Pemphigus foliaceus has been recognized in pet dogs, cats, and horses and is the most common autoimmune skin disease diagnosed in veterinary medicine. Pemphigus foliaceus in animals produces clusters of small vesicles that quickly evolve into pustules. Pustules may rupture, forming erosions or become crusted. Left untreated, pemphigus foliaceus in animals is life-threatening, leading to not only loss of condition but also secondary infection.

Pemphigus vulgaris is a very rare disorder described in pet dogs and cats. Paraneoplastic pemphigus has been identified in pet dogs.

In most cases of bullous pemphigoid, no clear precipitating factors are identified. Potential precipitating events that have been reported include exposure to ultraviolet light and radiation therapy. Onset of bullous pemphigoid has also been associated with certain drugs, including furosemide, and other nonsteroidal anti-inflammatory agents, captopril, penicillamine, and antibiotics.

IgA pemphigus is a subtype of pemphigus with two distinct forms:

- "Subcorneal pustular dermatosis" (also known as Sneddon–Wilkinson disease and pustulosis subcornealis) is skin condition that is a rare, chronic, recurrent, pustular eruption characterized histopathologically by subcorneal pustules that contain abundant neutrophils. This is distinct from and not to be confused with subcorneal pustular dermatosis type of IgA pemphigus. Sneddon's syndrome, also known as Ehrmann-Sneddon syndrome, is also a different syndrome.

- "Intraepidermal neutrophilic IgA dermatosis" is characterized histologically by intraepidermal bullae with neutrophils, some eosinophils, and acantholysis.

Bullous pemphigoid may be self-resolving in a period ranging from several months to many years even without treatment. Poor general health related to old age is associated with a poorer prognosis.

Types include:

- Acrodermatitis enteropathica

- Acropustulosis

- Acrodermatitis chronica atrophicans

- Papular acrodermatitis of childhood

- Dermatitis repens

Dermatitis herpetiformis generally responds well to medication and changes in diet. However, it is an autoimmune disease, and patients with DH are more likely than others to have thyroid problems and intestinal lymphoma.

Dermatitis herpetiformis does not usually cause complications on its own, without being associated with another condition. Complications from this condition, however, arise from the autoimmune character of the disease, as an overreacting immune system is a sign that something does not work well and might cause problems to other parts of the body that do not necessarily involve the digestive system.

Gluten intolerance and the body's reaction to it make the disease more worrying in what concerns the possible complications. This means that complications that may arise from dermatitis herpetiformis are the same as those resulting from coeliac disease, which include osteoporosis, certain kinds of gut cancer, and an increased risk of other autoimmune diseases such as thyroid disease.

The risks of developing complications from dermatitis herpetiformis decrease significantly if the affected individuals follow a gluten-free diet. The disease has been associated with autoimmune thyroid disease, insulin-dependent diabetes, lupus erythematosus, Sjögren's syndrome, sarcoidosis, vitiligo, and alopecia areata.

The forms of pemphigoid are considered to be connective tissue autoimmune skin diseases. There are several types:

- Gestational pemphigoid or Pemphigoid gestationis (PG) (formerly called Herpes gestationis)

- Bullous pemphigoid (BP) Rarely affect the mouth

- Mucous membrane pemphigoid, also known as Cicatricial pemphigoid (CP) (No skin involvement)

Bullous and Cicatricial pemphigoids usually affect persons who are over age 60. Gestational pemphigoid occurs during pregnancy, typically in the second or third trimester, and/or immediately following pregnancy.

Pemphigoid is a group of rare autoimmune blistering skin diseases. As its name indicates, pemphigoid is similar in general appearance to pemphigus, but, unlike pemphigus, pemphigoid does not feature acantholysis, a loss of connections between skin cells.

Pemphigoid is more common than pemphigus, and is slightly more common in women than in men. It is also more common in people over 60 years of age than it is in younger people.

A vesiculobullous disease is a type of mucocutaneous disease characterized by vesicles and bullae (i.e. blisters). Both vesicles and bullae are fluid-filled lesions, and they are distinguished by size (vesicles being less than 5–10 mm and bulla being larger than 5–10 mm, depending upon which definition is used). In the case of vesiculobullous diseases which are also immune disorders, the term "immunobullous" is sometimes used. Examples of vesiculobullous diseases include:

- "Infectious: (viral)"

- Herpes simplex

- Varicella-Zoster infection

- Hand, foot and mouth disease

- Herpangina

- Measles (Rubeola)

- "Immunobullous:"

- Pemphigus vulgaris

- Pemphigoid

- Dermatitis herpetiformis

- Linear immunoglobulin-A disease (linear IgA disease)

- "Genetic:"

- Epidermolysis bullosa

Some features are as follows:

Pemphigus ( or ) is a rare group of blistering autoimmune diseases that affect the skin and mucous membranes. The name is derived from the Greek root "pemphix" meaning "pustule".

In pemphigus, autoantibodies form against desmoglein. Desmoglein forms the "glue" that attaches adjacent epidermal cells via attachment points called desmosomes. When autoantibodies attack desmogleins, the cells become separated from each other and the epidermis becomes "unglued", a phenomenon called acantholysis. This causes blisters that slough off and turn into sores. In some cases, these blisters can cover a significant area of the skin.

Originally, the cause of this disease was unknown, and "pemphigus" was used to refer to any blistering disease of the skin and mucosa. In 1964, researchers found that the blood of patients with pemphigus contained antibodies to the layers of skin that separate to form the blisters. In 1971, an article investigating the autoimmune nature of this disease was published.

Adenocarcinoma of the bowel has been associated with coeliac disease.

Acrodermatitis /ac·ro·der·ma·ti·tis/ is a childhood form of dermatitis selectively affecting the hands and feet and may be accompanied by mild symptoms of fever and malaise. It may also be associated with hepatitis B and other viral infections.

The lesions appear as small coppery-red, flat-topped firm papules that appear in crops and sometimes in long linear strings, often symmetric.

It is a diffuse chronic skin disease usually confined to the limbs, seen mainly in women in Northern, Central, and Eastern Europe, and characterized initially by an erythematous, oedematous, pruritic phase followed by sclerosis and atrophy. It is caused by infection with "Borrelia burgdorferi".

The cause of prurigo nodularis is unknown, although other conditions may induce PN. PN has been linked to Becker's nevus, linear IgA disease, an autoimmune condition, liver disease and T cells. Systemic pruritus has been linked to cholestasis, thyroid disease, polycythaemia rubra vera, uraemia, Hodgkins disease, HIV and other immunodeficiency diseases. Internal malignancies, liver failure, renal failure, and psychiatric illnesses have been considered to induce PN, although more recent research has refuted a psychiatric cause for PN. Patients report an ongoing battle to distinguish themselves from those with psychiatric disorders such as delusions of parasitosis and other psychiatric conditions.

Linear IgA bullous dermatosis is frequently associated with medication exposure, especially vancomycin, with men and women being equally affected. It was first described by Tadeusz Chorzelski in 1979. Linear IgA dermatosis is a rare immune-mediated blistering skin disease that may be divided into two types:

- "Adult linear IgA disease" is an acquired, autoimmune blistering disease that may present with a clinical pattern of vesicles indistinguishable from dermatitis herpetiformis, or with vesicles and bullae in a bullous pemphigoid-like appearance. This disease can often be difficult to treat even with usually effective medications such as rituximab.

- "Childhood linear IgA disease" (also known as "Chronic bullous disease of childhood") is an acquired, self-limited bullous disease that may begin by the time the patient is age 2 to 3 and usually remits by age 13.

GSE can result in high risk pregnancies and infertility. Some infertile women have GSE and iron deficiency anemia others have zinc deficiency and birth defects may be attributed to folic acid deficiencies.

It has also been found to be a rare cause of amenorrhea.

Chronic and repetitive scratching, picking, or rubbing of the nodules may result in permanent changes to the skin, including nodular lichenification, hyperkeratosis, hyperpigmentation, and skin thickening. Unhealed, excoriated lesions are often scaly, crusted or scabbed. Many patients report a lack of wound healing even when medications relieve the itching and subsequent scratching.

Patients often:

- seek treatment during middle-age, although PN can occur at any age.

- have a history of chronic severe pruritus.

- have a significant medical history for unrelated conditions.

- suffer from liver or kidney dysfunctions.

- suffer secondary skin infections.

- have a personal or family history of atopic dermatitis.

- have other autoimmune disorders.

- have low vitamin D levels.

A survey of 10,000 American households revealed that the prevalence of diagnosed primary immunodeficiency approaches 1 in 1200. This figure does not take into account people with mild immune system defects who have not received a formal diagnosis.

Milder forms of primary immunodeficiency, such as selective immunoglobulin A deficiency, are fairly common, with random groups of people (such as otherwise healthy blood donors) having a rate of 1:600. Other disorders are distinctly more uncommon, with incidences between 1:100,000 and 1:2,000,000 being reported.

Prevalence varies by population, but is on the order of 1 in 100 to 1 in 1000 people, making it relatively common for a genetic disease.

SigAD occurs in 1 of 39 to 57 patients with celiac disease. This is much higher than the prevalence of selective IgA deficiency in the general population. It is also significantly more common in those with type 1 diabetes.

It is more common in males than in females.

Prognosis is excellent, although there is an association with autoimmune disease. Of note, selective IgA deficiency can complicate the diagnosis of one such condition, celiac disease, as the deficiency masks the high levels of certain IgA antibodies usually seen in celiac disease.

As opposed to the related condition CVID, selective IgA deficiency is not associated with an increased risk of cancer.

Patients with Selective IgA deficiency are at risk of anaphylaxis from blood transfusions. These patients should receive IgA free containing blood products and ideally blood from IgA-deficient donors.

Aside from the mosquito allergy cat, cats with EGC usually have allergy, ectoparasite infestation or possibly ringworm or other skin infection. Other implicated causes include traumatic damage, autoimmune disease or FeLV infection.

Urticaria is a vascular reaction of the skin characterized by the appearance of wheals, which are firm, elevated swelling of the skin. Angioedema, which can occur alone or with

urticaria, is characterized by a well-defined, edematous swelling that involves subcutaneous tissues, abdominal organs, or upper airway.

- Acquired C1 esterase inhibitor deficiency

- Acute urticaria

- Adrenergic urticaria

- Anaphylaxis

- Aquagenic urticaria

- Cholinergic urticaria

- Chronic urticaria (ordinary urticaria)

- Cold urticaria

- Dermatographism (dermographism)

- Episodic angioedema with eosinophilia (Gleich's syndrome)

- Exercise urticaria (exercise-induced urticaria)

- Galvanic urticaria

- Heat urticaria

- Hereditary angioedema (Quincke's edema)

- Localized heat contact urticaria

- Mast cell-independent urticaria

- Physical urticaria

- Primary cold contact urticaria

- Pressure urticaria (delayed pressure urticaria)

- Reflex cold urticaria

- Schnitzler syndrome

- Secondary cold contact urticaria

- Solar urticaria

- Systemic capillary leak syndrome

- Urticarial allergic eruption

- Urticaria-like follicular mucinosis

- Vibratory angioedema

Current research is aimed at studying large cohorts of people with CVID in an attempt to better understand age of onset, as well as mechanism, genetic factors, and progression of the disease.

Funding for research in the US is provided by the National Institutes of Health. Key research in the UK was previously funded by the Primary Immunodeficiency Association (PiA) until its closure in January 2012, and funding is raised through the annual Jeans for Genes campaign. Current efforts are aimed at studying the following:

- Causes of complications. Little is known about why such diverse complications arise during treatment

- Underlying genetic factors. Though many polymorphisms and mutations have been identified, their respective roles in CVID development are poorly understood, and not represented in all people with CVID.

- Finding new ways to study CVID. Given that CVID arises from more than one gene, gene knock-out methods are unlikely to be helpful. It is necessary to seek out disease related polymorphisms by screening large populations of people with CVID, but this is challenging given the rarity of the disease.

By definition, primary immune deficiencies are due to genetic causes. They may result from a single genetic defect, but most are multifactorial. They may be caused by recessive or dominant inheritance. Some are latent, and require a certain environmental trigger to become manifest, like the presence in the environment of a reactive allergen. Other problems become apparent due to aging of bodily and cellular maintenance processes.

Ionizing radiation-induced cutaneous conditions result from exposure to ionizing radiation.

- Acute radiodermatitis

- Chronic radiation keratosis

- Chronic radiodermatitis

- Eosinophilic, polymorphic, and pruritic eruption associated with radiotherapy

- Fluoroscopy burn

- Radiation acne

- Radiation cancer

- Radiation dermatitis (radiodermatitis)

- Radiation recall reaction

- Radiation-induced erythema multiforme

- Radiation-induced hypertrophic scar

- Radiation-induced keloid

- Radiation-induced morphea

Dapsone is an effective treatment in most people. Itching is typically reduced within 2–3 days. However, dapsone treatment has no effect on any intestinal damage that might be present.

Therefore, a strict gluten-free diet must also be followed, and this will usually be a lifelong requirement. This will reduce any associated intestinal damage and the risk of other complications. After some time on a gluten-free diet, the dosage of dapsone can usually be reduced or even stopped, although this can take many years.

Dapsone is an antibacterial, and its role in the treatment of DH, which is not caused by bacteria, is poorly understood. It can cause adverse effects on the blood, so regular blood monitoring is required.

Dapsone is the drug of choice. For individuals with DH unable to tolerate dapsone for any reason, alternative treatment options may include the following:

- colchicine

- lymecycline

- nicotinamide

- tetracycline

- sulfamethoxypyridazine

- sulfapyridine