PROCESSES, PATHWAYS, CAUSES AND EFFECTS, AND MECHANISMS

Prolonged stationary phase caused by protein synthesis inhibitors

A condition that results in the inhibition of lipoteichoic acid synthesis in Gram-positive bacteria

Inhibition of lipoteichoic acid synthesis

The process that results in an increase in wall-attached teichoic acids, promoting the attachment of LytA

Attachment of LytA

The effect that facilitates the breakdown of the bacterial cell wall

Bacterial cell to burst by weakening the cell wall and/or bacterial capsule

The effect of cell wall disruptors

Slowing down the metabolism of bacteria by disrupting protein synthesis

The effect of translation inhibitors

Resists high internal osmotic pressure (5-20 atm)

The primary function of the prokaryotic cell wall

Control and harness the osmotic pressure to propagate cells and push for binary fission and meiosis

The function a properly working bacterial cell wall performs on the highly pressurized internal environment

Determines the shape of the bacterial cell

The function of a proper bacterial cell wall based on its content

Enhance the ability of bacteria to cling to living tissue and cause disease

The role of virulence factors contained within the bacterial cell wall

Fosters the maturity of bacterial cells and allows expression of certain virulence factors

The function of a biofilm

Mitosis and meiosis is quite tricky

The biological process in Mycobacteria that is hindered by the presence of long, heavy mycolic acids in the cell wall

Eliciting a strong response from the body

The effect of lipopolysaccharides (LPS) when attached to the outer membrane of Gram-negative bacteria

Wall-attached teichoic acids

The molecule whose increase promotes the attachment of LytA, an autolysin, when lipoteichoic acid synthesis is inhibited

Inhibition makes the fungal cell wall weak and destroys the fungal filament

The result of inhibiting chitin synthesis

Inhibiting peptidoglycan from forming and lengthening the cross-links

The consequence of beta-lactam compounds covalently binding to and inhibiting Penicillin-Binding Protein (PBP)

Weakens the peptidoglycan cell wall

The overall effect of beta-lactam compounds inhibiting PBP

Inhibition of the elongation of the peptidoglycan filament/polymer

The mechanism of glycopeptides, such as Vancomycin

Binding to the D-Ala-D-Ala terminus with H-bonds, wrapping around it like a glove

The specific mechanism by which Vancomycin prevents further polypeptide attachment

Inhibits dephosphorylation of Bactoprenol

The mechanism of action of Bacitracin

Inhibiting the building blocks from reaching the construction site

The ultimate result of Bacitracin inhibiting the dephosphorylation of Bactoprenol

Inhibits conversion of L-Alanine to D-Alanine

The specific mechanism, called the cycloserine effect, of Cycloserine

Prevents D-Alanine dimer formation

The specific mechanism, called the ligase effect, of Cycloserine

D-Ala-D-Ala terminus is not synthesized

The consequence of Cycloserine's action on alanine racemase and D-alanyl-D-alanine ligase

Inhibits the attachment of phosphoenolpyruvate to GlcNaC

The mechanism of action of Fosfomycin

Blocks MurNac synthesis

The overall result of Fosfomycin inhibiting the attachment of phosphoenolpyruvate to GlcNaC

No functional building block is produced

The consequence of MurNac synthesis being blocked by Fosfomycin

Blocking protein synthesis or translation

The major action of translation inhibitors

Preventing attachment of the tRNA to the growing polypeptide chain

The specific result of translation inhibitors binding to the prokaryotic ribosome

No transpeptidation, no protein translation, and overall slowing down bacterial metabolism

The effects that result from translation inhibitors preventing tRNA attachment

Delay time for bacteria to return to log growth

The effect observed during the Post-Antibiotic Effect (PAE)

Slow recovery after reversible nonlethal damage to cell structures

One reason for the delayed return to log growth during PAE

Persistence of the drug at a binding site or within the periplasmic space

One reason for the delayed return to log growth during PAE

Need to synthesize new enzymes before growth can resume

One reason for the delayed return to log growth during PAE

Organisms become more susceptible to antibacterial activity after antibiotic exposure

The effect observed during Post-Antibiotic Leukocyte Enhancement (PALE)

Crossing the placenta and the intact blood-brain barrier

A characteristic feature of tetracyclines' pharmacokinetics

Bacterial cell "vomits out" tetracycline

The effect of bacterial efflux pumps, a mechanism of resistance to tetracyclines

Block the bacterial cell from expelling drugs

The function of efflux pump inhibitors like Capsaicin

Softening or creating small holes in the cell wall

The result of using permeabilizers like Cationic Antimicrobial Peptide and EDTA

Normal cell function is disrupted since the solute environment is disrupted

The consequence of permeabilizers softening the cell wall and allowing solutes to move freely

Inert bacterial cells are more likely to be phagocytosed since it is not actively producing toxins

The result of quorum sensing inhibitors convincing bacteria that they are alone

Preventing a type of pump from expelling contents

The function of Type III secretion system inhibitors like Coil A + Coil B

Inhibits transpeptidase

The specific action of beta-lactams in the cell wall space

Inhibits C55-P bactoprenol shuttle

The specific action of Bacitracin in the cell wall space

Inhibition of D-Ala-D-Ala terminus on both sides

The specific action of Glycopeptide (Vancomycin) in both the cytoplasm and cell wall space

Binds to the bacterial membrane and causes rapid depolarization

The mechanism of action of Daptomycin

Ca2+-dependent K+ efflux (formation of ion channel)

The specific process triggered by Daptomycin binding to the bacterial membrane

Destroy cell integrity

The ultimate effect of Daptomycin creating holes in the cell membrane

Bacteriostatic drug (e.g., tetracycline) interferes with the action of penicillin

An example of an antagonistic combination of antimicrobials

Penicillin requires bacterial growth for interference in the cell membrane

The condition required for penicillin's action that is blocked by bacteriostatic drugs

Competition of same class drugs for a common binding site

A mechanism of antagonism, such as with double beta-lactams

Inhibition of cell permeability to a second antimicrobial

A mechanism of antagonism in drug interaction

De-repression of resistance enzymes for a second drug

A mechanism of antagonism in drug interaction

Increases the uptake of aminoglycosides by activating P-glycoprotein mediated transporters

The synergistic mechanism observed when Penicillin and aminoglycosides are rationally combined

Inhibits protein synthesis

The mode of action of bacteriostatic drugs, allowing normal flora to destroy the bacteria over time

Immediate destruction of the cell

The mode of action of bactericidal drugs

Disrupt the cell wall causing immediate lysis and death

The specific mechanism by which Beta-lactams achieve immediate destruction

Interfere with DNA synthesis

The mechanism by which Quinolones, Rifampicin, and Nitroimidazoles achieve immediate destruction

Kills during the rapid growth phase

The time-related effect of drugs like Gentamicin, Quinolones, Piperacillin, and Cefotaxime

Affects microbes in the non-growing phase

The time-related effect of drugs like Aminoglycosides, Bacitracin, Quinolones, Beta-lactam antibiotics, Carbapenems, Daptomycin, and Rifampicin

Clinical efficacy is best predicted by the percentage of time that blood concentrations of a drug remain above the MIC

The key predictive measure for time-dependent antimicrobial strategy

Maximum effect is achieved by exposing the microbes at a concentration of antimicrobial that is slightly above the MIC

The optimal dosing strategy for time-dependent antimicrobial killing

Concentration of the drug should remain above the MIC for at least 70% of the dosing interval

The desired steady-state concentration for time-dependent killing

Antimicrobial control is achieved at a faster rate than just exposing the microbe to time above the MIC

The effect of concentration-dependent killing

Keeping maximum concentrations of the drug (at Cmax)

The ideal strategy for concentration-dependent antimicrobials

Antimicrobial concentration plotted over time, superimposed with the control of microbial growth

The graph used as a useful predictor of bactericidal activity

Period in which the antimicrobial coverage can inhibit growth

What the Area Under the Curve (AUC) represents

Determined by the urgency of the need to control infection

The factor that dictates the classification of an antimicrobial as bactericidal or bacteriostatic

Arrests the growth and replication of bacteria at serum levels achievable in the patient

The action of bacteriostatic antibiotics

Limits the spread of infection until the immune system attacks, immobilizes, and eliminates the pathogen

The overall goal achieved by bacteriostatic antibiotics

Requires the host defense mechanism to kill the bacteria

A requirement for an individual taking a bacteriostatic antibacterial drug

Kills bacteria at drug at serum levels achievable in the patients

The action of bactericidal antibiotics

Can handle infection even without a good working host defense mechanism

The function of bactericidal agents

Block formation of the initiation complex, cause misreading of the code on the mRNA template, and inhibit translocation

The three specific mechanisms by which Aminoglycosides, as protein synthesis inhibitors, work on the 30s ribosomal unit

Transport can be enhanced by cell wall synthesis inhibitors

A factor that increases the efficacy of Aminoglycosides

Inhibits protein translation

The overarching mechanism of action of Aminoglycosides and Tetracyclines

Block aminoacyl tRNA to the A-site

The mechanism of action of Tetracyclines on the 30s subunit

Blocks the formation of initiation complexes and translocation of the aminoacyl tRNA from the A-site

The mechanism of action of Macrolides, Chloramphenicol, Streptogramins, and Lincosamides on the 50s subunit

Blocks the assembly of the ribosome

The mechanism of action of Oxazolidinones on the 23s of the 50s rRNA subunit

Reduced cell permeability or active efflux

The main mechanism of bacterial resistance to Macrolides

Destroys the macrocyclic lactone ring

The effect of Enterobacteria esterases, a mechanism of Macrolide resistance

Modifies the macrolide target, making the drug unable to access its binding site in the bacterial ribosome

The effect of Target modification by methylase, a mechanism of Macrolide resistance

Inhibits the enzyme, remaining in the circulation longer, and is more effective

The consequence of Macrolides inhibiting Cytochrome P450 (CYP450) enzymes

Inactivated by glucuronidation in the liver

The process by which Chloramphenicol is metabolized

Inhibits human gonadal and adrenal steroid synthesis

The mechanism by which Ketoconazole causes side effects like gynecomastia and menstrual irregularities

Causes thrombophlebitis and pain with the intramuscular route

An adverse reaction associated with the administration of Tetracyclines

Causes diffuse vasodilation

The unclear mechanism thought to be responsible for "Red Man" syndrome

Disruption of the epithelial cytoskeleton, tight junction barrier loss, cytokine release, and apoptosis

The effects of toxins causing C. difficile colitis

Imbalance of bacteria in gut, vagina, mouth, or skin

The cause of conditions like mucosal pruritus and candidiasis due to Tetracyclines

Opens the surface/cavity to overpopulation of pathogenic bacteria

The result of Tetracyclines killing both native and pathogenic flora

Produces specific toxins

The mechanism stated by some references for Staphylococcus aureus causing Toxic Shock Syndrome

Staphylococcal debris causing toxic shock syndrome due to irritation

The mechanism noted by Doc Chua for Toxic Shock Syndrome

Creating biofilms

The method used by Staphylococci to cause Toxic Shock Syndrome in certain conditions

Neutropenia, Anemia, Thrombocytopenia

Three reversible hematologic disturbances caused by Flucytosine

Elevation of serum transaminases (ALT and AST) and Alkaline phosphatases (ALP)

The reversible hepatic dysfunction caused by Flucytosine

Caused by metabolism of toxic antineoplastic 5-fluorouracil (5-FU)

The reason for Flucytosine's adverse effects like hematologic and hepatic disturbances

Inhibition of ergosterol synthesis by blocking a fungal cytochrome P450 enzyme lanosterol 14 alpha-demethylase

The mechanism of action of Azoles

Blocks the demethylation of lanosterol to ergosterol

The specific step inhibited by Azoles in ergosterol synthesis

Leads to membrane fluidity, permeability, and inhibition of fungal cell growth and replication

The consequence of Azoles blocking ergosterol synthesis

Inhibits cell wall synthesis

The mechanism of action of Echinocandins

Inhibits the formation of glucans in the fungal cell wall

The specific mechanism of Echinocandins