Antimicrobial drugs

List the cellular targets of antibiotics and explain how they affect cellular processes of bacteria

Antibiotics target key bacterial processes: cell wall synthesis (penicillins weaken wall → lysis), plasma membrane (polymyxins disrupt membrane), nucleic acid synthesis (quinolones inhibit DNA gyrase; rifamycins inhibit RNA polymerase), protein synthesis (bind 30S or 50S ribosome), and folic acid synthesis (sulfa drugs block metabolism)

Describe the chemical structure of beta-lactam antibiotics and describe how they work

Beta-lactam antibiotics contain a beta-lactam ring that mimics peptidoglycan structure. They bind transpeptidase enzymes, preventing cross-linking of the cell wall, leading to weak walls and bacterial lysis

Explain why some antibiotics are more toxic than others

Some antibiotics are more toxic because they target structures similar to human cells or affect normal microbiota. Drugs with less selective toxicity (closer similarity to human cells) have more side effects.

Describe antibiotic resistance mechanisms that bacteria have developed

Bacteria resist antibiotics by producing enzymes (beta-lactamase), altering target sites (e.g., MRSA changes transpeptidase), pumping drugs out (efflux pumps), or reducing drug entry :contentReference[oaicite:2]{index=2}

Name some antibiotic-resistant bacteria and the diseases they might cause

Examples include MRSA (skin infections, pneumonia), CRE (UTIs, bloodstream infections), and Pseudomonas aeruginosa (lung infections, especially in cystic fibrosis) :contentReference[oaicite:3]{index=3}

Explain why it is difficult to find antivirals, antifungals, antiprotozoals, and / or antihelminthics that can be used as pharmaceuticals

These pathogens are eukaryotic or use host cell machinery, so they are very similar to human cells. This makes it hard to target them without harming the host (low selective toxicity).

Explain the concept of selective toxicity and be able to calculate a therapeutic index

Selective toxicity means the drug harms the pathogen but not the host. Therapeutic index = maximum safe dose ÷ minimum effective dose; a higher value means the drug is safer :contentReference[oaicite:4]{index=4}

Describe the viral propagation cycle and explain the impact of interrupting the different stages

The viral cycle includes attachment, penetration, uncoating, synthesis, assembly, and release. Drugs that block any step (e.g., entry or replication) stop virus production and spread :contentReference[oaicite:5]{index=5}

Choose one antiviral drug and become an expert on it

Acyclovir is an antiviral drug used to treat herpes simplex virus (HSV-1, HSV-2) and varicella-zoster virus (chickenpox and shingles). It works as a nucleoside analog that mimics a DNA building block. In infected cells, a viral enzyme (thymidine kinase) activates the drug, allowing it to inhibit viral DNA polymerase and stop DNA replication by causing chain termination. This selective activation makes it less toxic to human cells. It can be given orally, topically, or intravenously, and side effects are usually mild but may include kidney toxicity in severe cases.

What is interferon and how does it work?

Interferon is a host-produced protein that inhibits viral replication. It signals nearby cells to activate antiviral defenses and helps limit viral spread

Provide examples of cellular targets for antifungal drugs

Antifungals target cell walls (echinocandins inhibit beta-glucan) and cell membranes (azoles and allylamines inhibit ergosterol synthesis; polyenes bind ergosterol) :contentReference[oaicite:7]{index=7}

Why is Amphotericin B only used for life-threatening systemic infections?

Amphotericin B binds ergosterol but also affects human cells, causing toxicity (especially kidney damage), so it is reserved for severe infections

What cellular process does flucytosine inhibit?

Flucytosine inhibits nucleic acid synthesis by blocking DNA replication and transcription

Why is a two-pronged approach (e.g., Amphotericin B + flucytosine) thought to be more effective than either drug alone?

Combination therapy targets multiple pathways, increases effectiveness, and reduces resistance development, especially in severe fungal infections :contentReference[oaicite:10]{index=10}

Why are there so many antimalarial drugs but so few drugs that treat other protozoal diseases

Malaria is widespread and heavily researched, leading to many drugs, while other protozoal diseases are less studied and harder to target due to similarity to human cells :contentReference[oaicite:11]{index=11}

What are some common diseases treated by nitroimidazole drugs?

Nitroimidazoles (e.g., metronidazole) treat infections like Giardia, Trichomonas, Entamoeba, and Toxoplasma by inhibiting nucleic acid synthesis :contentReference[oaicite:12]{index=12}

Why is nitazoxanide relatively nontoxic? What diseases can it treat?

Nitazoxanide targets anaerobic energy metabolism unique to parasites, making it less harmful to humans. It treats Giardia, Cryptosporidium, and some worms :contentReference[oaicite:13]{index=13}

What diseases do albendazole, mebendazole, and praziquantel treat?

Albendazole and mebendazole treat roundworms by blocking glucose uptake, while praziquantel treats flukes and tapeworms by paralyzing them for removal