lyme disease
2016-12-27 12:49:36 0 举报AI智能生成
lyme disease B.burgdorferi
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host defense
innate immunity
complement
3 pathways
alternative
lectin
classical
proteolytic activation
result
formation of MAC
lysis
anaphylatoxin
C3a: stimulate acitivity of phagocytes
C5a: chemattractent: arrival of neutrophils
C3a and C5a induce vasodilation of endothelial cells in nearby blood vessels increasing vascular permeability
phagocytosis
lipoproteins stimulates TLR1 and TLR2 (e.g. OspA)
something stimulates TLR7 and TLR8
unmethylated CpG DNA stimulate TLR9 (mammalian CpG DNA is methylated)
adaptive immunity
antibodies against surface proteins
virulence factors
VLsE
surface lipoprotein
recombination, lead to antigenic diversity
B.burgdorferi has a plasmid that contains 15 silent vls cassettes and one functional copt of vlsE
egments of silent cassettes recombine with vlsE gene
thus invade host humoral immune system (antibody recognition)
CRASPs
complement susceptibility
resistant
sensitive
intermediate
complement regulator acquiring surface proteins
e.g. CspA CspZ ErpACP, are CRASP12345
target: human protein factor H
similar in nerisserial Factor H
nd to glycosaminoglycans (GAGs)
prevent damage by complement system
Osp lipoprotein
TLR2 ligands
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pathogen: borrelia burdorferi
basics
phylum: spirochaetes
morphorlogy
cork-screw
diderm (double mbn)
axial filaments
lengthwise between IM and OM in periplasm
twisting motion
No LPS detected in OM but other glycolipids
**compare cell envelops**
life style: free-living and anaerobic
virulence factors
lipoprotein
immunostimulatory molecule
induce inflammatory mediator by macrophages
production of superoxide by neutrophils
induction of NKFB, up regulation of inflammatory genes
differential expression
lipoprotein VLsE
antigenic variation
lipoprotein CRASPs
inhibit complement
Osp bind to TLR2
properties of disease
reservoirs
human (laten or active)
animal: zoonotic
any disease of infection that is naturally transmissible from vertebrate animals to humans'
examlples
anthrax
grazing herbivores. ingestion/contact of spores
leprosy
monkeys, rabbits. contact via urine, feces
cat-scratch disease
cats
bites or scratches
cryptococcosis
birds
inhaling fungi
non-living: ocntaminated water and soil by animal feces
vector
arthropodic: mosquitos and ticks
vector born disease
examples
malaria - mosquitos
yersinia pestis - rat fleas
causative agent: *borrelia burgdorferi*
transmission
bites of immature ticks (nymphs)
requisites
36-48h attachment
feed on summer
tiny
adult is easier to be seen
hard-to -see area
egg-larva-nymph-adult
transmission cycle
human is the incidental/dead end host
non-communicable between humans
3 hosts are involved
doctors
signs and synptoms
characteristic
skin rash called 'erythema migrans'
common
fatigue, fever, headache
lab characterize
based on symptoms and possible exposure
no reliable lab diagnostic marker thus far
after years of exposure, can see antibodies in western blot: OspBADC
if left untreated, induce autoimmune reaction, lead to juvenile arthritis
treatment
initial
antibiotics
resistance
later: spread to other tissues
joints heats CNS PNS more skins
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