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formation of membrane attack complex
outcome of complement system
alternative complement system
activated spontaneously by hydrolysis C3 and further triggered by structures on microorganisms and other foreign surfaces
lymphadenitis/scrofula
caused my MTB and NTM, enlarged lyphnodes after bacteria from lungs travels to lymph nodes
classical complement system
antibody-antigen complex binds C1 complex, most active in bacterial infections
lectin complement system
Pattern recognition receptors, such as mannose-binding lectin (MBL) bind to carbohydrates on pathogens.
toll like receptors
receptor that recognizes multiple targets
TLR2
recognizes gram positive and some gram negative bacteria peptidoglycan
TLR3
recognizes viral dsRNA
TLR4
recognizes gram negative LPS
TLR7 and TLR8
recognizes viral ssRNA
NOD-like receptors
cytoplasmic and recognize mostly bacteerial pathogens
RIG-like receptors
cytoplasmic sense viruses
C-type lectin receptor
targets microbial carbohydrates in bacterial, viral, and fungal cell membranes
TNF-a, IL-1, IL-6
major inflammatory cytokines
activate engothelial cells and resident immune cells, stimulat phagocytosis and production of prostaglandins
local affects of major inflammatory cytokines
act of hypothalamus as endogenous pyrogens (fever)
systeematic effects of major inflammatory cytokines
hypotension, intravascular thrombosis, cachexia (wasting of muscle and fat cells)
systematic effects of TNFa
IL-8 (CXCL8)
chemokines that recruites neutrophils
monocyte chemoattractant protein (MCP-1, CCL2)
chemokine that recruites monocytes
Dendritic cell, macrophage, mast cell
resident immune cells
dendritic cell
antigen preseeenting cell that activates B and T cells
mast cell
function in degranulation
biogenic amines (histamines)
released from mast cell cause vasodilation and vascular leak
cytokine (TNF)
released from mast cell cause inflammation
enzymes
released from mast cell cause tissue damage
neutrophils, monocytye/macrophage, natural killer cells, eosinophils, basophils
recruited inflammatory cells
macrophage
phagocytosis, ROS and NO killing, repair damaged tissues by stimulating angiogenesis and fibrosis
natural killer cells
kill infected cells and activate macrophages, perforin expression (holes in target membrane), and FcR expression (stimulate antibody-dependent cellular cytotoxicity (ADCC))
eosinophils
specialized to fight parasitic infections, active in allergic responses
basophils
infiltrate sites of allergic inflammation and release mediators and cytokines
Fc region
portion of antibody that interacts with cell surface receptors, common to all antibodies
fab region of antibody
what provides antibody specificity?
VDJ recombination
what provides diversity of antibodies?
IgM
pentameric or monomeric, first antibody secreted, activation of complement
IgG
monomeric, highest concentration in blood, diffuse into extravascular sites/ cross placenta (passive immunity), activation of complement
IgD
monomeric, least abundant, on B-cells
IgE
monomeric, binds to mast cell receptors (histamine release), parasidic response and allergic reactions
IgA
dimeric, passive immunity (breast milk), in mucous secretions, neutralization and agglutinating pathogens
IgG, IgD, IgE
monomeric antibody isotypes
IgM and IgG
which antibodies can activate complement
MHC I
presents antigen to CD8 T cell
MHC II
presents antigen to CD4 T cell
antigen small peptide presented on MHC of antigen presenting cell (dentritic cell)
How are antigen recognized by TCR
alloimune response
recipient T cells react to donor MHC molecules as foreignÂ
Graft versus host disease (GVHD)
donor T cells react to recipient MHC as foreign
Oral GVHD
painful sores in mouth as result of donor T cells reacting to recipient MHC as foreign
streptococci are catalase negative
difference between streptococci and staphlococci
streptococcus pyrogens (group a streptococcus)
beta-hemolytic streptococcus
viridans (s. mutans)
alpha hemolytic streptococcus part of normal oral flora
streptokinase
virulence factor of GAS dissolves blood clots to relaese additional bacteria
hyluaronidase
virulence factor of GAS breaks down hyaluronic acid in connective tissue
streptolysin
virulence factor of GAS toxic for neutrrophils, RBCs, and platelets
streptodornase
virulence factor of GAS the digests DNA
streeptococcal pyrogenic exotoxins (spe)
virulence factor of GAS, exotoxin, superantigen, causes scarlet fever
M protein
virulence factor of GAS provides resistance to phagocytosis
scarlet fever
caused by GAS exotoxin, circumoral pallor and strawberry tongue
Necrotizing fasciitis
severe rapidly progressing connective tissue infection due to GAS exotoxin, toxin production can lead to toxic shock
Streptococcal pharyngitis
GAS infection, symptoms include red swollen tonsils, fever, sore throat, red spots on roof of mouth
Impetigo
superficial skin GAS infection, skin ulceration on face and lower extremities
Post streptococcal glomerulonephritis (PSGN)
due to the immune response to infection following skin and pharyngeal infections (GAS infections ie. strep throat). characterized by DARK URINE
Acute rheumatic Fever (ARF)
multi organ inflammatory syndrome as an immune response to untreated GAS pharryngitis, aschoff bodies in heart skins brain and joints
S. aureus, streptococci, enterococci
most common causes of infective endicarrditis (IE)
S. aureus
most deadly cause of infective endocarditis, associated with healthcare infections
streptococcal
cause of infective endocarditis in oral cavity, poor dentition as risk factor, little pain or no symptoms
Mycobacterium tuberculosis (MTB)
Aerosolized respiratory droplet nuclei, contagious, from other humans, primary pathogen, latentency common
Nontuberculosis Mycobacterium (NTM)
Caused by M. avium complex, Non-contagois, Opportunistic pathogen, Found in water and soil, No latency
latent tuberculosis
ccurs after immune response at granulomas kills most of MTB, bacteria latent in granulomas, asymptomatic, non contagious, no symptoms
bacteroides, prevotella, fusobacterium, porphyromonas
Gram negative anerobes
B. fragilis
opportunistic pathogen (friend to foe) , B lactimase confers penicillin resistance
P. melanogenica
diagnostic marker for oral cancer
F. nucleatum
common cause of acute necrotizing gingivitis
Acute Necrotizing Ulcerative Gingivitis (ANUG)
associated with F. nucleatum, bleeding gingiva with abrupt onset, malaise/fever, excessive salivation and foul breath typically seen in people under 35
gentle debridement, mouth rinses, antibiotics
treatment for acute necrotizing Ulcerative gingivitis
C. perfingens
Which organism is mainly responsible for causing gas gangrene?
C. tetani
causes lock jaw, blocks inhibitory neurotransmitters, can be neonatally transferred through umbilical cord, immunizations only treatment option
C. botulinum
block release of acetylcholine, causes paralysis of muscles, associated with infant botulism
actinomyces
part of normal flora in oral, urinogenital, and GI tract, pathogenic after trauma (ex: extraction)
A. isralii
cause of cerevicofacial actinocmyces (pyogenic abceess “sulfur granules”)
H. influenzae, Strep. pneumoniae, Neisseria meningitidis
bacteria that cause bacterial meningitis
stiff calfs, can’t bend knees
kernigs sign of meningeal inflammation
stiff neck, legs fold when neck bends
bruzinski’s signs of meningeal inflammation
WBC increase
CSF cell count change with meningitis
elevated protein
CSF protein change with meningitis
low glucose
CSF glucose change with meningitis
vaccination
main prevention method of meningitis
IgA protease and polysaccharide capsule
N. meningitidis virulence factors
Elimination, substitution, engineering controls, administering controls, PPE
five rungs of hierarrchy of controls from most to least effective
befor and after touching patient, procedure, gloving/ungloving, body fluid exposure, touching surrounding
opportunities for hand washing
C. difficle, catheder associated infections, central line infections, surgical site infections, MRSA, COVID
key healthcare associated infections
increases patient suffering, lead to disability, increases healthcare cost, preventable
importance of healthcare-associated infections
HIV, Hep B, Hep C
most common bloodborne pathogens
Hep B
most infectious bloodborne pathogen
treat all patient as infectious, vaccination, standard precautions, immediate action after exposure
prevention of bloodborne pathogens
cleaning
removal of organic matter on soiled surfaces
Disinfection
eliminates most pathogenesis microorganism, some microbial forms remain
Sterilization
eliminates all forms of microbial lifeÂ
high level heat sterilization
level of disinfection needed for Instruments that penetrate soft tissue or bone, instruments that contact mucous membranes, dental handpieces
intermediate/ low level chemical disinfectant
level of disinfection needed for patient chair and room surfaces