Why does a reaction occur after a flea bite? - briefly
Flea saliva contains anticoagulant proteins that the immune system identifies as foreign, prompting an immediate hypersensitivity reaction with histamine release that produces redness, swelling, and itching. Repeated bites can intensify this response as the body becomes sensitized.
Why does a reaction occur after a flea bite? - in detail
When a flea pierces the skin, it injects saliva that contains anticoagulant enzymes, proteases, and allergenic proteins. These substances prevent blood clotting and facilitate feeding, but they also act as foreign antigens. The immune system recognizes the proteins as threats, triggering a cascade of events.
The immediate phase involves mast cells and basophils. Their surface receptors bind the flea salivary antigens, causing degranulation and release of histamine, serotonin, and leukotrienes. Histamine dilates capillaries, increases vascular permeability, and stimulates nerve endings, producing redness, swelling, and itching within minutes.
Later, antigen‑presenting cells such as dendritic cells capture the salivary proteins and migrate to regional lymph nodes. There they present peptide fragments to naïve T lymphocytes, prompting differentiation into Th2 cells. Th2 cells secrete interleukin‑4 (IL‑4) and interleukin‑13 (IL‑13), which drive B‑cell class switching to IgE production.
IgE antibodies bind to high‑affinity FcεRI receptors on mast cells and basophils. Upon subsequent flea bites, cross‑linking of surface‑bound IgE by the same salivary antigens causes rapid, amplified degranulation—a classic Type I hypersensitivity response. This secondary reaction is more intense, often lasting several hours to days, and may include papules, vesicles, or a wheal‑and‑flare pattern.
Additional contributors include:
- Proteolytic enzymes in flea saliva that degrade skin proteins, exposing additional epitopes.
- Cytokine release (e.g., IL‑31) that intensifies pruritus by acting on sensory neurons.
- Eosinophil recruitment driven by chemokines (e.g., eotaxin) that sustains inflammation during the late phase.
In individuals with prior sensitization, the immune system reacts more vigorously, whereas naïve hosts may experience only a mild, transient wheal. The overall reaction results from the combined effects of mechanical injury, salivary antigens, and the host’s adaptive immune response.