1
Q
What is Lyme’s disease and what does it do?
A
- Prototype emerging infectious disease (new disease)
- Multisystem disorder
- Presents bullseye rash (erythema migrans - getting bigger)
- Result of tick bite infected with the bacteria
- Bacteria spreading under skin
- Untreated = arthritis, carditis, nervous system manifestations
2
Q
What is the origin/epidemiology of Lyme’s?
A
- Most common vector-borne disease in North America
- Comes from town in Connecticut called Lyme, recognised in 1975 rural communities
- Epidemic of polyarthritis (arthritis in many locations) in children - arthritis doesn’t happen in epidemics!
- Misdiagnosed with autoimmune rheumatoid arthritis
- Many noted bullseye rash prior to symptoms, associated with tick bite
- Researchers isolate a spirochete (type of bacteria) from the ticks, and also isolated this organism from skin, blood, cerebral spinal fluid, from patients
3
Q
What bacteria is responsible for it, what are its characteristics?
How is it spread?
A
- Borrelia burgdorferi
- Gram negative spirochete, thin (0.5 micrometer) and long (> 10 micrometers!), spiral shaped
- Lyme Borrelia found in northern hemispheres
- Species other than B. burgdorferi cause Lyme disease (collectively called B. burgdorferi sensu lato) but are uncommon
- Spread by the bite of hard body ticks (Ixodes species)
- Thus it is a vector-borne disease
4
Q
What is the reservoir for B. burgdorferi?
A
- Transmitted to mammalian hosts through ticks, usually white footed mouse
- Must be mammal-tick-mammal transmission, bacteria are only found in vertebrate or arthropod hosts.
5
Q
What is the main tick genus that spreads Lyme’s, whats its life cycle?
How do ticks acquire the infection? At what point in the life cycle is the disease transmitted the most?
A
- Ixodes Tick (Black legged or deer tick)
- 2 main ones in North America (Ixodes scapularis -east and Ixodes pacifica -west)
- Different in Europe and Asia
- 3 stages Larva > Nymph > Adult
- Require one blood meal between stages
- Adults do not transmit bacteria to eggs, must be acquired from a mammalian host
- Most infections come from nymphs; feed in spring and smaller, therefore harder to see
6
Q
Transmission of Lyme’s disease
A
- Ticks do not jump or fly, they sit and wait to latch onto host
- Bite hard to see places (back, armpit, groin)
- Latch on and feed for days, appear grey when engorged
- Transmission chance increases after >24 of latching
- Pets can get Lyme disease
- No instance of person-person transmission
7
Q
Tick removal steps?
What should not be done?
A
- Use fine tipped tweezers
- Grasp tick as close to skin as possible
- Steadily pull upwards
- Wash area
- Keep tick
Do not squish tick, burn tick off, apply petroleum jelly
- Squish or burn causes stress and forces more organisms into the skin, same with the jelly which suffocates
8
Q
Following initial infection, what occurs?
A
- B. burgdorferi move around (disseminate) and propagate through life cycle
- Hematogenous dissemination (spreading by blood) is the main event in development, because the bacteria must be disseminated to be picked up by future ticks (in a mouse, for example)
9
Q
What does tick saliva do to immunity?
A
Inhibit DC function greatly: phagocytosis, maturation, inflammatory mediators, antigens
Helps the tick survive in skin (while feeding)
10
Q
What are special features of B. burgdorferi? Structural, Genetic?
A
- Periplasmic flagella (key virulence factor) called axial filaments
- Intracellular; located within periplasmic space - only possible since it is Gram negative
- Unusual outer membrane
- no LPS despite being Gram negative
- Unusual genetic structure
- Has circular and linear plasmids
11
Q
How do the B. burgdorferi flagella work?
A
- Wrap around bacterial cells to produce cork-screw shapes
- Rotation of axial filament causes the bacteria to move in a corkscrew like manner (twisting)
- Promotes movement of bacteria through extracellular matrix of host tissue and invasion of vasculature (blood vessels)
12
Q
What is expressed in B. burgdorferi in place of LPS?
A
- Surface lipoproteins are expressed that function as adhesins
- This causes drag (stationary adhesion), where they then turn on the flagella and escape
- Repetitive mobility/motility (“pounding”) is required to enter/leave the endothelium
13
Q
What are the effects of the linear and circular plasmids of B. burgdorferi?
How does this effect diagnosis?
A
- Limits metabolic capacity
- Has a small amount of DNA; it has lost a lot of genes so is limited in its life cycle and habitat choice
- Plasmids vary from strain to strain
- Some tests are based on genes from these plasmids = if you don’t have that gene, incorrect conclusion (i.e., the tests suck)
14
Q
Describe the early localised stage of infection
A
- Erythema migrans (bulls eye rash) - early in the groin, axilla, waist, back, legs, 1-2 weeks after tick bite,
- 25% do not have rash
- Rash CONFIRMS lyme infection but early treatment prevents lyme disease
- If untreated it can reach > 12 diameter
- Flu-like symptoms (fever, chills, fatigue, body aches)
15
Q
Describe the early disseminated stage of infection (days to weeks)
A
- Occurs in untreated patients
- Multiple rashes indicated dissemination of B. burgdorferi
- Pain and swelling of large joins
- Heart palpitations
- Meningitis
- Not your classic hyper-aggressive meningitis (rather, it is more chronic)
- Paracellular traversal
- Bell’s (facial) palsy occurs which is the loss of muscle tone on one or both sides of face
16
Q
Describe the late disseminated stage of infection (months to years later)
A
- Can cause serious long-term disability
- Require long course of ABx
- Symptoms
- Muscle pain, arthritis
- Severe pain and swelling in large joints
- 5% develop neurological problems (shooting pains, numbness, memory issues)
17
Q
What is post treatment Lyme disease? (medical condition)
A
- 10-20% experience symptoms following treatment with ABX (don’t know why)
- Lingering symptoms such as fatigue, muscle and joint pain, cognitive defects, sleep disturbances
- May involve autoimmune response or persistent infection
- Most patients recover from this (long-term ABx unhelpful)
18
Q
Lyme disease in Canada, how do you prevent getting it?
A
- Ticks moving north - on birds, in warmer weather, increases with mouse populations
- Cases rising but vastly under reported
- Risk areas dot the border
Prevention:
- Avoid wooded areas endemic with Lyme disease, stay on paths, avoid low lying brush and long grass
- Wear long pants and shirt, light coloured - Repellents (DEET) - Check for ticks, remove properly
19
Q
Diagnosis?
A
- Erthyema migrans and other typical symptoms
- Tick bite/reason to suspect exposure
- B. burgdorferi antibody tests
- Detect antibodies to a laboratory strain of B. burgdorferi
- False negatives usually due to early testing (no antibody response yet) and genetic diversity of the bacteria
- Sensitivity is controversial
- Submit the tick for testing! To the national microbiology laboratory
20
Q
Treatment?
A
- If bitten by a tick that carries, watch for a rash and symptoms
- Early diagnosis = recovery with 2-4 weeks of ABx
- No treatment = joint, heart, nervous problems
21
Q
Chronic Lyme disease?
A
- Very controversial
- Some think this is due to chronic infection by B. burgdorferi
- Problem: can be diagnosed without evidence of prior lyme disease or tick bite
- Persistent symptoms like fatigue, headache, sleep disturbance, cognitive dysfunction, neurological problems
- Long-term antimicrobial therapy is not helpful (4 clinical trials)
22
Q
Lyme’s disease vaccine?
A
- LYMErix was based on an outer membrane protein
- Human trial of 11,000 adults showed it to be 75% effective
- Should be considered for high risk areas but not recommended
- Claim/lawsuits that vaccine causes arthritis
- Placebo group got arthritis too
- No evidence
- Pulled from market due to lack of demand, now only approved for dogs
- Once pulled, does not come back
Bacteriology
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