Bacterial Pathogenesis II Flashcards
Fimbriae
Also called pili
Short “hair-like” structures that extend from the cell surface
This attachment is relatively non-specific and loose
Attaches to urethral mucosa for example – bacteria causes UTIs
Receptor Mediated Attachment
This attachment is both specific and tight/stronger
Adhesion interacts with proteins on surface of eukaryotic cell and acts like a lock and key
Biochemical, Physical, and Chemical Barriers
Lysozyme degrades the cell wall
Sebaceous glands – oil will help prevent attachment
Male genital tract is protected by spermine from bacterial attachment
Break in skin is usual cause of bacterial invasion
IgA coats the bacterial surface, therefore if coated then cannot attach to anything
Mucus, cilia, skin, acid in stomach, etc.
Pattern of Bacterial Growth
Bacterial growth can only increase so much before they plateau because there is a closed environment and the nutrients not only run out, but they begin to inhibit each other
Lag phase, logarithmic phase, stationary phase, and death phase
Barriers to Bacterial Growth
Nutrient Limitation: iron; lactoferrin (granule that is released by neutrophils) and hepcidin (limits iron release from stores) to prevent iron from being available
Hostile Environment: acid, bile, mucus, cilia
Host Immune System
Pathogenicity and Virulence
Pathogenic/Non-pathogenic: can the bacteria cause disease of not – (yes or no)
Virulent: ability of a microbe to cause disease – (more or less)
Virulence Determinant/Virulent Factor: any factor which increase the virulence of a pathogen
Endotoxin vs. Exotoxin
Endotoxin: stays attached to the bacteria until the bacteria bursts; induces cytokine release
Exotoxin: secreted toxins to disrupt normal functioning of a host cell
IgA Protease and Siderophore
IgA protease: enzyme that degrades host IgA to prevent coating of bacteria that facilitate attachment
Siderophore: binds to iron before it gets stored or used to make Hb for example; binds iron and brings it back to the bacteria
Capsule and Invasins
Capsule: always makes phagocytosis less efficient (not always prevents)
Invasins: any factor that helps a intracellular bacteria gain entry
LPS
LPS is “multi-alarm” signal of infection
Low levels – Stimulates protective response
Fever (TLRs)
Activation of immune and inflammatory response
High levels – Can be deadly High fever Vasodilation and hyotension Capilary leakage (petechiae) Disseminated intravascular coagulation
Responses to LPS
Increase in vascular permeability causing HTN and shock
DIC thrombosis from clot formation
Liver production of acute phase proteins to cause fever
Hypoglycemia
Alternative complement pathway activation to increase C3a and C5a causing shock
Exotoxins
Secreted toxins: produced by Gram-positive and Gram-negative bacteria
Often encoded on plasmid or lysogenic phage
Varied cellular targets and activities: ribosomes, transport mechanisms, regulatory proteins
Varied effects: diarrhea, loss of neural function, Death
Many are A and B subunits: A is Active subunit and B is Binding subunit
AB Exotoxins
Tells us how many A and B units the bacteria has
AB toxin = diphtheria
AB5 = cholera
A2B = anthrax
Superantigens
Non-specific activation of T-cells resulting in the release of large amounts of interleukins and pyogenic cytokine release
Can also lead to death of the T-cell resulting in loss of specific immunity
Responsible for Toxic Shock Syndrome (Staphylococcus aureus) via Staphylococcal Toxic shock syndrome Toxin-1
Streptococcal pyrogenic exotoxins (SPE)
Bacterial Conjugation
Pilus binds cells together until membranes fuse together
The bacteria receives the donor plasmid piece and the genes to make a plasmid so it can share the genetic information with other bacterial cells, therefore the recipient eventually becomes the donor
Note: Not all plasmids are mobile. If a plasmid is not mobile it can not be moved by conjugation
