Why is immunoglobulin needed after a tick bite?

Why is immunoglobulin needed after a tick bite? - briefly

Immunoglobulin supplies immediate antibodies that neutralize tick‑borne pathogens or their toxins, preventing infection before the active vaccine can induce a protective response. It is administered when recent exposure carries a high risk of disease, such as rabies.

Why is immunoglobulin needed after a tick bite? - in detail

A bite from a hard‑bodied arachnid can introduce a range of pathogens and, in some species, a neurotoxic protein that causes rapid muscle weakness. Immediate neutralisation of these agents is often the only reliable way to prevent severe disease, which is why passive antibody therapy is sometimes required after exposure.

The principal reasons for administering immunoglobulin after such an encounter are:

  • Neutralisation of tick‑derived neurotoxins – Certain ticks secrete a paralytic toxin that interferes with neuromuscular transmission. Human anti‑tick‑paralysis immunoglobulin binds the toxin, halting progression of weakness and allowing recovery once the tick is removed.
  • Post‑exposure prophylaxis for tick‑borne encephalitis (TBE) – In endemic regions, individuals at high risk may receive hyper‑immune TBE immunoglobulin within 72 hours of a bite. The antibodies provide immediate protection while the active vaccine response develops.
  • Severe systemic infections – Rare cases of fulminant anaplasmosis, babesiosis, or relapsing fever may be refractory to antibiotics. Intravenous immunoglobulin (IVIG) supplies a broad spectrum of antibodies that enhance opsonisation and complement activation, supporting the host’s immune clearance.
  • Rabies risk – If a tick is found attached to a rabid animal, rabies immune globulin is administered alongside the vaccine to deliver immediate neutralising antibodies at the wound site.

Mechanistically, immunoglobulin achieves protection by:

  1. Binding to specific antigens on pathogens or toxins, preventing attachment to host cells.
  2. Marking the complex for phagocytosis through Fc‑mediated opsonisation.
  3. Activating the complement cascade, leading to lysis of susceptible organisms.
  4. Modulating the inflammatory response, which can mitigate tissue damage in severe infections.

The therapeutic window is narrow: antibodies must be present before the toxin or pathogen disseminates. Consequently, clinicians assess exposure risk, local disease prevalence, and symptom onset to decide whether passive immunisation is warranted. When indicated, a single dose of appropriate hyper‑immune globulin is given intramuscularly or intravenously, followed by observation for adverse reactions and, when relevant, initiation of active vaccination to sustain long‑term immunity.