3. Lyme Disease is caused by a
spirochete bacteria Borrelia
burgdorferi
Ticks are the vectors
The “Deer Tick” Ixodes
scapularis
THE USUAL SUSPECT
4.
5. Hard tick
Anal groove present
Eyes are absent
Not ornate, No festoons
Palpi longer than wide
Tick Key, Experts
IDENTIFICATION
6.
7. INITIAL PATHOGENESIS
Tick is infected with Borrelia burgdorferi during feeding.
Transmitted into the dog by a bite through the skin.
Tick “cements” itself to the host in order to feed.
Blood meal begins 30 min later.
Usually takes around 8 hours to transmit Borrelia burgdorferi
8. KEYS TO SUCCESS
Saliva!
An anesthetic to numb and reduce pain
An antihistamine to reduce allergic reaction or itching
An anticoagulant to stop bleeding
An anti-inflammatory to reduce swelling
An immunosuppressant to help aid in the transmission of the
pathogens
10. BORRELIA CONT.
OSP can be altered to avoid
detection from host immune
system
Can change shape
Hides between cellular folds
11. PATHOLOGY
Travels through the bloodstream
Bacterial dissemination to the skin, heart, kidneys, peripheral and
central nervous systems and the joints.
Three major focus are the CNS, Joints, and the Kidneys
12.
13. Induce astrogliosis in the
astrocytes, (proliferation &
apoptosis).
Blood-brain barrier weakend
Compromise nutrient supply,
and ion balance.
CNS
14. CNS CONT.
Induce astrocytes and microglia to produce toxic substances
Quinolinic acid , cytokines, interleukin-6, and Tumor necrosis
factor-alpha
Nerve cell damage leads to fatigue, malaise, and cognitive deficits.
Increase stress hormones that interfere with neurotransmitter
efficacy.
15. JOINTS
Chronic Lyme disease causes
Induced autoimmune conditions or
Acute pro-inflammatory action
Research is still ongoing
Severity of joint disease and pain varies among indviiduals
19. History
ELISA Test
Indirect Fluorescent Antibody (IFA)
Test
Western Immunoblot Test
Corroborate equivocal or positive
results
TX Response
DIAGNOSIS
20. VACCINATION
3 types currently available
The killed whole spirochete vaccine (Fort Dodge)
Can lead to vaccine reaction
The recombinant vaccine (Merial)
Generates antibodies against Osp A
Osp A used to attach to tick host
21. VACCINATION CONT.
Prevent from exiting tick into dog
Osp A DNA used so less chance for reaction
Third type of vaccine (Intervet-Schering-Plough)
Targets Osp C and Osp A
Kills any bacteria that was not hindered by Osp A antibodies
22. RESOURCES
All pictures from google images
Atlantic Veterinary College lectures
Canine Lyme Disease http://www.lymeinfo.ca/default.aspx 2013.
A Lyme Disease Primer
http://www.marvistavet.com/html/body_lyme_disease.html 2010
Borrelia burgdorferi and Lyme Disease
http://www.textbookofbacteriology.net/Lyme.html 2008-2012
23. RESOURCES CONT.
A Practical Guide to Lyme Disease http://lymediseaseguide.org/
2013
Lyme Disease http://www.capcvet.org/capc-
recommendations/lyme-disease2013
Stage One - Eggs The adult female tick lays her eggs on the ground in the spring.
Stage Two - Larva The egg hatches into larva and finds its first wildlife hosts (usually a mouse or other small mammal). After a blood meal, the larva detaches and falls to the ground, where it lies dormant during the winter.
Stage Three - Nymphs Larva develop into nymphs and begin feeding again on a variety of hosts (mice, deer, humans, dogs) that may be infected with a bacteria called Borrelia burgdorferi that causes Lyme disease.
Stage Four - Adults Feed on many different hosts, many of which in Lyme disease areas are infected with the Lyme bacteria organism. Ticks ultimately infect other hosts such as deer, humans and dogs.
The inflammatory B-cell response in the CSF in response to the CNS infection. Borrelia are recognized by monocytic cells (1), which produce the B-cell–attracting chemokine CXCL13 (2). B cells immigrate into the CSF (3) and mature to plasma cells (4). These plasma cells can produce B.b.-specific antibodies (5) that can eventually destroy the invaded spirochetes (6).
Mild focal meningitis and encephalitis without concomitant neurologic signs have been described in experimentally, but not naturally, infected dogs.
where the fluid in the joints, and the joint capsule is irrevocably damaged
After dissemination of the spirochete from the skin to the joint, the synovial tissue is infiltrated by mononuclear cells, including macrophages, T cells, B cells and plasma cells. Joint fluid, which accumulates in the joint space, contains large numbers of neutrophils8, immune complexes30, complement components31 and inflammatory cytokines32, 33, 34. B. burgdorferi-specific T helper 1 (TH1) inflammatory responses are concentrated in joint fluid35, 36, and in the joint, B. burgdorferi-specific T cells of the V1 subset might aid in the regulation of these responses through interactions of FAS (CD95) and FAS ligand (CD95L)37, 38. In addition, patients with Lyme arthritis have high levels of Borrelia-specific antibody28, 39, some of which might be produced locally. BCR, B-cell receptor; IFN-, interferon-; TCR, T-cell receptor; TNF, tumour-necrosis factor.
The lesion consisted of glomerulonephritis, diffuse tubular necrosis with regeneration, and interstitial inflammation. The clinical course of the disease involved a rapid progression of glomerular disease that proved fatal in all of the dogs affected. Nearly 90% of the dogs had immune-mediated membranoproliferative glomerulonephritis, with the remainder suffering from membranous glomerulonephritis and amyloidosis.
