Rheumatologic

Manifestations of Lyme
Disease

Andrea Gaito, MD
Lyme Arthritis

Lyme Arthritis occurs in 60% of patients

with untreated Lyme disease

Can be a mono,oligo or polyarthritis

Bb rapidly disseminates to joints by inducing
cytokines that induce vascular permeability

The persistence of the organism stimulates
both an inflammatory and an autoimmune
response
Case report

18 year old white female presents with 2

month history of right knee pain,
accompanied by fatigue and headache and
blurry vision. No known tick bite or rash.
Seen by orthopedist, knee aspirated, fluid
not tested.

Labs: Lyme Elisa: positive 1.50, western
blot:IgM +23,41 IgG 41, Rf: 15, ANA 1:40

Sed rate: 32
Diagnostic Evaluation

History: tick exposure, sports
injuries,structural issues: Osgood Schlatter,
chondromalacia

Family History: All autoimmune disorders,

esp. RA, SLE, hypothyroidism,Crohns,UC

Medication History: Use of antibiotics,

NSAIDS
Physical Exam

Vital to perform a full physical exam on
every patient, disrobed

Spine: alignment, scoliosis,kyphosis

Range of Motion: most important diagnostic
criteria in peripheral joints exam,know
standard values for age groups

Presence of synovitis: differentiates
arthralgia from arthritis, with or without
joint effusion
Physical Exam,
(continued)

Head and Neck: hair loss, oral ulcerations,
conjunctival injection, cranial nerve abnormalities,
oral thrush, enlarged thyroid, submandibular lymph
nodes

Skin: vitiligo, hyperpigmentation, fibrosis, rashes,
Raynaud’s stigmata, spider angiomas, mottling

General: dysrhythmias, hepatomegaly,
splenomegaly, lymphadenopathy,hypereflexia

Gait evaluation: limping, ataxia, dysequilibrium
Laboratory Evaluation

Lyme tests: western blot IgM, IgG,

C6peptide,PCR

Coinfections: Bartonella IgM/IgG,PCR

Ehrlichia chaffeenis & Anaplasmosis,

Babesia,Rickettsia,Tularemia

Viruses: Parvo, Hepatitis,etc
Laboratory Tests,
(continued)

ANA (with titer)
Anti-RNP ab

Sedimentation rate
Anti-Smith ab

RF (with titer)
SSA, SSB ab

CPK
Anticardiolipin ab,

CRP IgM,IgG,IgA

Anti-dsDNA
IL-6

Anti-CCP antibody
Tissue
transglutaminase
ab
Radiographic Evaluation

Xrays:

soft tissue swelling

joint space narrowing

sclerosis

erosions
MRI

Highly effective in differentiating Lyme

arthritis from septic arthritis or structural
damage

Can distinguish joint effusions, synovial
thickness, marrow and muscle edema, and
menisceal tears.

3 features highly suggestive of Lyme:
myositis, adenopathy and lack of
subcutaneous edema
Synovial Fluid Analysis
Normal Joint Fluid Lyme Arthritis

Amber colored Yellow color

Thick viscosity Thin viscosity

Clear Turbid

WBC < 2,000 WBC 5,000-50,000

Mononuclear cells Leukocytes
+ Lyme C6peptide,
elisa,PCR
Treatment of Lyme
Arthritis

IV Rocephin, 2 grams daily until
resolution of the effusion

NSAIDS?

Repeat joint aspiration?

Steroids?

Physical therapy?
Treatment of Lyme
disease with arthralgia

Antibiotic choices: Doxycycline, Ceftin,
and Biaxin, most effective for joint
symptoms

Treat coinfections simultaneously

Placquinil,NSAIDS, etc.
Common Rheumatologic
Disorders Associated with
Lyme Disease

Rheumatoid Arthritis

Systemic Lupus Erythematosus

Polymyositis and Dermatomyositis

Polymyalgia Rheumatica

Antiphospholipid antibody disorders

Celiac disease

Crohns disease and ulcerative colitis
Autoimmunity in Lyme
Disease

In addition to the inflammatory response,
the persistence of the Lyme bacteria can
induce an autoimmune response

The human lymphocyte function antigen
(hlFA 1 alpha) contains a peptide with
homolgy to OSPA 165-173,(Lyme vaccine)

Autoantibodies are produced as a secondary
process which further promotes a variety of
systemic responses
The Inflammatory
Response

Spirochetal lipoproteins are potent inducers
of many proinflammatory cytokines: TNF
alpha & IL-6,

TNF alpha & IL-6 then stimulate T and B cell
production, which causes further tissue
destruction

Pathophysiology is most similar to
rheumatoid arthritis not osteoarthritis

The occurrence of this phenomena
correlates with the frequency of certain
MHC classes, HLA DR, HLA DB
Management of Lyme
Disease and Autoimmune
Disorders
Lyme Disease and
Rheumatoid Arthritis

Treatments options:

Nsaids

Placquinil

Biologics: Enbrel, Humira,
Remicade,Orencia, Cimzia, etc.

Methotrexate

Imuran

steroids
Lyme Disease and
Generalized autoimmune
disorders

Lyme and SLE: antibiotics + placquinil

Lyme and Sjogrens: antibiotics
+placquinil

Lyme and myositis: antibiotics +lowest
dose steroids,consider mtx as steroid
sparing agent

Lyme and antiphospholipid disorders:
antibiotics + aspirin, others as needed
Synovectomy

May be necessary if patient does not

respond to treatment.

May also contribute to diagnosis in
seronegative patients

May temporize joint damage to avoid
replacement
Case Reports

Osteoblastic lesions secondary to ACA

Borrelial Lymphocytoma

Nodular Fascitis

Wegner’s Granulomatosis with AV
block

Lyme arthritis secondary to autologous
chondrocyte transplanation
Lyme disease can manifest in a diverse
array of inflammatory and autoimmune
disorders. Most are triggered and driven
by the persistence of bacterial proteins in
host tissue. The successful treatment of
the patient with Lyme disease involves
treating the primary infection as well as
identifying and treating the secondary
rheumatologic disorder if present.