Borrelioses. Lyme disease. Flashcards
what is the etiology of lyme disease ?
Borrelia burgdorferi
what are the characteristics of lyme disease ?
afastidious microaerophilic spirochete bacteria
Atypical and cystic forms of B. burgdorferi can persist in the body for years.
what is the epidemiology
lyme disease is now the most common vector-borne disease in the United States and Europe
human infection is caused primarily by three pathogenic genospecies:
B. burgdorferi sensu stricto in USA and westerN EUROPE
Borrelia garinii,
and Borrelia afzelii,
IN Eurasia.
which have different geographic distribution
incidence of Lyme disease is highest between April and October (especially from June to August)
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vectors according to geographic location
lxodes ricinus - europe
lxodes persulcatus - asia and easter europe
lxodes scapulars - north america
lxodes pacificus - north america
ticks of l ricinus complex have larval , nymphal and adult stages = each of the the requires blood meal at each stage
nymphal ticks peaks during early summer months - and usually the main vector
they increase with human outdoor activities
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reservoir
Peromyscus leucopus, the white‑footed mouse, is the primary reservoir of B. burgdorferi in the US.
other reservoir hosts - deer, cattle
how is lyme borreliosis transmitted ?
BY BITES OF INFECTED NYMPHAL TICKS OR LXODES RICINUS COMPLES (black legged deer ticks)
they are a vector
what are the risk factors of lyme disease ?
being outdoors while hiking and gardening
occupational exposure - landscapers and ranger
age group 5-15 years of age
45-55 years of age
summer months - june and july
what is the pathogenesis of lyme disease ?
for b burgodorferi to maintain its lifecycle it must adapt tot two different environments - Tick and Malian host
ticks carry the pathogen in their midgut
they get this be feeding on an infected host during any of the 3 stages of their life
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before nymph can transmit the disease they must be attached to host for a long period around 36-48 hours since the blood meal has to trigger reproduction of the borrelia and for the infection size to be large enough to be infective
if tiki’s removed before the 36th hour - no clinical manifestation can occur
the pathogen enters as spirochetes translocated fro the gut then to the salivary glands and to the tick bite site
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body reaction to the tick bite can have 3 courses
1) spirochete eliminated by the host defence
2) spirochete remain viable and localised in the skin
producing erythema migrant - characteristic skin lesion for lyme disease
3) within days to weeks , spirochete may disseminate through lymphatic system and blood
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spirochete shows distinctive tropism fr he skin , heart , cns , joints , eyes - esp to bind with the collagen fibrils
what is the incubation period for borrelia burgforedi ?
3-32 days
what are the three stages of clinical manifestation in borrelia burgforedi?
1) early localised
characteristic a painless rash called erythema
chronicum migrans
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usually begins as a red macule or papule at the site of the tick
bite
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it later expands to an annular rash (90%)
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it increases in size and develops a bright red
outer border and partial central clearing
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->sometimes described as a
“bull’s-eye” rash
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Nonspecific symptoms: Fatigue, Myalgias,
Arthralgias, Headache, Fever, Chills, Neck
stiffness
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2) early disseminated
after 3-10wks
clinical manifestations differ in Europe and the United States:
• in Europe more affected are asymptomatic relatively to those in the US
Weeks to months after tick bite
if localized infection is not treated it may spread to many sites
most common symptoms:
1) rheumatologic
Migratory arthralgia: can progress to Lyme arthritis
Generally in large joints (especially knee or elbow)
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2) Early neuroborreliosis
Cranial nerve disorders
Most commonly peripheral facial nerve palsy
Nocturnal radicular pain, paresthesia, and paresis
Meningitis that may cause benign intracranial hypertension
Polyneuropathy
in europe Meningopolyradiculitis (Bannwarth’s syndrome), a manifestation of stage 2 neuroborreliosis, which is characterized by severe radicular pain
in children the optic nerve may be affected because of inflammation or increased intracranial pressure which may lead to blindness
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then dermatologic
(disseminated EM),
Multiple erythema migrans lesions
in Europe, 2 dermatological manifestations have been present which are
not seen in North America:
borrelial lymphocytoma
(a purplish nodula swelling usually occurring on the earlobe or nipple in stage 2 disease)
and
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cardiac
(AV block, myopericarditis)
Adams-Stokes syndrome
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occular - including conjunctivitis, retinal vasculitis, optic neuropathy, and uveitis
early signs may vary, but only fatigue and lethargy are constant
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3) chronic disseminated
months after infection with no antibiotic treatment
patients develop frank
arthritis esp. in the knees (=lyme arthritis - hallmark for this stage)
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dermatologic,
acrodermatitis chronica atrophicans - ONLY IN EUROPE AND ASIA
due to infection with Borrelia afzelii
commonly affects women > 40 years
which occurs over extensor
surfaces of the extremities
1) Edematous stage with inflammatory reaction (livid discoloration)
2) Atrophic stage: hairless, sclerotic skin plaques
rheumatologic
late neuroborreliosis Aseptic (lymphocytic) meningitis Progressive encephalomyelitis Cognitive impairment Gait abnormality Bladder dysfunction Psychiatric abnormalities (cranial nerve palsy, ataxia, spastic paresis, encephalomyelitis)
what is the diagnosis of borrelia ?
primarly based on clinical findings
wo‑step serological testing
Initial test: enzyme‑linked immunosorbent assay (ELISA)
Confirmatory test: Western blot
Detect IgG and IgM antibodies against Borrelia
Results are only significant with corresponding clinical symptoms because:
Positive results only demonstrate exposure to Borrelia (not necessarily current infection).
False negative results are possible if seroconversion has not yet occurred (may take up to 8 weeks).
Various diseases can lead to a false positive serology as a result of cross-reactions, including: Syphilis Rocky Mountain spotted fever Systemic lupus erythematosus Rheumatoid arthritis
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(the culture of B. burgdorferi in Barbour-Stoenner-Kelly (BSK) medium
permits definitive diagnosis)
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an enzyme-linked immunosorbent assay (ELISA) but the antibodies can only
be found 21 days after tick bite
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Western blot test
what is the treatmnet approach of borrelia burgfordi ?
If stage I Lyme disease is likely (e.g., EM is present), start empiric antibiotics without further testing.
If symptoms of Lyme disease arise in a patient with possible exposure (especially if recently traveled to an endemic area), conduct two-step serological testing.
all 3 stages of clinical manifestation are curable with antibiotics if untreated dissemination is likely to occur
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Localized Lyme disease \+ Disseminated Lyme disease ( Isolated CN palsy Mild carditis Borrelial lymphocytoma Initial arthralgia/arthritis Acrodermatitis chronica atrophicans) 14- 21 days
First-line oral antibiotics
Doxycycline >9yrs
Amoxicillin
Cefuroxime axetil
Therapy in pregnant/nursing patients <9 yrs
Amoxicillin
Cefuroxime axetil
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Disseminated Lyme disease
Hospitalize patient Intravenous antibiotics Drug of choice: ceftriaxone Cefotaxime Penicillin G
what is post lyme syndrome ?
in this stage, there are generalized symptoms:
marked fatigue,
severe headache,
diffuse musculoskeletal pain, multiple symmetric tender
points,
pain and stiffness in many joints,
diffuse paresthesias,
difficulty with concentration, and sleep disturbances
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late manifestations of Lyme disease, including arthritis, encephalopathy,
and neuropathy are not so severe
what is dd
erythema migrans
Cellulitis
Contact dermatitis (discoid eczema)
Erythema marginatum (rheumatic fever)
facial palsy can also be caused by Herpes simplex virus type 1 (Bell’s
palsy) and varicella-zoster virus (Ramsay Hunt syndrome)
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most common is the chronic fatigue syndrome or fibromyalgia
what is the prevention for lyme disease ?
no approved vaccine
avoid prime habitats in areas known for Lyme disease.
Tick bite prevention: Prevent and properly manage tick bites to avoid exposure.
Wear protective clothing: e.g., long-sleeved shirts, long pants, and light colors.
Use tick repellent and pesticides.
Check body for tick bites.
Remove ticks immediately!
Grasp the tick with tweezers directly above the skin’s surface.
Carefully pull upward with even pressure.
Do not use nail polish remover, adhesives, oils, or similar substances to remove the tick. The tick should be removed quickly rather than waiting for it to detach slowly.
Disinfect the site of the bite and dispose of the tick
Observe the bite site for early detection of EM.
Post‑exposure prophylaxis for Lyme disease
Although controversial, post-exposure prophylaxis may be considered for patients who meet all of the following criteria:
The attached tick can be identified as an adult or nymphal Ixodes scapularis tick.
The tick has been attached for ≥ 36 hours (based on degree of engorgement or amount of time since exposure).
Prophylaxis can be started within 72 hours of tick removal.
The patient can take doxycycline
what is Jarisch-Herxheimer-
like reaction?
during the first 24 h of
therapy approximately 15% of patients experience this
reaction to endotoxin-like products released by the death of harmful microorganisms within the body during antibiotic treatment.
as fever, chills, rigor, hypotension, headache, tachycardia, hyperventilation, vasodilation with flushing, myalgia (muscle pain), exacerbation of skin lesions and anxiety.
shock
