NAVLE Multisystemic

Equine Borreliosis (Lyme Disease) Study Guide

Equine borreliosis (Lyme disease) is a tick-borne infection caused by the spirochete bacterium Borrelia burgdorferi. While exposure to this organism is common in horses residing in endemic regions, clinical disease is considered rare.

Overview and Clinical Importance

Equine borreliosis (Lyme disease) is a tick-borne infection caused by the spirochete bacterium Borrelia burgdorferi. While exposure to this organism is common in horses residing in endemic regions, clinical disease is considered rare. The distinction between exposure (seropositive) and clinical disease is crucial for the NAVLE. This condition represents a significant diagnostic challenge because clinical signs are vague and nonspecific, and positive serology only indicates exposure, not active disease.

The disease is primarily transmitted by Ixodes scapularis (blacklegged or deer tick) in the northeastern and midwestern United States and Ixodes pacificus on the West Coast. Understanding the documented clinical syndromes, appropriate diagnostic approach, and treatment protocols is essential for board examination success.

Component Details
Primary Vector (Eastern US) Ixodes scapularis (blacklegged/deer tick)
Primary Vector (Western US) Ixodes pacificus
Tick Life Cycle 2-year cycle: egg, larva, nymph, adult; each mobile stage feeds on a different host
Reservoir Host White-footed mice and other small mammals (NOT deer; deer are hosts for adult ticks but do not carry Borrelia)
Transmission Time Tick must be attached for at least 18-24 hours for transmission to occur
Peak Transmission Nymphs: late spring/summer; Adults: fall and early spring
Endemic Regions Northeastern US, mid-Atlantic states, upper Midwest, Pacific Coast

Etiology and Pathophysiology

Causative Agent

Borrelia burgdorferi is a Gram-negative spirochete bacterium characterized by its distinctive spiral or corkscrew shape. Key microbiological features include flagella enclosed between outer and inner membranes (endoflagella), a flexible cell wall measuring approximately 0.3 micrometers wide and 5-20 micrometers in length, and the ability to alter outer surface proteins (Osp) depending on host environment.

Transmission and Vector Biology

NAVLE TipA tick must be attached for at least 18-24 hours to transmit B. burgdorferi. Prompt tick removal can prevent infection! Adult females and nymphs are primarily responsible for transmission to horses.

Pathogenesis

After transmission, B. burgdorferi enters the skin and undergoes a sophisticated process of upregulating and downregulating specific outer surface protein antigens. The spirochetes then migrate through the skin and connective tissue to joint and synovial membranes, meninges (brain and spinal cord coverings), and eyes. The most common histopathologic lesion is lymphohistiocytic and plasmacytic infiltrate in affected tissues.

Key pathogenic concepts: The disease severity is believed to be related to the host inflammatory response rather than direct damage by the spirochete. Antibodies can be detected 3-6 weeks after infection. Most infected horses remain asymptomatic and never develop clinical disease.

Syndrome Clinical Signs Prognosis
Neuroborreliosis CNS/neurologic: Ataxia, behavioral changes, cranial nerve deficits (facial palsy), dysphagia, neck stiffness, hyperesthesia (skin sensitivity), muscle atrophy/weight loss, fasciculations, episodic respiratory distress (laryngeal dysfunction) POOR - Only ONE successful treatment outcome documented in literature
Borrelia-Associated Uveitis Ocular: Severe bilateral uveitis (rapid onset), yellow-green fibrinoid aqueous humor, aqueous flare, synechiae, miosis, preiridal fibrovascular membrane, rubeosis iridis, loss of corpora nigra POOR for vision restoration; may precede neuroborreliosis
Cutaneous Pseudolymphoma Dermatologic: Dermal papular to nodular lesions at tick bite site; histologically may mimic lymphoma but immunohistochemistry reveals mixed lymphoid hyperplasia GOOD - Responds well to antibiotic treatment

Clinical Presentation

Documented Clinical Syndromes

The ACVIM consensus statement identifies three well-documented clinical syndromes attributed to B. burgdorferi infection in horses. These are the only syndromes with strong scientific evidence linking them to Borrelia infection.

Undocumented but Possible Clinical Signs

The following signs are often attributed to equine Lyme disease but lack strong scientific documentation. Many other diseases are MORE LIKELY causes of these signs:

  • Shifting leg lameness and joint swelling/effusion
  • Muscle stiffness and soreness
  • Low-grade fever
  • Chronic weight loss and poor performance
  • Behavioral changes (irritability, depression)
  • Laminitis (rare association)

Exam Focus: Neuroborreliosis signs can mimic EPM (Equine Protozoal Myeloencephalitis), cervical vertebral stenotic myelopathy (wobblers), and EHV-1 myeloencephalopathy. These conditions must be ruled out before diagnosing Lyme disease. The key distinguishing feature of neuroborreliosis is meningeal thickening (dural thickening) seen on postmortem examination.

Test Description Clinical Utility
Lyme Multiplex Assay (Cornell) Quantitative detection of antibodies to OspA, OspC, and OspF antigens; can be performed on serum and CSF Can differentiate infection stage; OspC = early/recent infection; OspF = chronic infection; OspA = vaccination or chronic disease
C6 ELISA/SNAP Test Detects antibodies to C6 peptide (invariable region of VlsE protein); qualitative Indicates exposure only; limited sensitivity in horses (approximately 63%)
Western Blot Confirmatory test detecting antibodies to multiple B. burgdorferi proteins More specific than screening ELISA; used for confirmation
PCR Detects B. burgdorferi DNA in tissue, synovial fluid, or CSF Can confirm active infection but has LOW sensitivity; organism present in low numbers

Diagnosis

Diagnostic Criteria

Lyme disease is a DIAGNOSIS OF EXCLUSION. Diagnosis requires ALL of the following criteria:

  • Horse lives in or has traveled to an endemic region for Ixodes ticks
  • Clinical signs compatible with documented Lyme disease syndromes
  • Positive serologic test for B. burgdorferi antibodies
  • Other causes of clinical signs have been RULED OUT

Serologic Testing

High-YieldA positive antibody test ONLY indicates exposure, NOT active disease. Antibodies can be detected 3-6 weeks after infection. Many horses (30-75% in endemic regions) are seropositive but never develop clinical disease. Routine serologic testing of healthy horses is NOT recommended, nor is treatment of seropositive but clinically healthy horses.

Lyme Multiplex Assay Interpretation

Diagnosing Neuroborreliosis

For horses with neurologic signs suspicious for neuroborreliosis:

  • CSF analysis: Typically shows neutrophilic or lymphocytic pleocytosis
  • Paired serum and CSF: Submit simultaneously for Lyme Multiplex; local antibody production in CNS supports diagnosis
  • Rule out differentials: EPM, EHV-1, wobblers (cervical vertebral malformation), WNV
  • Postmortem: Meningeal thickening (dural inflammation), lymphohistiocytic and plasmacytic infiltrates
Antibody Pattern Interpretation
OspC positive, OspF negative Early/recent infection (within 3-5 weeks); easier to treat at this stage
OspC positive, OspF positive Active or ongoing infection
OspC negative, OspF positive Chronic/past infection
OspA positive (non-vaccinated) May indicate chronicity and disease severity; associated with treatment-resistant disease in humans

Treatment

Antibiotic Therapy

Treatment should ONLY be initiated in horses with clinical signs compatible with Lyme disease, positive serology, AND after ruling out other causes. The ideal treatment regimen is unknown due to lack of controlled clinical trials.

Treatment Duration and Protocols

Recommended protocol: IV oxytetracycline for 7 days followed by oral doxycycline or minocycline for 3-6 weeks. Treatment duration is often longer in horses than humans because infection is typically present longer before diagnosis.

For neuroborreliosis: Consider parenteral beta-lactams (penicillin G, ceftriaxone, cefotaxime) that cross the blood-brain barrier, similar to human protocols. However, successful treatment outcomes remain rare.

Adjunctive Therapy

  • NSAIDs: Flunixin meglumine or firocoxib for pain, lameness, or uveitis
  • Dexamethasone: Consider in acute, severe neuroborreliosis or uveitis (controversial; mixed outcomes in humans)
  • Joint support: Chondroprotective agents if joint involvement present
NAVLE TipIV tetracycline is the MOST EFFECTIVE treatment based on experimental studies (100% clearance vs. 25% for oral doxycycline). Remember that tetracyclines also have anti-inflammatory properties that may contribute to clinical improvement independent of antibacterial effects. Response to antibiotic treatment alone is NOT sufficient to confirm Lyme disease diagnosis.
Drug Dose Route Notes
Oxytetracycline 6.6 mg/kg q24h IV MOST EFFECTIVE in experimental studies; achieved 100% clearance
Doxycycline 10 mg/kg q12h PO Low bioavailability in horses (20-30%); inconsistent clearance
Minocycline 4 mg/kg q12h PO Better bioavailability than doxycycline; alternative when IV not feasible
Ceftiofur 2.2 mg/kg q24h IM Inconsistent clearance in studies (50%); reserve as second-line

Prevention

Tick Control and Environmental Management

  • Environmental modification: Mow pastures regularly, remove brush/leaf litter, eliminate rodent habitats
  • Topical repellents: Permethrin-based products applied regularly
  • Daily tick checks: Thorough grooming and inspection, especially ears, mane, tail base, and ventral areas
  • Prompt tick removal: Remove ticks within 24 hours using fine-tipped tweezers; grasp close to skin and pull straight out

Vaccination

There is NO approved Lyme vaccine for horses. Off-label use of canine Lyme vaccines is practiced by some veterinarians in endemic areas. Studies suggest proper vaccination could prevent infection, but data on equine-specific efficacy is limited. Many horses show low and short-lasting antibody responses to canine vaccines.

Syndrome Prognosis
B. burgdorferi infection (no clinical signs) EXCELLENT - Most exposed horses never develop clinical disease
Cutaneous pseudolymphoma GOOD - Excellent response to antibiotic treatment
Borrelia-associated uveitis POOR for vision restoration
Neuroborreliosis POOR - Only ONE documented successful treatment; many horses succumb despite prolonged antibiotic therapy

Prognosis

Memory Aids

LYME = "Lots of Your tests Mean Exposure only" L - Lives in endemic region Y - Yes to compatible clinical signs M - Must have positive serology E - Exclude other diseases FIRST

The "NUP" Syndromes (Documented Equine Lyme Disease): N - Neuroborreliosis (POOR prognosis) U - Uveitis (POOR prognosis for vision) P - Pseudolymphoma (GOOD prognosis)

Tick Transmission Timeline: "24 to Transmit" Ticks must be attached for at least 24 hours to transmit B. burgdorferi. Daily tick checks can prevent infection!

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