Bacterial Pathogenesis Flashcards
Low Virulence
- Streptococcus salivarius:
- -Present in Oropharyngeal Flora
- -If lands on a damaged heart valve during bacteremia, it can stick and destroy it.
Moderate Virulence
- Escherichia coli:
- -Found in colon
- -If gets access to bladder, causes acute infection
High Virulence
- Bordetella pertussis:
- -Whooping cough
- -Not in normal flora
- -Highly infectious
- -Causes disease in almost every non-immune person it contacts
Extremely High Virulence
- Yersinia pestis:
- -Plague
- -Highly infectious
- -Leads to death in a Few Days in over 70% of cases
Types of Human - Bacteria Relationships
Commensals Coexist:
–Humans have Normal Flora, mostly Bacterial
Opportunistic Pathogens:
- -Take advantage of breaks in defense (e.g. surgery, AIDS)
- *Candida albicans (oral thrush)
Primary Pathogens:
- -Cause disease on their own.
- -Able to replicate, survive, and be transmitted to another host.
- -Breach barriers to do this.
- -Never members of normal flora
Examples:
- *Neisseria gonorrhoeae
- *Typhoid bacillus (Salmonella typhi) (Typhoid Fever)
- *Tubercle Bacillus
Human Behavior and Bacterial Disease
- Legionella pneumophila:
- -Aerosolization created by cooling towers causes transmission to humans.
- Staph aureus: Toxic Shock Syndrome
- -Development of super absorbent tampons, production of a toxin by some strains of S. aureus.
Food Poisoning:
- -By *E. coli O157:H7, *Campylobacter, *Salmonella
- -Due to food technology distribution networks.
Entry: Beating Host Defenses
Microbes gain access from the environment.
Skin.
Secretions coat mucosal epithelium (secretory IgA, mucus, etc.)
Some bacteria excrete IgA *Protease.
Infecting Dose
Environmental or Animal Reservoirs:
–*Vibrio cholerae
(100,000,000 organisms)
Drink contaminated water.
Growth in Food may deliver high numbers:
–*Salmonella
(100,000 organisms)
Contaminated food.
No reservoir, requires the lowest infecting doses:
–*Mycobacterium tuberculosis (1-10 organisms)
Cough onto person.
Adherence
Requirements:
1) An *Adhesin on the invading Microbe
2) A *Receptor on the Host cell.
The adhesion is exposed on the bacterial surface alone or with Pili.
Two of the Most Common Receptors:
–Mannose and Fibronectin
–Are on Epithelial Host cell surfaces.
(*Borrelia burgdoferi binds to Fibronectin and Factor H to interfere with Complement Deposition. Down-regulates immune response.)
Pili:
- -Mediate Attachment
- -Also Mediate Movement across the cell surface (twitching motility):
- Neisseria gonorrhoeae (gonococcus)
Strategies for Survival
Some Exotoxin-mediated bacterial diseases can produce injury without moving: *Diphtheria,
*Bordetella pertussis (Whooping Cough)
- Bordetella pertussis toxin paralyzes the ciliary epithelium in the Respiratory tract, preventing the function of the Mucociliary escalator that is supposed to keep the lungs sterile.
- Diphtheria secretes AB toxin; A subunit blocks protein synthesis in our cells, killing the cells.
Invasion
Invasins:
Either direct bacterial entry into cells,
Or provide direct contact between bacteria and Host cell Membrane.
Binding of a microbe to an Integrin-like molecules on the Host cell surface may trigger a Host cell signal that causes uptake.
Bacteria enter cells initially within a membrane-bound, host vesicle, but then follow one of two distinct pathways:
1) (*Listeria, Shigella) Enzymatically lyse the Phagosome membrane and Escape to the host cell Cytosol.
2) (Salmonella typhi, *Mycobacterium tuberculosis) Remain in the phagosome and replicate.
Apoptosis
One of the most common tactics is to induce programmed cell death (apoptosis).
The invading bacteria that induce apoptosis nullify the signaling of necrotic death.
Necrosis: destruction. This would cause a large release of signals from dying cell, to which the body would respond.
Apoptosis: programmed cell death. Very quiet. Not a huge release of molecules; so body may not realize and may not respond.
Anti-Phagocytic Activity
Avoiding phagocytosis by using an Anti-phagocytic Capsule.
- -*Streptococcus pneumoniae
- -*Bacteroides fragilis (meningitis)
This polysaccharide capsule interferes with Complement Deposition on the bacterial cell surface by binding Regulators of C3b.
*Neisseria gonorrhoeae up-regulates catalase production after it is phagocytosed, to avoid ROS-mediated destruction.
Wikipedia:
A popular mnemonic to remember most of the encapsulated bacteria is the SHiNE SKiS bacteria
SHiNE: Streptococcus pneumoniae (pneumococcus) Hemophilus influenzae type b (Hib) Neisseria meningitidis (meningococcus)
SKiS:
Salmonella typhi
Klebsiella pneumoniae
Group B Streptococcus (GBS)
(S. pneumo, Hib, N. meningitidis, E. Coli, Salmonella, Klebsiella, Group B Strep).
Antigenic Variation
Varying surface antigens
- Neisseria Gonorrhea:
- -No natural immunity
- -Reinfections are common
An immune response can be mounted to the Surface Pili and Outer Membrane proteins of N. gono, but the organism is continuously varying them.
This happens even in the course of a single infection.
A-B Exotoxins
B (Binding) Subunit:
–Binding Specificity to the Host cell
A (Active) Subunit:
- -Catalytic domain
- -Catalyzes the modification of a *Target Protein; the most common is *ADP-Ribosylation
Cholera Toxin:
- -Affects a G protein that regulates a secretory pathway.
- -Results in Hypersecretion of electrolytes, Severe Dehydration, Diarrhea.
Example:
*Corynebacterium Diphtheriae
