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Unit 10: Principles of Pathogenesis - Coggle Diagram
Unit 10: Principles of Pathogenesis
Terminology
Primary pathogen
Can make an otherwise heathy person sick
Opportunist
Opportunistic pathogen - causes disease only when body's innate or adaptive defenses are compromised
Virulence
Refers to degree of pathogenicity
Infectious dose
number of microbes necessary to establish infection (lower number --> more dangerous)
Incubation period-->prodormal phase-->being sick-->convalesncence (recovery)-->(carriers)
Infections
Acute
illness is short-term, symptoms develop quickly, last a short time (strep throat)
Chronic
symptoms develop slowly, last for months or years (tuberculosis, HIV)
Latent
Never completely eliminated, microbes exists in host tissues without causing symptoms (not contagious when latent)
Bacterial pathogens
Islands
Genomic islands
Large blocks of newly acquired genes
Pathogenicity islands
Large blocks of newly acquired genes that are involved in disease (type III secretion system for example)
How are genes acquired
Competence/transformation
Protein complexes in the membrane that actibely pump naked DNA into their cytoplasm
Phage transduction
Phages graps bacterial DNA from the cell to make virions which deliver a segment of DNA from the previously infected cell (instead of infection)
Conjugation (jumoing plasmids)
DNA injects itself into the cell
Phase encoded genes (lysogeny)
Some phages choose to integrate their own DNA into the host DNA --> lysogeny :
Prophages
Can carry DNA segments (viral) to other organisms
Establishing an infection in a host
Mechanisms of pathogens
Penetrating the skin
Crossing the epithelial barrier, rely on skin injuries (ticks)
Penetrating the mucous membranes
Pathogen induces non-phagocytic cells to engulf via endocytosis
MALT --> pathogens use M cells to cross intestinal barrier, most are destroyed by macrophages
Some microbes avoid or exploit macrophages (Shigella)
Some invade by alveolar macrophages (tuberculosis)
Colonize mucous membranes, proudce toxins
Invade host tissues, produce toxins
Invade host tissues, avoid defenses
Adherence
Adhesins attach host cell receptors
First-line defence sweep microbes away
Colonization
Growth in biofilms
Dealing with host immunity
Iron limiting
secretory IgA avoidance (proteases, pili turnover)
Type III secretion systems in infection
delivering toxins (effector proteins) directly into host cells
In gram-negatives, effector proteins induce change in host cell (uptake of bacterial cells)
E-coli make actin pedestal on host cells
Avoiding immune detection
Complement system (MAC) proteins
Bind complement regulatory proteins to avoid activation of membrane attack complex (MAC)
Antibodies
IgA protease --> cleaves IgA
Antigenic variation --> alter structure of surface antigens
Mimicking host molecules
Destruction by phagocytes
Avoid the encounter
C5a peptidase, membrane-damaging toxins
Avoid recognition and attachement
Capsules which interfere with opsonization
M protein which inactivates C3b
Fc receptors which bind Fc region of antibodies
Survive within phagocytes
Prevent phagosome-lysosome fusion
Survive within phagolysosome, delay fusion
Causing disease
Exotoxins (protein toxins)
When secreted outside of the bacterial cell
Cause damage during an infection
Food can be sterile but still give food poisoning
Can act locally or systemically
A-B toxins (A is toxic, B binds to cell)
Endotoxins
lipopolysaccharide (LPS)
outer layer of gram-negative outer membrane
The toxic component is the lipid A part
when localized, response helps clear infection
When systemic, causes widespread response, septic or endotoxic shock
How inflammation and antibodies cause damage
Phagocytic cells can release enzymes and toxic products
Antibody-antigen complexes can from, settle in kidneys and joints, and activate the complement system leading to inflammation
Cross-reactive antibodies may bind ti body's own tissues, promote autoimmune response
Exotoxin groups
Neurotoxins
Damage nervous system
Botulism (Clostridium botulinum)
Tetanus (clostridium tetani)
Enterotoxins
Cause intestinal disturbance
Cholera
Cytotoxins
Damage variety of cell types
Shiga toxin
Effectors - proteins injected directly into host cells by complex secretion systems