Non-Bacterial Antimicrobials

Pharmacology — Antivirals, Antifungals and Antiparasitics, NMC MBBS licence examination syllabus (Nepal Medical Council).

Antivirals, antifungals and antiparasitics

The antimicrobials where the drug is closer to being poisonous to you as well.

The antibiotics chapter rests on a comfortable fact: bacteria are structurally different enough from us that a drug can attack them and leave us largely alone. Cell walls, distinct ribosomes, and folate synthesis pathways we do not possess give plenty to aim at.

None of that holds for the organisms in this chapter. Viruses replicate inside our cells using our machinery. Fungi and parasites are eukaryotes, built much as we are. The consequence runs through everything here: fewer selective targets, narrower safety margins, more toxicity, and more monitoring.

🩺 Where this lives: The commonest antimicrobial error in the world is giving an antibiotic for a viral illness, and understanding why it is useless requires knowing what antibiotics actually target. A drug that disrupts bacterial cell wall synthesis has nothing to act on in a virus that has no cell wall and is replicating inside a human cell. The prescription changes nothing for that patient and contributes to resistance that will affect someone else — usually while the clinician feels they have done something helpful under real pressure to act.

💡 A note on drugs and doses. This chapter gives no doses, no treatment durations and almost no named individual agents. Antiviral and antifungal selection is highly indication-specific and changes with resistance and availability, and naming agents in a revision resource invites their use without checking a current source. Take every choice from national guidance. Antibacterials are covered in the Antibiotics chapter, HIV therapy in HIV and Viral Hepatitis, antimalarials in Malaria and Dengue, and TB regimens in the Tuberculosis chapter.

Why selectivity is harder here

This single idea predicts most of what follows. Because there are fewer targets unique to the organism, these drugs interfere with processes our own cells also use — so renal impairment, hepatotoxicity, marrow suppression and electrolyte disturbance are expected rather than surprising. The practical consequence is that monitoring is part of the prescription in a way it usually is not for a short antibacterial course.

WHAT EACH GROUP CAN ACTUALLY BE ATTACKED AT VIRUSES They have almost no metabolism of their own. The exploitable targets are the few VIRUS-SPECIFIC ENZYMES needed for replication, and the steps of entry and release. CONSEQUENCE: antivirals are narrow-spectrum — a drug for one virus family does nothing for another — and they work only while the virus is actively replicating. FUNGI Eukaryotic cells much like ours. The main exploitable difference is ERGOSTEROL in the fungal cell membrane where ours contains cholesterol, plus the fungal cell wall. CONSEQUENCE: antifungals aimed at membranes affect ours to some degree, which is why systemic agents carry significant toxicity. PARASITES Also eukaryotes, and often large multicellular organisms with complex life cycles. CONSEQUENCE: drugs may act only on particular life-cycle stages, which is why some regimens are repeated, and why killing the parasite can itself cause harm through inflammation. THE GENERAL RULE: expect more toxicity, expect monitoring, and expect the drug choice to depend far more precisely on which organism is involved than it does with antibacterials.

Antivirals

💡 Exam angle: two properties are examined repeatedly. Timing — most antivirals act only during active replication, so the window from symptom onset is short and starting late achieves little. And suppression versus cure — herpes viruses remain latent for life, HIV requires lifelong therapy, and hepatitis B is suppressed rather than eradicated. Hepatitis C is the exception: modern direct-acting antiviral therapy is curative, which is why finding it is now worthwhile in a way it was not a decade ago.

Antifungals

Two safety points carry the section. Azoles cause many drug interactions through hepatic enzyme inhibition — which links directly to the prescribing safety chapter, where an enzyme inhibitor added to warfarin causes bleeding at an unchanged dose. And amphotericin is nephrotoxic and causes electrolyte loss, so renal function and potassium are monitored throughout. Note also that invasive fungal infection usually implies an immunocompromised host — finding it should prompt the question of why, including HIV testing.

Antiparasitics

TWO POINTS WORTH KNOWING PRECISELY DEWORMING AND REINFECTION Soil-transmitted helminths cause anaemia, malnutrition and impaired growth and learning in children, and mass deworming programmes are cheap and effective. But the drug treats the child, not the environment. Without improved sanitation, reinfection follows — which is why deworming sits alongside water and sanitation programmes rather than replacing them. See the environmental health and enteric infection chapters. KILLING THE PARASITE CAN CAUSE HARM In NEUROCYSTICERCOSIS, dying cysts provoke an inflammatory response in the brain, which can worsen seizures and raise intracranial pressure. Treatment is therefore a specialist decision, given with anti-inflammatory cover and anticonvulsant management — never an empirical prescription. A similar principle appears elsewhere: in some parasitic infections the host response to dying organisms is the dangerous part. AND CONSIDER THE HOST: unusual or severe parasitic disease should prompt the question of immunosuppression, as with fungal infection.

When none of them is indicated

💡 Exam angle: the expected answer to a stem describing a self-limiting viral illness with a patient requesting antibiotics is not simply "refuse". It is to explain the expected course, give clear safety-netting advice about what would change the assessment, and document the reasoning. Framing it as a decision that has been explained rather than a request that has been denied is both better medicine and, in an examination, the higher-scoring answer.

Clinical reasoning: four presentations

🔍 Case 1 — antibiotics for a cold

PresentationA man with three days of sore throat, cough and coryza asks for antibiotics, saying they always help. He is systemically well with no red flags. An antibiotic is prescribed to save time and avoid an argument.

ProblemNo benefit, real cost.

ReasoningAntibacterials target structures viruses do not possess, so the prescription cannot help. It exposes him to adverse effects, reinforces the expectation for next time, and selects resistance affecting others.

AnswerExplain the expected course and why an antibiotic will not shorten it, give specific safety-netting advice about what would change the assessment, and document it. This takes longer than prescribing and is the correct answer.

🔍 Case 2 — bleeding after an antifungal

PresentationA man stable on warfarin for years is started on an oral azole antifungal. Within days he develops bruising and a markedly raised INR. His warfarin dose is unchanged.

MechanismEnzyme inhibition.

ReasoningAzoles inhibit hepatic enzymes, slowing warfarin metabolism so its level rises at an unchanged dose. Warfarin has a narrow therapeutic index, which is exactly the group in which interactions matter — see the prescribing safety chapter.

AnswerManage the raised INR and bleeding per protocol, review the antifungal, and check interactions before adding any drug to warfarin.

🔍 Case 3 — creatinine rising on treatment

PresentationA patient receiving amphotericin for invasive fungal infection has a rising creatinine and a falling potassium. The infusion continues unchanged and electrolytes are checked twice weekly.

IssuePredictable toxicity, inadequately monitored.

ReasoningAmphotericin is nephrotoxic and causes renal potassium and magnesium wasting. These are expected effects requiring close monitoring and active replacement, not incidental findings.

AnswerMonitor renal function and electrolytes frequently per protocol, replace potassium and magnesium, and discuss formulation or agent with the specialist team. Also ask why this patient has invasive fungal disease.

🔍 Case 4 — treating the cyst

PresentationA patient with seizures is found to have a cerebral cyst suggestive of neurocysticercosis. Antiparasitic treatment is started empirically in the outpatient clinic without further discussion.

RiskThe host response to dying cysts.

ReasoningKilling the parasite provokes inflammation around the lesion, which can worsen seizures and raise intracranial pressure. Treatment requires anti-inflammatory cover and anticonvulsant management.

AnswerRefer for specialist assessment rather than treating empirically. Sometimes the parasite is not the most urgent problem — the reaction to killing it is.

Commonly confused

Confusion	The distinction	Why it matters
Antibacterial vs antiviral targets	Viruses have no cell wall or ribosomes of their own	Antibiotics cannot help a viral illness.
Selectivity in bacteria vs fungi	Fungi are eukaryotes like us	Expect more toxicity and monitoring.
Suppression vs cure	Most antivirals suppress	Hepatitis C is the curable exception.
Early vs late antiviral	They act during active replication	Started late they achieve little.
Azole vs other antifungals	Azoles inhibit hepatic enzymes	Major interaction risk with warfarin.
Amphotericin efficacy vs toxicity	Nephrotoxic with electrolyte loss	Monitoring is part of the prescription.
Deworming vs sanitation	The drug treats the child, not the soil	Reinfection follows without both.
Killing the parasite vs the host response	Dying cysts provoke inflammation	Treatment can worsen symptoms.

Rapid revision

MUST-KNOW FACTS 1. Bacteria have structures we lack — so antibacterials are selective. 2. VIRUSES replicate inside our cells using our machinery. 3. Antiviral targets are the few VIRUS-SPECIFIC enzymes. 4. FUNGI and PARASITES are EUKARYOTES, built much as we are. 5. The main fungal target is ERGOSTEROL in the cell membrane. 6. LESS SELECTIVITY MEANS MORE TOXICITY AND MORE MONITORING. 7. Expect renal, hepatic and marrow effects. 8. Antivirals are NARROW-SPECTRUM — one family only. 9. Most work only during ACTIVE REPLICATION — start early. 10. Most SUPPRESS rather than eradicate. 11. Herpes viruses remain LATENT for life. 12. HIV requires LIFELONG combination therapy. 13. HIV MONOTHERAPY selects resistance rapidly. 14. HEPATITIS C IS THE EXCEPTION — modern therapy is CURATIVE. 15. AZOLES inhibit hepatic enzymes — MANY INTERACTIONS. 16. An azole added to warfarin raises the INR at an unchanged dose. 17. Azoles are also hepatotoxic; some are avoided in pregnancy. 18. AMPHOTERICIN is NEPHROTOXIC with electrolyte loss. 19. Monitor renal function, potassium and magnesium throughout. 20. TOPICAL agents suffice for most superficial fungal infection. 21. INVASIVE fungal disease implies an IMMUNOCOMPROMISED host — ask why. 22. Soil-transmitted helminths cause ANAEMIA and impaired growth. 23. Mass deworming is cheap and effective. 24. But REINFECTION follows without improved SANITATION. 25. NEUROCYSTICERCOSIS: killing cysts provokes INFLAMMATION. 26. It can worsen seizures and raise intracranial pressure. 27. Treatment is a specialist decision, never empirical. 28. THE COMMONEST ERROR IS AN ANTIBIOTIC FOR A VIRAL ILLNESS. 29. It cannot help and it selects resistance. 30. Explain the course and safety-net rather than simply refusing. 31. Take every agent, dose and duration from national guidance.

💡 Exam angle: one idea unlocks this chapter — the closer an organism is to us biologically, the more toxic the drug that kills it. From that, the monitoring requirements, the narrow spectra and the interaction risks all follow without memorisation.

Syllabus points

Why bacteria are easy targets
Why viruses offer few targets
Fungi and parasites as eukaryotes
Less selectivity, more toxicity
Why antivirals are narrow-spectrum
Timing and active replication
Suppression versus cure
Hepatitis C as the curable exception
Azoles and enzyme inhibition
Amphotericin nephrotoxicity
Invasive fungal disease implies immunocompromise
Deworming and reinfection
Why killing a parasite can harm
Declining an antibiotic well

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