1 Flashcards
Six steps in the infectious diseases process
Encounter Entry Colonization and/or invasion Multiplication and/or spread Damage Outcome
some infections are
endogenous
Nonspecific Adherence.
Reversible
Docking
Examples:
-Brownian movement (i.e., random interactions)
-electrostatic attractions
-interactions with glycocalyx or extraceullar matrices
Nonspecific adherence more info
Nonspecific adherence involves nonspecific attractive forces which allow approach of the bacterium to the eucaryotic cell surface. Possible interactions and forces involved are:
- hydrophobic interactions
- electrostatic attractions
- atomic and molecular vibrations resulting from fluctuating dipoles of similar frequencies
- Brownian movement
- recruitment and trapping by biofilm polymers interacting with the bacterial glycocalyx (capsule)
Specific adherence
involves adhesins:
Adhesins are substances on the surface of microbes that are involved with adherence to host tissue.
Often found on fimbrae (a.k.a. pili), but can be found in capsules or cell surface.
Interactions are specific – adhesin receptors are specific for adhesins.
Streptococcus mutans (the cause of carries) binds to tooth pellicle. Why
The adhesin is Glucosyl transferase which binds to a salivary protein that is involved in pellicle formation.
Colonization
To colonize, the pathogen must be adapted for growth in a given niche.
E.g., Skin pathogens must withstand skin environment and must be able to garner enough nutrients to survive.
How do bacteria “take-up” nutrients?
Carrier-mediated diffusion (facilitated)
- Phosphorylation-linked transport (group translocation)
- Active transport (energy dependent)
Invasion
: To invade, pathogens must have specific virulence factors that allows them to invade the host (generally referred to as “Invasins”.
Hyaluronidase
breaks down hyaluronic acid, which destroys tight junctions
Lateral propogation to contiguous tissues
multiply then spread
Dissemination to distant sites
spread then multiply
Disease symptoms are often dependent upon
pathogen density
Host response
to infection
Phagocytes
Cytotoxic T cell activity-kills host cells, not virus. Takes away viral mech, but if the immune cell becomes too active, it kills too many cells. Damaged caused by immune system, not virus. This is immunopathology
Infectious organism
Lytic viral infections - causes host cell to lyse.
Invasins damage host tissue.
Toxin producing microbes
Endotoxins
Component of cell wall
The term endotoxin generally reserved for lipopolysaccharide
Exotoxins
Soluble substances secreted into host tissues Cytotoxins: lyse cells Hemolysis: lyse red blood cells Leukocidins lyse white blood cells Enterotoxins: affect intestinal cells Neurotoxins: affect neurons
So, what makes a microbe a pathogen?
Ability to adhere to host. Ability to colonize the host. Ability to replicate within given niche. Ability to cause damage. Invasion Production of toxin Activation of the immune system
Important difference b/t prokaryotes and eukaryotes
the fact that eukaryotic cells have microtubules, which help maintain shape. Prokaryotes don’t have this. Thus, they have different strategies to maintain their shape and not explode.
Strict aerobes
must have oxygen to grow
Obligate anaerobes
cannot tolerate oxygen
Facultative anaerobes
can grow with or without
oxygen (most medically important bacteria)
Between cell membrane and murein layer, you have
periplasmic space. A lot of antibiotics target activities in this space
The structure of
Lipopolysaccharide
(LPS)
Lipid A - fatty acids attached to a phosphorylated disaccharide
Polysaccharide core – very similar between Gm- bacteria, but has sugars
that are somewhat unique to bacteria.
O-antigen - highly variable repeating sugar subunits.
O-antigen is the main reason for the different antigenic specificities among Gram-negative bacteria.
