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Lyme Disease
April 29, 2003
Madina Agenor
Sogole Moin
Disease History
• In the early 1900s, manifestation first reported in Europe
– associated it with tick bites
• In 1975, outbreak in Lyme, Connecticut
– Believed to be juvenile rheumatoid arthritis
• In 1982, spirochetes were identified in the midgut of the blacklegged tick (Ixodes scapularis) and named Borrelia
burgdorferi.
• In 1984, Borrelia burgdorferi was isolated from the blood of
patients with EM and from the rash lesion itself.
– Determined etiologic agent
• Today, it is the most common tick-borne infection in the U.S.
– more than 16,000 infections each year.
Distribution
• Mostly localized
to states in the
northeastern,
mid-Atlantic, and
north-central
regions, and to
several counties
in northwestern
California
http://www.cdc.gov/ncidod/dvbid/lyme/
• In 1996-1999, the states with the highest
reported number of Lyme disease cases were:
New York, Connecticut, Pennsylvania, New
Jersey, Wisconsin, Maryland and Rhode Island
• Also reported in Europe, Asia and Australia
• Where suburban and country residential
dwellings encroach on wooded areas
• Most common during late spring and summer
Causative Agent
• Borrelia burgdorferi sensu stricto
• Spirochete: slender helical
shaped bacteria
• Gram negative
• Motile
http://www.cdc.gov/ncidod/dvbid/lyme/
• Extracellular pathogen
• Aerobic or microaerophilic
• .2um to 5um in width and 10 to 25 um in
length
• Protoplasmic cylinder
• Cell membrane
• Outer membrane
• 7 to 11 flagella
• Cell division after 12 to 24 hours of elongation
• Optimal temperature is 33C
• Incubation period of 3 to 32 days after
infecting the human host through a tick bite
• Genome: linear chromosome and numerous
linear/circular plasmids
• Plasmids encode key genes involved in
virulence
• B. burgdorferi discovered in 1982
• Isolated and cultured from the tick Ixodes
scapularis
• Midgut contents of the tick removed and
cultured on BSKII medium
• Motile spirochetes isolated and observed by
dark field microscopy
• Spirochetes identified as B. burgdorferi
• U.S.: B. burgdorferi sensu stricto
• Europe: B. burgdorferi sensu stricto, B.
garinii, and B. afzelii
• Asia: B. garinii and B. afzelii
Methods of Transmission
• Vector-borne disease
• Vector is deer or black-legged tick (Ixodes scapularis)
or by the western black-legged tick (Ixodes pacificus)
on the Pacific Coast.
• Transmits B. burgdorferi while feeding on an
uninfected host
– the spirochetes are present in the midgut and migrate during
blood feeding to the salivary glands, from which they are
transmitted to the host via saliva.
• B. burgdorferi cannot penetrate intact skin
• Two-year life cycle of
tick
– Larval, nymphal and
adult stages
http://www.cdc.gov/ncidod/dvbid/lyme
• Nymphal ticks are size of
poppy seeds
• Reservoir for B. burgdoferi is deer
or white-footed mouse
• Human contact can occur through pets
and outdoor activities in wooded areas
• If tick is attached for less than 24 hours,
risk of acquiring Lyme disease is
significantly reduced.
• Once in the host, B. burgdorferi recognizes
polysaccharides on the surface of mammalian
cells
Symptoms
• Symptoms of B. burgdorferi
• Stage 1
– Localized erythema migrans (EM) http://www.cdc.gov/ncidod/dv
bid/lyme/diagnosis.htm
– Red macule/papule
– Round lesion that measures 5cm to 15cm.
• Stage 2
– Early disseminated infection
• multiple secondary erythema migrans lesions
• systemic non specific symptoms
– Persistent or late infection
•
•
•
•
Symptoms of neurologic disease
Symptoms of musculoskeletal disease
Symptoms of cardiac disease
Chronic inflammatory eye disease
• Stage 3
– 6 months after primary skin lesion
• Swelling and pain in large weight-bearing joints, especially
in the knee.
• Chronic arthritis
– Years after infection, if left untreated:
• Late neurological syndrome
• Post-Lyme disease syndrome
– Persistent disease after antibiotic treatment
– Controversial
• Some infected individuals show asymptomatic
infection
• Some only manifest nonspecific symptoms
Diagnosis
• Serologic data by IFA, ELISA and immmunoblotting
techniques.
– Detect presence of IgM or IgG antibodies in patient’s
serum against Borrelia burgdorferi
– Tests are insensitive the first several weeks of infection
– Western blot is more accurate and is used 6-12 weeks after
infection to confirm results
• Direct Isolation
– Biopsies of the skin lesions may yield the organism in 50%
or more of cases
Cure
• Antibiotic therapy
• Doxycycline and amoxicillin are used for two to four
weeks in early cases
• Doxycycline is also effective against human
granulocytic ehrlichiosis
• Cefuroxime axetil or erythromycin can be used for
patients who are allergic to penicillin or who cannot
take tetracyclines.
• More developed cases, may require treatment with
intravenous ceftriaxone or penicillin for 4 weeks or
more
Prevention
• Avoid tick habitats
• Wear appropriate barrier clothing that follow personal
protection procedures
• Apply insect repellent containing DEET to skin
• Apply permethrin to clothes
• Perform regular body checks for ticks
• Remove ticks promptly with tweezers and clean area
with antiseptic
• Education of the general public
• Lyme disease vaccine: LYMErix
– Recommended to 15-70 year olds living in endemic
areas
– Recommended to those who are at risk due to
occupation
– Only suggested to those who have a seasonal
problem of infection greater than 1%
– No longer commercially available since February
25, 2002
Control
• Habitat modification for ticks
-Clear trees and brush
•
Chemical control of tick populations
-Apply pesticides to residential properties
• Habitat modification for deer and rodents
-Keep rodents and deer away from houses and gardens
• Host management
-Deer feeding stations equipped with pesticide applicators
-Baited devices to kill ticks on rodents
Works Cited
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Bacon, R.M., B.J. Biggerstaff, M.E. Schriefer ME, R.D. Gilmore Jr, M.T. Philipp, A.C.
Steere, G.P. Wormser, A.R. Marques, B.J. Johnson. “Serodiagnosis of Lyme Disease by
Kinetic Enzyme-Linked Immunosorbent Assay Using Recombinant VlsE1 or Peptide
Antigens of Borrelia burgdorferi Compared with 2-Tiered Testing Using Whole-Cell
Lysates.” Journal of Infectious Diseases. 2003 Apr 15;187(8):1187-99.
Benenson, Abram. Ed. Control of Communicable Diseases Manual. Washington, DC:
American Public Health Association, 1995.
Crippa, M., O. Rais and L. Gern. “Investigations on the mode and dynamics of
transmission and infectivity of Borrelia burgdorferi sensu stricto and Borrelia afzelii in
Ixodes ricinus ticks.” Vector Borne Zoonotic Diseases. 2002 Spring;2(1):3-9.
Durham, Jerry D. and Felissa R. Lashley. Emerging Infectious Diseases: Trends and
Issues. New York: Springer Publishing Co., 2002.
Parveen, N., M. Caimano, J.D. Radolf, J.M. Leong. “Adaptation of the Lyme disease
spirochaete to the mammalian host environment results in enhanced glycosaminoglycan
and host cell binding.” Molecular. Microbiology. 2003 Mar;47(5):1433-44.
Perry, Jerome, James Staley, Stephen Lory. Microbial Life. Sunderland, MA: Sinauer
Associates, Publishers, 2002.
CDC Lyme Disease Home Page. http://www.cdc.gov/ncidod/dvbid/lyme/
Zeus Scientific, Inc. “IFA Assays – Bacterial Diseases”.
http://www.zeusscientific.com/ifabact.html. 23 April 2003.