Pharmacology of Antibacterial Drugs

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Questions and Answers

A patient with a severe bacterial infection is prescribed an antibiotic that inhibits cell wall synthesis by binding to the D-Ala-D-Ala terminus of peptidoglycan precursors. Which of the following antibiotics is most likely being used?

  • Vancomycin (correct)
  • Azithromycin
  • Gentamicin
  • Ciprofloxacin

A researcher is studying a new antibacterial drug that inhibits bacterial DNA synthesis. Which of the following mechanisms of action would NOT be consistent with this type of drug?

  • Binding to the 30S ribosomal subunit (correct)
  • Inhibition of topoisomerase II (DNA gyrase)
  • Inhibition of dihydrofolate reductase
  • Inhibition of dihydropteroate synthase

A patient develops Clostridioides difficile infection following antibiotic treatment. Which of the following mechanisms is the MOST likely cause of this infection?

  • Disruption of the normal gut microbiota (correct)
  • Decreased drug accumulation
  • Enzymatic inactivation of the antibiotic
  • Alteration of the drug target

A virologist is investigating a novel antiviral drug that prevents viral entry into the host cell by targeting host cell receptors. Which of the following drugs utilizes a similar mechanism of action?

<p>Maraviroc (A)</p> Signup and view all the answers

An HIV-positive patient is prescribed a drug that inhibits viral integrase. Which of the following enzymes is directly affected by this drug?

<p>Integrase (C)</p> Signup and view all the answers

A patient with influenza is prescribed a neuraminidase inhibitor. What is the primary mechanism by which this drug reduces the spread of the virus?

<p>Preventing the release of viruses from infected cells (D)</p> Signup and view all the answers

A patient with a systemic fungal infection is treated with a drug that binds to ergosterol in the fungal cell membrane, forming pores that disrupt membrane integrity. Which of the following antifungal drugs is most likely being used?

<p>Amphotericin B (A)</p> Signup and view all the answers

A researcher is developing a new antifungal drug that specifically targets the synthesis of beta-1,3-glucan. Which class of antifungal drugs is the researcher most likely studying?

<p>Echinocandins (B)</p> Signup and view all the answers

A patient with a fungal infection is prescribed flucytosine. What is the mechanism by which this drug inhibits fungal growth?

<p>Inhibiting fungal DNA and RNA synthesis (D)</p> Signup and view all the answers

A patient with malaria is treated with chloroquine. What is the primary mechanism by which chloroquine affects the malaria parasite?

<p>Inhibiting heme polymerization (B)</p> Signup and view all the answers

A veterinarian is treating a dog infected with parasitic worms and prescribes ivermectin. How does ivermectin work to eliminate the worms?

<p>Enhancing glutamate-gated chloride channels (C)</p> Signup and view all the answers

A patient is diagnosed with a Giardia infection and prescribed metronidazole. What is the mechanism by which metronidazole eradicates the protozoa?

<p>Damaging protozoal DNA (D)</p> Signup and view all the answers

Which of the following mechanisms of antibacterial resistance involves the production of enzymes that chemically modify the antibiotic, rendering it inactive?

<p>Enzymatic inactivation of the drug (D)</p> Signup and view all the answers

A patient undergoing antiviral therapy develops resistance to a non-nucleoside reverse transcriptase inhibitor (NNRTI). What is the most likely mechanism contributing to this resistance?

<p>Mutations in viral genes encoding reverse transcriptase (B)</p> Signup and view all the answers

A transplant patient on long-term antifungal medication begins to show signs of nephrotoxicity. Which class of antifungals is most likely contributing to this adverse effect?

<p>Polyenes (D)</p> Signup and view all the answers

Which of the following scenarios would MOST likely lead to the selection of antibiotic-resistant bacteria within a patient?

<p>Prescribing antibiotics for a suspected viral infection (B)</p> Signup and view all the answers

A researcher is exploring a new target for antiviral drugs that aims to prevent the cleavage of viral polyproteins into functional components. Which viral enzyme would this drug MOST likely inhibit?

<p>Protease (A)</p> Signup and view all the answers

A patient on antifungal therapy exhibits increased levels of liver enzymes and complains of abdominal pain. Which antifungal is mostly likely contributing to these symptoms?

<p>Itraconazole (A)</p> Signup and view all the answers

Which of the following antiparasitic drugs is thought to generate free radicals that damage the target parasite's proteins as its primary mechanism of action?

<p>Artemisinins (A)</p> Signup and view all the answers

A patient is prescribed doxycycline for a bacterial infection. Which cellular process is MOST directly inhibited by this medication?

<p>Protein synthesis (A)</p> Signup and view all the answers

Which antibiotic is LEAST likely to be effective against a bacterial strain that has developed resistance through the production of beta-lactamase?

<p>Penicillin (B)</p> Signup and view all the answers

A patient who is HIV positive and has been responding well to antiretroviral therapy suddenly experiences a resurgence of viral load. Resistance testing reveals a mutation in the gene encoding reverse transcriptase. Which class of drugs is MOST likely to have reduced efficacy?

<p>Non-nucleoside reverse transcriptase inhibitors (C)</p> Signup and view all the answers

Which of the following antifungal drug resistance mechanisms would be MOST effective against azole antifungals?

<p>Increased efflux of the drug (A)</p> Signup and view all the answers

A patient being treated for a parasitic worm infection shows signs of neurotoxicity, including seizures. Which of the following antihelminthic drugs, known for its potential neurotoxic effects due to its mechanism of action on chloride channels, might be the cause?

<p>Ivermectin (D)</p> Signup and view all the answers

A microbiologist discovers a bacterial strain that is resistant to multiple antibiotics. Genetic analysis reveals the presence of an efflux pump that expels a wide range of structurally unrelated antibiotics. Which resistance mechanism is MOST likely at play?

<p>Multidrug resistance (B)</p> Signup and view all the answers

Which of the following mechanisms of action is NOT typically associated with antibacterial drugs that target protein synthesis?

<p>Inhibiting peptidoglycan cross-linking (A)</p> Signup and view all the answers

A patient with HSV-1 is prescribed valacyclovir. Which of the following best describes the mechanism of action of this drug?

<p>Inhibits viral DNA polymerase (C)</p> Signup and view all the answers

Which of the following is likely to be the MOST significant consequence of widespread use of broad-spectrum antibiotics?

<p>Disruption of normal microbiota and increased risk of secondary infections (A)</p> Signup and view all the answers

An investigational drug is found to selectively inhibit the synthesis of squalene epoxidase in fungi. Which of the following classes of antifungals has a similar mechanism of action?

<p>Allylamines (B)</p> Signup and view all the answers

Why is it important to consider the potential for disrupting the normal gut microbiota when prescribing antibacterial drugs?

<p>To reduce the risk of Clostridioides difficile infection (D)</p> Signup and view all the answers

A researcher is studying a potential new antimalarial drug that targets the parasite's ability to detoxify heme. Which of the following existing drugs works through a similar mechanism?

<p>Chloroquine (B)</p> Signup and view all the answers

A patient presents with a systemic fungal infection and the physician is considering the use of amphotericin B. What is the MOST critical potential adverse effect that the physician must closely monitor during the course of treatment?

<p>Nephrotoxicity (C)</p> Signup and view all the answers

A patient is diagnosed with a Trichomonas infection. Which of the following drugs is MOST appropriate for treating this condition?

<p>Metronidazole (A)</p> Signup and view all the answers

A bacterial strain exhibits resistance to aminoglycosides. Which of the following mechanisms would MOST directly account for this resistance?

<p>Alteration of the 30S ribosomal subunit (A)</p> Signup and view all the answers

Which of the following steps in the viral life cycle is targeted by fusion inhibitors such as enfuvirtide?

<p>Fusion of the viral and cellular membranes to enter the host cell (A)</p> Signup and view all the answers

Why are interferons sometimes used in the treatment of viral infections like hepatitis B and C?

<p>To stimulate the host's immune system to fight the virus (C)</p> Signup and view all the answers

A patient is being treated with mebendazole for a helminth infection. What is the MOST likely mechanism of action of this drug?

<p>Inhibiting microtubule polymerization in the worm's cells (B)</p> Signup and view all the answers

A bacterium has developed resistance to sulfonamides. Which mechanism is MOST likely responsible for this resistance?

<p>Mutation of dihydropteroate synthase (D)</p> Signup and view all the answers

A researcher is investigating a novel antibacterial compound that demonstrates selective toxicity towards Gram-negative bacteria. The compound disrupts the function of lipopolysaccharide (LPS) transport proteins, leading to LPS accumulation within the bacterial cytoplasm. Which of the following mechanisms of action would MOST likely explain the selective toxicity of this compound?

<p>Impairment of the LPS transport system, disrupting outer membrane assembly. (D)</p> Signup and view all the answers

A researcher is developing a new antiviral drug to combat a rapidly mutating RNA virus. The drug is designed to target a highly conserved region within the viral RNA-dependent RNA polymerase (RdRp) that is essential for its function. However, during in vitro testing, the virus rapidly develops resistance to the drug. Which of the following mechanisms is MOST likely responsible for the rapid development of resistance?

<p>Mutation within the targeted conserved region of RdRp that does not abolish its function. (B)</p> Signup and view all the answers

A patient with a severe systemic fungal infection is being treated with a combination of amphotericin B and flucytosine. While amphotericin B is known to disrupt fungal cell membrane integrity, the addition of flucytosine aims to enhance the overall efficacy of the treatment. Which of the following mechanisms explains the MOST likely synergistic effect of this drug combination?

<p>Amphotericin B increases the permeability of the fungal cell membrane, facilitating the entry of flucytosine. (B)</p> Signup and view all the answers

An immunocompromised patient is diagnosed with a disseminated parasitic infection caused by an intracellular protozoan. The chosen treatment regimen involves a combination of antiparasitic drugs that target different stages of the parasite's life cycle. Which of the following strategies would MOST likely lead to a synergistic effect, maximizing parasite eradication while minimizing host toxicity?

<p>Using a drug that prevents parasite entry into host cells combined with a drug that inhibits parasite replication within host cells. (D)</p> Signup and view all the answers

A research team is investigating a novel strategy to combat antimicrobial resistance by developing a compound that inhibits bacterial efflux pumps. The hypothesis is that by blocking these pumps, intracellular concentrations of antibiotics will increase, restoring their efficacy. Which of the following mechanisms would MOST likely contribute to the success of this strategy in overcoming antibiotic resistance?

<p>Reduced export of antibiotics from the bacterial cell, leading to increased intracellular concentrations. (D)</p> Signup and view all the answers

Flashcards

Pharmacology of Infectious Diseases

Drugs targeting and eradicating or controlling pathogenic microorganisms within a host.

Antibacterial Drugs

Drugs used to treat bacterial infections.

Beta-Lactam Antibiotics

Inhibit bacterial cell wall synthesis by binding to penicillin-binding proteins (PBPs).

Glycopeptide Antibiotics

Inhibit cell wall synthesis by binding to the D-Ala-D-Ala terminus of peptidoglycan precursors.

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Aminoglycosides

Inhibit bacterial protein synthesis by binding to the 30S ribosomal subunit, causing misreading of mRNA.

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Tetracyclines

Inhibit protein synthesis by binding to the 30S ribosomal subunit and preventing tRNA attachment.

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Macrolides

Inhibit protein synthesis by binding to the 23S rRNA of the 50S ribosomal subunit, blocking translocation.

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Fluoroquinolones

Inhibit bacterial DNA synthesis by targeting topoisomerase II (DNA gyrase) and topoisomerase IV.

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Sulfonamides and Trimethoprim

Inhibit folate synthesis, essential for bacterial DNA synthesis.

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Antibacterial Resistance

Mechanisms include enzymatic inactivation, target alteration, decreased accumulation and bypass of the metabolic pathway.

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Adverse Effects of Antibacterials

Include nausea, diarrhea, allergic reactions, and potential for Clostridioides difficile infection.

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Antiviral Drugs

Drugs used to treat viral infections by targeting specific steps in the viral replication cycle.

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NRTIs and NtRTIs

Inhibit reverse transcriptase, acting as chain terminators when incorporated into viral DNA.

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NNRTIs

Inhibit reverse transcriptase by binding to a different site, causing a conformational change and disrupting its activity.

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Protease Inhibitors (PIs)

Inhibit viral protease, needed to cleave viral polyproteins into functional proteins.

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Integrase Inhibitors

Inhibit viral integrase, which integrates viral DNA into the host cell's DNA.

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Fusion Inhibitors

Prevent viral entry into the host cell by blocking the fusion of the viral and cellular membranes.

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Neuraminidase Inhibitors

Inhibit neuraminidase, allowing influenza viruses to be released from infected cells.

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Viral Entry Inhibitors

Block viral entry into the host cell by targeting host cell receptors.

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Acyclovir and Derivatives

Inhibit viral DNA polymerase in herpesviruses.

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Interferons

Cytokines with antiviral, immunomodulatory, and antiproliferative effects.

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Antiviral Resistance

Mutations in viral genes encoding drug targets.

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Adverse Effects of Antivirals

Include gastrointestinal disturbances, neurological effects, and hematological abnormalities.

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Antifungal Drugs

Drugs used to treat fungal infections.

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Azoles

Inhibit ergosterol synthesis by inhibiting lanosterol 14-alpha demethylase.

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Polyenes

Bind to ergosterol, forming pores that disrupt membrane integrity.

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Allylamines

Inhibit squalene epoxidase, involved in ergosterol synthesis.

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Echinocandins

Inhibit synthesis of beta-1,3-glucan, a component of the fungal cell wall.

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Griseofulvin

Disrupts fungal mitosis by interacting with microtubules.

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Flucytosine

Pyrimidine analog that inhibits fungal DNA and RNA synthesis.

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Antifungal Resistance

Alterations in drug target, increased efflux, and bypass of metabolic pathway.

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Adverse Effects of Antifungals

Include gastrointestinal disturbances, liver toxicity, and nephrotoxicity.

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Antiparasitic Drugs

Drugs to treat parasitic infections caused by protozoa, helminths, or ectoparasites.

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Antimalarial Drugs

Drugs used to treat malaria.

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Chloroquine

Inhibits heme polymerization in the parasite's food vacuole.

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Artemisinins

Generate free radicals that damage parasite proteins.

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Antihelminthic Drugs

Drugs used to treat infections caused by parasitic worms.

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Mebendazole and Albendazole

Inhibit microtubule polymerization in the worm's cells.

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Ivermectin

Paralyzes worms by enhancing the effect of glutamate-gated chloride channels.

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Antiprotozoal Drugs

Drugs used to treat infections caused by protozoa.

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Metronidazole and Tinidazole

Reduced to toxic products that damage protozoal DNA.

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Antiparasitic Resistance

Alterations in drug target, decreased drug accumulation, and increased drug metabolism.

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Adverse Effects of Antiparasitics

Include gastrointestinal disturbances, neurological effects, and skin reactions.

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Study Notes

  • The pharmacology of infectious diseases involves the use of drugs to target and eradicate or control pathogenic microorganisms like bacteria, viruses, fungi, and parasites within a host organism.

Antibacterial Drugs

  • Antibacterial drugs, also known as antibiotics, are used to treat bacterial infections.
  • Antibacterial drugs are classified based on their mechanism of action; this includes the inhibition of cell wall synthesis, protein synthesis, nucleic acid synthesis, or other metabolic pathways.
  • Beta-lactam antibiotics like penicillins, cephalosporins, and carbapenems inhibit bacterial cell wall synthesis.
  • These antibiotics bind to penicillin-binding proteins (PBPs), preventing peptidoglycan cross-linking.
  • Glycopeptide antibiotics like vancomycin also inhibit cell wall synthesis.
  • Glycopeptide antibioitics bind to the D-Ala-D-Ala terminus of peptidoglycan precursors, preventing their incorporation into the cell wall.
  • Aminoglycosides like gentamicin and tobramycin inhibit bacterial protein synthesis by binding to the 30S ribosomal subunit, causing misreading of mRNA.
  • Tetracyclines like doxycycline and minocycline inhibit protein synthesis by binding to the 30S ribosomal subunit, preventing tRNA attachment.
  • Macrolides like erythromycin and azithromycin inhibit protein synthesis by binding to the 23S rRNA of the 50S ribosomal subunit and blocking translocation.
  • Fluoroquinolones like ciprofloxacin and levofloxacin inhibit bacterial DNA synthesis by targeting topoisomerase II (DNA gyrase) and topoisomerase IV.
  • Sulfonamides and trimethoprim inhibit folate synthesis, essential for bacterial DNA synthesis.
  • Sulfonamides inhibit dihydropteroate synthase, while trimethoprim inhibits dihydrofolate reductase.
  • Resistance to antibacterial drugs occurs through various mechanisms, including enzymatic inactivation of the drug, alteration of the drug target, decreased drug accumulation, and bypass of the inhibited metabolic pathway.
  • Common adverse effects of antibacterial drugs include gastrointestinal disturbances, allergic reactions, and the potential for Clostridioides difficile infection due to disruption of the normal gut microbiota.

Antiviral Drugs

  • Antiviral drugs treat viral infections by targeting specific steps in the viral replication cycle.
  • Nucleoside and nucleotide reverse transcriptase inhibitors (NRTIs and NtRTIs) like zidovudine and tenofovir inhibit reverse transcriptase.
  • Reverse transcriptase is an enzyme essential for retroviruses like HIV to replicate, and NRTIs/NtRTIs act as chain terminators when incorporated into the viral DNA.
  • Non-nucleoside reverse transcriptase inhibitors (NNRTIs) like efavirenz and nevirapine also inhibit reverse transcriptase.
  • NNRTIs bind to a different site on the enzyme, causing a conformational change that disrupts its activity.
  • Protease inhibitors (PIs) like lopinavir and ritonavir inhibit viral protease.
  • Viral protease is an enzyme needed to cleave viral polyproteins into functional proteins.
  • Integrase inhibitors like raltegravir and dolutegravir inhibit viral integrase.
  • Viral integrase is an enzyme that integrates viral DNA into the host cell's DNA.
  • Fusion inhibitors like enfuvirtide prevent viral entry into the host cell by blocking the fusion of the viral and cellular membranes.
  • Neuraminidase inhibitors like oseltamivir and zanamivir inhibit neuraminidase, an enzyme that allows influenza viruses to be released from infected cells.
  • Viral entry inhibitors like maraviroc block viral entry into the host cell by targeting host cell receptors.
  • Acyclovir and its derivatives like valacyclovir and famciclovir inhibit viral DNA polymerase in herpesviruses.
  • Interferons are cytokines that have antiviral, immunomodulatory, and antiproliferative effects.
  • Interferons treat certain viral infections, such as hepatitis B and C.
  • Resistance to antiviral drugs occurs through mutations in viral genes that encode drug targets.
  • Common adverse effects of antiviral drugs vary depending on the specific drug but can include gastrointestinal disturbances, neurological effects, and hematological abnormalities.

Antifungal Drugs

  • Antifungal drugs treat fungal infections, which can be superficial or systemic.
  • Azoles like fluconazole, itraconazole, and voriconazole inhibit the synthesis of ergosterol, a crucial component of the fungal cell membrane.
  • Azoles inhibit the enzyme lanosterol 14-alpha demethylase.
  • Polyenes like amphotericin B and nystatin bind to ergosterol in the fungal cell membrane, forming pores that disrupt membrane integrity and cause cell death.
  • Allylamines like terbinafine inhibit squalene epoxidase, an enzyme involved in ergosterol synthesis.
  • Echinocandins like caspofungin and micafungin inhibit the synthesis of beta-1,3-glucan, a component of the fungal cell wall.
  • Griseofulvin disrupts fungal mitosis by interacting with microtubules.
  • Flucytosine is a pyrimidine analog, once converted to 5-fluorouracil within the fungal cell, inhibits fungal DNA and RNA synthesis.
  • Resistance to antifungal drugs occurs through various mechanisms, including alterations in the drug target, increased efflux of the drug, and bypass of the inhibited metabolic pathway.
  • Common adverse effects of antifungal drugs include gastrointestinal disturbances, liver toxicity, and nephrotoxicity, particularly with amphotericin B.

Antiparasitic Drugs

  • Antiparasitic drugs treat parasitic infections caused by protozoa, helminths, or ectoparasites.
  • Antimalarial drugs like chloroquine, quinine, and artemisinins treat malaria, a parasitic disease caused by Plasmodium species.
  • Chloroquine inhibits heme polymerization in the parasite's food vacuole, leading to the accumulation of toxic heme.
  • Artemisinins are thought to generate free radicals that damage parasite proteins.
  • Antihelminthic drugs like mebendazole, albendazole, and ivermectin treat infections caused by parasitic worms.
  • Mebendazole and albendazole inhibit microtubule polymerization in the worm's cells, disrupting their function.
  • Ivermectin paralyzes worms by enhancing the effect of glutamate-gated chloride channels.
  • Antiprotozoal drugs like metronidazole and tinidazole treat infections caused by protozoa, such as Giardia and Trichomonas.
  • Metronidazole and tinidazole are reduced to toxic products that damage protozoal DNA.
  • Resistance to antiparasitic drugs can occur through various mechanisms, including alterations in the drug target, decreased drug accumulation, and increased drug metabolism.
  • Common adverse effects of antiparasitic drugs vary depending on the specific drug but can include gastrointestinal disturbances, neurological effects, and skin reactions.

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