Which immunoglobulin is prescribed after a tick bite?

Understanding Tick Bites and Potential Risks

Identifying the Dangers of Tick-borne Diseases

Common Pathogens Transmitted by Ticks

Ticks transmit a diverse array of microorganisms that cause acute and chronic illnesses in humans. The most frequently encountered agents include:

Borrelia burgdorferi – spirochete responsible for Lyme disease; early infection presents with erythema migrans and flu‑like symptoms.
Rickettsia rickettsii – obligate intracellular bacterium causing Rocky Mountain spotted fever; characterized by fever, headache, and a maculopapular rash.
Ehrlichia chaffeensis and Anaplasma phagocytophilum – agents of human ehrlichiosis and anaplasmosis; produce leukopenia, thrombocytopenia, and elevated liver enzymes.
Babesia microti – intra‑erythrocytic protozoan causing babesiosis; manifests as hemolytic anemia and febrile illness.
Francisella tularensis – causative organism of tularemia; leads to ulceroglandular lesions and systemic infection.
Powassan virus – flavivirus transmitted by Ixodes species; can cause encephalitis and meningitis.
Tick‑borne encephalitis virus (TBEV) – flavivirus prevalent in Eurasia; results in meningitis, encephalitis, or meningoencephalitis.
Borrelia hermsii and related species – agents of relapsing fever; produce recurrent episodes of high fever and headache.

Additional pathogens reported in limited regions include Coxiella burnetii (Q fever), Hepatozoon spp., and various Rickettsia species causing spotted fevers. Recognizing these organisms guides diagnostic testing and informs therapeutic decisions after a tick exposure.

Symptoms of Tick-borne Infections

Tick bites introduce a range of bacterial, viral, and protozoan pathogens; recognizing the clinical picture promptly guides effective management.

Common tick‑borne infections present with distinct but sometimes overlapping signs:

Lyme disease – expanding erythema migrans lesion, fever, fatigue, headache, arthralgia, possible facial nerve palsy.
Anaplasmosis – abrupt fever, chills, severe headache, myalgia, leukopenia, elevated liver enzymes.
Babesiosis – hemolytic anemia, fever, chills, sweats, malaise, occasional jaundice.
Rocky Mountain spotted fever – high fever, headache, nausea, a maculopapular rash that begins on wrists and ankles and spreads centrally, possible confusion.
Ehrlichiosis – fever, rash, thrombocytopenia, elevated transaminases, mild respiratory symptoms.
Tularemia – ulceroglandular lesion, tender lymphadenopathy, fever, chills, sometimes pneumonia.

Symptom onset varies: erythema migrans may appear within 3–30 days, while fever and systemic signs of anaplasmosis or ehrlichiosis typically emerge 1–2 weeks after exposure. Early rash or localized inflammation often precedes systemic involvement.

Delayed treatment can lead to arthritis, neurological deficits, cardiac conduction abnormalities, or severe hemolysis, underscoring the need for timely diagnosis.

In selected high‑risk exposures, passive immunization with specific immunoglobulin preparations may be administered shortly after the bite to prevent disease progression; however, clinical assessment of symptoms remains the primary tool for deciding therapeutic intervention.

Immunoglobulin Therapy: A Closer Look

What is Immunoglobulin?

Types of Immunoglobulins

Immunoglobulins are glycoprotein molecules produced by B‑lymphocytes that recognize specific antigens and mediate immune responses. Five distinct classes circulate in human serum, each possessing unique structural features and functional specializations.

IgG – most abundant class; crosses placental barrier; mediates opsonization, complement activation, and neutralization; long half‑life enables sustained protection.
IgM – first antibody produced during primary exposure; exists as a pentamer; efficiently activates complement and agglutinates pathogens.
IgA – predominant in mucosal secretions; dimeric form resists proteolysis; protects respiratory, gastrointestinal, and genitourinary tracts.
IgE – binds high‑affinity receptors on mast cells and basophils; triggers degranulation upon allergen encounter; also participates in defense against parasites.
IgD – low‑level serum presence; functions primarily as a receptor on naïve B cells, facilitating antigen recognition.

Following a bite from an arthropod that can transmit infectious agents, passive immunotherapy relies on the IgG class. Human immune globulin preparations, composed of pooled IgG antibodies, are administered to provide immediate neutralizing activity while the host generates its own response. IgM, IgA, IgE, and IgD are not employed for this purpose because they lack the pharmacokinetic profile and broad-spectrum neutralizing capacity required for rapid prophylaxis.

Mechanism of Action

Rabies immune globulin is administered when a tick bite raises the possibility of rabies exposure. The preparation contains high‑titer anti‑rabies IgG harvested from human donors. Its therapeutic effect derives from immediate passive immunity.

Antibodies bind the rabies virion at the inoculation site, blocking attachment to neuronal receptors.
Neutralized virus is unable to enter peripheral nerves, halting retrograde axonal transport toward the central nervous system.
Fc regions engage complement and Fc‑γ receptors on phagocytes, promoting opsonization and clearance of viral particles.
The administered IgG persists in circulation for several weeks, maintaining protective titers until active vaccination induces endogenous antibody production.

Together, these actions provide rapid containment of the virus, buying time for the host’s active immune response to develop following the vaccine series.

Specific Immunoglobulins for Tick Bites

Human Immunoglobulin for Tick-borne Encephalitis (TBE)

Human anti‑tick‑borne encephalitis (TBE) immunoglobulin is the specific preparation administered after a suspected exposure to TBE‑infected ticks. It consists of purified IgG antibodies obtained from donors with high titres against the TBE virus and is supplied as a sterile solution for intramuscular injection.

The product is indicated for passive immunisation when a person has been bitten by a tick in a TBE‑endemic area and cannot receive the active vaccine promptly, or when vaccination is contraindicated. The recommended schedule consists of a single dose of 0.2 mL per kilogram of body weight, not exceeding 20 mL, injected into the deltoid or gluteal muscle within 72 hours of the bite. In cases of delayed presentation, the dose may be repeated after 7 days, although efficacy declines with time.

Clinical studies demonstrate that passive immunisation reduces the incidence of symptomatic TBE by approximately 80 % when administered within the optimal window. Adverse reactions are generally mild and include local soreness, transient fever, and headache. Severe hypersensitivity responses are rare; a history of severe allergic reactions to human immunoglobulins contraindicates use.

Key considerations for clinicians:

Verify exposure in a recognized TBE risk zone.
Assess eligibility for active vaccination; reserve immunoglobulin for those unable to be vaccinated.
Calculate dose based on exact body weight; avoid exceeding the maximum volume.
Observe the patient for at least 30 minutes post‑injection to detect immediate hypersensitivity.
Document administration in the patient’s record and advise follow‑up serology to confirm passive protection.

Human anti‑TBE immunoglobulin provides rapid, short‑term protection and is the standard passive prophylactic agent following tick exposure in regions where TBE is endemic.

When is TBE Immunoglobulin Administered?

TBE immunoglobulin (TBE‑IG) provides passive protection against tick‑borne encephalitis when active vaccination is unavailable or insufficient. It is indicated for individuals who have been bitten by a tick in regions where TBE is endemic and who meet specific risk criteria.

Unvaccinated persons or those with incomplete TBE vaccination series.
Exposure to a tick identified as Ixodes ricinus or Ixodes persulcatus, the primary vectors of TBE.
Bite occurring within 72 hours before presentation.
High‑risk scenarios, such as prolonged outdoor activity in forested areas during peak transmission months.

Administration should occur as early as possible after the bite. The optimal window is the first 24 hours; efficacy remains acceptable up to 48 hours and declines sharply after 72 hours. Delayed treatment beyond this period is generally not recommended.

The standard regimen consists of a single intramuscular dose of 250 IU per kilogram of body weight, administered in the deltoid muscle. No routine booster doses are required; repeat dosing is reserved for repeated high‑risk exposures within a short interval.

Contraindications include known hypersensitivity to human immunoglobulin preparations and severe IgA deficiency. In cases where TBE‑IG is contraindicated, immediate active immunization with the TBE vaccine should be initiated, acknowledging the delayed onset of protective immunity.

Efficacy and Limitations

The immunoglobulin administered after a tick exposure provides immediate passive immunity by delivering high‑titer neutralizing antibodies directly into the circulation. This rapid serologic boost bridges the gap before the active vaccine series can elicit a protective response, reducing the risk of disease onset during the incubation window. Clinical data demonstrate that, when combined with the appropriate vaccine, the passive product lowers the incidence of infection by more than 95 % in high‑risk cohorts.

Limitations include:

Passive protection lasts only weeks; it does not replace the need for a full vaccine schedule to achieve lasting immunity.
Supply constraints restrict availability in many regions, especially for formulations targeting tick‑borne encephalitis.
Intravenous or intramuscular administration carries a risk of hypersensitivity reactions, ranging from mild local irritation to systemic anaphylaxis.
High cost limits routine use in low‑resource settings.
Evidence of efficacy is primarily derived from rabies and tick‑borne encephalitis post‑exposure protocols; data for other tick‑borne pathogens remain sparse.

Effective use therefore requires timely administration, concurrent vaccination, and careful monitoring for adverse events.

Other Immunoglobulin Treatments (If Applicable)

After a tick bite, the primary passive‑immunity product is rabies immune globulin, administered when the animal is suspected of being rabid. In cases where additional immunoglobulin therapy may be considered, clinicians evaluate the following options:

Tetanus immune globulin (TIG). Indicated when the bite results in a deep, contaminated wound and the patient’s tetanus vaccination status is incomplete or unknown. A single dose of 250 IU is given intramuscularly, followed by the appropriate tetanus toxoid vaccine series.
Hyperimmune globulin against specific pathogens. Rarely employed for tick‑borne diseases; for example, equine anti‑Borrelia globulin has been used experimentally in severe, refractory Lyme disease, but it is not part of standard guidelines.
Antivenom immunoglobulin preparations. Applicable only for tick species that deliver potent toxins, such as certain Argasidae ticks in tropical regions. Antivenom is administered intravenously under close monitoring for hypersensitivity.
Intravenous immunoglobulin (IVIG). Considered when a patient develops an autoimmune complication triggered by tick exposure, such as immune‑mediated thrombocytopenia or Guillain‑Barré syndrome. Dose regimens follow established protocols for the underlying autoimmune condition.

Each alternative immunoglobulin is selected based on the bite’s clinical context, the patient’s immunization history, and the presence of secondary complications. The decision to use any of these products requires adherence to current infectious‑disease guidelines and consultation with specialists in toxicology or immunology when appropriate.

Important Considerations for Post-Tick Bite Management

When to Seek Medical Attention

After a tick attachment, immediate evaluation is essential whenever specific clinical or exposure criteria are met. The following situations demand prompt medical consultation:

Tick remains attached for more than 24 hours, indicating prolonged feeding and higher pathogen transmission risk.
The bite occurs in a region endemic for Lyme disease, Rocky Mountain spotted fever, or other tick‑borne infections, and the tick species is identified as a known vector.
The patient develops a rash, especially an expanding erythema migrans lesion, or any other cutaneous changes at the bite site.
Systemic symptoms appear within days of the bite, including fever, chills, headache, myalgia, arthralgia, or fatigue.
Neurological signs emerge, such as facial palsy, meningitis‑like symptoms, or peripheral neuropathy.
Cardiac manifestations arise, for example, palpitations, chest pain, or evidence of heart block.
The individual is immunocompromised, pregnant, or a child under eight years of age, because these groups have reduced capacity to contain infection.
The bite occurs in a setting with known exposure to rabies‑carrying wildlife, prompting consideration of rabies immunoglobulin administration.

In each case, early assessment allows clinicians to determine whether prophylactic therapy—often a single dose of doxycycline for Lyme disease prevention—or specific immunoglobulin treatment is warranted. Delayed intervention increases the probability of severe complications and reduces the effectiveness of both antibiotic and antibody‑based regimens. Prompt medical attention therefore minimizes morbidity and supports optimal recovery.

Diagnostic Procedures

After a tick attachment, clinicians must confirm or exclude infectious agents before considering any passive immunotherapy. The evaluation begins with a thorough history of exposure, tick identification, and a focused physical examination for erythema migrans, neurologic deficits, or systemic signs.

Key diagnostic procedures include:

Serologic testing for Borrelia burgdorferi – initial enzyme‑linked immunosorbent assay (ELISA) followed by confirmatory immunoblot; recommended when the bite occurred ≥ 5 days prior or when a rash is absent.
Polymerase chain reaction (PCR) of skin biopsy – useful for early localized disease when serology may be negative; specimen taken from the border of the lesion.
Blood culture and PCR for Anaplasma, Ehrlichia, and Rickettsia – indicated when fever, leukopenia, or thrombocytopenia accompany the bite.
Serology for tick‑borne encephalitis virus – performed in endemic regions; IgM and IgG titers measured in serum or cerebrospinal fluid if neurologic symptoms appear.
Complete blood count and liver function tests – identify hematologic or hepatic involvement that may influence therapeutic choices.

Interpretation of results guides therapy. Positive Borrelia serology or PCR confirms Lyme disease, for which oral doxycycline or intravenous ceftriaxone is indicated; immunoglobulin preparation is not recommended. Detection of viral encephalitis or severe bacterial sepsis may prompt supportive care and, in rare cases, administration of pathogen‑specific immunoglobulin when such products exist. Rabies immune globulin is reserved for mammalian bites from animals suspected of rabies exposure; tick bites do not trigger its use.

The diagnostic pathway ensures that passive immunotherapy is employed only when a specific indication exists, preventing unnecessary treatment and focusing resources on proven antimicrobial or antiviral regimens.

Alternative and Supportive Treatments

After a tick attachment, the primary prophylactic agent is a specific immunoglobulin administered to neutralize pathogen transmission. When this therapy is unavailable, contraindicated, or supplemented, clinicians rely on alternative and supportive measures.

Proper tick extraction reduces pathogen load. Use fine-point tweezers, grasp the mouthparts close to the skin, and pull upward with steady pressure. Disinfect the site immediately with an antiseptic such as chlorhexidine. Observing the bite for signs of erythema, swelling, or a target lesion guides further action.

Adjunctive pharmacologic options include:

A single dose of doxycycline (200 mg) within 72 hours of removal for high-risk exposure to Borrelia species.
Oral azithromycin (500 mg on day 1, then 250 mg daily for two days) as an alternative when doxycycline is contraindicated.
Non‑steroidal anti‑inflammatory drugs to control localized pain and inflammation.

Supportive care focuses on symptom monitoring and patient education. Advise daily inspection of the bite area for expanding rash, fever, or joint pain. Prompt reporting of systemic manifestations enables early initiation of targeted antimicrobial therapy.

When immunoglobulin administration is delayed, passive immunization may be considered through hyperimmune serum derived from donors exposed to tick‑borne pathogens, though availability is limited and efficacy varies. In such cases, reinforce the above measures while arranging definitive treatment.