Lyme Borreliosis¶
Chapter 191 | Part 5: Infectious Diseases
KEY CLINICAL POINTS¶
- Lyme borreliosis is caused by Borrelia burgdorferi sensu lato, transmitted via Ixodes ticks.
- Clinical stages include localized (erythema migrans), disseminated (neurological, cardiac, arthritis), and persistent (chronic arthritis, neuroborreliosis).
- Doxycycline is the preferred treatment for early-stage disease; ceftriaxone for severe neurologic involvement.
- Posttreatment Lyme disease syndrome (PTLDS) may occur in 10–20% of patients despite adequate antibiotic therapy.
- The Jarisch-Herxheimer reaction (JHR) is common during treatment, requiring close monitoring.
1. DEFINITION & OVERVIEW¶
Lyme borreliosis is a multisystem spirochetal infection caused by Borrelia burgdorferi sensu lato, transmitted via Ixodes ticks. It presents with a characteristic erythema migrans lesion (EM) in stage 1, followed by disseminated infection (stage 2) and persistent infection (stage 3).
Table 191-1 Algorithm for Testing for and Treating Lyme Disease¶
| PRETEST PROBABILITY | EXAMPLE | RECOMMENDATION |
|---|---|---|
| High | Patients with erythema migrans | Empirical antibiotic treatment without serologic testing |
| Intermediate | Patients with oligoarticular arthritis | Serologic testing and antibiotic treatment if test results are positive |
| Low | Patients with nonspecific symptoms (myalgias, arthralgias, fatigue) | Neither serologic testing nor antibiotic treatment |
1.1 Etiologic Agent¶
Borrelia burgdorferi sensu lato (B. burgdorferi, B. garinii, B. afzelii, B. bavariensis) are fastidious, microaerophilic spirochetes with a genome of ~1.5 Mb. They possess over 100 lipoproteins, many of which are immunogenic.
1.2 Transmission¶
Ixodes ticks (Ixodes scapularis in North America, I. ricinus in Europe) transmit the spirochete. Nymphal ticks are primarily responsible for human transmission, peaking in early summer.
2. EPIDEMIOLOGY¶
Lyme disease is the most common vector-borne infection in the U.S. and Europe. Incidence peaks in endemic regions (e.g., northeastern U.S., Europe). Risk factors include tick exposure, outdoor activities, and immunocompromised status. Annual cases in the U.S. exceed 476,000, with 30,000 reported annually.
2.1 Geographical Distribution¶
B. burgdorferi (U.S.), B. afzelii/B. garinii (Europe), and B. miyamotoi (Asia) are regional variants. Ixodes persulcatus vectors are found in eastern Russia, China, and Japan.
2.2 Risk Factors¶
Residing in wooded areas, tick bites, immunosuppression, and co-infections (e.g., anaplasmosis, babesiosis).
3. ETIOLOGY & PATHOPHYSIOLOGY¶
B. burgdorferi survives in ticks and mammals, adapting to different environments. It expresses outer-surface protein A (OspA) in ticks and OspC in mammals. Virulence factors include surface proteins that bind host tissues and evade immune responses.
3.1 Immune Evasion¶
Spirochetes downregulate OspC and upregulate VlsE for antigenic variation. Complement resistance via Factor H binding and surface proteins.
3.2 Pathogenesis¶
Dissemination via hematogenous spread leads to arthritis, neuroborreliosis, and carditis. Persistent infection may cause chronic symptoms due to immune dysregulation.
4. CLINICAL FEATURES¶
Early: EM (stage 1), disseminated infection (stage 2) with arthritis, neurologic symptoms, or carditis. Late: Persistent arthritis, chronic neurologic disease, or acrodermatitis chronica atrophicans.
4.1 Early Infection (Stage 1)¶
EM: expanding erythematous lesion with central clearing. Often asymptomatic, but may present with fatigue, headache, or mild fever.
4.2 Disseminated Infection (Stage 2)¶
Arthritis (oligoarticular), meningitis, cranial neuritis, carditis, and migratory musculoskeletal pain. JHR may occur.
4.3 Persistent Infection (Stage 3)¶
Chronic arthritis, encephalopathy, polyneuropathy, or acrodermatitis. PTLDS may develop with fatigue, cognitive dysfunction, or musculoskeletal pain.
5. DIFFERENTIAL DIAGNOSIS¶
Erythema multiforme, cellulitis, staphylococcal scalded skin syndrome, other tick-borne infections (e.g., anaplasmosis, babesiosis), and autoimmune disorders.
5.1 Mimicking Conditions¶
Bell’s palsy (facial palsy without EM), rheumatoid arthritis, systemic lupus erythematosus, and fibromyalgia.
5.2 Atypical Presentations¶
STARI (tick-associated rash illness) with EM-like rash but no B. burgdorferi DNA. Co-infections with Ehrlichia or Babesia may complicate diagnosis.
6. INVESTIGATIONS & DIAGNOSIS¶
Serologic testing (ELISA, Western blot) for IgM/IgG. PCR for B. burgdorferi DNA in joint fluid or CSF. Cultures in BSK medium are less practical.
Western Blot Bands for Lyme Disease¶
| IgM Bands (kDa) | IgG Bands (kDa) |
|---|---|
| 23, 39, 41 | 18, 23, 28, 30, 39, 41, 45, 58, 66, 93 |
6.1 Serologic Testing¶
Two-step approach: ELISA followed by Western blot. IgM positive in early stages, IgG in later stages. False positives may occur with co-infections.
6.2 PCR and Imaging¶
PCR detects B. burgdorferi DNA in joint fluid or CSF. MRI may show meningeal or spinal cord inflammation in neuroborreliosis.
7. MANAGEMENT & TREATMENT¶
Antibiotic therapy is effective for early-stage disease. IV antibiotics for severe neurologic/cardiac involvement. PTLDS is managed with symptomatic treatment.
Treatment Algorithm for Lyme Disease Manifestations¶
| Manifestation | Recommended Therapy |
|---|---|
| Skin infection | Oral doxycycline 100 mg bid x14–21 days |
| Arthritis | Oral doxycycline 100 mg bid x28–30 days |
| Neuroborreliosis | IV ceftriaxone 2 g qd x14–28 days |
| Carditis | IV ceftriaxone 2 g qd x14–28 days |
7.1 Early-Stage Treatment¶
Doxycycline (100 mg bid) for 14–21 days. Alternatives: amoxicillin (500 mg tid) or cefuroxime axetil (500 mg bid).
7.2 Neurologic/Cardiac Involvement¶
IV ceftriaxone (2 g qd) or penicillin G (5 million units q6h) for 14–28 days. Monitor for JHR and cardiac arrhythmias.
7.3 Chronic Symptoms (PTLDS)¶
No proven benefit from prolonged antibiotics. Symptomatic management with NSAIDs, physical therapy, or cognitive behavioral therapy.
8. PROGNOSIS & COMPLICATIONS¶
Mortality is <2% with treatment. Complications include arthritis, neuroborreliosis, carditis, and PTLDS. Untreated, mortality ranges from 10–70%.
8.1 Complications¶
Chronic arthritis, encephalopathy, polyneuropathy, acrodermatitis, and cardiac arrhythmias. Co-infections may worsen outcomes.
8.2 Pregnancy¶
Lyme disease may cause abortion or stillbirth. Avoid doxycycline; use amoxicillin or ceftriaxone.
9. SPECIAL CONSIDERATIONS¶
Avoid doxycycline in pregnancy. Use alternative antibiotics for renal impairment. Monitor for JHR and cardiac arrhythmias during treatment.
9.1 Pediatric Considerations¶
Amoxicillin is preferred in children. Avoid doxycycline in children <8 years old.
9.2 Co-Infections¶
Anaplasmosis, babesiosis, and ehrlichiosis may co-occur. PCR and blood smear testing are essential for diagnosis.
10. KEY POINTS & CLINICAL PEARLS¶
- Early EM is the hallmark of Lyme disease. 2. Doxycycline is first-line for early-stage infection. 3. JHR is common during treatment. 4. PTLDS is managed with symptomatic care. 5. Serologic testing has limited utility in early stages.