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Pod Med > Other Arthritides > Flashcards

Other Arthritides Flashcards

1
Q

Other Causes of Arthritis

A
  • Sarcoidosis
    • Systemic Sclerosis
    • Systemic Lupus Erythematosus (SLE)
  • Sjogren’s syndrome
    • Lyme disease
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2
Q

Sarcoidosis

• Chronic systemic granulomatous disease – Multiple organ involvement

A
  • Characterized by disseminated, noncaseating granulomas
    – Suggests infection as a likely cause
  • Mimics rheumatologic diseases
    – Fever, arthritis, uveitis, myositis, rash or neurologic deficits
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3
Q

Sarcoidosis

• Affects young adults in their 20’s and 30’s

A

• Most common in US
– 8x more common in African Americans than Caucasian Americams
– 40 cases/100,000
• Woman> men

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4
Q

Sarcoidosis Pathogenesis

A

Etiology unknown
Immune response plays a central role in pathogenesis

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5
Q

Sarcoidosis

• Recruit inflammatory cells
– Injury to local tissue

A

• Increase growth factors
– Produce fibrosis

• Hypercalcemia
– Increase absorption of calcium in intestine that results from overproduction of a metabolite of vitamin D by activated macrophages

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6
Q

Sarcoidosis

• Depressed cellular immunity – Lymphopenia

A

• Increased humoral immunity

– Autoantibody production and hypergammaglobulinemia
– (+) RF or ANA – 20-30% of patients

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7
Q

Sarcoid Granulomas

A

• Contains a central core of epitheloid cells (modified macrophages) and multi- nucleated giant cells
– Surrounded by lymphocytes, macrophages, monocytes, and fibroblasts
• Affects lungs liver, and lymph nodes

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8
Q

Distribution of Sarcoid Granulomas

A
  • Lung 86%
    • Liver 86%
    • Lymph nodes 86%

* Spleen 63%
• Heart 20%
• Kidney 19%
• Bone marrow 17% • Pancreas 6%

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9
Q

Sarcoidosis Clinical Presentation

A
  1. Pulmonary symptoms (40-45%)
  2. Asymptomatic hilar adenopathy on chest x-ray (5-10%)
  3. Constitutional symptoms (25%)
  4. Extrathoracicinflammation(25%)
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10
Q

Sarcoidosis Pulmonary Symptoms

** picture-> large lymph nodes

A

Respiratory symptoms are the most common complaint
Dry cough
 Dyspnea
Nonspecific chest pain
Hemoptysis (rare initially)
Pleural effusion (rare)

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11
Q

Abnormal chest x-ray >90%

A

Regardless of initial symptoms

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12
Q

Sarcoidosis

Constitutional Symptoms (25%)

A
  • Fever
    -Seen more so with hepatic involvement
  • Weight loss
  • Fatigue
    -Malaise
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13
Q

Sarcoidosis

• Rheumatologic manifestations

A

• Arthritis occurs 10 – 15% of patients
• Two patterns of joint disease
-Early onset
-Late onset

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14
Q

Sarcoidosis

Early onset arthritis (Most Common)

A

Within 6 months of disease onset

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15
Q

Sarcoidosis (Early)

A
  • Erythema nodosum common (66%)
  • Monoarthritis unusual
    – Usually 2-6 joints
    • Often begins in feet and ankles
    • May spread to knees, PIPJ’s, MCPJ’s, wrists, and elbows
    • Axial skeleton is spared
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16
Q

Sarcoidosis (Early)

A
  • Periarticular swelling common
  • Non-inflammatory effusions
    • Tenosynovitis
    • Heel pain
    • Joint pain
    – Pain greater than clinical signs of inflammation would suggest
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17
Q

Sarcoidosis (Early)

A

• Radiographic presentation
– Rarely bone or cartilage damage noted
• Duration of arthritis
– Several weeks
• May be as long a 3 months

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18
Q

Lofgren’s Syndrome

** erythema nodosum seen in Crohns, sarcoidosis, lofgrens

A

• Acute arthritis
• Erythema nodosum
• Bilateral hilar adenopathy

90% remission rate

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19
Q

Sarcoidosis (Late)

• 6 months after onset of disease

A

• Mono arthritis more common than in EARLY stage
– But usually 2 or 3 joints
• Less severe/widespread
• Transient or chronic
• Knee joint (most commonly involved)
– Followed by ankles and PIPJs
• Synovial effusions
– Mildly inflammatory

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20
Q

Sarcoidosis (Late)

• Chronic cutaneous sarcoidosis

A

• NO erythema nodosum
• Dactylitis
• Pain is not as severe

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21
Q

Sarcoidosis (Late)

A

• Radiographic changes are uncommon

– Cystic changes in middle and distal phalanx of hand
– Trabecular changes
- Honeycomb pattern

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22
Q

Sarcoidosis

• Other rheumatologic manifestation

A

– Eye disease (22%)
• Uveitis

– Myositis
– rotid gland enlargement
– Mononeuritis multiplex
– Facial nerve palsy

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23
Q

Sarcoidosis

  • Extrathoracic manifestations
    – Peripheral lymphadenopathy – 75%
    – Skin involvement – 33%
  • macular or papular sarcoidosis
  • erythema nodusom
    • lupus pernio
A

– Hepatic granulomas – 86%

– Neurosarcoidosis- 5%
– Other manifestations
• Myocardial
• Renal involvement

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24
Q

Lupus Pernio

A

• Potentially disfiguring red to violaceous plaques and nodules
• Resemble frostbite
• Usually affects the nose, cheeks, and ears

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25
Q

Erythema Nodosum

A

• Inflammation of the fat cells under the skin (panniculitis)
• Tender,rednodules that are usually seen on both shins

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26
Q

Sarcoidosis

A

– No single finding or lab test establishes a diagnosis
– Diagnosis depends on the clinical picture
• At least 2 organ systems are affected
• Evidence of noncaseating granulomas
• Exclusion of other possible causes

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27
Q

Sarcoidosis

• Lab Tests

A
  • Increase ACE levels (66%)
    • Increase in serum calcium (19%)
  • Leukopenia (28%)
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28
Q

Sarcoidosis

Diagnosis

A

– No single finding or lab test establishes a diagnosis
– Diagnosis depends on the clinical picture
• At least 2 organ systems are affected
• Evidence of noncaseating granulomas
• Exclusion of other possible causes

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29
Q

Sarcoidosis
• Lab Tests

A
  • Increase ACE levels (66%)
    • Increase in serum calcium (19%)
  • Leukopenia (28%)
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30
Q

Sarcoidosis
• Imaging/Procedures

A

• Chest x-ray
• Transbronchial lung biopsy
• (+) Kveim-Siltzbach test (intradermal sarcoid spleen extract)

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31
Q

Sarcoidosis Treatment

A
  • Asymptomatic hilar adenopathy

* No treatment
• NSAID’s
• Corticosteroids
• Immunosuppressive drugs
-Efficacy has not been established

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32
Q

Systemic Sclerosis

A

AKA Scleroderma

“Hard Skin

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33
Q

Systemic Sclerosis

A

• Multisystem disease (hallmark)
– Functional and structural abnormalities of small blood vessels
– Fibrosis of the skin and internal organs
– Inflammation
– Autoimmunity

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34
Q

Etiology Unknown

A

Potential triggers
Infectious agents,
environmental toxins, and drugs,
microchimerism

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35
Q

Epidemiology of Scleroderma

A

• Acquired, noncontageous, progressive, rare disease
– 19 cases per 1 million per year in US
• Peak age of onset 35-50 years
• Blacks are at moderately increased risk
• Female-to-male ratio 3-7:1

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36
Q

Systemic Sclerosis

A
  1. Diffuse scleroderma
  2. Limited scleroderma

- CREST syndrome
3. Localized scleroderma

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37
Q

Diffuse Scleroderma

A

• Proximal skin thickening
• Rapid onset following appearance of Raynaud’s phenomenon
• Significant vessel disease – Lung, heart, GI, kidney
• Associated with ANA and absence of aniticentromere antibody
• Poor prognosis
– 10-year survival 40-60%

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38
Q

Limited Scleroderma

A

Milder symptoms
Slower onset and progression
Mainly affects extremities distal to the elbows and/or knees
Internal organ involvement is less severe CREST Syndrome
Good prognosis
10-year survival >70%

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39
Q

CREST Syndrome

• Calcinosis
– Calcium deposits in skin
• Raynaud’s Phenomenon
– Spasm of blood vessel in response to cold or stress

A

• Esophageal dysfunction
– Acid reflux
– Decrease in motility of esophagus
• Sclerodactyly
– Thickening and tightning of skin on fingers and hands
• Telangiectasias
– Dilation of capillaries causing red marks on surface of skin

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40
Q

Localized Scleroderma

A

 Morphea
-Patches of fibrotic skin and subcutaneous tissues w/o systemic disease
 Linear
-Longitudinal fibrotic bands that occur predominantly on the extremities and involve the feet

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41
Q

Raynaud’s Phenomenon

A

• Vasospasticdisorder
– Associated with discoloration of the digits

• Coldtemperaturesor emotional stress triggers the attacks

42
Q

Raynaud’s Phenomenon

A

Vasospams
Pallor & Cyanosis
Hyperemic phase
White, Blue, Red

43
Q

Raynaud’s Phenomenon

A

• Primary syndrome
• Secondary syndrome

44
Q

Primary

A

• Symmetric episodic attacks of acral pallor or cyanosis
• Absence of PVD
• Absence of tissue necrosis
• Normal nail-fold capillary
• Neg ANA
• Normal ESR
• Patients are usually younger

45
Q

Secondary

A

• More severe
• Ischemicchanges/necrosis • Digitalulceration
• Associated
– Scleroderma, SLE, myositis, Sjogren’s syndrome, RA, mixed connective tissue disease
• Laterageofonset
• Asymmetric finger involvement • Abnormalnail-foldcapillary

46
Q

Raynaud’s Phenomenon Treatment

A
  • Conservative,non-pharmacologic
    • Avoid exposure to cold temperatures
  • Avoid vasoconstrictors
    – Decongestants, amphetamines, beta-blockers, caffeine, and smoking
    • Calcium channel blockers – Nifedipine 30-180 mg daily – Amlodipine 5-20 mg daily
    • Directvasodilator– Topical nitroglycerin
    • Low-dose aspirin
47
Q

Systemic Sclerosis

A

• Cutaneous involvement
• Diffuse pruritus
• Non-pitting edema
• Progressive skin tightness & decreased flexibility
• Varying degrees of hypo or hyperpigmentations

48
Q

Systemic Sclerosis

A

• Subcutaneous calcinosis
• Telangiectasias

Dilated capillary loops and areas of loss of capillaries in the skin of the nail fold are characteristic

49
Q

Telangiectasia

Clinical Presentation

A

• Musculoskeletal
– Earliest symptoms
• Nonspecific arthralgias and myaligias • Pain with motion of joints
– Secondary to inflammation and fibrosis of tendon sheath or adjacent tissue
– Late
• Atrophy and weakness

50
Q

Other features

A

Pulmonary disease Leading cause of mortality GI dysfunction
 Esophageal
Other systems are affected Cardiovascular and renal

51
Q

Systemic Sclerosis
• Diagnosis
-Clinical suspicion
-No single finding or lab test establishes a diagnosis

A

• Lab tests
-Increased sedimentation rate

  • (+) ANA in speckled or nucleolar pattern (95%)
  • (+) anticentromere antibodies in about 60-90% of limited disease
    -(+)Scl70
52
Q

Systemic Sclerosis

• Radiographs

A

• Calcinosis and resorption of the distal tufts • Contractures with joint space narrowing
• Osteopenia

53
Q

Systemic Sclerosis

 Treatment  DMARDs

A

 MSK
 NSAIDs
 Corticosteroids
 Skin
 Topical emollients  Topical steroids
 Raynaud’s
 Avoid cold exposure
 Calcium channel blockers

54
Q

Systemic Lupus Erythematosus (SLE)

A

Autoimmune disease multisystem involvement
Clinical manifestations of the disease are diverse

55
Q

Systemic Lupus Erythematosus (SLE)
• Epidemiology

A
  • Predominantly occurs in women
  • Male approx 10%
    • Peak incidence is 15-40 years of age
    • More common in African Americans and Hispanic-Americans vs Caucasians
    • Strong family association
56
Q

Systemic Lupus Erythematosus (SLE)

Exact etiology unknown

Most common presentation – Constitutional symptoms

A
  • Fever, fatigue and/or weight loss, lymphadenopathy, splenomegaly
    – Cutaneous manifestations
  • Skin rash
    – Articular manifestations
  • Arthritis and/or arthralgia
57
Q

Cutaneous Manifestations of SLE

A
  • Acute Lupus Erythematosus
    • Subacute Lupus Erythematosus

* Chronic Lupus Erythematosus

58
Q

Cutaneous Manifestations of SLE

• AcuteLupusErythematosus – Localalized lesions

A

• Hallmark “butterfly rash”
– Localized to malar region
– Confluent, macular or papular erythema on the nose and
cheeks (spares the nasolabial folds)
– Lasts days to weeks
– Generalized lesions
• Macular or maculopapular erythema occurring in a
photosensitive distribution on any area of the body
• Commonly involves palmar surfaces, dorsum of the hands,
and extensor surfaces of the fingers – Skin lesions heal w/o scarring

59
Q

Cutaneous Manifestations of SLE
Subacute Lupus Erythematosus

A

– Nonscarring, photosensitive
– Last for weeks to months
– Back, neck, shoulders and extensor surfaces
– Some drugs can induce these lesions
– Can occur in annular form
• May be mistaken for
– Fungal rash, Lyme ds, psoriasis

60
Q

Cutaneous Manifestations of SLE
• ChronicLupusErythematosus
– Photosensitive lesions that can lead to skin atrophy – Scar producing
– May persist for several months.
– Discoid Lupus Erythematosus

A

• Most common subtype of chronic SLE
• Term “discoid” refers to the sharply demarcated disk-shaped
appearance of the lesions
• Raised, erythematosus plaques with adherent scale that
commonly occur on the scalp, face, and neck
• Assoc with squamous cell carcinoma

61
Q

Systemic Lupus Erythematosus (SLE)

A

 Alopecia
Assoc with discoid lupus
 Photosensitivity
Skin rash as a result of unusual reaction to sunlight
Mucosal lesions Mouth and nose ulcers

62
Q

Systemic Lupus Erythematosus (SLE)
 Musculoskeletal
 Very common (90%)
 Symmetric, inflammatory arthritis predominantly affecting the knees, wrists, and small joints of the hands

A

 No erosive changes
 Avascular Necrosis
 Most commonly affects femoral heads, tibial plateaus, and femoral condyles
 Myalgias and muscle weakness
 Mild joint effusions

63
Q

Systemic Lupus Erythematosus (SLE)
Jaccoud’s arthropathy

Resembles RA

A

 Non-erosive hand
deformities Ulnar deviation  Hyperflexion
 Hyperextension
 Reducible deformities secondary to involvement of the peri-articular tissue

64
Q

Systemic Lupus Erythematosus (SLE)
• Renal

A

• Kidney is the most commonly affected organ
• Approximately 50% of patients develop clinically evident renal disease
• Neuropsychiatric
• Mood disorders, anxiety and psychosis • Seizures
• Headaches
• Mononeuritis

65
Q

Systemic Lupus Erythematosus (SLE)
 Cardiopulmonary  Pericarditis

A

 Pleurisy
 Other organ systems GI
 abdominal pain  Ocular
 cotton wool spots  Hematology
 Leukopenia and lymphopenia  Anemia

66
Q

Systemic Lupus Erythematosus (SLE)
• Diagnosis
• Clinical suspicion with support of laboratory tests
• Laboratory test

A

• CBC with diff, Cr, urinalysis, urine/cr ratio • Serologic tests
• ANA, anti-dsDNA, anti-Ro, anti-La, anti-Smith, anti-RNP, direct Coombs, antiphospholopid antibodies, C3, C4
 Autoantibodies are present for 5-7 years before clinical onsent of SLE

67
Q

American College of Rheumatology Diagnostic Criteria
Need 4 out of 11

A
  1. Malar rash
  2. Discoid rash
  3. Photosensitivity
  4. Oral ulcers
  5. Arthritis
  6. Serositis
  7. Renal disorder
  8. Neurologic disorder
  9. Hematologic disorder
  10. Immunologic disorder
  11. Antinuclear antiboidy
68
Q

Systemic Lupus Erythematosus (SLE)
• Recommendations

A

• Avoid intense sun exposure • Yearly influenza vaccination

69
Q

Systemic Lupus Erythematosus (SLE)
• Treatment • NSAID’s

A

• Corticosteroids
• Medrol dosepack, prednisone
• Antimalarial agents
• Hydroxychloroquine (Plaquenil) 200 mg BID • Prevents 50% of SLE flares
• Immunosuppressants
• Methotrexate, leflunomide, azathioprine, mycophenolate
mofetil, cyclophosphamide
• Others
• Rituximab, belimumab

70
Q

10% of SLE patients will develop Sjogren’s Syndrome

A

10% of SLE patients will develop Sjogren’s Syndrome

71
Q

Sjogren’s Syndrome

Debilitating autoimmune disorder

A

Associated with non-Hodgkins lymphoma
Sicca Complex
Xerostomia (dry mouth)
Xerophthalmia (dry eyes)
Lymphocytic infiltration of the exocrine glands

72
Q

Sjogren’s Syndrome
• Insidious onset

A
  • Occurs with any age
    – Peak incidence during midlife
    – Increases with age
    • Affects 0.05-4.8% of population
  • Affects all races
    • Female-to-male ratio is 9:1
73
Q

Sjogren’s Syndrome
• Etiology unknown

A

– Possible environmental agent may trigger cascade of events
– Multiple viruses
• Predilection for causing Sjogren’s syndrome
– Hormones ???
– Genetic factors

74
Q

Sjogren’s Syndrome

Primary Sjogren’s

A

No other underlying rheumatic disorder is present
Secondary Sjogren’s  Associated
Systemic lupus erythematosus Rheumatoid arthritis
 Scleroderma

75
Q

Cardinal Manifestations of Sjogren’s Syndrome
• Ocularsymptoms

A

– Decrease aqueous component of tears
• Visual acuity and discomfort occurs
– Burning
• Relieved by artificial tears – Dryness
– Inflammation of eyelids – Foreign-body sensation – Red eye
– Painful eye

76
Q

Cardinal Manifestations of Sjogren’s Syndrome
• Oral

A

– Dryness (xerostomia)
– Dental caries
• Gum line
– Sudden increase in salivary gland pain or size
– Enlarged
• Salivary and parotid glands
– Oral candidiasis

77
Q

Other Manifestations of Sjogren’s Syndrome

• Cutaneous

A

– Dry skin (dec secretion of sebaceous gland)
– Vasculitis
– Periungual telangiectasis
• If in large numbers, increase chance of developing scleroderma

• Neurologic
– Peripheral neuropathy

78
Q

Other Manifestations of Sjogren’s Syndrome

Musculoskeletal
• Myalgias

A
  • Arthralgias

* Arthritis
-Symmetrical polyarthritis
-Resembles RA but nondeforming

79
Q

Sjogren’s Syndrome Labs

A

RF 90%

ANA 80%

80
Q

Sjogren’s Syndrome Treatment
• Artificial tears
• Stimulate tear production
– Restasis (cyclosporine) eye drops

A

• Artificial saliva
• Frequent dental care
– Flouride treatment and antimicrobial rinses
• Increases salivary secretion
– Pilocarpine
– Evoxac (cevimeline) 30 mg TID
• Antifungals
• NDAID’s
• Corticosteroids
• Immunosuppressants

81
Q

Lyme Disease

A

Multisystem inflammatory disease
Tick-borne spirochete Borrelia burgdorferi

82
Q

Lyme Disease

93 % of all Lyme disease in US

A

are in 11 states NY, NJ, CT, RI, MA, PA, WI, MN, MD, NH, ME

83
Q

Lyme Disease

Diagnosed based on symptoms

A

Lyme Disease
ONLY Ixodid ticks are known to spread
B. P

Pathogenesis unclear

84
Q

Increase in Incidence of Lyme Disease

A

Growth of deer and tick population

– Expansion of endemic areas
– People moving into endemic areas
– Increase in recognition

85
Q

Clinical Presentation of Lyme Disease

Three stages (variable, w/ overlapping symptoms)

A

Early localized Early disseminated Late disease

86
Q

Early Localized
• Erythema migrans (Hallmark)
– Present 80%
– Within a month of a tick bite – May feel warm to touch
– Rarely itching or painful
– “bulls eye”

A

• May expand upto12inch
• Flu-like symptoms
– Fever, chills, headache, fatigue, muscle and joint aches
• Also may have swollen lymph nodes

87
Q

Early Disseminated Lyme Disease

 Within weeks of onset of infection
 Systems affected
 Skin
 Multiple erythema migrans lesions

A

 Heart
 AV block
 light-headedness, fainting, shortness of breath, heart palpitations, or chest pain
 1% of Lyme ds cases
 Nervous systems
 Cranial nerve palsy
 Bell’s palsy
 dysfunction of the cranial nerve VII (the facial nerve)
 Meningitis

88
Q

Early disseminated Lyme disease;

A

multiple red lesions with dusky centers

89
Q

Late Disease
• Months after onset of disease

A
  • Severe headaches and neck stiffness
  • MSK
    – Arthritis with severe joint pain and swelling, particularly the knees and other large joints
    • Peripheral sensory neuropathy (60%)
    • “stocking and glove” distribution
      • Reduced vibratory sensation
90
Q

Lyme Disease

Muscluloskeletal compliants reported in 80% of people with Erythema migrans

A

Muscluloskeletal compliants reported in 80% of people with Erythema migrans

91
Q

Musculoskeletal Manifestations of Lyme Disease
• Common in all 3 stages

A
  • Migratory pain in joint, tendons, bursae and muscle
    – Pain last for hrs to few days in one location
  • Arthritis begins months or year after infection
    – Monoarthritis or oligoarthritis
    – Knee most common joint affected
92
Q

Lyme Disease Diagnosis
• Based on clinical history and exposure to the tick

A

• Serologic tests to confirm disease
• ELISA (enzyme linked immunosorbent assay)
• Western blot
• Joint aspiration or spinal fluid
• Inflammation fluid

93
Q

Immunoblot tests for Lyme disease testin – IgM and IgG

A
  • IgM antibodies are made sooner
    – Helpful for identifying patients during the first few weeks
    of infection.
    – Downside of testing for IgM antibodies is that they are
    more likely to give false positive results.
  • IgG antibodies are more reliable
    – Can take 4-6 weeks for the body to produce in large enough quantities for the test to detect them.
94
Q

False positive results
• Tick-borne relapsing fever
• Syphilis

A

• Anaplasmosis(formerlyknownasgranulocytic ehrlichiosis)
• Leptospirosis
• Some autoimmune disorders(e.g.,lupus)
• Bacterial endocarditis
• Infection with Helicobacterpylori, EpsteinBarr virus, or Treponema denticola (bacteria found in the mouth that can cause gum disease and/or infection after dental procedures)

95
Q

Best Treatment

Prevention

A

Best Treatment

Prevention

96
Q

Prevent Lyme Disease

• Insect repellent
– with DEET or Permethrin
– 20 to 30% DEET (N, N-diethyl-m-toluamide
– Treat clothing and gear, such as boots, pants, socks and tents
with products containing 0.5% permethrin.

A

• Remove tick promptly
– Conduct a full-body tick check using a hand-held or full-length mirror to view all parts of your body upon return from tick- infested areas.
• Apply pesticides
• Reduce tick habitat
– Clear tall grasses and brush around homes and at the edge of lawns.
– Place a 3-ft wide barrier of wood chips or gravel between lawns and wooded areas and around patios and play equipment. This will restrict tick migration into recreational areas.

97
Q

Removing a tick
• Usefine-tippedtweezerstograspthetickas close to the skin’s surface as possible
• Pull upward with steady, even pressure.

A

Don’t twist or jerk the tick; this can cause the mouth- parts to break off and remain in the skin. If this happens, remove the mouth-parts with tweezers. After removing the tick, thoroughly clean the bite area and your hands with rubbing alcohol, an iodine scrub, or soap and water

• Dispose of alive tick by submersing it in alcohol, placing it in a sealed bag/container, wrapping it tightly in tape, or flushing it down the toilet. Never crush a tick with your fingers

98
Q

If you remove a tick quickly (within 24 hours), you can greatly reduce your chances of getting Lyme disease.

A

If you remove a tick quickly (within 24 hours), you can greatly reduce your chances of getting Lyme disease.

99
Q

Prevention

• Most humans are infected through the bites of immature ticks called nymphs

– Nymphs are tiny (less than 2 mm) and difficult to see
– They feed during the spring and summer months

A

• Adult ticks can also transmit Lyme disease
bacteria
– Much larger and are more likely to be discovered and removed before they have had time to transmit the bacteria
– Adult Ixodes ticks are most active during the cooler months of the year

100
Q

Prevent Lyme Disease
• Insect repellent
– with DEET or Permethrin
– 20 to 30% DEET (N, N-diethyl-m-toluamide
– Treat clothing and gear, such as boots, pants, socks and tents
with products containing 0.5% permethrin.

A

• Remove tick promptly
– Conduct a full-body tick check using a hand-held or full-length mirror to view all parts of your body upon return from tick- infested areas.
• Apply pesticides
• Reduce tick habitat
– Clear tall grasses and brush around homes and at the edge of lawns.
– Place a 3-ft wide barrier of wood chips or gravel between lawns and wooded areas and around patios and play equipment. This will restrict tick migration into recreational areas.

101
Q

Treatment of Lyme Disease
• Early localized
– Oral Antibiotic treatment (2-3 wks)

A

• Curative
• Doxycycline, amoxicillin, cefuroxime

• Early disseminated and Late
– IV antibiotics (2-4 wks)
• Cefotaxime • Penicillin G

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