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LYME DISEASE Epidemiology Clinical Manifestations

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Presentation on theme: "LYME DISEASE Epidemiology Clinical Manifestations"— Presentation transcript:

1 LYME DISEASE Epidemiology Clinical Manifestations
Differential Diagnosis Diagnosis Treatment Prevention

2 EPIDEMIOLOGY Caused by spirochete Borrelia burgdorferi
Transmitted by Ixodes ticks Nymph-stage ticks feed on humans May through July - transmit spirochete Endemic areas Northeastern coastal states Wisconsin & Minnesota Coast of Oregon & northern California

3 Ixodes scapularis ticks
The percentage of nymphs infected with the spirochete is only half that of adult ticks. Nonetheless, 90% or more of cases of Lyme disease are spread by nymphs because adults are less abundant, larger (found and removed more quickly and easily), and active at a time when fewer people are outside. The tick takes 24 hours or longer to attach. During that time B. burgdorferi lies dormant on the inner aspect of the tick's midgut. As the blood meal reaches the midgut, spirochetes proliferate and escape the gut, ultimately reaching the tick's salivary glands, where the excess water of the blood meal is passed back into the host along with the spirochete. (Courtesy of Leonard Sigal.)

4 Larva, nymph, and adult female and male Ixodes dammini ticks
Figure Larva, nymph, and adult female and male Ixodes dammini ticks (from right to left). The larva (far left) is approximately 1 mm in diameter. I. dammini is the principal vector for transmission of Lyme disease in the eastern and midwestern United States. (From Rahn [51]; courtesy of Marge Anderson, Pfitzer Central Research, Groton, CT.)

5 EPIDEMIOLOGY (cont) >  of dear ticks carry spirochete
Rising frequency attributed to enlarging deer population & concurrent suburbanization High risk areas - wooded or brushy, unkempt grassy areas & fringe of these areas Lower risk on lawns that are mowed

6 MAJOR RISK FACTORS Geographical Occupational Recreational
Northeast, north-central (Wisconsin, Minnesota) coastal regions of California & Oregon Occupational Landscaper, forester, outdoor Recreational hiking, camping, fishing, hunting

Stage 1 - Acute, localized disease Stage 2 - Subacute, disseminated disease Stage 3 - Chronic or late persistent infection

8 ACUTE INFECTION Tick must have been feeding for at least 24-48 hrs
Erythema migrans develops 1 to 4 weeks after bite Without treatment rash clears within 3 to 4 weeks About 50% of pts will also c/o flulike illness - fever, H/A, chills, myalgia

9 DISSEMINATED DISEASE May develop in wks to mos in untreated pts
Symptoms usually involve skin, CNS, musculoskeletal system, & cardiac Dermatological manifestations new skin lesions, smaller and less migratory than initial Erythema and urticaria have been noted

10 DISSEMINATED (cont) Neurologic complications
Occurs wks to mos later in about 15% to 20% of untreated Symptoms Lyme meningitis mild encephalopathy unilateral or bilateral Bell’s palsy peripheral neuritis

11 Left facial palsy (Bell's palsy) in early Lyme disease
Figure Left facial palsy (Bell's palsy) in early Lyme disease. The left facial droop reflects a seventh nerve palsy (Bell's palsy), an early neurologic manifestation of Lyme disease, and one that may be bilateral. Other neurologic manifestations include lymphocytic meningitis or meningoencephalitis and other cranial or peripheral neuritis. They typically occur 2 to 8 weeks after infection. (From Klempner [52]; with permission.)

12 DISSEMINATED (cont) Musculoskeletal symptoms
Symptoms evolve into frank arthritis in up to 60% of untreated pts Onset averages 6 mos from initial infection Symptoms migratory joint, muscle, & tendon pain knee most common site no more than 3 joints involved during course lasts several days to few weeks then joint returns to normal

13 DISSEMINATED (cont) Cardiac involvement
Noted in about 5% to 10% beginning several wks after infection Transient heart block may be consequence Range from asymptomatic to first-degree heart block to complete Cardiac phase lasts from 3 to 6 wks

Follows latent period of several mos to a yr after initial infection 60% to 80% will have musculoskeletal complaints Most common; arthritis of knee - may also occur in ankle, elbow, hip, shoulder

15 CHRONIC (cont) Neurologic impairment distal paresthesias
radicular pain memory loss fatigue

16 NATURAL HISTORY Without treatment will see disseminated disease in about 80% of pts Oligoarthritis - 60% to 80% Chronic neurologic & persistent joint symptoms - 5% to 10%

17 Clinical stages of Lyme disease
Stage III or the chronic stage is also referred to as the "late neurologic stage." This stage is characterized by chronic or late persistent infection of the nervous system. Syndromes included in this stage are encephalopathy, encephalomyelopathy, and polyneuropathy. The encephalopathy is characterized by memory and other cognitive dysfunction. The encephalomyelopathic signs are combined with progressive long tract signs and optic nerve involvement. White matter lesions may be visible on magnetic resonance imaging of the brain. The late polyneuropathy is primarily sensory. (Adapted from Davis [229].)

Human babesiosis fever, chills, sweats, arthralgias, headache, lassitude pts with both appear to have more severe Lyme disease Ehrlichiosis described as “rashless Lyme disease” high fever & chills & may become prostrate in day or two

Acute & early disseminated stages Rocky Mountain spotted fever human babiosis summertime viral illnesses viral encephalitis bacterial meningitis

20 DIFFERENTIAL (cont) Late disseminated & chronic stages gout pseudogout
Reiter’s syndrome, psoriatic arthritis, ankylosing spondylitis rheumatoid arthritis depression fibromyalgia chronic fatigue syndrome

21 DIAGNOSIS Clues to early disease EPIDEMIOLOGIC
travel or residence in endemic area within past month h/o tick bite (especially within past 2 weeks) late spring or early summer (June, July, August)

expanding lesion over days (rather than hours or stable over months) central clearing or target appearance minimal pruritis or tenderness central papular erythema, pigmentation, or scaling at sit of tick bite lack of scaling location at sites unusual for bacterial cellulitis (usually axillae, popliteal fossae, groin, waist

23 Erythema (chronicum) migrans
Figure Erythema (chronicum) migrans. Erythema migrans (EM), the pathognomonic skin lesion of Lyme disease, appears as an expanding erythematous lesion, often with central clearing, around the site of the tick bite. Rare lesions of EM can have erythematous and indurated centers resembling streptococcal cellulitis or vesicular and necrotic centers. EM is reported in 60% to 80% of patients. Common sites are the thigh, groin, trunk, and axilla. (From Steere et al. [51]; with permission.)

24 Single erythema migrans
An example of single erythema migrans is shown on the back with the appearance of a "bull's eye." The lesion occurred at the site of a tick bite and slowly spread over the course of a few days. (Courtesy of Leonard Sigal.)

25 EARLY DISEASE (cont) ASSOCIATED SYMPTOMS fatigue myalgia/arthralgia
headache fever and/or chills stiff neck respiratory & GI complaints are infrequent

26 EARLY DISEASE (cont) PHYSICAL EXAM Regional lymphadenopathy
Multiple erythema migrans lesion Fever

27 DISSEMINATED DISEASE Clinical presentation can make diagnosis
epidemiological inquiry review of key historic features physical findings serum for antibody testing spinal tap

28 LATE DISEASE Careful attention to musculoskeletal & neurologic symptoms Differentiating Lyme from fibromyalgia & CFS oligoarticular musculoskeletal complaints that include signs of joint inflammation limited & specific neuro deficits abnormalities of CFS absence of disturbed sleep, chronic H/A, depression, tender points

29 ANTIBODY TESTING Testing with ELISA is not required to confirm diagnosis Pts with objective clinical signs have high pretest probability of disease Tests are not sensitive in very early disease Should not use is pt without subjective symptoms of Lyme

30 TESTING(cont) A + test in person with low probability of disease risks false + rather than true + Test when pts fall between these two extremes pt with lesion or symptoms without known endemic exposure (new area) pretest probability now has high sensitivity & specificity

31 TESTING (cont) For a positive or equivocal ELISA or IFA CDC recommends Western blot Testing cannot determine cure as pt remains antibody + PCR is being developed - still considered investigational

32 TREATMENT Early Lyme disease doxycycline, 100 mg BID for 21 to 18 days
amoxicillin, 500 mg TID for 21 to 28 days cefuroxime, 500 mg BID for 21 days

33 PREVENTION Wear light-colored clothes - easier to spot tick
Wear long pants, long sleeves Use tick repellent, such as permethrin, on clothes Use DEET on skin Check for ticks after being outside Remove ticks immediately by head


35 WEST NILE VIRUS Summer first detected in NYC & Western hemisphere 59 hospitalized - epicenter Queens - 7 died Summer epicenter Staten Island - 19 hospitalized - 2 died For states, 3737 confirmed cases, 214 deaths

36 INFECTIOUS AGENT Member of family Filaviviridae
Belongs to Japanese encephalitis complex Before 1999 outbreaks seen only in Africa, Asia, Middle East, rarely Europe Reservoir & Mode of transmission wild birds primary reservoir & Culex spp. major mosquito vector

Incubation usually 6 days (range 3-15) Symptoms milder: fever, headache, myalgias, arthralgias, lymphadenopathy, maculopapular or roseolar rash affecting trunk & extremities occasionally reported: pancreatitis, hepatitis, myocarditis CNS involvement rare & usually in elderly

38 TREATMENT No known effective antiviral therapy or vaccine
Intensive supportive in more severe cases

Enteroviruses Herpes simplex virus Varicella

40 TESTING Lab conformation based on following criteria:
isolating West Nile virus from or demonstrating viral antigen or genomic sequences in tissue, blood, CSF, or other body fluid demonstrating IgM antibody to West Nile virus in CSF by ELISA demonstrating 4-fold serial change in plaque reduction neutralization test (PRNT) antibody to West Nile virus in paired, acute & convalescent serum samples demonstrating both West Nile virus-specific IgM & IgG antibody in single serum specimen using ELISA & PRNT

41 Must report suspected cases of West Nile to the NYC Department of Health
During business hours call Communicable Disease Program (212) At all other times call Poison Control Center - (212)

Infectious mononucleosis - designates the clinical syndrome of prolonged fever, pharyngitis, lymphadenopathy Epstein-Barr virus-associated infectious mononucleosis (EBV-IM) non Epstein-Barr virus-associated infectious mononucleosis (non-EBV-IM) approximately 10-20% have

43 EPIDEMIOLOGY >90% of adults have serologic evidence of prior EBV infection Mean age of infection varies In US 50% of 5-year-old children & 50-70% of first-year college students have evidence of prior infection Infection in children most prevalent amongst lower socioeconomic peak rate of EBV-IM

44 Chance of acute EBV infection leading to IM  with age
Good sanitation & uncrowded living conditions  risk of EBV-IM

45 OTHER CAUSES OF IM CMV Human herpesvirus 6 HIV Adenovirus Toxo
Corynebacterium diptheriae Hep A Rubella Coxiella burnetii

Classic triad - fever, pharyngitis, lymphadenopathy Prodrome- malaise, anorexia, fatigue, headache, fever Symptoms usually peak 7 days after onset &  over next 1-3 wks Splenic enlargement %

47 Less common clinical features
upper airway compromise abdominal pain rash (ampicillin  risk of) hepatomegaly jaundice eyelid edema

48 DIAGNOSTIC TESTING Serologic test for heterophil antibodies
Percentage with antibodies higher > 4yrs old % of persons who are + at 1 week varies with test (1 study - 69% + at 1 wk; 80% + by 3 wks) False +s rare

49 If heterophil antibody continues neg & still suspect;
serum for viral capsis antigen (VCA) IgG & IgM & for EBV nuclear antigen (EBNA) IgG VCA antibodies + in many at onset

Total leukocyte count  usually > 50% of total leukocytes consist of lymphocytes possible mild thrombocytopenia  LFTs fold abnormalities on UA

51 IM IN OLDER ADULTS 3-10% of persons >40 are susceptible
Presenting S & S different Fever present but few have pharyngitis & lymphadenopathy Jaundice in >20% R/O; hepatobiliary disease, neoplasms, collagen vascular diseases, bacterial infections

52 MANAGEMENT Supportive NSAIDs or tylenol - no ASA
Bedrest during febrile stage If have splenomegaly avoid vigorous activity for 3-4 wks No evidence that steroids or antivirals are of benefit

Has been called: chronic EBV syndrome, postviral fatigue syndrome, “yuppie flu” 1988 CDC convened researchers & clinicians to define & classify CFS 1994 international group proposed guidelines for CFS CDC reported prevalence of 4-11 cases/100,000 population In US most cases occur in young to middle-aged white women

54 ETIOLOGY No cause identified Postulated infective neuromuscular
immunologic neurologic psychiatric

Fatigue criteria Must not be lifelong Must be persistent, relapsing & unexplained Must not be result of ongoing exertion & cannot be relieved by rest

56 Symptom Criteria Sore throat
Short-term memory or concentration impairment Tender cervical or axillary lymph nodes Headaches of a new type, pattern, or severity Unrefreshing sleep Postexertional malaise lasting > 24 hrs Multijoint pain without joint swelling or inflammation Muscle pain

57 Exclusion Criteria Past or current diagnosis of major depression with psychotic or melancholic features, bipolar disorder, schizophrenia, delusional disorders, dementia, bulimia nervosa, anorexia nervosa Active medical conditions Previously diagnosed conditions with unclear resolution (malignancies, hepatitis B or C) Alcohol or substance abuse within 2 yrs of onset of fatigue Severe obesity (BMI  45)

58 Detailed medical history Complete physical Labs
CBC ESR TSH UA Serum chem for electrolytes, BUN, cr, glucose, calcium, phosphorus, alk phos, total protein, albumen, globulin, LFTs

59 MANAGEMENT Goal: Restore pts occupational & social functioning & prevent further disability. Guidelines Establish diagnosis Prevent further disability If indicated, start medication ASAP Warn about unproven therapies Initiate psychological intervention

60 PHARMACOTHERAPY Antivirals Immunomodulators Psychotropic agents
Pain medications Antiallergy medications Acetylcholinesterase inhibitors Agents used in alternative medicine

Exercise Cognitive behavior therapy Self-help groups Work as therapeutic modality

62 DIFFERENTIAL Fibromyalgia Endocrine Chronic viral infections
Malignancy Sleep disorders causing fatigue Connective tissue diseases Body weight changes Side effects of medications Other illnesses

Major depressive episodes Anxiety disorders Delusional disorders Bipolar disorder Schizophrenia Eating disorders Dementias Sleep disorders Substance use disorders

64 HERPES ZOSTER Represents reactivation of varicell-zoster virus
Latently resides in a dorsal root or cranial nervie ganglia Multiple erythematous plaques with clustered vesicles Vesicles begin to dry & crust in 7-10 days, clear within 2-3 wks, new may continue to appear for up to 1 wk

65 COMMON DISTRIBUTION Thoracic dermatome 50% Cervical dermatome 20%
Trigeminal dermatome 15% Lumbosacral dermatome 10%

Prodrome Vesicular rash Diagnosis - presentation

67 Herpes zoster Figure Herpes zoster. Reoccurrence of the varicella virus. Vesicles usually appear in a dermatomal distribution.

68 Acute herpes zoster ophthalmicus
Figure Acute herpes zoster ophthalmicus. An elderly woman presented with tingling and subsequent pain on the left side of her forehead. She developed vesicular lesions over the distribution of the ophthalmic branch of the trigeminal nerve. The involvement of the tip of her nose (Hutchinson's sign) suggests involvement of the nasociliary nerve, a nerve that also supplies the cornea. In this case, the cornea has become inflamed, the eye is red, and there is a danger that glaucoma will develop. Patients with acute herpes zoster ophthalmicus should be treated with acyclovir, 800 mg five times a day for 5 days, beginning within 72 hours of the onset of symptoms; this reduces the incidence of ocular involvement, but it does not alter the course of postherpetic neuralgia.

Trigeminal dermatome may affect second branch associated with involvement of eye keratitis, uveitis, secondary glaucoma, iridocyclitis Ramsay-Hunt syndrome affects facial & auditory nerves facial palsy with cutaneous zoster of external ear or TM, with associated tinnitus, vertigo, &/or hearing loss

70 TREATMENT Early treatment Acyclovir (Zovirax) Valacyclovir (Valtrex)
within hrs Acyclovir (Zovirax) 800mg 3x/day Valacyclovir (Valtrex) 1,000mg 3x/day Famciclovir (Famvir) 500mg 3x/day

Famvir and Valtrex  incidence Capsaicin cream (Zostrix 0.025% & Zostrix HP 0.075%) 4x/day Amitriptyline Gabapentin Often remits spontaneously after 6 months Pain referral

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