topic 9/10 Flashcards
What are the 3 main ways in which bacteria are classified?
Shape (coccus, rods, spirals/helical)
arrangement (how the different rods/coccus, etc. fit together, spacing, etc.)
Staining (gram positive (purple), gram negative (red), acid fast (tuberculosis)
what are 4 additional ways in which bacteria are classified?
colony morphology (how they look on a petri dish-color, contour, consistency, “streak for isolation”
metabolic rxns (aerobic +/-, carb utilization, enzymes produce)
serology (Ab directed against cell structures)
genetics (DNA homology)
What are the structural differences in gram positive and negative cells
Gram positive-Thick peptidoglycan cell wall (tough to break through) bound together and to cell membrane by techoic and lipotechoic acid.
Gram negative-thinner peptidoglycan cell wall between inner and outer cell membranes. Bound to outer membrane by lipoproteins. Outer membrane surrounded by lipopolysaccharides (LPS).
What are the parts of an LPS? Which part gives specifity?
Lipid near the membrane, then a core polysaccharide, then an o-specific side chain polysaccharide which lends to specifity.
What determines which kinds of cells a bacterium affects?
The bacteria needs to adhere to the cell and it does so by having the specific necessary ligands. These are things that are on the bacterial surface such as pili, adhesins, and flagella.
What are the different typical phases of bacterial growth? What are the doubling times of e. coli and of tuberculosis?
Lag phase–>log phase–>stationary phase–>death phase
e. coli doubling time=20 minutes
m. tuberculosis= >24 hrs
What are general characteristics of normal flora?
• Mostly bacteria – some fungi
• Commensals: orgs that dine together
• Found at sites in contact or communication with the outside world (skin, eyes, R.T., G.I., G.U.)
• Permanent “residents” or “transients” or “carriers”
• Internal organs - ~sterile
• Specific organisms present are not rigidly defined – to each his own
– physiology, diet, age, geographical habitat
• But knowing the typical n-flora at a bodily site, provides an understanding of the possible infections from injury to that site.
• AND the possible significance when isolated.
Why don’t we worry so much about normal flora that can be harmful?
• For instance, 10% of the population have the
meningococcus (Neisseria meningitidis) and the
pneumococcus (Streptococcus pneumoniae) as normal flora – these folks are colonized!
But no harm is usually done = “carrier state”
- Colonization is necessary but insufficient for disease.
- Even though these are very pathogenic organisms.
• So the properties of not just the organism but the
state of host defenses are both important in clinical
outcome, plus “unknown” factors!
What are some beneficial effects of normal flora?
• Act as host defense mechanism – by occupying attachment sites – competing with pathogens for nutrition – produce antimicrobial substances – So it’s no wonder that if suppressed, pathogens take over
• Antibiotic suppresion of G.I/G.U. flora
• Stimulate development of Immunity
– Germ-free animal studies=no immune system in animals
• Possible nutritional role - not essential (fat vs. skinny normal flora)
What are some harmful effects of normal flora?
• Harmful Effects -
– compromised patients
• Smokers, alcoholics, stroke victims – URT
• Malignancy, diseases, immunosupprressive drugs
– when displaced from their usual location(usually the case)
• Dental surgery;main vascular lines, catheterization
– when suppressed, others may take over
• Antibiotic suppresion of G.I/G.U. flora
What are the stages of bacterial disease (its pathogenesis)?
- Transmission - source to portal of entry
- Evasion of host defenses (virulence factors)
- Adhesion to host tissue (virulence factors)
- Colonization and Spread (virulence factors)
• Damage - toxins, invasiveness & inflammation
(virulence factors)
- Host Response to Infection (good & bad)
- Progression or Resolution of disease
What parts of bacteria are involved in adhesion to host tissue? What are two things that can happen after adhesion?
- Adhesion: adhesins-pili, capsules, glycocalyx, LPS O antigen chains, flagella, M protein, Other surface proteins, invasins
- Without them sometimes no disease
The bacteria itself could invade the cell or it could secrete toxins into the cell.
What causes staph. scalded skin syndrome? What is an exotoxin/endotoxin/enterotoxin
It is caused by staphylococcus aureus exotoxins which are serine proteases which selectively recognize and hydrolyze desmosomal proteins in the skin.
exo=secreted
endotoxin=within bacteria
enterotoxin=related to gi tract
What are some ways in which bacteria cause damage and some examples of each?
– Alterations of Metabolism
• toxins that block metabolism/cell functions-Inhibit protein synthesis; nerve function; cAMP, LPS (gram negative)
– Cell death
• lysis by toxins (Clostridia)
• lysis by intracellular growth (rickettsia)
• lysis by cell-mediated immune response (TB)
• apoptosis (shigella)
– Mechanical - obstructions
