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.

Dapsone has been the world wide standard for treatment of leprosy. The other agents listed are used in treatment of tuberculosis.

Zidovudine (ZDV,) formerly called azidothymidine, is active orally and is distributed to most tissues. The primary toxic side effect of ZDV is bone marrow suppression leading to anemia and neutropenia, which may require transfusions. Additional side effects include thrombocytopenia, gastrointestinal distress, headache, myalgia, acute cholestatic hepatitis, agitation, and insomnia. 

The other choices are incorrect. Acyclovir is commonly used for the treatment of mucocutaneous and genital herpes lesions and for prophylaxis in AIDS. Acyclovir has no significant toxicity on the bone marrow. Nelfinavir is a protease inhibitor that is characterized by a short half-life and has a number of drug interactions but its primary adverse effect is diarrhea and it has the most favorable safety profile in pregnancy. It is not associated with bone marrow suppression. Lamivudine is a nucleoside inhibitor and is an active inhibitor of HIV reverse transcriptase. It is used in the treatment of hepatitis B virus infection. The drug is remarkably nontoxic and adverse effects are mild. Tenofovir is a nucleoside reverse transcriptase inhibitor and anti-HIV drug that competitively inhibits reverse transcriptase and causes chain termination after incorporation into DNA. Adverse side effects include gastrointestinal distress, asthenia, and headache but not anemia, leukopenia, or thrombocytopenia.

The chemical type of an antiviral compound is often important in determining its potential mechanisms and, therefore, its utility against specific types of viruses. Interferon is a glycoprotein produced by many types of mammalian cells. It stimulates host mechanisms to prevent viral penetration and also inhibits viral protein synthesis. Idoxuridine, as its name implies, is a pyrimidine, which inhibits viral DNA polymerase. Zidovudine and zalcitabine are also pyrimidines, but they inhibit reverse transcriptase and act as chain terminators. Only acyclovir is a purine that requires viral thymidine kinase to be converted to an active phosphorylated form, which then inhibits viral DNA polymerase.

Suramin must be administered intravenously and should be used cautiously in patients with kidney disease. It inhibits protein kinases and dihydrofolate reductase and reduces ATP synthesis. It is used in the treatment of certain extra-intestinal nematodes and is probably one of the most toxic anthelminthic agents.

 The other choices are incorrect. Diethylcarbamazine is rapidly absorbed following oral administration and increases the susceptibility of extra-intestinal nematodes to host antibodies. Ivermectin is used to treat O. volvulus in humans and is rapidly absorbed following oral administration. The primary use of praziquantel, which is rapidly absorbed orally, is in the treatment of infection from flat worms and flukes where it reduces the resistance of the parasite to host immune mechanisms. Zidovudine is also administered orally, but is used for treatment of AIDS, where most of its toxic symptoms are hematologic.