There are several diseases that are caused by avian reovirus, which includes, avian arthritis/tenosynovitis, runting-stunting syndrome, and blue wing disease in chickens. Blue wing disease affects young broiler chickens and has an average mortality rate of 10%. It causes intramuscular and subcutaneous hemorrhages and atrophy of the spleen, bursa of Fabricius, and thymus. When young chickens are experimentally infected with avian reovirus, it is spread rapidly throughout all tissues. This virus is spread most frequently in the skin and muscles, which is also the most obvious site for lesions. Avian arthritis causes significant lameness in joints, specifically the hock joints. In the most severe cases, viral arthritis has caused the tendon to rupture. Chickens that have contracted runting-stunting syndrome cause a number of individuals in a flock to appear noticeably small due to its delayed growth. Diseased chicks are typically pale, dirty, wet, and may have a distending abdomen. Some individuals may display “helicopter-like” feathers in their wings and other feather abnormalities. The virus has also been shown to cause osteoporosis.

Avian reoviruses belong to the genus "Orthoreovirus", and "Reoviridae" family. They are non-enveloped viruses that undergo replication in the cytoplasm of infected cells. It has icosahedral symmetry and contains a double-shelled arrangement of surface protein. Virus particles can range between 70–80 nm. Morphologically, the virus is a double stranded RNA virus that is composed of ten segments. The genome and proteins that are encoded by the genome can be separated into three different sizes ranging from small, medium, or large. Of the eleven proteins that are encoded for by the genome, two are nonstructural, while the remaining nine are structural.

Avian reoviruses can withstand a pH range of 3.0–9.0. Ambient temperatures are suitable for the survival of these viruses, which become inactive at 56 °C in less than an hour. Common areas where this virus can survive include galvanized metal, glass, rubber, feathers, and wood shavings. Avian reovirus can survive for up to ten days on these common areas in addition to up to ten weeks in water.

Cultivation and observation of the effects of avian reovirus is most often performed in chicken embryos. If infected into the yolk sac, the embryo will succumb to death accompanied by hemorrhaging of the embryos and cause the foci on the liver to appear yellowish-green. There are several primary chicken cell cultures/areas that are susceptible to avian reoviruses, which include the lungs, liver, kidney, and fibroblasts of the chick embryo. Of the following susceptible areas, liver cells from the chick embryo have been found to be the most sensitive for primary isolation from clinical material.

Typically, the CPE effect of avian reoviruses is the production of syncytia. CPE, or cytopathic effects are the visible changes in a host cell that takes place because of viral infection. Syncytia is a single cell or cytoplasmic mass containing several nuclei, formed by fusion of cells or by division of nuclei.

Psittacine beak and feather disease (PBFD) is a viral disease affecting all Old World and New World parrots. The causative virus–beak and feather disease virus (BFDV)—belongs to the taxonomic genus Circovirus, family Circoviridae. It attacks the feather follicles and the beak and claw matrices of the bird, causing progressive feather, claw and beak malformation and necrosis. In later stages of the disease, feather shaft constriction occurs, hampering development until eventually all feather growth stops. It occurs in an acutely fatal form and a chronic form.

Cracking and peeling of the outer layers of the claws and beak make tissues vulnerable to . Because the virus also affects the thymus and Bursa of Fabricius, slowing lymphocyte production, immunosuppression occurs and the bird becomes more vulnerable to secondary infections. Beak fractures and necrosis of the hard palate can prevent the bird from eating.

The acute form of the disease is manifested by lethargy, loss of appetite, vomiting and diarrhea. Due to the severe immune system suppression, multiple secondary infections develop, causing death within two to four weeks. Typical confirmation of the acute form of the disease is by necropsy, because it progresses too quickly for the normal signs such as feather loss and beak deformity to appear.

The chronic form occurs if the bird's immune system manages to mount a reaction to the virus and any secondary infections. The characteristic feather symptoms need time to develop, as they only appear during the first moult after infection. In those species having powder down, signs may be visible immediately, as powder down feathers are continually replenished.

The acute stage of the disease, occurring most often in the spring and summer, begins one to three weeks after infection and lasts for two to four weeks. Clinical signs include a fever, petechiae, bleeding disorders, vasculitis, lymphadenopathy, discharge from the nose and eyes, and edema of the legs and scrotum. There are no outward signs of the subclinical phase. Clinical signs of the chronic phase include weight loss, pale gums due to anemia, bleeding due to thrombocytopenia, vasculitis, lymphadenopathy, dyspnea, coughing, polyuria, polydipsia, lameness, ophthalmic diseases such as retinal hemorrhage and anterior uveitis, and neurological disease. Dogs that are severely affected can die from this disease.

Although people can get ehrlichiosis, dogs do not transmit the bacteria to humans; rather, ticks pass on the "ehrlichia" organism. Clinical signs of human ehrlichiosis include fever, headache, eye pain, and gastrointestinal upset. It is quite similar to Rocky Mountain spotted fever, but rash is not seen in patients.

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.

It is also called the hematic phase. The most common findings are fever (usually sustained, but with temperature no greater than 102 °F (39 °C)), pale appearance, malaise, painless liver enlargement, jaundice, enlarged lymph nodes, and enlarged spleen. This phase is characterized by severe hemolytic anemia and transient immunosuppression. The case fatality ratios of untreated patients exceeded 40% but reach around 90% when opportunistic infection with "Salmonella spp" occurs. In a recent study, the attack rate was 13.8% (123 cases) and the case-fatality rate was 0.7%.

Other symptoms include a headache, muscle aches, and general abdominal pain. Some studies have suggested a link between Carrion's disease and heart murmurs due to the disease's impact on the circulatory system. In children, symptoms of anorexia, nausea, and vomiting have been investigated as possible symptoms of the disease.

Most of the mortality of Carrion's disease occurs during the acute phase. Studies vary in their estimates of mortality. In one study, mortality has been estimated as low as just 1% in studies of hospitalized patients, to as high as 88% in untreated, unhospitalized patients. In developed countries, where the disease rarely occurs, it is recommended to seek the advice of a specialist in infectious disease when diagnosed. Mortality is often thought to be due to subsequent infections due to the weakened immune symptoms and opportunistic pathogen invasion, or consequences of malnutrition due to weight loss in children. In a study focusing on pediatric and gestational effects of the disease, mortality rates for pregnant women with the acute phase were been estimated at 40% and rates of spontaneous abortion in another 40%.

It is also called the eruptive phase or tissue phase, in which the patients develop a cutaneous rash produced by a proliferation of endothelial cells and is known as "Peruvian warts" or "verruga peruana". Depending on the size and characteristics of the lesions, there are three types: miliary (1–4 mm), nodular or subdermic, and mular (>5mm). Miliary lesions are the most common. The lesions often ulcerate and bleed.

The most common findings are bleeding of verrugas, fever, malaise, arthralgias (joint pain), anorexia, myalgias, pallor, lymphadenopathy, and liver and spleen enlargement.

On microscopic examination, the chronic phase and its rash are produced by angioblastic hyperplasia, or the increased rates and volume of cell growth in the tissues that form blood vessels. This results in a loss of contact between cells and a loss of normal functioning.

The chronic phase is the more common phase. Mortality during the chronic phase is very low.

Pythiosis of the skin in dogs is rare, and appears as ulcerated lumps. Primary infection can also occur in the bones and lungs. Dogs with the gastrointestinal form of pythiosis have severe thickening of one or more portions of the gastrointestinal tract that may include the stomach, small intestine, colon, rectum, or in rare cases, even the esophagus. The resulting pathology results in anorexia, vomiting, diarrhea (sometimes bloody), and abdominal straining. Extensive weight loss may be evident.

In cats, pythioisis is almost always confined to the skin as hairless and edematous lesions. It is usually found on the limbs, perineum, and at the base of the tail. Lesions may also develop in the nasopharynx.

The only animals that have been successfully infected with the disease are rabbits which are used for "in vivo" studies of the disease.

Other animals reported to have contracted pythiosis are bears, jaguars, camels, and birds, although these have only been singular events.

There are a large number of immunodeficiency syndromes that present clinical and laboratory characteristics of autoimmunity. The decreased ability of the immune system to clear infections in these patients may be responsible for causing autoimmunity through perpetual immune system activation.

One example is common variable immunodeficiency (CVID) where multiple autoimmune diseases are seen, e.g., inflammatory bowel disease, autoimmune thrombocytopenia and autoimmune thyroid disease.

Familial hemophagocytic lymphohistiocytosis, an autosomal recessive primary immunodeficiency, is another example. Pancytopenia, rashes, lymphadenopathy and hepatosplenomegaly are commonly seen in these patients. Presence of multiple uncleared viral infections due to lack of perforin are thought to be responsible.

In addition to chronic and/or recurrent infections many autoimmune diseases including arthritis, autoimmune hemolytic anemia, scleroderma and type 1 diabetes are also seen in X-linked agammaglobulinemia (XLA).

Recurrent bacterial and fungal infections and chronic inflammation of the gut and lungs are seen in chronic granulomatous disease (CGD) as well. CGD is caused by a decreased production of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase by neutrophils.

Hypomorphic RAG mutations are seen in patients with midline granulomatous disease; an autoimmune disorder that is commonly seen in patients with granulomatosis with polyangiitis (Wegner’s disease) and NK/T cell lymphomas.

Wiskott-Aldrich syndrome (WAS) patients also present with eczema, autoimmune manifestations, recurrent bacterial infections and lymphoma.

In autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) also autoimmunity and infections coexist: organ-specific autoimmune manifestations (e.g., hypoparathyroidism and adrenocortical failure) and chronic mucocutaneous candidiasis.

Finally, IgA deficiency is also sometimes associated with the development of autoimmune and atopic phenomena.

In reality, immunodeficiency often affects multiple components, with notable examples including severe combined immunodeficiency (which is primary) and acquired immune deficiency syndrome (which is secondary).

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.

Although symptoms can vary greatly between affected individuals, even those within the same family, symptoms normally begin in infancy and are typically a result of thickening skin and mucous membranes. The first symptom is often a weak cry or a hoarse voice due to a thickening of the vocal cords. The hoarse voice can be one of the most striking clinical manifestations of the disease. Lesions and scars also appear on the skin, usually the face and the distal parts of the limbs. This is often the result of poor wound healing and the scarring continues to increase as the patient ages, leaving the skin with a waxy appearance. Skin may be easily damaged as a result of only a minor trauma or injury, leaving many blisters and additional scars. The skin is also usually very dry and wrinkly. White or yellow infiltrates form on the lips, buccal mucosa, tonsils, uvula, epiglottis and frenulum of the tongue. This can lead to upper respiratory tract infection and sometimes requires tracheostomy to relieve the symptom. Too much thickening of the frenulum can restrict tongue movement and may result in speech impediments. Beading of the papules around the eyelids is a very common symptom and is often used as part of a diagnosis of the disease. Some other dermatological symptoms that are sometimes seen but less common include hair loss, parotitis and other dental abnormalities, corneal ulceration, and focal degeneration of the macula.

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.

The characteristic symptom of Degos disease is the development of papules. Initially, individuals may have skin lesions or rashes, but they will proceed to develop distinct bumps, or papules. Papules are circular in shape, have a porcelain-white center and red border. As papules age, the white centers will skin in and only the border will remain raised. Typically, papules range from 0.5 to 1 cm in width. Papules appear on the trunk and upper extremities and are not found on the individual's palms, soles, scalp, or face.

Depending on whether an individual has the benign variant or malignant variant of the disease symptoms will vary. Both the benign and malignant forms have development of the characteristic papules. Individuals with the benign form will have the typical papules persisting anywhere from a few years to throughout their whole lives. In the benign form, no inner organs are affected. If an individual develops the malignant form, it means that not only are the papules present, but inner organs are involved. Most malignant cases involve problems of the gastrointestinal tract leading to small intestine lesions, abdominal pain, diarrhea, and bowel perforation. If the central nervous system is involved, symptoms can include headaches, dizziness, seizures, paralysis of cranial nerves, weakness, stroke, damage to small areas of the brain due to artery blockage (cerebral infarcts, and cerebral hemorrhage). Additional organs commonly impacted include the heart, lungs, and kidneys. Symptoms that may develop from damage to these organs include double vision (diploplia), clouding of lenses of eyes, swelling of the optic disc (papilledema), partial loss of vision, shortness of breath, chest pain, epilepsy,and thickening of pericardium.

Someone with the benign form may suddenly develop symptoms of the malignant form. Symptoms can last anywhere from a few weeks to several years. Onset of symptoms typically begins to manifest between the ages of 20-50. A few cases of this condition in newborns have also been described.

Urbach–Wiethe disease is characterized by both neurological and dermatological symptoms.

Symptoms start with slowly developing dysarthria (difficulty speaking) and cerebellar ataxia (unsteadiness) and then the progressive dementia becomes more evident. Loss of memory can be the first symptom of GSS. Extrapyramidal and pyramidal symptoms and signs may occur and the disease may mimic spinocerebellar ataxias in the beginning stages. Myoclonus (spasmodic muscle contraction) is less frequently seen than in Creutzfeldt–Jakob disease. Many patients also exhibit nystagmus (involuntary movement of the eyes), visual disturbances, and even blindness or deafness. The neuropathological findings of GSS include widespread deposition of amyloid plaques composed of abnormally folded prion protein.

Like other mitochrondrial diseases, "MNGIE is a multisystem disorder". MNGIE primarily affects the gastrointestinal and neurological systems. Gastrointestinal symptoms may include gastrointestinal dysmotility, due to inefficient peristalsis, which may result in pseudo-obstruction and cause malabsorption of nutrients. Additionally, gastrointestinal symptoms such as borborygmi, early satiety, diarrhea, constipation, gastroparesis, nausea, vomiting, weight loss, and diverticulitis may be present in MNGIE patients. Neurological symptoms may include diffuse leukoencephalopathy, peripheral neuropathy, and myopathy. Ocular symptoms may include retinal degeneration, ophthalmoplegia, and ptosis. Those with MNGIE are often thin and experience continuous weight loss. The characteristic thinness of MNGIE patients is caused by multiple factors including inadequate caloric intake due to gastrointestinal symptoms and discomfort, malabsorption of food from bacterial overgrowth due to decreased motility, as well as an increased metabolic demand due to inefficient production of ATP by the mitochondria.

Livedo reticularis is a common skin finding consisting of a mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin. The discoloration is caused by swelling of the venules owing to obstruction of capillaries by small blood clots. The blood clots in the small blood vessels can be a secondary effect of a condition that increases a person's risk of forming blood clots, including a wide array of pathological and nonpathological conditions . Examples include hyperlipidemia, microvascular hematological or anemia states, nutritional deficiencies, hyper- and autoimmune diseases, and drugs/toxins.

The condition may be normal or related to more severe underlying pathology. Its differential diagnosis is broadly divided into possible blood diseases, autoimmune (rheumatologic) diseases, cardiovascular diseases, cancers, and endocrine disorders. It can usually (in 80% of cases) be diagnosed by biopsy.

It may be aggravated by exposure to cold, and occurs most often in the lower extremities.

The condition's name derives from the Latin "livere" meaning bluish and "reticular" which refers to the net-like appearance.

Liver disease (also called hepatic disease) is a type of damage to or disease of the liver.

MCD clinical features range from waxing and waning mild enlargement of the lymph nodes with B symptoms to more severe cases involving intense inflammation, widespread enlargement of lymph nodes enlargement of the liver and spleen, vascular leak syndrome with anasarca, fluid collections in the space around the lungs, and fluid collection in the abdomen's peritoneal space, organ failure, and even death. The most common 'B Symptoms' of MCD are high fevers, night sweats, weight loss, and loss of appetite. Acute episodes can display significant clinical overlap with acute viral illnesses, autoimmune diseases, hematologic malignancies, and even sepsis. Laboratory findings commonly include low red blood cell count, low or high platelet counts, low albumin, high gamma globulin levels, elevated C-reactive protein levels, elevated erythrocyte sedimentation rate, IL-6, vascular endothelial growth factor (VEGF), and fibrinogen; positive anti-nuclear antibody, anti-erythrocyte autoantibodies, and anti-platelet antibodies; and protein spilling into the urine, and polyclonal marrow plasmacytosis. Castleman disease is seen in POEMS syndrome and is implicated in 10% of cases of paraneoplastic pemphigus.

Castleman disease, also known as giant lymph node hyperplasia, lymphoid hamartoma, or angiofollicular lymph node hyperplasia, is a group of uncommon lymphoproliferative disorders that share common lymph node histological features. The disease is named after Benjamin Castleman.

Castleman's disease has two main forms: It may be localized to a single lymph node (unicentric) or occur systemically (multicentric).

The unicentric form can usually be cured by surgically removing the lymph node, with a 10-year survival of 95%.

Multicentric Castleman disease (MCD) involves hyperactivation of the immune system, excessive release of proinflammatory chemicals (cytokines), proliferation of immune cells (B cells and T cells), and multiple organ system dysfunction. Castleman disease must be distinguished from other disorders that can demonstrate "Castleman-like" lymph node features, including reactive lymph node hyperplasia, autoimmune disorders, and malignancies. Multicentric Castleman's disease is associated with lymphoma and Kaposi's sarcoma.

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.

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.