Infection Pathogenesis Flashcards
Virulence Def
Capacity of a microbe to cause disease
Pathogenesis Def
Development of disease
Realtionship between infection progression and host immune response
Average inividual: immune response should slow disease progression (doe not occur in immunocompromised individuals). Immune response sometimes can hurt host eg liquid filling lungs in Covid
How do organisms of low virulence/pathogenicity cause ingredients
host immune system compromised and presence of an anatomical legion
Portals of Entry
oral + GIT (ingestion), nasal + respiratory tract (inhalation), skin (penetration), urogenital tract (sexual) and transplacental
Virulence factors that allow attachment to host cells (entry to infection)
Pilli, adhesions and biofilm
Pilli Outline
Adhesive tips on pathogen flagella that attach to antigens on host cells. Found mostly in gram negative bacteria. Some bacteria can switch pilli allowing access to more host cell binding and escaping detection from immune system
Bacterial Adhesions Outline
Protein/glycoprotein molecules on bacterial membrane/fligilli tips
Biofilm Outline
Self-produced extracellular polymer matrix typically in eviorments with a lot of shear (eg blood vessels, heart chamber). Bacteria display an altered genotype (microcolony). Biofilm matures overtime. Decreased antibiotic penetration (neutralised) and altered physiology of bacteria in biofil
Biofilm Formation
Primary attachment (of single prokaryotic cell), accumulation (of other cells), microcolony formation (biofilm excretion)
Most common biofilm infections
Line (medical device) associated (eg pacemakers,urinary cathetars), skin (staph arreus) and soft tissue (open wounds) infections
Cystic Fibrosis Biofilm infections
Pseudomonas aeruginosa forms biofilms in bronchi
Endocarditis Biofilm infections
Biofilms formed in heart valves
Intracellular Pathogens Outline
Bacteria that grow in host cells. Masked from immune system, provided with nutrients and shielded from antibiotics.
Virulence that allows pathogens to enter cells
Invasions. Proteins on bacteria surface activates host’s cytoskeleton machinery enabling bacterial entry by endocytosis. Bacteria stays in vesicles
How do bacteria prevent phagocytosis
Anti-phagocytic virulence on bacterial cell.
Anti-phagocytic Components
polysaccharide capsules (S pnuemoniae and haemophilus influenza), fimbriae (group A streptococci), biofilm (pseudomonas areguinosa), LPS O polysccaride (E Coli) and protein A (s arreus)
What virulence can kill white blood cells
leucocidins. Eg S arreus
What virulence kills erythrocytes
Hemolysins. E Coli
What virulence kills macrophages
Exotoxin A. P aerguinosa
How bacterial cells bind to iron
Siderophores bind to iron in proteins allowing them to internalise
Endotoxins Outlines
Components on cell membrane that causes damage to host and induce inflammation
Exotoxins Outline
Components produced in cell excreted from pathogen to induce inflammation
Bacterial Enzymes Outline
Digestive enzymes in cell. Can be weaponised against host cell eg lipase breaks into cell membrane
Endotoxin LPS Outline
Lipopolysaccharide. Expressed on membrane of gram negative cells. Contain 2 components O and A. Has pro-inflammatory properties
Reaction to gram negative LPS bind to TLR4 receptors
Release cytokines IL6, II8, TNF alpha. Stimulates inflammation, coagulation pathways and complement pathways
Characteristics of tolerable inflammation
Low lps. Localised, protective response. Increased permeability and dilation of blood vessels. Defence chemicals and immune cells cane enter tissues. Pathogen is destroyed and removed. Moderate inflammation and fever
Characteristics of pathogenic/severe inflammation
High LPS due to high bacterial conc. Risk of intravscular clotting and damage to blood vessels. Results in sepsis. Septic shock (circulatory collapse), respiratory distress, dcreased cardoac output. Organ failure
Teichoic acids and lipoteichoic acids, gram positive outline
Binds to TLR2. Releases IL2, II4 and TNF-alpha. Triggers excessive inflammation, intravascular coagulation and tissue damage
3 types of exotoxin
A-B toxins, phospholipase and superantingens
A-B Toxin Outline
B component brings toxin to cell (by receptor binding stimulated endocytosis) and A component damages cell (by binding to intracellular machinary). Eg C diphtheriae
Phospholipase Outline
Breaks down cell membranes. Hydrolysis of phosphatidylcholine and sphingomyelin, resulting in cell lysis eg phospholipase C, C perifinges
Superantigens Outline
Proteins excreted from cells. Activate many different types of immune cell by non-specific t-cell activation. Excessive immune response. Uncontrolled release of cytokines. Eg Toxic Shock Syndrome, S aureus
3 exotoxins
Cytotoxins (effect cells), neurotoxins (effect neurons) and enterotoxins (cells of the GIT)
Clostridium Tetani Toxin Outline
Spores contaminate opening in skin. Spores germinate. Spores can remain latent for up to 10 years and release toxin on lysis. Toxin targets spinal chord and brain stem. Symptoms: trismus (lock jaw), spasms of limbs and trunk, death by respiration complications
Clostridium Botulinum Toxin Outline
Spores can be ingested (eg canned foods) or enter through open wounds. Blocks nerve signals to muscles. Results in muscle weakness, paralysis and respiratory failure
Cholera Toxin Outline
Produced by vibro cholera (gram negative). Uncontrolled GIT water secretion
Bacterial Enzymes
Collagenase, streptokinase, lecithinase, hyaluronidase and urease
Collagenase Outline
Breaks down collagen (skin, bone and cartilage) allowing bacterial entry eg C perferinges
Streptokinase Outline
Dissolves fibrin clots. Allows bacteria to spread through tissue eg streptococcus pyognes
Lecithinase Outline
Breaks down lecithin (cell membrane component) eg listeria
Hyrulonidase Outline
Breaks down hyruloric acid (cement between tissues and cells).
