The correct answer is "inhibition of topoisomerase II," as this is the mechanism of action of fluoroquinolone antibiotics, such as levofloxacin.

The other choices are incorrect for the following reasons:

Blockage of tRNA-ribosome-mRNA complex binding is the mechanism of action of tetracycline antibiotics. 

Disruption of mycolic acid synthesis is the mechanism of action of various anti-fungal agents.

Disruption of peptidoglycan cross-linkage is the mechanism of action of vancomycin.

Inhibition of peptidoglycan synthesis is the mechanism of action of beta-lactam antibiotics.

Acyclovir is converted to acyclovir-triphosphate and incorporated into the synthetic pathway for viral DNA as a guanosine molecule. The initial phosphorylation of acyclovir is carried out by viral thymidine kinase. Acyclovir has a higher affinity for viral thymidine kinase than mammalian thymidine kinase. Therefore, acyclovir is specifically effective in virally infected cells.

Methisazone blocks synthesis of viral mRNA and proteins. This is especially evident in pox viruses. Methisazone has been used to treat small pox.

Amantadine affects the central nervous system, producing mild, reversible disturbances. High dosages have been reported to induce seizures

The opportunistic mycoses are a group of fungal infections that occur almost exclusively in immunocompromised patients. A host of fungi, previously thought to be nonpathogenic, are known to be the etiologic agents of the opportunistic fungal infections. A certain few mycoses are seen with the greatest frequency and include zygomycosis, candidiasis, cryptococcosis, and aspergillosis. Aspergilli are widespread in the environment, and their conidia are easily dispersed and inhaled. These organisms are capable of causing a pulmonary infection in the immunocompromised patient, which rapidly disseminates and causes infection in virtually every organ. The drug of choice for the treatment of these infections is amphotericin B. A polyene macrolide antibiotic, amphotericin B works by forming pores in the fungal cell membrane. The other listed compounds are antifungal agents; however, their selectivity makes them unsuitable for the treatment of aspergillosis.

Gentamicin belongs to the aminoglycoside antimicrobial agents. It is a bactericidal agent with a wide spectrum of activity against Gram-negative and Gram-positive organisms. It irreversibly inhibits protein biosynthesis by acting directly on the ribosome. Gentamicin binds receptors on the 30S subunit of the bacterial ribosome and inhibits protein synthesis through interference with the initiation complex, misreading of the code on the mRNA template, and causing polysomes to dissociate into nonfunctional monosomes.

Ototoxicity and nephrotoxicity are the most serious adverse effects of gentamicin. Ototoxicity is manifested as vestibular dysfunction, which may be due to destruction of hair cells. If renal failure is present, the probability of ototoxicity is greater.

Nephrotoxicity is more common with gentamicin than with any of the other aminoglycosides. It can produce acute renal insufficiency and tubular necrosis.

The amino glycoside antibiotics include gentamicin, streptomycin, neomycin, tobramycin, kanamycin, amikacin, and netilmicin. All these drugs contain amino sugars linked to an aminocyclitol ring by glycosidic bonds. They are used primarily to treat infections caused by aerobic gram-negative bacteria, where they act to interfere with protein synthesis. The aminoglycosides diffuse through channels in the outer membrane of the bacteria and enter the periplasmic space. Subsequently, the drugs are transported across the cytoplasmic membrane by an energy-dependent transport system, which requires the bacteria to utilize oxygen. Once inside the bacterium, they bind to the 30 S ribosomal subunit and block the initiation of protein synthesis. Bacteria may acquire resistance to the action of the aminoglycosides by several different mechanisms. Penetration of the drug through the pores in the outer membrane may become retarded, but resistance of this type is unimportant clinically. Natural resistance to the aminoglycoside antibiotics can be caused by the failure of the drug to penetrate the cytoplasmic membrane. As the transport mechanism requires the utilization of oxygen, this explains the resistance of anaerobic bacteria and facultative bacteria grown under anaerobic conditions. However, the importance of this mechanism on clinically-important acquired-resistance does not appear to be significant. Resistance resulting from alterations in ribosomal structure is less clinically relevant for most infections. While an alteration in ribosomal structure can prevent binding of the drug, these alterations are not widespread. The most clinically relevant mechanism for acquired-resistance to the aminoglycoside antibiotics is the plasmid-mediated elaboration of inactivating enzymes. These enzymes may phosphorylate, adenylate, or acetylate the aminoglycoside, resulting in loss of function. This has become a source of special concern with regard to enterococcal infections, many of which are highly resistant to all aminoglycosides.

Initial treatment for pulmonary or extrapulmonary tuberculosis is isoniazid (INH), rifampin (RMP), and pyrazinamide (PZA) as a short-course intensive daily regimen for 2 months, followed by INH and RMP for 4 more months. The most common side effects of rifampin are reddish urine and stool, saliva, sweat, tears, diarrhea, joint pain, back pain, swelling of feet and/or legs, and blood in urine. Hyperuricemia is a major toxic effect of pyrazinamide; other toxic effects include fever, indigestion, urticaria, photosensitivity, and joint pain. Isoniazid can cause polyneuropathy, jaundice, muscle pain, confusion, and unsteady walk.

Tenofovir is categorized as a nucleoside analogue reverse transcriptase inhibitor (NRTIs). An NRTI’s mechanism of action is to block reverse transcriptase, an enzyme that enables the human immunodeficiency virus 1 (HIV-1) to flourish. This enzyme aids the HIV virus in making a copy of DNA from the viral RNA, and this DNA is incorporated into the host genome. The effectiveness has been found in a review conducted by the Centers for Disease Control and Prevention to be so effective that “pre-exposure prophylaxis can potentially be a vital option for HIV prevention in pearly at very high risk for infection, whether through sexual transmission or injecting drug use.”

In regards to Post-Exposure Prophylaxis (PEP), The United States Public Health Service recommend the use of tenofovir, emtricitabine, or a combination drug of these two medications—plus raltegravir for PEP in occupational exposure scenarios.

All of the drugs are antifungal agents but only flucytosine has been associated with bone marrow suppression and synergizes with other drugs which suppress bone marrow functions. Miconazole and ketoconazole may produce hepatotoxicity, gastro-intestinal upset and headaches. Amphotericin B may produce nephrotoxicity while itraconazole is associated with gastro-intestinal upset and rare liver dysfunction.