Infectious Disease Part 1 Flashcards
(6) factors influencing infection
- communicability
- infectivity
- virulence
- pathogenicity
- toxigenicity
- port of entry
structures of bacterium
prokaryotes (no nucleus)
aerobic, anerobic
gram + gram-
motile inmotile
toxin production
binary fission
can acquire new genetic info and evolve
endotoxin
(Lipopolysaccharides)–structural portion of the cell wall which activates the inflammatory response and produces fever (produced by Gram-negative bacteria)
exotoxin
enzymes that can damage the plasma membranes of host cells or can inactivate enzymes critical to protein synthesis (produced by Gram-negative or positive bacteria)
bacterial modes of transmission
contact e.g. gonerrhea, streptococco
airborn e.g. TB legionella
droplet e.g. pertussis, meningecoco
vector e.g. lyme disease
vehicle e.g. Campylobacter(food), trachoma (fomites)
treatment approach 3 steps
Step 1: Identify the source of infectionand individual
patient considerations
Step 2: Identify the organism
Step 3: Selection of appropriate antimicrobial therapy
Gram negative bacterial are harder to treat because
Peptidoglycan layer is thinner compared to Gram-positive bacteria and has a protective outer lipid barrier composed of lipopolysaccharides (LPS) impermeable to most penicillin and cephalosporin antibiotics
LPS layer produces ______ which trigger release of pro-inflammatory cytokines, leading to inflammation, tissue damage, sepsis and potential death
endotoxins
Some broad-spectrum penicillins(i.e., ampicillin, amoxicillin) and 3rd generation cephalosporins are more_________ and can penetrate the ______ through _______ to enter the cell, inhibiting
hydrophilic
LPS barrier
porin channels
cell wall synthesis = cell death
Some Gram-negative bacteria may produce ______________ –combining penicillin with a B-lactamase inhibitor like clavulanic acid inactivates this enzyme [i.e., amoxicillin/clavulanate (Clavulin)]
B-lactamase (penicillin-destroying enzyme)
mechanisms of antibacterial resistance (innate and acquired)
(4)
1.Reduction of drug concentration by impairing uptake or expelling drug from cell
2. Alteration of drug target site
3. Production of antagonist compounds or drug-metabolizing enzymes
4. NDM-1 gene (encodes a potent form of beta-lactamase enzyme to create resistance to beta-lactam antibiotics)
Superinfection:
abx stewardship
The coordinated effort to optimize antibiotic use for infections
what are the goals of abx stewardship
Improve patient outcomes
*
Reduce microbial resistance + superinfections
*
Decrease the spread of multi-drug-resistant infections
*
Selection of appropriate drug (narrowest spectrum), dose (lowest), and duration (shortest)
*
Minimize unnecessary or inappropriate use
patient factors when selecting abx
Allergies/hypersensitivities
Age
Pregnancy/lactation
(decrease oral contraceptive effect when on abx)
Drug Interactions
important pmHX when selecting abx
Immune: immune-compromise may require increased dose or longer course
Hematologic: caution with bone marrow suppression
Cardiac: history of prolonged QT interval, or use of QT-prolonging medication
Renal: consider eGFR and calculate creatinine clearance, may need reduced dose
Hepatic: may need reduced dose if
history of hepatic
dysfunction + drug
metabolization in liver
MSK: caution with tendon rupture or tendonitis
