate and pleuritis and adhesions are common. The pleural exudates may have solidified forming a gelatinous covering.

Histological examination of the lung tissues may show acute serofibrinous to chronic fibrino-necrotic pleuropneumonia with neutrophilic inflammation in the alveoli, bronchioles, interstitial septae and subpleural connective tissue.

Symptoms are different for every person depending on the type of rat-bite fever with which the person is infected. Both spirillary and streptobacillary rat-bite fever have a few individual symptoms, although most symptoms are shared. Streptobacillosis is most commonly found in the United States and spirillary rat-bite fever is generally diagnosed in patients in Africa. Rat-bite symptoms are visually seen in most cases and include inflammation around the open sore. A rash can also spread around the area and appear red or purple. Other symptoms associated with streptobacillary rat-bite fever include chills, fever, vomiting, headaches, and muscle aches. Joints can also become painfully swollen and pain can be experienced in the back. Skin irritations such as ulcers or inflammation can develop on the hands and feet. Wounds heal slowly, so symptoms possibly come and go over the course of a few months.

Symptoms associated with spirillary rat-bite fever include issues with the lymph nodes, which often swell or become inflamed as a reaction to the infection. The most common locations of lymph node swelling are in the neck, groin, and underarm. Symptoms generally appear within 2 to 10 days of exposure to the infected animal. It begins with the fever and progresses to the rash on the hands and feet within 2 to 4 days. Rash appears all over the body with this form, but rarely causes joint pain.

Equine venereal diseases are sexually transmitted infections in horses. They include contagious equine metritis (CEM) (caused by "Taylorella equigenitalis") and equine coital exanthema (caused by equine herpesvirus 3).

The streptobacillosis form of rat-bite fever is known by the alternative names Haverhill fever and epidemic arthritic erythema. It is a severe disease caused by "Streptobacillus moniliformis", transmitted either by rat bite or ingestion of contaminated products (Haverhill fever). After an incubation period of 2–10 days, Haverhill fever begins with high prostrating fevers, rigors (shivering), headache, and polyarthralgia (joint pain). Soon, an exanthem (widespread rash) appears, either maculopapular (flat red with bumps) or petechial (red or purple spots) and arthritis of large joints can be seen. The organism can be cultivated in blood or articular fluid. The disease can be fatal if untreated in 20% of cases due to malignant endocarditis, meningoencephalitis, or septic shock. Treatment is with penicillin, tetracycline, or doxycycline.

In cattle, the main signs of paratuberculosis are diarrhea and wasting. Most cases are seen in 2- to 6-year-old animals. The initial signs can be subtle, and may be limited to weight loss, decreased milk production, or roughening of the hair coat. The diarrhea is usually thick, without blood, mucus, or epithelial debris, and may be intermittent. Several weeks after the onset of diarrhea, a soft swelling may occur under the jaw. Known as "bottle jaw" or intermandibular edema, this symptom is due to protein loss from the bloodstream into the digestive tract. Paratuberculosis is progressive; affected animals become increasingly emaciated and usually die as the result of dehydration and severe cachexia.

Signs are rarely evident until two or more years after the initial infection, which usually occurs shortly after birth. Animals are most susceptible to the infection in the first year of life. Newborns most often become infected by swallowing small amounts of infected manure from the birthing environment or udder of the mother. In addition, newborns may become infected while in the uterus or by swallowing bacteria passed in milk and colostrum. Animals exposed at an older age, or exposed to a very small dose of bacteria at a young age, are not likely to develop clinical disease until they are much older than two years.

The clinical signs are similar in other ruminants. In sheep and goats, the wool or hair is often damaged and easily shed, and diarrhea is uncommon. In deer, paratuberculosis can progress rapidly. Intestinal disease has also been reported in rabbits and nonhuman primates.

Unlike cattle and sheep, infections in deer often present with clinical illness in animals under one year of age.

Paratuberculosis or Johne's disease is a contagious, chronic and sometimes fatal infection that primarily affects the small intestine of ruminants. It is caused by the bacterium "Mycobacterium avium" subspecies "paratuberculosis". Infections normally affect ruminants (mammals that have four compartments of their stomachs, of which the rumen is one), but have also been seen in a variety of nonruminant species, including rabbits, foxes, and birds. Horses, dogs, and nonhuman primates have been infected experimentally. Paratuberculosis is found worldwide, with some states in Australia (where it is usually called bovine Johne's disease or BJD) as the only areas proven to be free of the disease.

Some sources define "paratuberculosis" by the lack of "Mycobacterium tuberculosis", rather than the presence of any specific infectious agent, leaving ambiguous the appropriateness of the term to describe Buruli ulcer or Lady Windermere syndrome.

Contagious caprine pleuropneumonia (CCPP) is a cause of major economic losses to goat producers in Africa, Asia and the Middle East.

Disease is caused by members of the Mycoplasma genus - usually "Mycoplasma capricolum subsp. capricolum" but sometimes by "M. mycoides" subsp. "capri" or "M. mycoides" subsp. "mycoides". It is extremely contagious with very high morbidity and mortality rates, causing an interstitial fibrinous pleuropneumonia in infected goats. Infection is spread by close-contact aerosol, therefore overcrowding and confinement increases disease incidence. Stress factors such as malnutrition and long transport can also predispose animals to disease.

Goats are the only species affected, therefore the disease is not a zoonosis. There is no age breed or sex predilection, but clinical signs are often worse in younger animals.

Cuterebriasis is a parasitic disease affecting rodents, lagomorphs (hares, rabbits, pikas), felines and canines. The etiologic agent is the larval development of bot flies within the "Cuterebra" or "Trypoderma" genera, which occurs obligatorily in rodents and lagomorphs, respectively. Felines and canines serve as accidental hosts, but research suggests only by "Trypoderma" spp. Entrance into the body by first instar larva occurs via mucous membranes of natural orifices or open wounds as opposed to direct dermic penetration.

"Rabbits, Hares & Lagomorphs"

Usually there do not appear to be any clinical signs. Subcutaneous cysts, warbles, may present upon larval deposition out of the body at maturation.

"Felines & Canines"

There are three forms in which Cuterebriasis may present:

- Myasis

- Cerebrospinal

- Respiratory

Myasis involves subcutaneous cyst formation due to 3rd larval instar maturation, occurring ~30 days post-entry into the body. Cysts are often found on the face, neck and trunk, but location varies with larval migration within the host. Serous discharge may be observed from these cysts, which are typically 3-5mm in diameter and include a central pore through which the larvae respire. This pore also serves as a means of exit for the larvae, which occurs anywhere between 3 and 8 weeks post-entry.

Cerebrospinal cuterebriasis results from larval migration to the brain. This is seen in cats, and is the proposed cause for feline ischemic encephalopathy and a suggestive causative agent of feline idiopathic vestibular disease. Symptoms of this type of presentation include lethargy, seizures, blindness, abnormal vocalization or gait, circling, and abnormal or no reflex responses. When affecting the central nervous system, cats are known to exhibit violent sneezing attacks that can onset weeks prior to manifestation of other clinical signs.

Respiratory disease results when larval migration occurs through the trachea, pharynx, diaphragm, or lungs. Cuterebriasis has been increasingly noted as a cause for dyspnea in felines.

Trombiculosis, trombiculiasis, or trombiculidiasis is a rash caused by trombiculid mites which is often referred to as a chigger bite.

Cryptococcosis, also known as cryptococcal disease, is a potentially fatal fungal disease. It is caused by one of two species; "Cryptococcus neoformans" and "Cryptococcus gattii". These were all previously thought to be subspecies of "C. neoformans" but have now been identified as distinct species.

Cryptococcosis is believed to be acquired by inhalation of the infectious propagule from the environment. Although the exact nature of the infectious propagule is unknown, the leading hypothesis is the basidiospore created through sexual or asexual reproduction.

Cryptococcosis is a defining opportunistic infection for AIDS, and is the second-most-common AIDS-defining illness in Africa. Other conditions that pose an increased risk include certain lymphomas (e.g., Hodgkin's lymphoma), sarcoidosis, liver cirrhosis, and patients on long-term corticosteroid therapy.

Distribution is worldwide in soil. The prevalence of cryptococcosis has been increasing over the past 20 years for many reasons, including the increase in incidence of AIDS and the expanded use of immunosuppressive drugs.

In humans, "C. neoformans" causes three types of infections:

- Wound or cutaneous cryptococcosis

- Pulmonary cryptococcosis

- Cryptococcal meningitis.

Cryptococcal meningitis (infection of the meninges, the tissue covering the brain) is believed to result from dissemination of the fungus from either an observed or unappreciated pulmonary infection. Often there is also silent dissemination throughout the brain when meningitis is present. "Cryptococcus gattii" causes infections in immunocompetent people (fully functioning immune system), but "C. neoformans v. grubii", and "v. neoformans" usually only cause clinically evident infections in persons with some form of defect in their immune systems (immunocompromised persons). People with defects in their cell-mediated immunity, for example, people with AIDS, are especially susceptible to disseminated cryptococcosis. Cryptococcosis is often fatal, even if treated. It is estimated that the three-month case-fatality rate is 9% in high-income regions, 55% in low/middle-income regions, and 70% in sub-Saharan Africa. As of 2009 there were globally approximately 958,000 annual cases and 625,000 deaths within three months after infection.

Although the most common presentation of cryptococcosis is of "C. neoformans" infection in an immunocompromised person (such as persons living with AIDS), the "C. gattii" is being increasingly recognised as a pathogen in what is presumed to be immunocompetent hosts, especially in Canada and Australia. This may be due to rare exposure and high pathogenicity, or to unrecognised isolated defects in immunity, specific for this organism.

Beech bark disease is a disease that causes mortality and defects in beech trees in the eastern United States and Europe. In North America, the disease occurs after extensive bark invasion by the beech scale insect, "Cryptococcus fagisuga". Through a presently unknown mechanism, excessive feeding by this insect causes two different fungi ("Neonectria faginata" (previously "Nectria coccinea var. faginata") and "Neonectria ditissima" (previously "Nectria galligena")) to produce annual cankers on the bark of the tree. The continuous formation of lesions around the tree eventually girdles it, resulting in canopy death. In Europe, "N. coccinea" is the primary fungus causing the infection. Infection in European trees occurs in the same manner as it does in North American trees. Though the disease still appears in Europe, it is less serious today than it once was.

The first visible sign of a beech scale insect infestation is a woolly, white, waxy covering that the insect secretes. This sign can be observed covering small areas or most of the tree. The amount of waxy material observed depends on the population of the beech scale insect on that tree. The "Neonectria" fungi also show signs of its presence. An early sign is what looks like a bleeding spot on the tree. A reddish-brown fluid will ooze from the wound site, giving it this appearance. Later, perithecia will form around the dead spot, which is another sign of the disease.

Symptoms of beech bark disease can be observed in the foliage and on the bole of the tree. Foliage may become small, sparse and yellowed. Trees that display a thin, weak crown may persist for several years but may also die without displaying any symptoms. Noticeable symptoms on the bole are the cracking of the bark, the formation of cankers, and beech snap. Beech snap is a result of the fungi and insect weakening the wood, which makes it susceptible to being blown over by wind.

Clinical diagnostic features are lifelong eruptions of pityriasis versicolor-like macules, flat wart-like papules, one to many cutaneous horn-like lesions, and development of cutaneous carcinomas.

Patients present with flat, slightly scaly, red-brown macules on the face, neck, and body, recurring especially around the penial area, or verruca-like papillomatous lesions, seborrheic keratosis-like lesions, and pinkish-red plane papules on the hands, upper and lower extremities, and face. The initial form of EV presents with only flat, wart-like lesions over the body, whereas the malignant form shows a higher rate of polymorphic skin lesions and development of multiple cutaneous tumors.

Generally, cutaneous lesions are spread over the body, but some cases have only a few lesions which are limited to one extremity.

Epidermodysplasia verruciformis (EV), also known as treeman syndrome, is an extremely rare autosomal recessive hereditary skin disorder associated with a high risk of skin cancer. It is characterized by abnormal susceptibility to human papillomaviruses (HPVs) of the skin. The resulting uncontrolled HPV infections result in the growth of scaly macules and papules, particularly on the hands and feet. It is typically associated with HPV types 5 and 8, which are found in about 80% of the normal population as asymptomatic infections, although other types may also contribute.

The condition usually has an onset of between the ages of one and 20 but can occasionally present in middle age. The condition is also known as Lewandowsky–Lutz dysplasia – named after the physicians who first documented it, Felix Lewandowsky and Wilhelm Lutz.

Women with aerobic vaginitis usually present with a thinned reddish vaginal mucosa, sometimes with extensive erosions or ulcerations and abundant yellowish discharge (without the fishy amine odour, typical of bacterial vaginosis). The pH is usually high. Symptoms can include burning, stinging and dyspareunia. The symptoms can last for long periods of time—sometimes even years. Typically, patients have been treated several times with antimycotic and antibiotic drugs without relief. In asymptomatic cases, there is microscopic evidence but no symptoms. The prevalence of asymptomatic cases is unknown.

Symptoms of BCD include:

- Crystals in the cornea (the clear covering of the eye)

- Yellow, shiny deposits on the retina

- Progressive atrophy of the retina, choriocapillaries and choroid (the back layers of the eye). This tends to lead to progressive night blindness and visual field constriction.

Like many other genetic disorders that affect lipid metabolism, there are several forms of MLD, which are late infantile, juvenile, and adult.

- In the "late infantile form", which is the most common form of MLD (50–60%), affected children begin having difficulty walking after the first year of life, usually at 15–24 months. Symptoms include muscle wasting and weakness, muscle rigidity, developmental delays, progressive loss of vision leading to blindness, convulsions, impaired swallowing, paralysis, and dementia. Children may become comatose. Untreated, most children with this form of MLD die by age 5, often much sooner.

- Children with the "juvenile form" of MLD (onset between 3 and 10 years of age) usually begin with impaired school performance, mental deterioration, and dementia and then develop symptoms similar to the late infantile form but with slower progression. Age of death is variable, but normally within 10 to 15 years of symptom onset although some juveniles can live for several decades or longer after onset.

- The "adult form" commonly begins after age 16 often with an onset in the 4th or 5th decade of life and presents as a psychiatric disorder or progressive dementia. Adult-onset MLD usually progresses more slowly than the late infantile and juvenile forms, with a protracted course of a decade or more.

Palliative care can help with many of the symptoms and usually improves quality of life and longevity.

Carriers have low enzyme levels compared to their family population ("normal" levels vary from family to family) but even low enzyme levels are adequate to process the body's sulfatide.

Symptoms of the most common (and most serious) form of Canavan disease typically appear in early infancy usually between the first three to six months of age. Canavan disease then progresses rapidly from that stage, with typical cases involving intellectual disability, loss of previously acquired motor skills, feeding difficulties, abnormal muscle tone (i.e., floppiness or stiffness; hypotonia), poor head control, and megalocephaly (abnormally enlarged head). Paralysis, blindness, or seizures may also occur.

There exists a less common variant of Canavan disease which is generally much less serious, and involves later onset of symptoms, which are often mild and nonspecific enough to go unrecognized as manifestations of Canavan's disease. This variant does not seem to have any effect on lifespan, and is typically limited to minor cases of speech and motor skill development delay.

There is a recurrent acute and chronic inflammation and thrombosis of arteries and veins of the hands and feet. The main symptom is pain in the affected areas, at rest and while walking (claudication). The impaired circulation increases sensitivity to cold. Peripheral pulses are diminished or absent. There are color changes in the extremities. The colour may range from cyanotic blue to reddish blue. Skin becomes thin and shiny. Hair growth is reduced. Ulcerations and gangrene in the extremities are common complications, often resulting in the need for amputation of the involved extremity.

Metachromatic leukodystrophy (MLD, also called arylsulfatase A deficiency) is a lysosomal storage disease which is commonly listed in the family of leukodystrophies as well as among the sphingolipidoses as it affects the metabolism of sphingolipids. Leukodystrophies affect the growth and/or development of myelin, the fatty covering which acts as an insulator around nerve fibers throughout the central and peripheral nervous systems. MLD involves cerebroside sulfate accumulation. Metachromatic leukodystrophy, like most enzyme deficiencies, has an autosomal recessive inheritance pattern.