Antibiotics and resistance microbio study

Chemotherapeutic agent

powerful medications used to treat cancer by stopping or slowing the growth of cancer cells.

Antibiotic

powerful medicines that treat bacterial infections by killing bacteria or stopping them from growing

Selective toxicity

the ability of a chemical or drug to harm an infecting pathogen or target cell without causing significant damage to the host organism

Spectrum of action

the range of bacterial types—such as gram-positive, gram-negative, or anaerobic strains—that a specific drug can kill or stop from growing. Antibiotics are grouped by this range into narrow-spectrum, broad-spectrum, and extended-spectrum categories

Therapeutic index

a ratio that compares the toxic dose of a drug to its effective therapeutic dose

Therapeutic window

the safe and effective range of a drug's concentration in the body, bounded by the minimum effective concentration and the maximum tolerated concentration. Doses kept inside this range heal the patient while avoiding harm

Synergism

happens when two or more drugs work together to create an effect that is much greater than the sum of their separate effects

Why is selective toxicity possible

because drugs exploit structural and biochemical differences between pathogens (or abnormal cells) and the host. By targeting components unique to the pathogen—such as bacterial cell walls, distinct ribosomal structures, or specialized enzymes—treatments can destroy the invader while leaving normal human cells unharmed.

Which microorganisms would be the easiest to develop selective toxicity treatments for?

Bacteria (Prokaryotes), because the fundamental biological differences between bacterial cells and human (host) cells provide numerous unique and safe targets that can be attacked without harming the patient

Cell wall synthesis inhibition

Drugs targeting the synthesis of the bacterial cell wall.

Cell membrane disruption

Drugs that damage or disrupt the structure of the microbial cell membrane.

Protein synthesis inhibition

Drugs that interfere with the function of bacterial ribosomes (70S ribosomes), which are different from human ribosomes (80S ribosomes).

Nucleic Acid Synthesis Inhibition

Drugs that interfere with the synthesis or function of DNA or RNA.

Metabolic Pathway Interference

Drugs that block essential metabolic pathways, such as folic acid synthesis. Bacteria synthesize their own folic acid, while humans obtain it from their diet.

Attachment Blockage

Some antiviral drugs prevent viruses from attaching to host cells.

Does exposure to an antibiotic result in resistance or does it merely select for resistance?

Treatment with antibiotics selects for resistance; it does not cause it directly. A population of bacteria with a few resistant individuals will see the sensitive ones die off when exposed to the antibiotic, allowing the resistant ones to multiply.

Alteration of the Drug Target

Mechanism of resistance where the bacterial target (e.g., ribosome, enzyme) is modified so the drug can no longer bind effectively.

Example of Drug Target alteration

Azithromycin resistance due to altered ribosome structure; Fluoroquinolone resistance due to altered DNA gyrase.

Alteration of a Metabolic Pathway

Mechanism of resistance in which overproduction of an enzyme in a pathway can overcome inhibition

Example of metabolic pathway alteration

Sulfonamide resistance due to overproduction of dihydropteroate synthase (DHPS).

Alteration of drug permeability

Mechanism of resistance in which changes in the bacterial cell membrane prevent the drug from entering the cell

Example of drug permeability alteration

Colistin resistance due to changes preventing entry

Exportation of the drug (Efflux pumps)

Mechanism of resistance in which Bacteria actively pump the drug out of the cell

Example of drug exportation

Tetracycline resistance via efflux pumps

Inactivation of the drug

Mechanism of resistance in which Bacteria produce enzymes that break down or inactivate the antibiotic

Example of drug inactivation

Beta-lactamase enzymes inactivate penicillin like drugs

The Target Exists

The mechanism must match a structure the bug actually has. (e.g., Penicillin does nothing to Mycoplasma because it has no cell wall).

The drug reaches it

Route of administration and tissue distribution determine where the drug goes. (e.g., The blood-brain barrier makes treating meningitis difficult).

The dose stays safe

The dose must be within the therapeutic range, between the effective dose and the toxic dose. (Therapeutic range < toxic dose, also known as the therapeutic index).

Horizontal gene transfer

Bacteria can acquire resistance through transfer of genetic material between bacteria.

Random mutations

Bacteria can acquire resistance through errors during DNA replication.

Tetracyclines in pregnancy

Affect teeth and bone development

Fluoroquinolones in pregnancy

Can affect cartilage development

Aminoglycosides in pregnancy

Can cause fetal hearing damage

Sulfonamides in pregnancy

Risk of kernicterus near term

Macrolides (e.g., Azithromycin) in pregnancy

often considered acceptable in pregnancy as they target protein synthesis and are generally considered safer for the fetus than the other listed classes.

Would penicillin have any effect on fungal infections?

No, because penicillin is exclusively an antibacterial medication and It works by targeting and inhibiting the synthesis of peptidoglycan, a complex polymer that makes up the cell walls of bacteria