The tetracycline antibiotics possess a wide range of antimicrobial activity against gram-positive and gram-negative bacteria, as well as Rickettsia, Mycoplasma, Chlamydia, Ureaplasma, some atypical mycobacteria, and amoebae. These drugs are primarily bacteriostatic and act by inhibiting microbial protein synthesis. The tetracyclines, after active transport into the cell, bind to the 30 S ribosomal subunit. This prevents the access of aminoacyl tRNA to the acceptor site on the mRNA-ribosome complex, inhibiting the addition of amino acids to the growing peptide chain. This effect is, for the most part, reversible and removal of the drug results in loss of action.

The other mechanisms listed are utilized by other antimicrobial agents. For example, all beta-lactam drugs are selective inhibitors of cell wall synthesis, and therefore active against growing bacteria. Sulfonamides are structural analogs of PABA that is necessary for folic acid synthesis. By competitive inhibition, the drug interferes with folic acid synthesis. Folic acid is an important precursor to the synthesis of nucleic acids. Quinolones are examples of antibiotics which inhibit bacterial DNA synthesis by blocking of the DNA gyrase. Antibiotics—polymyxin and colistin—and the antifungal agent amphotericin B act by inhibiting cell membrane function.

Amantadine only works after viral attachment to the cell, preventing viral uncoating. It is also believed to interfere with viral mRNA production. Amantadine is effective against influenza virus A.

Transport antibiotics act as carriers of ions across membranes (e.g. valinomycin) or by forming channels in the membrane that allow ions to cross the membrane (example-gramicidin A). Gramicidin affects cell membrane permeability while polymyxin B interferes with bacterial cell wall production. These transport antibiotics, also called ionophores, are secreted by many microorganisms and disable other species by making their membranes permeable to ions. These antibiotics show high specificity for specific ions. Carriers bind ions on one side of the membrane and shuttle the ion across the membrane. The carrier antibiotics are donut shaped with a hydrophilic center where the ion binds and a hydrophobic periphery that allows the antibiotic to traverse the membrane.

The channel forming antibiotics form a β-helix that forms a "hole" in the membrane through which ions can move. These channels open and close and the accompanying ion movements can be detected by measuring the conductance across the membrane. The transport antibiotics have been a very useful tool for cell biologists and physiologists studying the movement of ions across biological membranes under a variety of conditions. Both types of antibiotics insert into the lipid bilayer but do not alter the composition of the membrane lipids. Penicillin is an antibiotic that acts by inhibiting cell wall synthesis by inhibiting the enzyme glycopeptide transpeptidase. Neomycin is an aminoglycoside antibiotic that binds to the 30S subunit of the ribosome inhibiting protein synthesis.

3'-azido-3'-deoxythymidine (AZT) is a nucleoside analog that blocks HIV replication by inhibiting the RNA-dependent polymerase, HIV-DNA polymerase. The DNA polymerase from HIV is 100-fold more sensitive to AZT than the host polymerase. AZT is a pyrimidine analog that is phosphorylated to AZT-triphosphate by cellular enzymes and acts as a competitive inhibitor of the reverse transcriptase. AZT can be incorporated into viral DNA and cause chain termination because its structure lacks the 2' hydroxyl needed for addition of the next nucleotide by the polymerase.

In addition to nucleoside analogues, HAART also contains non-nucleoside reverse transcriptase inhibitors and protease inhibitors that block cleavage of the precursors of the viral coat proteins, preventing proper viral assembly. Maraviroc blocks a specific cell receptor needed by HIV to enter the host cell.

Amikacin binds to the 30S ribosomal sub-unit, not the 50S.

Enzymatic hydrolysis by % lactamase-producing bacteria targets penicillins.

Bacterial resistance to amikacin can be mediated through loss of a receptor by which amikacin binds the 30S ribosomal subunit, interference with membrane transport, and bacterial acetylation, adenylation, or phosphorylation.

Amikacin is resistant to peroxidase.

Amikacin is only marginally soluble in the bacterial cell membrane to begin with.

The mechanism of amphotericin B involves ergosterol, but the mechanism is not related to ergosterol synthesis. Amphotericin B binds to ergosterol in the cell membrane, disrupting its permeability to ions. Ketoconazole and other imidazoles interact with cytochrome P-450 to inhibit P-450 dependent synthesis of ergosterol by sterol 14-demethylase. Griseofulvin interacts with microtubular protein to inhibit fungal mitosis. Flucytosine incorporates into RNA and disrupts fungal protein synthesis. Zidovudine is used primarily as an antibiotic and not as an antifungal agent.

Vancomycin is the correct answer. Antibiotics that inhibit bacterial cell wall synthesis include the beta-lactam antibiotics (penicillins and cephalosporins), vancomycin, and bacitracin. Synthesis of the bacterial cell wall takes place in 4 steps: 1) Precursors of the cell wall are synthesized within the bacterial cytoplasm. 2) The precursors are transported across the cell membrane. 3) Outside the cell membrane, the precursors are linked together to form chains called peptidoglycans. 4) The peptidoglycan chains are cross-linked to form a rigid, stable cell wall.

• Beta-lactam antibiotics act by inhibiting step 4, the cross-linking of peptidoglycans. They also activate hydrolytic enzymes, which degrade already-existing cell walls. This usually results in lysis and death of the bacteria. (Mutant bacterial strains, which lack the hydrolytic enzyme, are not killed by beta-lactams, but their growth is arrested)
• Vancomycin inhibits step 3, the elongation of the peptidoglycan chains
• Bacitracin interferes with step 2, the transport of precursors across the cell membrane

Aminoglycosides, tetracyclines, macrolides (erythromycin and its relatives), clindamycin, and chloramphenicol are inhibitors of bacterial protein synthesis. They act by binding to ribosomal subunits.

• Aminoglycosides bind to several sites on the bacterial ribosome. They interfere with the movement of ribosomes along the strand of mRNA. They also induce misreading of the mRNA so that incorrect amino acids are incorporated into the elongating peptide chain
• Tetracyclines bind to the 30S ribosomal subunit. Macrolides, clindamycin, and chloramphenicol bind to the 50S subunit. These antibiotics interfere with the attachment of tRNA to the ribosome, thus preventing the addition of amino acids to the peptide chain

Sulfonamides and trimethoprim act by inhibiting the synthesis of folic acid. Certain bacteria synthesize folic acid from precursors by a series of enzyme-catalyzed reactions. Sulfonamides and trimethoprim block different steps in this synthetic pathway by binding competitively to different enzymes. When used together, their actions are synergistic (mammals do not synthesize folic acid, but require it as a vitamin; therefore, these drugs do not interfere with metabolism in mammalian cells).

Quinolones (e.g. norfloxacin and ciprofloxacin) inhibit bacterial nucleic acid synthesis by interfering with DNA gyrase, a bacterial enzyme that catalyzes supercoiling of DNA.

Polymyxins have a detergent action that disrupts bacterial cell membranes. They can also have the same toxic effect on mammalian cells; for this reason, they are seldom used except in topical preparations.

All the listed agents are synthetic analogues, except interferon, which is a glycoprotein produced by many types of mammalian cells. It has been shown to be useful in treatment of hepatitis, papilloma viruses, hairy-cell leukemia and AIDS-related Kaposi's sarcoma. Idoxuridine, as its name implies, is a synthetic pyrimidine analog, which inhibits viral DNA polymerase. Zidovudine and zalcitabine are also synthetic pyrimidine analogs but they inhibit reverse transcriptase and act as chain terminators. Acyclovir is a synthetic purine analog which requires viral thymidine kinase to be converted to an active phosphorylated form, which then, inhibits viral DNA polymerase.

Loa loa is an extra-intestinal nematode, which may migrate to the CNS, causing encephalitis. Diethylcarbamazine is successful in treating Loa loa but will exacerbate the encephalitis unless steroids are used first to treat the symptoms of the encephalitis. Other side effects of diethylcarbamazine may be due to rapid death of nematodes and release of various toxic substances. Symptomatic treatment might be appropriate with a number of pharmacological classes, but most symptoms will resolve as the body is cleared of dead and dying nematodes.

Metronidazole is correct. The patient is infected with Clostridium difficile, a Gram-positive, spore-forming bacillus. It is manifested by watery diarrhea, which left untreated can progress to fulminant colitis. Previous antibiotic use is the leading cause of Clostridium difficile, as the use of antibiotics alters the normal colonic flora, allowing Clostridium difficile to proliferate. Patients who have confirmed infection should first discontinue any offending antibiotics. The patient is then treated with either oral metronidazole or oral vancomycin. Due to its cost, oral vancomycin is typically reserved for severe or recurrent cases of Clostridium difficile.

The other choices are incorrect. Loperamide and lomotil are incorrect. These medications are both anti-motility agents. Their use is not recommended in the treatment of Clostridium difficile, as anti-motility agents have been associated with the development of toxic megacolon and systemic infection. Prednisone is incorrect. While corticosteroids have been used in severe Clostridium difficile colitis as adjunctive treatment to reduce inflammation, their use is not recommended for first-line treatment. In order to clear Clostridium difficile, the patient must undergo treatment with either metronidazole or vancomycin. Clindamycin is incorrect. Clindamycin is not active against Clostridium difficile. In fact, its use has been associated with development of Clostridium difficile.