Bacterial Pathogenesis II Flashcards Preview

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Flashcards in Bacterial Pathogenesis II Deck (19):


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 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
Alternative complement pathway activation to increase C3a and C5a causing shock



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



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



DNA is secreted via syringe style when it attaches to another bacteria

Has gene a from the bacteriophage and is assembled the new DNA in its current DNA
Sharing of genes between bacterial species mediated by a bacteriophage via homologous replication
Bacteriophage is basically a virus that infects a bacteria



Fragment of DNA is picked up from the environment and incorporated into the bacterial chromosome (DNA)



"Hopping Gene"
Transposon can “hop” from one location to another via self excision
Can jump from one plasmid into another plasmid, or within the same plasmid
Copy paste mechanism is also possible


Virulence: Immune Modulation

Innate Immunity: modify environment and destroy physical barriers

Phagocytosis: prevention (capsule), damage phagocyte (toxin), hijack phagocyte

Complement: mis-regulate, destroy components