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41 Cards in this Set

  • Front
  • Back
Endotoxin
LPS; Lipid A: repsonsible for toxicoty, Poly O: Protective, antigenic, determinint of strain
Only Gram Negative
Integral part of outer membrane
Always on a chromosome
Weakly antigenic (O side)
Cannot be converted to toxoid
Weakly neutralized by antibody
Stable with stands high temp
Effects similr regardless of bacrerial origin
Exotoxin
Produced by both gram + and -
Extracellular, usually secreted
Phage or plasmid encoded
Highly antigenic
Converttable to non-toxic toxoids
Readlily neutralized by antibody
Unstable cannot stand high temp
Effects vary upon type
Type 3 cytotoxins
Bacteria binds to cell and inserets tube to inject toxins
Proteins never see the environment cant make toxoids against it
How does Toxic Shock Syndrom Toxin (TSST) enter the body?
Mucoasl infection through the vaginal tract
Superantigens
Bind to MHC class II and T Cell Receptors
Binding NOT antigen specific
T-Cells stimulated to produce IL-2, TNF, Il-1, Il-6, INF-Gamma
Results in toxic shock
Staphylococcus Aureus TSST-1
Found in women who used High Absorbency Tampons
Staphylococcus Enterotoxins
Intoxication of contaminated food
Causes vomiting and diarrhea
Resistant to heat and digestive enzymes
Streptpcpccus Pyogenes Pyrogenic Exotoxins
Responsible for rash in scarlet fever
Diptheria
Controlled by low iron levels
Acts primarily on throat
Cholera
Increases cAMP levels which increase ion secretion and water leading to watery diarrhea
Tetanus, Tetani
Neurotoxin
Reaches CNS through motor nerves
Causes spastic paralysis (lockjaw; arching of back)
How does virulence transfer between bacteria?
By way of horizontal gene transfer mechanisms
Endogeneous
Normal flora get somewhere sterile
Exogeneous
Contact from food born, respiratory, sexual, vector, zoonoses
Congenital
Passed from mother to fetus
Colonization
First stage of microbial infection
Establishment of the pathogen at its point of entry
Receptor mediated binding of the bacteria
Requires:
Adhesion, most commmon example is with the pili
Receptor, specific carb or peptide that resides on surface of the host cell
Non-specific Binding
Bind to host by secrition of viscous substances(biofilm, slime layer)
Invasion
Penetation of host cells and tissue
Mediated by INVASION by phagocytosis
Gives advantage by supplying bacterium with nutrients from host
Dissemination
Entrance of a bacterium into the blood stream
Example of a invasion by a bacteria
What do all bacteria require for growth
Iron
Acquistion by eithier Siderophores or iron binding outer membrance proteins
Siderophores
Iron binding chemicals that compete for iron bound to tansferin, Hb, or lactoferin
Exotoxins
Secreted by both
Can be easily converted to toxoid
Three types:
Local, systemic, superantigens (incude uncontrolled T cell cytokine release)
O polysaccharide
Major antigenic determinant; antibody binding site
Endotoxin
Gram (-)
Cannnot be converted to toxoid
No plasmid encoded
Outer membrane
Stable to boiling
Clinical manifestation; shock and fever
Immunopathogenesis
Damaged caused by the IS
Ex: Gram-bacterial sepsis, and Tuberculosis
How can bacterial avoid immune repsponses?
Avoid contact
Inhibition of phagocytic engulfment by capsules
Coat with IgA antibodies or inactivate C5A or C3A
Bind antibody inappropriately by binding Fc of Ab
Intracellular residence
What is one of the most important virulence factors?
Encapsulation
Enterotoxins
Special exotoxins in the gut
LPS
Lipid A causes toxicity
CD14 interacts with TLR 4
Leads to activation of TNF and IL-1
Causes hypotention and shock
Disseminated Intravascular Coagulation (DIC)
Activation of Factor XII (hageman factor) and causes occlusion of small vessels
Classification of Exotoxins
A-B subunit
B- Binding subunit mediates adherence of toxin complex to host cell and aids in transplocation of A
A- Active subunit possesses the toxic activity; mediates host cell damage
Diphtheria toxin
Catalyzes ADP ribosylation of EF2
Acts primarily on throat
Encoded on a prophage
Maximal effects under LOW IRON levels
Cholera Toxin
Increase adenylate cyclase
Increasing cAMP levels
Increased secretion of ions and water leads to DIARRHEA
Petussis Toxin
Similar effect on Adenylate Cyclase but through Gi G protein receptor
Increases respiratory secretion
Whooping cough
Shiga Toxin
EHEC produces this toxin
Results in bloody diareha
Deadenylates 28S rRNA blocking pretein synthesis
Bordetella Adenylate Cyclase Toxin
Increased cAMP
Forms pores
2 toxins that interfere with phagocytosis
Clostridium Difficile Cytotoxins A and B
Part of some peoples normal gut flora which can overgrow forming a enterotoxin
calls in PMNs leading to diarrhea
Alpha Toxin of Staphylococcus Aureus
Toxic to RBC
Streptococcus Pneumonia
Toxic to ciliary action of pulmonary cells
Clostridium Perfringes Alpha Toxin
Causes detruction of all types of cells (RBC, WBC, platlets,muscle, endothelium, etc.)