Review for exam #1

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 foreign 

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 life 

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