9.1 Hypersensitivity

A type of hypersensitivity reaction characterized by skin reactions that are usually papular and erythematous and may involve the feet, eyes, ears, and axile or perianal area.

This skin condition in dogs often shows poor response to corticosteroids.

This breed is particularly prone to Atopic Dermatitis.

A common trigger for Atopic Dermatitis in dogs, these microscopic creatures are found in house dust.

A common symptom of Atopic Dermatitis in dogs, this indicates intense itching.

Chronic licking and scratching can lead to these skin problems in dogs with Atopic Dermatitis.

The release of histamine from mast cells and basophils is the primary cause of this type of hypersensitivity reaction.

Also known as cytotoxic hypersensitivity reactions, this type of hypersensitivity involves the destruction of cells.

This is a necessary condition for hypersensitivity reactions to occur, involving a primed immune system.

This type of hypersensitivity is primarily mediated by immunoglobulin E (IgE) antibodies.

A widely used classification system for hypersensitivity reactions, named after the scientists who developed it.

This type of hypersensitivity is primarily characterized by complement fixation, involving a component of the immune system.

This can be triggered by events like the rupture of a hydatid cyst or blood transfusions from infected dogs, leading to a severe allergic reaction.

Allergies to parasites often involve this type of hypersensitivity reaction.

The rapid elimination of transfused red blood cells in genetically different individuals is caused by this process.

This type of hypersensitivity is involved in the rapid elimination of transfused red blood cells in genetically different individuals.

This is the consequence of the elimination of transfused red blood cells in genetically different individuals, involving both intravascular and extravascular destruction.

This type of hypersensitivity is associated with red cell antigens and antibody-mediated hypersensitivity reactions.

These cells are primarily involved in the tuberculin reaction, a type of delayed hypersensitivity.

These cells present antigen to memory T cells after tuberculin is injected intradermally, initiating the reaction.

These cytokines promote the activation of T cells, macrophages, and basophils in response to tuberculin, amplifying the reaction.

Macrophages play a crucial role in this type of hypersensitivity reaction, responsible for causing tissue damage.

When an animal is exposed to M. tuberculosis, these specialized cells are generated, enabling a faster response to future encounters with the bacterium.

The tuberculin reaction is categorized as this type of hypersensitivity reaction, characterized by a delayed response.

These cells play a primary role in the Arthus reaction, phagocytising immune complexes.

Staphylococcal hypersensitivity is primarily associated with this type of hypersensitivity reaction, involving immune complexes.

The interactions between injected antigen, antigen-presenting cells, and T cells ultimately lead to this type of reaction.

This reaction is crucial for eliminating antigens that resist conventional acute inflammatory processes, promoting a delayed immune response.

In the Arthus reaction, these cells release neutrophil chemotactic factor and proteases, contributing to the inflammatory response.

This type of hypersensitivity is the primary cause of pruritic pustular dermatitis in dogs, involving immune complexes.

These IgE-mediated responses play a crucial role in type I hypersensitivity, primarily controlling parasitic infections.

These are major components of the granules released during eosinophil degranulation, playing a role in fighting parasites.

In type I hypersensitivity, clinical signs result from the release of these inflammatory mediators from mast cells, eosinophils, and basophils.

This type of immune response is characterized by eosinophil degranulation in response to IgE-coated parasites, playing a key role in parasite defense.

Eosinophils destroy large parasites primarily through this mechanism, involving the release of substances that damage the parasite.

These cells, including Th cells and mast cells, produce molecules that stimulate the release of eosinophils into the bloodstream, boosting the immune response.

Allergic dermatitis is responsible for a significant portion of skin diseases in dogs, reflecting the prevalence of allergic reactions.

This type of food is frequently involved in food allergies in dogs, leading to allergic reactions.

Atopic Dermatitis in dogs is associated with this type of hypersensitivity reaction, involving IgE antibodies.

These anatomical areas are commonly affected by skin reactions in dogs with food allergies, showing the impact of allergies on specific areas.

These are organs that can be affected by inhaled antigens in acute anaphylaxis, showing the breadth of the allergic reaction.

This organ is the major shock organ in dogs during acute anaphylaxis, reflecting the severity of the reaction.

Only a small percentage of ingested protein is absorbed as peptide fragments large enough to be recognized as foreign, explaining the rarity of food allergies.

Vasoactive molecules binding to their receptors is the primary reason for the symptoms experienced during acute anaphylaxis, highlighting the chemical basis of allergic reactions.

The clinical course of acute anaphylaxis depends on this factor, underlining the importance of understanding the spread of the reaction.

The primary component of tuberculin used in skin tests, this substance is derived from M. tuberculosis.