Fluoroquinolone resistance US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Fluoroquinolone resistance. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Fluoroquinolone resistance US Medical PG Question 1: A 22-year-old female with no past medical history presents to her primary care physician with a 3-day history of knee pain. She denies any recent injury or trauma. On physical examination her knee is warm, erythematous, and has diminished range of movement. The patient reports having multiple sexual partners over the last year and does not use protection regularly. Her blood pressure is 124/85 mmHg, heart rate is 76/min, and temperature is 38.3℃ (101.0℉). A joint aspiration is performed and a growth of gram-negative diplococci is noted on bacterial culture. What is the treatment of choice for this patient's condition?
- A. Vancomycin monotherapy
- B. Fluoroquinolones
- C. Nafcillin monotherapy and joint aspiration
- D. Oxacillin and ceftriaxone
- E. Ceftriaxone monotherapy and joint aspiration (Correct Answer)
Fluoroquinolone resistance Explanation: ***Ceftriaxone monotherapy and joint aspiration***
- The patient's presentation with **acute monoarthritis**, fever, and **gram-negative diplococci** on joint culture is highly suggestive of **gonococcal arthritis**. Intravenous ceftriaxone is the treatment of choice for disseminated gonococcal infection.
- While joint aspiration confirms the diagnosis and can relieve pressure, definitive treatment requires systemic antibiotics to clear the infection.
*Vancomycin monotherapy*
- **Vancomycin** is primarily effective against **gram-positive bacteria**, particularly MRSA, and would not adequately cover the gram-negative diplococci found in this case.
- Using vancomycin alone would leave the patient's gonococcal infection untreated, potentially leading to worsening of symptoms or complications.
*Fluoroquinolones*
- While some fluoroquinolones have activity against *Neisseria gonorrhoeae*, **widespread resistance** to this class of antibiotics has emerged, making them an unreliable choice for empiric or first-line treatment of gonococcal infections.
- The CDC no longer recommends fluoroquinolones for gonococcal infections due to high rates of resistance.
*Nafcillin monotherapy and joint aspiration*
- **Nafcillin** is a narrow-spectrum penicillin effective primarily against **methicillin-sensitive *Staphylococcus aureus*** and other gram-positive organisms.
- It would not provide appropriate coverage for the **gram-negative diplococci** identified in this patient's joint fluid.
*Oxacillin and ceftriaxone*
- While **ceftriaxone** is appropriate, the addition of **oxacillin** (another anti-staphylococcal penicillin) would be unnecessary.
- Oxacillin is primarily used for gram-positive infections and would not add benefit against **gonococcal arthritis**, increasing the risk of adverse effects without improving efficacy.
Fluoroquinolone resistance US Medical PG Question 2: A 67-year-old man presents to the physician with profuse watery diarrhea along with fever and crampy abdominal pain. He has been taking an antibiotic course of cefixime for about a week to treat a respiratory tract infection. At the doctor’s office, his pulse is 112/min, the blood pressure is 100/66 mm Hg, the respirations are 22/min, and the temperature is 38.9°C (102.0°F). His oral mucosa appears dry and his abdomen is soft with vague diffuse tenderness. A digital rectal examination is normal. Laboratory studies show:
Hemoglobin 11.1 g/dL
Hematocrit 33%
Total leucocyte count 16,000/mm3
Serum lactate 0.9 mmol/L
Serum creatinine 1.1 mg/dL
What is most likely to confirm the diagnosis?
- A. Identification of C. difficile toxin in stool (Correct Answer)
- B. Colonoscopy
- C. CT scan of the abdomen
- D. Abdominal X-ray
- E. Stool culture
Fluoroquinolone resistance Explanation: ***Identification of C. difficile toxin in stool***
- The patient's presentation with **profuse watery diarrhea**, fever, and abdominal pain following a course of **antibiotics (cefixime)** is highly suggestive of *Clostridioides difficile* infection (CDI).
- **Detecting *C. difficile* toxins A or B in stool** is the most reliable and definitive method to confirm the diagnosis of CDI.
*Colonoscopy*
- While colonoscopy can reveal **pseudomembranes** characteristic of severe *C. difficile* colitis, it is an **invasive procedure** and not the primary diagnostic tool.
- Endoscopy is typically reserved for cases where the diagnosis is uncertain despite positive toxin tests, or to assess severity when there is concern for complications like **toxic megacolon**.
*CT scan of the abdomen*
- A CT scan may show signs of colitis, such as **bowel wall thickening**, but it cannot definitively diagnose *C. difficile* infection.
- It is more useful for identifying **complications** like toxic megacolon, bowel perforation, or ascites, rather than initial diagnosis.
*Abdominal X-ray*
- An abdominal X-ray is primarily used to look for signs of **toxic megacolon** or **bowel perforation** (e.g., free air under the diaphragm).
- It is **not diagnostic for *C. difficile* infection itself** and would not confirm the presence of the pathogen or its toxins.
*Stool culture*
- A stool culture for common bacterial pathogens would likely be **negative** in a case of *C. difficile* infection, as *C. difficile* is a distinct entity.
- While *C. difficile* can be cultured, **toxin detection** is preferred for diagnosis because not all *C. difficile* strains produce toxins, and asymptomatic carriage can occur.
Fluoroquinolone resistance US Medical PG Question 3: An 18-year old college freshman presents to his university clinic because he has not been feeling well for the past two weeks. He has had a persistent headache, occasional cough, and chills without rigors. The patient’s vital signs are normal and physical exam is unremarkable. His radiograph shows patchy interstitial lung infiltrates and he is diagnosed with atypical pneumonia. The patient is prescribed azithromycin and takes his medication as instructed. Despite adherence to his drug regimen, he returns to the clinic one week later because his symptoms have not improved. The organism responsible for this infection is likely resistant to azithromycin through which mechanism?
- A. Mutation in topoisomerase II
- B. Methylation of ribosomal binding site
- C. Presence of a beta-lactamase
- D. Decreased binding to RNA polymerase
- E. Insertion of drug efflux pumps (Correct Answer)
Fluoroquinolone resistance Explanation: ***Insertion of drug efflux pumps***
- **Azithromycin** is a macrolide antibiotic that inhibits bacterial protein synthesis by binding to the **50S ribosomal subunit**.
- In **Mycoplasma pneumoniae** (the most common cause of atypical pneumonia in young adults), the **most common** mechanism of macrolide resistance is through **efflux pumps**, particularly the **mef genes**.
- These efflux pumps actively transport macrolides out of the bacterial cell, reducing intracellular drug concentration and conferring resistance.
- This mechanism is responsible for the majority of macrolide-resistant *M. pneumoniae* isolates worldwide.
*Methylation of ribosomal binding site*
- **Methylation** of the ribosomal binding site (specifically the **23S rRNA** via erm genes) does prevent azithromycin from binding effectively.
- While this is a valid macrolide resistance mechanism seen in organisms like *Streptococcus pneumoniae* and *Streptococcus pyogenes*, it is **less common** in *Mycoplasma pneumoniae*.
- Efflux pumps (mef) are the predominant mechanism in *M. pneumoniae* resistant strains.
*Mutation in topoisomerase II*
- **Topoisomerase II** (DNA gyrase) is the target of **fluoroquinolone antibiotics**, not macrolides.
- Mutations in this enzyme lead to resistance against fluoroquinolones, such as **ciprofloxacin**.
*Presence of a beta-lactamase*
- **Beta-lactamase enzymes** inactivate **beta-lactam antibiotics** (e.g., penicillin, cephalosporins) by hydrolyzing their beta-lactam ring.
- Additionally, *Mycoplasma pneumoniae* **lacks a cell wall**, making it inherently resistant to all beta-lactam antibiotics regardless of beta-lactamase production.
*Decreased binding to RNA polymerase*
- **RNA polymerase** is the target for antibiotics like **rifampin**, which inhibits bacterial transcription.
- Decreased binding to RNA polymerase would lead to rifampin resistance, not azithromycin resistance.
Fluoroquinolone resistance US Medical PG Question 4: A scientist is studying the mechanisms by which bacteria become resistant to antibiotics. She begins by obtaining a culture of vancomycin-resistant Enterococcus faecalis and conducts replicate plating experiments. In these experiments, colonies are inoculated onto a membrane and smeared on 2 separate plates, 1 containing vancomycin and the other with no antibiotics. She finds that all of the bacterial colonies are vancomycin resistant because they grow on both plates. She then maintains the bacteria in liquid culture without vancomycin while she performs her other studies. Fifteen generations of bacteria later, she conducts replicate plating experiments again and finds that 20% of the colonies are now sensitive to vancomycin. Which of the following mechanisms is the most likely explanation for why these colonies have become vancomycin sensitive?
- A. Point mutation
- B. Gain of function mutation
- C. Viral infection
- D. Plasmid loss (Correct Answer)
- E. Loss of function mutation
Fluoroquinolone resistance Explanation: ***Plasmid loss***
- The initial **vancomycin resistance** in *Enterococcus faecalis* is often mediated by genes located on **plasmids**, which are extrachromosomal DNA.
- In the absence of selective pressure (vancomycin), bacteria that lose the plasmid (and thus the resistance genes) have a **growth advantage** over those that retain the energetically costly plasmid, leading to an increase in sensitive colonies over generations.
*Point mutation*
- A **point mutation** typically involves a change in a single nucleotide and could lead to loss of resistance if it occurred in a gene conferring resistance.
- However, since there was no selective pressure for loss of resistance, it is less likely that 20% of the population would acquire such a specific point mutation to revert resistance.
*Gain of function mutation*
- A **gain of function mutation** would imply that the bacteria acquired a *new* advantageous trait, not the *loss* of resistance.
- This type of mutation would not explain why some colonies became sensitive to vancomycin after the drug was removed.
*Viral infection*
- **Viral infection** (bacteriophages) can transfer genes through transduction or cause bacterial lysis, but it's not the primary mechanism for a widespread reversion of resistance in the absence of antibiotic pressure.
- It would not explain the observed increase in vancomycin-sensitive colonies due to evolutionary pressure.
*Loss of function mutation*
- While a **loss of function mutation** in a gene conferring resistance could lead to sensitivity, it's generally less likely to explain a 20% shift without selective pressure than **plasmid loss**.
- Plasmids are often unstable and are easily lost in the absence of selection, whereas a specific gene mutation causing loss of function would need to arise and become prevalent in the population.
Fluoroquinolone resistance US Medical PG Question 5: A 15-year-old boy presents with his father to the urgent care department with a 5-day history of frequent diarrhea, occasionally mixed with streaks of blood. Stool cultures are pending, but preliminary stool samples demonstrate fecal leukocytes and erythrocytes. The patient's vital signs are within normal limits, and he is started on outpatient therapy for presumed Shigella infection. Which of the following was the young man most likely started on?
- A. Oral vancomycin
- B. Oral erythromycin
- C. Oral metronidazole
- D. An oral quinolone
- E. Oral trimethoprim-sulfamethoxazole (TMP-SMX) (Correct Answer)
Fluoroquinolone resistance Explanation: **Oral trimethoprim-sulfamethoxazole (TMP-SMX)**
- **TMP-SMX** is a traditional first-line treatment for **Shigella infection** in settings where susceptibility is expected or confirmed.
- The patient's presentation with **bloody diarrhea**, **fecal leukocytes**, and **erythrocytes** is classic for **Shigella dysentery**.
- While **resistance rates vary by region**, TMP-SMX remains an appropriate choice when local susceptibility patterns support its use.
- It is cost-effective, well-tolerated, and appropriate for outpatient management of uncomplicated cases.
*Oral vancomycin*
- Vancomycin is specifically used for **Clostridioides difficile infection** and does not treat Shigella.
- It has **poor oral absorption** and no activity against Gram-negative enteric pathogens like Shigella.
*Oral erythromycin*
- Erythromycin is primarily effective against **Campylobacter jejuni** and respiratory pathogens.
- It has **limited activity against Shigella** and resistance rates are high, making it an inappropriate choice.
*Oral metronidazole*
- Metronidazole treats **anaerobic bacteria** and protozoal infections (*Giardia*, *Entamoeba histolytica*).
- It has **no significant activity against Shigella**, a facultative anaerobic Gram-negative bacillus.
*An oral quinolone*
- **Fluoroquinolones** (e.g., ciprofloxacin) are highly effective against Shigella and often used as first-line therapy, particularly in areas with high TMP-SMX resistance.
- They are increasingly preferred in current guidelines due to rising resistance to TMP-SMX.
- However, in the context of empiric outpatient treatment where susceptibility is presumed, **TMP-SMX** may still be chosen initially as a narrower-spectrum, cost-effective option, with fluoroquinolones reserved based on culture results or treatment failure.
Fluoroquinolone resistance US Medical PG Question 6: A 67-year-old male with a past medical history of diabetes type II, obesity, and hyperlipidemia presents to the general medical clinic with bilateral hearing loss. He also reports new onset vertigo and ataxia. The symptoms started a day after undergoing an uncomplicated cholecystectomy. If a drug given prophylactically just prior to surgery has caused this patient’s symptoms, what is the mechanism of action of the drug?
- A. Formation of free radical toxic metabolites that damage DNA
- B. Inhibition of the formation of the translation initiation complex (Correct Answer)
- C. Inhibition of DNA gyrase
- D. Inhibition of cell wall synthesis
- E. Inhibition of DNA-dependent RNA polymerase
Fluoroquinolone resistance Explanation: **Correct: Inhibition of the formation of the translation initiation complex**
- The symptoms of **bilateral hearing loss**, **vertigo**, and **ataxia** point to **ototoxicity** and **vestibulotoxicity**, which are classic side effects of **aminoglycoside antibiotics**.
- Aminoglycosides, such as gentamicin, are known to **inhibit bacterial protein synthesis** by binding to the **30S ribosomal subunit**, thereby **inhibiting the formation of the translation initiation complex**. They are sometimes used prophylactically, though less commonly for cholecystectomy.
*Incorrect: Formation of free radical toxic metabolites that damage DNA*
- This mechanism is characteristic of **nitrofurans** (e.g., nitrofurantoin) and some **antimalarials**, which are not typically used for surgical prophylaxis.
- While these drugs can cause various adverse effects, this specific mechanism does not lead to the described triad of ototoxicity and vestibulotoxicity.
*Incorrect: Inhibition of DNA gyrase*
- This is the mechanism of action for **fluoroquinolone antibiotics** (e.g., ciprofloxacin, levofloxacin).
- While fluoroquinolones can cause adverse effects like tendinopathy and CNS disturbances, they are not typically associated with the pronounced ototoxicity and vestibulotoxicity seen in this patient.
*Incorrect: Inhibition of cell wall synthesis*
- This is the mechanism of action for **beta-lactam antibiotics** (e.g., penicillin, cephalosporins) and **vancomycin**, which are common choices for surgical prophylaxis.
- Though some of these drugs can have side effects (e.g., vancomycin's "red man syndrome" or ototoxicity in specific cases), the combination of bilateral hearing loss, vertigo, and ataxia is not their characteristic adverse effect profile.
*Incorrect: Inhibition of DNA-dependent RNA polymerase*
- This is the mechanism of action for **rifamycins** (e.g., rifampin).
- Rifampin is primarily used for tuberculosis and some other serious infections, not typically for routine surgical prophylaxis, and its side effect profile does not include this specific constellation of ototoxicity and vestibulotoxicity.
Fluoroquinolone resistance US Medical PG Question 7: A 24-year-old woman presents to her physician's office complaining of a worsening cough with large volumes of mucoid sputum every morning and thick, foul-smelling sputum almost every time she coughs. She says that this cough started about one month ago and has been increasing in intensity. Over-the-counter medications are ineffective. Past medical history is significant for cystic fibrosis diagnosed at the age of 6 years, and pneumonia twice in the past 2 years. Other than a cough, she has no fever or any other concerns. A sputum sample grows aerobic, non-lactose fermenting, oxidase-positive, gram-negative bacillus. Which of the following treatment regimens is the most beneficial for her at this time?
- A. Postural drainage of the chest
- B. Surgical therapy
- C. Trimethoprim and sulfamethoxazole
- D. Intravenous ciprofloxacin (Correct Answer)
- E. Amoxicillin and clavulanic acid
Fluoroquinolone resistance Explanation: ***Intravenous ciprofloxacin***
- The patient's history of **cystic fibrosis** with recurrent respiratory infections and the isolation of an **aerobic, non-lactose fermenting, oxidase-positive, gram-negative bacillus** (consistent with *Pseudomonas aeruginosa*) strongly indicates the need for targeted antibiotic therapy.
- **Ciprofloxacin** is a fluoroquinolone antibiotic with good activity against *Pseudomonas aeruginosa*, and intravenous administration is appropriate for pulmonary exacerbations in CF patients.
- The worsening cough with large volumes of mucoid and foul-smelling sputum indicates a significant **pulmonary exacerbation** due to bacterial infection, necessitating effective antibiotic coverage.
- While **combination therapy** (typically an anti-pseudomonal beta-lactam plus an aminoglycoside or fluoroquinolone) is often preferred for Pseudomonas exacerbations in CF, **ciprofloxacin is the best option among those listed** as it provides reliable Pseudomonas coverage.
*Postural drainage of the chest*
- **Postural drainage** is an important component of airway clearance therapy in patients with cystic fibrosis and bronchiectasis, helping to mobilize secretions.
- While beneficial for symptom management and part of comprehensive CF care, it is not a primary treatment for an acute bacterial exacerbation and does not address the underlying **bacterial infection**.
*Surgical therapy*
- **Surgical therapy**, such as lung transplantation, is considered for end-stage lung disease in cystic fibrosis or for localized complications like severe bronchiectasis or massive hemoptysis refractory to medical management.
- It is not the initial or primary treatment for an acute infectious exacerbation, especially in a patient without indications for emergent surgical intervention.
*Trimethoprim and sulfamethoxazole*
- **Trimethoprim-sulfamethoxazole (TMP/SMX)** is a broad-spectrum antibiotic effective against many gram-positive and gram-negative organisms.
- However, it has **poor activity against Pseudomonas aeruginosa**, particularly the strains commonly found in cystic fibrosis patients, which often demonstrate intrinsic or acquired resistance to TMP/SMX.
- This makes it an inappropriate choice for treating Pseudomonas pulmonary exacerbations in CF.
*Amoxicillin and clavulanic acid*
- **Amoxicillin-clavulanic acid** is effective against many gram-positive bacteria and some gram-negative organisms, including *Haemophilus influenzae* and *Moraxella catarrhalis*.
- However, it has **minimal to no activity against Pseudomonas aeruginosa**, which is a common and highly virulent pathogen in cystic fibrosis patients, making it an unsuitable choice for this specific infection.
Fluoroquinolone resistance US Medical PG Question 8: A 61-year-old woman who recently emigrated from India comes to the physician because of a 2-month history of fever, fatigue, night sweats, and a productive cough. She has had a 5-kg (11-lb) weight loss during this period. She has a history of type 2 diabetes mellitus and poorly controlled asthma. She has had multiple asthma exacerbations in the past year that were treated with glucocorticoids. An x-ray of the chest shows a cavitary lesion of the posterior apical segment of the left upper lobe with consolidation of the surrounding parenchyma. The pathogen identified on sputum culture is found to be resistant to multiple drugs, including streptomycin. Which of the following mechanisms is most likely involved in bacterial resistance to this drug?
- A. Alteration in the sequence of gyrA genes
- B. Upregulation of arabinosyl transferase production
- C. Upregulation of mycolic acid synthesis
- D. Alteration in 30S ribosomal subunit (Correct Answer)
- E. Inhibition of bacterial synthesis of RNA
Fluoroquinolone resistance Explanation: ***Alteration in 30S ribosomal subunit***
- Streptomycin is an **aminoglycoside antibiotic** that acts by binding to the **16S rRNA of the 30S ribosomal subunit**, which interferes with bacterial protein synthesis.
- **Resistance to streptomycin** most commonly arises from mutations in the genes encoding ribosomal proteins (e.g., *rpsL*) or the 16S rRNA that alter the drug's binding site on the 30S ribosomal subunit, preventing its inhibitory effect.
*Alteration in the sequence of gyrA genes*
- Mutations in the *gyrA* gene typically confer resistance to **fluoroquinolone antibiotics**, such as ciprofloxacin and levofloxacin.
- Fluoroquinolones target **DNA gyrase (topoisomerase II)**, which is encoded by *gyrA*, not the ribosomes.
*Upregulation of arabinosyl transferase production*
- **Arabinogalactan**, a major component of the mycobacterial cell wall, is synthesized by **arabinosyl transferases** (e.g., EmbB).
- Resistance to **ethambutol** is often associated with mutations or upregulation of these enzymes, leading to increased synthesis of the arabinogalactan layer.
*Upregulation of mycolic acid synthesis*
- **Mycolic acid** is a crucial component of the mycobacterial cell wall, and its synthesis is inhibited by drugs like **isoniazid**.
- Upregulation of mycolic acid synthesis or mutations in genes related to its production (e.g., *kasA*) can lead to **isoniazid resistance**, but not directly to streptomycin resistance.
*Inhibition of bacterial synthesis of RNA*
- **Rifampin** is an antibiotic that inhibits bacterial RNA synthesis by binding to the **DNA-dependent RNA polymerase**.
- While resistance to rifampin often involves mutations in the *rpoB* gene, this mechanism is specific to rifampin and not streptomycin.
Fluoroquinolone resistance US Medical PG Question 9: A 23-year-old woman presents to your office for a gynecological exam. She says that she has been in good health and has no complaints. She has been in a steady monogamous relationship for the past year. Physical examination was unremarkable. Screening tests are performed and return positive for gonorrhea. You treat her with an intramuscular injection of ceftriaxone and 7 day course of doxycycline. What else is recommended for this case?
- A. Perform an abdominal ultrasonography in order to rule out pelvic inflammatory disease
- B. Recheck her in 1 week for gonorrhea and chlamydia
- C. Treat her partner for gonorrhea and chlamydia (Correct Answer)
- D. Treatment with penicillin G for potential co-infection with syphilis
- E. Inform her that her partner is likely cheating on her
Fluoroquinolone resistance Explanation: ***Treat her partner for gonorrhea and chlamydia***
- **Expedited partner therapy (EPT)** is recommended for all partners of individuals diagnosed with gonorrhea and chlamydia to prevent reinfection and further spread.
- This involves providing medication or a prescription to the patient to take to their partner without prior medical evaluation of the partner.
*Perform an abdominal ultrasonography in order to rule out pelvic inflammatory disease*
- While **pelvic inflammatory disease (PID)** is a potential complication of untreated gonorrhea, the patient is asymptomatic and has no signs on physical exam.
- Imaging is typically reserved for patients with symptoms suggestive of PID, such as pelvic pain, fever, or adnexal tenderness.
*Recheck her in 1 week for gonorrhea and chlamydia*
- A **"test of cure"** (retesting after treatment) is not routinely recommended for uncomplicated urogenital or rectal gonorrhea treated with recommended regimens unless specific concerns exist (e.g., treatment with an alternative regimen, pharyngeal infection).
- Re-testing for infection (specifically for reinfection) is recommended approximately **3 months** after treatment, not 1 week.
*Treatment with penicillin G for potential co-infection with syphilis*
- While syphilis screening is important, there is no indication for empirical treatment with **penicillin G** in this asymptomatic patient without a positive syphilis test result.
- Syphilis co-infection is usually identified through serological testing (e.g., RPR, VDRL) and then treated based on the stage of syphilis.
*Inform her that her partner is likely cheating on her*
- It is inappropriate and unprofessional for a healthcare provider to make assumptions or accusations about a patient's relationship status or partner's fidelity.
- The focus should remain on providing medical care and appropriate disease management, including partner treatment and education about safer sex practices.
Fluoroquinolone resistance US Medical PG Question 10: An investigator studying fungal growth isolates organisms from an infant with diaper rash. The isolate is cultured and exposed to increasing concentrations of nystatin. Selected colonies continue to grow and replicate even at high concentrations of the drug. Which of the following is the most likely explanation for this finding?
- A. Mutation of the β-glucan gene
- B. Inactivation of cytosine permease
- C. Altered binding site of squalene epoxidase
- D. Expression of dysfunctional cytochrome P-450 enzymes
- E. Reduced ergosterol content in cell membrane (Correct Answer)
Fluoroquinolone resistance Explanation: ***Reduced ergosterol content in cell membrane***
- **Nystatin** is a **polyene antifungal** that binds to **ergosterol** in the fungal cell membrane, forming pores and disrupting membrane integrity.
- Reduced ergosterol content means there are fewer binding sites for nystatin, leading to **resistance** and continued fungal growth even at high drug concentrations.
*Mutation of the β-glucan gene*
- **β-glucan** is a component of the fungal cell wall, targeted by **echinocandins**, not nystatin.
- A mutation in this gene would primarily confer resistance to echinocandins, not polyenes like nystatin.
*Inactivation of cytosine permease*
- **Cytosine permease** is involved in the uptake of **flucytosine**, an antimetabolite antifungal.
- Inactivation of this enzyme would primarily lead to resistance against **flucytosine**, not nystatin.
*Altered binding site of squalene epoxidase*
- **Squalene epoxidase** is an enzyme in the ergosterol biosynthesis pathway, targeted by **allylamines** (e.g., terbinafine).
- An altered binding site would confer resistance to allylamines, not nystatin, which directly targets ergosterol.
*Expression of dysfunctional cytochrome P-450 enzymes*
- **Cytochrome P-450 enzymes** (specifically lanosterol 14-α-demethylase) are targeted by **azoles** (e.g., fluconazole, itraconazole).
- Dysfunctional enzymes would primarily lead to resistance against **azoles**, not nystatin which has a different mechanism of action.
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