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what pathogen causes lyme disease?
borrelia burgdorferi
characteristics of borrelia burgdorferi
0.2-0.5 um wide and 2-30 um long
gram negative
obligate pathogens in a variety of vertebrate hosts
true or false: borrelia are longer and wider than other spirochetes.
true
what reveals the spirals and motility of borrelia burgdorferi?
dark field examination
spirochetes of borrelia burgdorferi are transmitted and maintained by
ticks
what is the most prevalent vector-borne disease in the Northern hemisphere?
lyme disease
lifecycle of ixodes scapularis
adult females drop off host to lay eggs
eggs hatch into larvae
larvae attach to and feed on first host (rodent)
larvae turn into nymphs after leaving first host
infected nymphs feed on humans
nymphs attach to and feed on second host (rodent)
nymphs turn into adults after leaving second host
infected adults feed on dogs
adults attach to their host for feeding
early localized stage of lyme disease in humans
3-30 days post tick bite
red, expanding rash: erythema migrans
fatigue, chills, fever, headache, muscle and joint aches, and swollen lymph nodes
early disseminated stage of lyme disease in humans
days to weeks post-tick bite
facial or bell’s palsy
severe headaches and neck stiffness
pain and swelling in the large joints
shooting pains that may interfere with sleep
late disseminated stage of lyme disease in humans
months to years post tick bite
arthritis with severe joint pain and swelling
up to 5% of untreated patients may develop chronic neurological complaints months to years after infection
lyme disease in dogs
70-90% of all dogs in endemic areas are seropositive
clinical signs are observed in <10% of exposed dogs
clinical illness is seen 2-5 months after tick exposure
clinical syndrome → polyarthritis and glomerulopathy
lyme arthritis clinical signs
fever
shifting leg lameness
articular swelling
polyarthritis
lymphadenomegaly
anorexia
general malaise
lymph nephritis clinical signs
sudden onset of anorexia, vomiting, lethargy, and weight loss
uremia, hyperphosphatemia, and severe protein-losing nephropathy
lodging of immune complexes in kidneys
labs, golden retrievers, and bernese mountain dogs
lyme disease in horses
50% of all horses in endemic areas are seropositive
clinical signs are observed in <10% of exposed horses
clinical signs of lyme disease in horses
chronic weight loss, sporadic lameness, shifting leg lameness, low-grade fever, muscle tenderness, poor performance, swollen joints
changes in behavior and skin sensitivity, both with rapid onset
neurological signs → depression, dysphagia, head tilt and encephalitis were reported in chronic cases
clinical lab findings for lyme disease
no specific hematologic or biochemical changes are pathognomonic of borreliosis
if a dog in a lyme endemic area has leukopenia or thrombocytopenia → caused by co-infection
synovial fluids of lyme arthritic dogs have increased cell counts
serological testing of lyme
seropositivity = exposure
whole-cell ELISA
C6 peptide based assays
multiplex assay
whole-cell ELISA
antibody measurements using whole spirochetes
cross-reactivity with leptospira-positive sera
whole cell-immunoblotting
helps identify sera that produce false-positive results in whole-spirochete assays
C6-peptide based assays
detect antibodies against C6-peptide
can differentiate between vaccinated and naturally infected dogs
does not react with sera from healthy dogs or infected with other diseases
C6-peptide based commercial assays
SNAP 4Dx plus test
lyme quant C6 test
treatment and control of lyme disease
acute cases responds to beta-lactams and tetracyclines
chronic cases require longer therapy
tick control
vaccines, bacterins, and subunit vaccines available
important tick-borne disease for humans
prevention of lyme by tick control in dogs
collars
topical powders, shampoos
daily combing and tick removal
prevention of lyme by tick control in the environment
targeting mice population
prevention of lyme disease by vaccines
recombinant, subunit vaccine
killed, whole-cell, bivalent bacterin