Chapter 38 — Antiparasitic Drugs — Module 4 — Ectoparasiticides and Special Populations
1. Permethrin is the first-line topical agent for scabies and head lice. Permethrin belongs to a class of insecticides called pyrethroids. By what mechanism does permethrin kill the parasite?
A) It inhibits acetylcholinesterase, the enzyme that breaks down the neurotransmitter acetylcholine, causing acetylcholine to accumulate at nerve junctions
B) It binds to voltage-gated sodium channels in the parasite's nerve membranes and prolongs their open state, causing repetitive nerve firing, paralysis, and death
C) It opens glutamate-gated chloride channels (an ion channel found only in invertebrates), causing nerve cell inhibition and paralysis
D) It physically blocks the breathing pores (spiracles) of the parasite, causing death by suffocation
E) It blocks GABA-A receptors (the receptor for the main inhibitory neurotransmitter), causing uncontrolled excitation
ANSWER: B
Rationale:
Permethrin and the other pyrethroids act on voltage-gated sodium channels in the axon membrane of the parasite. Normally these channels open for only 1 to 2 milliseconds during a nerve impulse and then rapidly close (inactivate). Permethrin binding prevents that inactivation, so sodium continues to flow inward, producing repetitive firing, hyperexcitation, paralysis, and death of the mite or louse. This sodium-channel target is also the basis for the safety margin in humans, because mammals metabolize pyrethroids rapidly and warm body temperature speeds channel recovery.
Option A: Option A is incorrect: acetylcholinesterase inhibition is the mechanism of malathion (an organophosphate), not permethrin.
Option C: Option C is incorrect: opening glutamate-gated chloride channels is the mechanism of ivermectin, not permethrin.
Option D: Option D is incorrect: physical suffocation by blocking spiracles is the mechanism of benzyl alcohol, not permethrin.
Option E: Option E is incorrect: GABA-A receptor blockade describes lindane, not permethrin; in fact permethrin does not act at GABA receptors at all.
2. A healthy adult is diagnosed with common scabies (infestation by the mite Sarcoptes scabiei). Which agent is the standard first-line treatment?
A) Oral metronidazole tablets taken for 7 days
B) Lindane 1% lotion applied to the whole body
C) Oral albendazole 400 mg as a single dose
D) Permethrin 5% cream applied from the neck down, left on 8 to 14 hours, then washed off and repeated in 1 week
E) Benznidazole 5 mg/kg/day taken for 60 days
ANSWER: D
Rationale:
Permethrin 5% cream is the first-line treatment for common scabies in adults and children above 2 months of age in most countries. It is applied from the neck down (including skin folds, under the fingernails, and between the toes), left on for 8 to 14 hours, washed off, and the full application is repeated in 1 week to kill mites that hatch from eggs after the first application, because permethrin is not reliably ovicidal. Two correctly applied treatments cure more than 90 percent of immunocompetent patients.
Option A: Option A is incorrect: metronidazole treats protozoal and anaerobic bacterial infections, not the scabies mite.
Option B: Option B is incorrect: lindane is a second- or third-line agent that has been largely abandoned and banned in many countries because of central nervous system (CNS) neurotoxicity; it is not first-line.
Option C: Option C is incorrect: albendazole treats helminth (worm) infections, not the scabies mite.
Option E: Option E is incorrect: benznidazole treats Chagas disease (American trypanosomiasis), not scabies.
3. Oral ivermectin is a useful alternative to topical permethrin for scabies, especially in nursing-home outbreaks or when a patient cannot reliably apply a cream. What is the standard oral ivermectin regimen for scabies?
A) 200 micrograms per kilogram as a single oral dose, repeated in 1 to 2 weeks
B) 50 micrograms per kilogram once, with no repeat dose needed
C) 1 gram per kilogram daily for 10 consecutive days
D) A single 2-gram dose with no weight-based adjustment
E) 200 micrograms per kilogram once daily for 30 days
ANSWER: A
Rationale:
The standard oral ivermectin regimen for common scabies is 200 micrograms per kilogram given as a single oral dose and then repeated in 1 to 2 weeks. The second dose is needed because ivermectin does not reliably kill eggs, so it must catch mites that hatch after the first dose. Two-dose ivermectin achieves cure rates comparable to two applications of permethrin 5% cream in head-to-head trials, and taking it with food increases absorption roughly 2.5-fold.
Option B: Option B is incorrect: 50 micrograms per kilogram is below the effective dose, and a single dose without a repeat does not eradicate newly hatched mites.
Option C: Option C is incorrect: 1 gram per kilogram is roughly 5,000 times the correct dose and would be grossly toxic; ivermectin is dosed in micrograms, not grams, per kilogram.
Option D: Option D is incorrect: ivermectin is dosed by body weight, not as a fixed 2-gram dose, and the dose is in micrograms per kilogram.
Option E: Option E is incorrect: ivermectin for scabies is not given daily for a month; it is a single weight-based dose repeated once after 1 to 2 weeks.
4. Crusted scabies (also called Norwegian scabies) is a severe form in which the mite burden can reach the millions rather than the 10 to 15 mites of typical scabies. Which type of patient is most likely to develop crusted scabies?
A) A healthy young adult athlete with no medical problems
B) A child with a simple, recently acquired head lice infestation
C) A patient who is immunocompromised or neurologically impaired, such as someone with advanced HIV infection, an organ transplant recipient, or a person with dementia
D) A pregnant woman in her second trimester with otherwise normal immunity
E) A patient with seasonal allergic rhinitis taking antihistamines
ANSWER: C
Rationale:
Crusted scabies develops in patients whose normal defenses against the mite are impaired. This includes immunocompromised patients (advanced human immunodeficiency virus (HIV) infection, organ transplant recipients, hematologic malignancy), neurologically impaired patients (dementia, Down syndrome, spinal cord injury with sensory loss, so the patient does not feel the itch and does not scratch off mites), and the extremely debilitated. The failure of the normal itch-and-scratch response and the failure of cell-mediated immunity allow the mite population to explode, producing thick hyperkeratotic crusts teeming with mites.
Option A: Option A is incorrect: a healthy person with intact immunity and a normal itch response mounts the defenses that keep the mite burden low, so crusted scabies is not expected.
Option B: Option B is incorrect: head lice are a separate parasite (Pediculus), not Sarcoptes scabiei, and ordinary lice infestation does not produce crusted scabies.
Option D: Option D is incorrect: normal pregnancy does not by itself cause the profound immune impairment required for crusted scabies.
Option E: Option E is incorrect: allergic rhinitis and ordinary antihistamine use do not impair the immune or neurologic function in the way crusted scabies requires.
5. Benzyl benzoate 25% lotion is an older scabicide. In what clinical situation is it most commonly chosen today?
A) As the preferred agent for crusted scabies, used alone without any other drug
B) As the single safest choice for scabies during the first trimester of pregnancy
C) As the agent of choice specifically because it causes no skin irritation
D) As the first-line agent in wealthy countries with full access to newer drugs
E) As a low-cost, widely available alternative in resource-limited settings where it is cheaper and easier to obtain than permethrin
ANSWER: E
Rationale:
Benzyl benzoate is used mainly in resource-limited settings (much of sub-Saharan Africa and parts of Asia) because it is inexpensive and widely available where permethrin may not be. It is applied from the neck down for 24 hours, washed off, and reapplied the next day, with the course repeated after a week. It works by disrupting octopamine receptor signaling, an invertebrate-specific target.
Option A: Option A is incorrect: crusted scabies requires combination therapy (oral ivermectin plus topical permethrin plus a keratolytic); no single topical agent, including benzyl benzoate, is adequate alone.
Option B: Option B is incorrect: benzyl benzoate's pregnancy safety profile is not well established, and permethrin — not benzyl benzoate — is the preferred scabicide in pregnancy; benzyl benzoate is not the agent specifically recommended for this setting.
Option C: Option C is incorrect: benzyl benzoate is in fact more irritating than permethrin and causes a burning sensation on application, which can reduce compliance.
Option D: Option D is incorrect: in well-resourced settings permethrin (or oral ivermectin) is preferred; benzyl benzoate is chosen mainly where cost and availability drive the decision.
6. A patient is treated for scabies with a single application of permethrin 5% cream. Why is a second application about 1 week later routinely recommended?
A) Because the first application is washed off too quickly to have any effect at all
B) Because permethrin does not reliably kill the eggs, so a second application is needed to kill mites that hatch after the first treatment
C) Because permethrin loses all activity within 24 hours and must be reloaded to maintain a blood level
D) Because the second dose treats a completely different parasite than the first dose
E) Because a single application causes resistance, and the second application reverses it
ANSWER: B
Rationale:
Permethrin is reliably effective against the live mite but is not reliably ovicidal (it does not dependably kill eggs). Eggs already laid in the skin can hatch in the days after the first application. The repeat application about 1 week later kills these newly hatched mites before they mature and lay new eggs, breaking the life cycle. This same egg-survival logic explains why oral ivermectin and permethrin head-lice rinses are also given in two doses spaced about a week apart.
Option A: Option A is incorrect: a single neck-down application left on for 8 to 14 hours is highly effective against live mites; it is not washed off too soon to work.
Option C: Option C is incorrect: permethrin is a topical agent acting locally on the parasite, not a systemic drug maintained by a blood level, and it does not lose all activity within 24 hours.
Option D: Option D is incorrect: both applications target the same organism (Sarcoptes scabiei); the second dose addresses newly hatched mites of the same species, not a different parasite.
Option E: Option E is incorrect: repeat dosing does not reverse resistance; resistance to permethrin arises from sodium-channel mutations and is not created or reversed by a second application.
7. Malathion 0.5% lotion is an effective agent for head lice. Malathion is an organophosphate. By what mechanism does it kill lice?
A) It inhibits acetylcholinesterase, the enzyme that normally breaks down the neurotransmitter acetylcholine, so acetylcholine accumulates and overstimulates the louse nervous system
B) It prolongs the open state of voltage-gated sodium channels, like the pyrethroids
C) It blocks GABA-A receptors, removing inhibition in the nervous system
D) It physically suffocates the louse by blocking its breathing pores
E) It chelates iron, starving the louse of an essential nutrient
ANSWER: A
Rationale:
Malathion is an organophosphate cholinesterase inhibitor. It inhibits acetylcholinesterase (AChE) in the louse nervous system, so the neurotransmitter acetylcholine (ACh) is not broken down and accumulates at cholinergic synapses. The resulting overstimulation of acetylcholine receptors paralyzes and kills the louse. Because this mechanism is completely independent of the sodium channel, malathion remains effective against lice that are resistant to pyrethroids.
Option B: Option B is incorrect: prolonging sodium-channel opening is the pyrethroid (permethrin) mechanism, not the malathion mechanism.
Option C: Option C is incorrect: GABA-A receptor blockade is the mechanism of lindane, not malathion.
Option D: Option D is incorrect: physical suffocation by blocking spiracles is the mechanism of benzyl alcohol, not malathion.
Option E: Option E is incorrect: malathion does not work by iron chelation; it acts on acetylcholinesterase.
8. Spinosad 0.9% topical suspension is a newer agent for head lice, derived from a soil bacterium. By what mechanism does spinosad kill lice?
A) It inhibits acetylcholinesterase, causing acetylcholine to accumulate
B) It blocks the louse from absorbing folate, halting DNA synthesis
C) It prolongs the open state of voltage-gated sodium channels
D) It activates the louse nicotinic acetylcholine receptors and glutamate-gated chloride channels, causing neuromuscular hyperexcitation and paralysis
E) It physically blocks the breathing pores (spiracles), causing suffocation
ANSWER: D
Rationale:
Spinosad binds to and activates insect nicotinic acetylcholine receptors (nAChR) and glutamate-gated chloride channels in the louse, producing neuromuscular hyperexcitation followed by paralysis and death. Because this target is distinct from the sodium channel, spinosad retains full activity against pyrethroid-resistant (kdr) lice. Spinosad is also ovicidal, so a single application is usually sufficient, unlike permethrin, which requires a mandatory second application.
Option A: Option A is incorrect: acetylcholinesterase inhibition is the malathion mechanism, not the spinosad mechanism.
Option B: Option B is incorrect: blocking folate metabolism describes antifolate drugs such as pyrimethamine, not spinosad, and lice are not killed by folate blockade in this way.
Option C: Option C is incorrect: prolonging sodium-channel opening is the pyrethroid (permethrin) mechanism; spinosad does not act there, which is why it works against kdr-resistant lice.
Option E: Option E is incorrect: physical suffocation through the spiracles is the mechanism of benzyl alcohol, not spinosad.
9. Benzyl alcohol 5% lotion treats head lice by a mechanism that is unusual among the antiparasitic agents. Which statement correctly describes how it works and its resistance profile?
A) It inhibits acetylcholinesterase, and lice readily develop resistance to it
B) It prolongs sodium-channel opening, so it shares cross-resistance with the pyrethroids
C) It physically suffocates lice by blocking their breathing pores (spiracles), a mechanical action with no known resistance risk
D) It activates glutamate-gated chloride channels, and resistance is widespread
E) It blocks GABA-A receptors, and resistance emerges rapidly with repeated use
ANSWER: C
Rationale:
Benzyl alcohol works by a physical rather than a neurotoxic mechanism: it blocks the spiracles (breathing pores) of the louse, preventing air exchange and asphyxiating the parasite. Because killing is mechanical rather than dependent on a specific molecular target, there is no known mechanism for the louse to develop resistance to it. This makes it a useful option when pyrethroids have failed because of resistance.
Option A: Option A is incorrect: acetylcholinesterase inhibition is the malathion mechanism, and benzyl alcohol does not act on that enzyme; its physical mechanism is not prone to resistance.
Option B: Option B is incorrect: sodium-channel prolongation is the pyrethroid mechanism; benzyl alcohol does not act there and therefore does not share pyrethroid cross-resistance.
Option D: Option D is incorrect: activating glutamate-gated chloride channels is the ivermectin and spinosad mechanism, not benzyl alcohol, and benzyl alcohol has no known resistance problem.
Option E: Option E is incorrect: GABA-A receptor blockade is the lindane mechanism, not benzyl alcohol; benzyl alcohol acts physically and has no recognized resistance.
10. Permethrin treatment for head lice increasingly fails in many regions because of a resistance mechanism called knockdown resistance (kdr). What is the molecular basis of kdr?
A) The louse produces an enzyme that chemically destroys permethrin before it can act
B) The louse pumps permethrin out of its cells using a drug-efflux transporter
C) The louse thickens its outer cuticle so permethrin cannot penetrate
D) The louse increases the number of sodium channels so that permethrin is diluted out
E) A point mutation in the louse voltage-gated sodium channel gene (such as T929I or L932F) changes the permethrin binding site so the drug binds poorly, while the channel still works normally
ANSWER: E
Rationale:
Knockdown resistance (kdr) is caused by specific point mutations in the gene for the voltage-gated sodium channel, most commonly at amino acid positions 929 (T929I) and 932 (L932F) in lice. These mutations alter the site where permethrin binds, reducing its binding affinity, while leaving the channel's normal electrical function largely intact. Because the resistance is due to a change in the drug's target site, it confers cross-resistance to all pyrethrins and pyrethroids and cannot be overcome by raising the dose; the solution is to switch to an agent with a different mechanism (malathion, spinosad, or benzyl alcohol).
Option A: Option A is incorrect: enzymatic destruction of the drug is a metabolic resistance mechanism, but kdr specifically refers to target-site mutation of the sodium channel, not drug-degrading enzymes.
Option B: Option B is incorrect: drug efflux by a transporter is a different resistance strategy; kdr is defined by sodium-channel mutation, not efflux.
Option C: Option C is incorrect: reduced cuticular penetration is a separate possible resistance route, but it is not what kdr means.
Option D: Option D is incorrect: kdr does not work by increasing channel number; it changes the binding site on existing channels through mutation.
11. In a region where many head lice carry the kdr sodium-channel mutation that makes them resistant to permethrin, why does malathion still work against those same lice?
A) Because malathion is a stronger pyrethroid that overwhelms the mutated sodium channel
B) Because malathion kills lice by inhibiting acetylcholinesterase, a mechanism that does not depend on the sodium channel, so a sodium-channel mutation does not protect the louse from it
C) Because malathion reverses the kdr mutation and restores the louse sodium channel to normal
D) Because malathion blocks the same sodium-channel site as permethrin but binds more tightly
E) Because malathion prevents the louse from reproducing rather than killing the adult
ANSWER: B
Rationale:
The kdr mutation specifically protects the louse against drugs that act on the voltage-gated sodium channel, namely the pyrethroids. Malathion kills by a completely different route, inhibiting acetylcholinesterase so that acetylcholine accumulates and overstimulates the nervous system. Because malathion's target is the enzyme, not the sodium channel, a sodium-channel mutation gives the louse no protection against it. This is why malathion (and likewise spinosad and benzyl alcohol) retains full activity against kdr-resistant lice.
Option A: Option A is incorrect: malathion is not a pyrethroid at all; it is an organophosphate, and it does not act on the sodium channel.
Option C: Option C is incorrect: malathion does not repair or reverse the genetic mutation; it simply acts on a different target.
Option D: Option D is incorrect: malathion does not bind the sodium channel; it inhibits acetylcholinesterase, so it shares no binding site with permethrin.
Option E: Option E is incorrect: malathion kills adult lice through acetylcholinesterase inhibition; it is not merely a reproductive inhibitor.
12. Body lice differ from head lice in where they live. The body louse spends most of its life in the seams of clothing rather than on the skin. What is the primary treatment for body lice infestation?
A) Environmental decontamination, meaning hot-laundering or discarding the infested clothing and bedding, because that is where the lice actually live
B) A single oral dose of albendazole
C) Daily application of a topical corticosteroid to the skin for 2 weeks
D) Lifelong suppressive therapy with oral ivermectin
E) Surgical removal of affected skin
ANSWER: A
Rationale:
Because the body louse lives and lays its eggs in the seams of clothing and comes onto the skin only to feed, the key intervention is environmental: hot-laundering (or discarding) the infested clothing and bedding eliminates the louse population at its source. Topical permethrin applied to the body and clothing can be used as an adjunct, but environmental decontamination is the primary treatment. This is also clinically important because body lice can transmit serious infections such as epidemic typhus and trench fever in crowded conditions.
Option B: Option B is incorrect: albendazole treats helminth (worm) infections, not louse infestation.
Option C: Option C is incorrect: a topical corticosteroid reduces inflammation and itch but does not kill lice or eradicate them from clothing.
Option D: Option D is incorrect: body lice are eradicated by treating the clothing and environment, not by lifelong drug suppression.
Option E: Option E is incorrect: body lice infestation is not a surgical condition; no skin removal is involved.
13. A patient treated correctly for scabies returns 10 days later still itching and is worried the treatment failed. The skin shows no new burrows and no live mites. What is the best explanation and action?
A) The treatment failed; immediately repeat the full course of a different scabicide
B) The itch proves permethrin resistance; switch to lindane right away
C) The patient was reinfected; no further evaluation of contacts is needed
D) Itching commonly persists for 2 to 4 weeks after a successful cure because of an ongoing hypersensitivity reaction to dead mite material, so reassurance and symptom control are appropriate rather than retreatment
E) The persistent itch means the mites have spread internally and systemic therapy is required
ANSWER: D
Rationale:
Pruritus typically continues for 2 to 4 weeks after successful scabies treatment, driven by a delayed-type hypersensitivity reaction to mite antigens, feces, and dead mite material that remain in the skin even after the mites are eradicated. In the absence of new burrows or confirmed live mites, this post-scabietic itch should be managed with reassurance, oral antihistamines, and topical corticosteroids, not by repeating scabicide. Failing to counsel patients about this leads to unnecessary retreatment.
Option A: Option A is incorrect: with no new lesions or live mites, persistent itch alone does not indicate treatment failure, so immediate retreatment is not warranted.
Option B: Option B is incorrect: itch alone does not demonstrate resistance, and lindane is a neurotoxic, largely abandoned agent that would not be the appropriate next step here.
Option C: Option C is incorrect: while reinfection from an untreated contact is one cause of true failure, evaluating and treating close contacts is precisely what should be done if true failure occurs; ignoring contacts is wrong.
Option E: Option E is incorrect: the scabies mite remains in the epidermis and does not spread internally, so systemic spread is not the explanation.
14. Pyrimethamine, used to treat toxoplasmosis, inhibits dihydrofolate reductase (DHFR) — the enzyme that regenerates the active form of folate needed for DNA synthesis. Because it also affects this enzyme in human bone marrow cells, what supportive measure is mandatory during treatment?
A) Daily potassium supplementation to prevent low potassium
B) Routine iron infusions to prevent iron deficiency
C) Co-administration of folinic acid (leucovorin) to protect human bone marrow from the antifolate effect, with periodic complete blood count monitoring
D) High-dose vitamin C to enhance drug absorption
E) Continuous proton pump inhibitor therapy to protect the stomach
ANSWER: C
Rationale:
Pyrimethamine inhibits dihydrofolate reductase (DHFR) in human bone marrow precursor cells as well as in the parasite, which can cause megaloblastic anemia, leukopenia, and thrombocytopenia. Folinic acid (leucovorin) supplies a form of folate that human cells can use without needing DHFR, so it rescues the bone marrow while leaving the antiparasitic effect intact. Folinic acid co-administration is mandatory, and a complete blood count (CBC) is monitored periodically (weekly during acute treatment) to detect marrow suppression early.
Option A: Option A is incorrect: pyrimethamine toxicity is bone marrow suppression from folate antagonism, not potassium loss, so potassium supplementation is not the protective measure.
Option B: Option B is incorrect: the anemia from pyrimethamine is megaloblastic (folate-related), not iron-deficiency anemia, so iron infusions do not address the mechanism.
Option D: Option D is incorrect: vitamin C does not protect the marrow from antifolate toxicity and is not used for this purpose.
Option E: Option E is incorrect: a proton pump inhibitor protects the gastric mucosa but does nothing to counter folate-antagonist bone marrow suppression.
15. Mefloquine, an antimalarial, carries a boxed warning (the strongest warning on a drug label) about a particular category of adverse effect. In which patient is mefloquine contraindicated because of this warning?
A) A patient with mild seasonal allergies and no other history
B) A patient with well-controlled high blood pressure
C) A patient with a remote history of a single kidney stone
D) A patient with mild lactose intolerance
E) A patient with a history of psychiatric illness or a seizure disorder, because mefloquine can cause serious neuropsychiatric effects and lowers the seizure threshold
ANSWER: E
Rationale:
Mefloquine's boxed warning concerns neuropsychiatric adverse effects, which range from anxiety, vivid nightmares, dizziness, and insomnia to, rarely, psychosis, seizures, and encephalopathy. Because of this, mefloquine is contraindicated in patients with a history of psychiatric illness, a seizure disorder, or cardiac conduction abnormalities, and the neuropsychiatric risk must be disclosed before prescribing. A patient with a prior psychiatric or seizure history is therefore the one in whom the drug should be avoided.
Option A: Option A is incorrect: seasonal allergies are unrelated to mefloquine's neuropsychiatric contraindication.
Option B: Option B is incorrect: well-controlled hypertension is not the basis for the boxed-warning contraindication, which is neuropsychiatric.
Option C: Option C is incorrect: a remote single kidney stone does not relate to the neuropsychiatric and seizure concerns that drive the contraindication.
Option D: Option D is incorrect: lactose intolerance is a benign gastrointestinal condition unrelated to mefloquine's central nervous system risks.
16. A child is treated for head lice with permethrin 1% rinse twice, applied correctly, but live lice remain. The family lives in a region where the kdr sodium-channel mutation is common. Applying the mechanisms covered earlier in this set, which choice is the best next step?
A) Repeat permethrin a third time at a higher concentration, since enough doses will overcome any resistance
B) Switch to spinosad, which kills lice through nicotinic acetylcholine receptor and chloride-channel activation, a mechanism unaffected by the sodium-channel kdr mutation
C) Switch to a different pyrethroid product, since another pyrethroid will bypass the kdr mutation
D) Add an oral antihistamine as the definitive treatment for the infestation
E) Conclude the child cannot be cured and stop all treatment
ANSWER: B
Rationale:
The kdr mutation alters the sodium-channel binding site, conferring cross-resistance to all pyrethrins and pyrethroids, and it cannot be overcome by a higher dose or by switching to another pyrethroid. The rational move is to choose an agent with a different mechanism. Spinosad activates nicotinic acetylcholine receptors and glutamate-gated chloride channels, a target unrelated to the sodium channel, so it retains full activity against kdr-resistant lice (malathion and benzyl alcohol would be equally rational alternatives for the same reason).
Option A: Option A is incorrect: because kdr is a target-site change, raising the permethrin concentration does not restore efficacy; cross-resistance applies regardless of dose.
Option C: Option C is incorrect: all pyrethroids share the same sodium-channel target, so kdr confers cross-resistance to the whole class; switching pyrethroids does not help.
Option D: Option D is incorrect: an antihistamine may relieve itch but does not kill lice and is not a treatment for the infestation.
Option E: Option E is incorrect: the infestation is readily curable with a different-mechanism agent such as spinosad, so abandoning treatment is unjustified.
17. A clinician is choosing a scabies treatment for a 3-year-old child and considers lindane. Recalling that lindane kills parasites by blocking GABA-A receptors (the receptors for the main inhibitory neurotransmitter in the nervous system), why is lindane contraindicated in all children?
A) Because lindane is absorbed through the skin and the same GABA-A blockade that kills the mite can cause central nervous system toxicity and seizures in the child, a risk that is greatest in young children whose skin is more permeable and whose nervous system is still developing
B) Because lindane is completely ineffective against the scabies mite
C) Because lindane is a pyrethroid and shares cross-resistance with permethrin
D) Because lindane must be given intravenously, which is impractical in children
E) Because lindane is safe in children but simply more expensive than permethrin
ANSWER: A
Rationale:
Lindane kills parasites by antagonizing GABA-A receptors, blocking inhibitory chloride channels and producing nervous-system hyperexcitation. The problem is selectivity: lindane is absorbed through human skin, and the same GABA-A blockade can produce central nervous system (CNS) toxicity and seizures in the patient. Children are especially vulnerable because their skin is more permeable and their CNS is still developing, so lindane is contraindicated in all children (and is banned in many countries). Seizures in children have been reported after dermal absorption.
Option B: Option B is incorrect: lindane does have scabicidal activity; the reason it is avoided is toxicity, not lack of efficacy.
Option C: Option C is incorrect: lindane is an organochlorine acting at GABA-A receptors, not a pyrethroid, and does not share the pyrethroid sodium-channel mechanism or its cross-resistance.
Option D: Option D is incorrect: lindane is a topical agent, not an intravenous drug; the contraindication is about neurotoxicity from dermal absorption, not the route being impractical.
Option E: Option E is incorrect: lindane is not safe in children; cost is not the issue, neurotoxicity is.
18. A pregnant woman in her second trimester is diagnosed with scabies. Considering that permethrin has very low absorption through the skin (less than 2 percent), which agent is preferred for treating her scabies?
A) Lindane lotion, because pregnancy increases its safety margin
B) Oral ivermectin as the routine first choice in any pregnancy
C) Diethylcarbamazine, because it is specifically indicated in pregnancy
D) Permethrin 5% cream, which is the preferred scabicide in pregnancy because its very low dermal absorption means little drug reaches the systemic circulation or the fetus
E) No treatment at all, because scabies should never be treated during pregnancy
ANSWER: D
Rationale:
Permethrin 5% cream is the preferred scabicide in pregnancy. Its dermal absorption is below 2 percent, so very little drug reaches the maternal circulation or the fetus, and it has a long record of safe use. Scabies should be treated in pregnancy, and permethrin is the agent of choice for doing so.
Option A: Option A is incorrect: lindane is contraindicated in pregnancy because of significant central nervous system absorption and neurotoxicity; pregnancy does not make it safer.
Option B: Option B is incorrect: ivermectin has limited pregnancy safety data and is generally avoided for elective use in pregnancy, reserved for life-threatening indications; it is not the routine first choice.
Option C: Option C is incorrect: diethylcarbamazine (DEC) is used for lymphatic filariasis and is contraindicated in pregnancy; it is not a scabies treatment.
Option E: Option E is incorrect: scabies can and should be treated in pregnancy, using a safe agent such as permethrin; withholding treatment is not appropriate.
19. A 10-kg infant has common scabies. Oral ivermectin is approved for children weighing 15 kg or more, in part because younger infants have a more permeable blood-brain barrier (the protective layer that normally keeps drugs out of the brain). What is the preferred treatment for this infant?
A) Oral ivermectin at the standard adult dose
B) Lindane lotion applied to the whole body
C) Topical permethrin 5% cream, which is the preferred agent for scabies in a child below 15 kg
D) Oral mefloquine
E) No treatment until the child reaches 15 kg
ANSWER: C
Rationale:
For scabies in a child below 15 kg, topical permethrin 5% cream is the preferred agent. Oral ivermectin is generally reserved for children of at least 15 kg (about 2 years of age) because limited data and a more permeable blood-brain barrier in young infants raise concern about central nervous system toxicity. Permethrin's low systemic absorption makes it the safer, effective choice here. (For infants, application is extended to include the face and scalp.)
Option A: Option A is incorrect: ivermectin is not recommended below 15 kg outside of life-threatening situations, and an adult dose would be inappropriate for a 10-kg infant.
Option B: Option B is incorrect: lindane is contraindicated in all children because of central nervous system neurotoxicity from dermal absorption.
Option D: Option D is incorrect: mefloquine is an antimalarial and is not a treatment for scabies.
Option E: Option E is incorrect: scabies in an infant should be treated promptly with a safe agent such as topical permethrin; waiting until the child reaches 15 kg is not appropriate.
20. Praziquantel is broken down in the liver by the enzyme CYP3A4. A patient who needs praziquantel is also taking rifampicin, a drug that strongly increases the amount of CYP3A4 the liver produces (a process called enzyme induction). What is the consequence, and what should be done?
A) Rifampicin raises praziquantel levels dangerously, so the praziquantel dose should be cut in half
B) There is no interaction, because praziquantel is not metabolized by CYP3A4
C) Rifampicin and praziquantel bind to each other in the gut, so they should simply be taken 2 hours apart
D) Rifampicin increases praziquantel absorption, improving its effect, so no change is needed
E) Rifampicin induces CYP3A4 and accelerates praziquantel breakdown, lowering praziquantel levels by about 85 percent and risking treatment failure, so the two should not be co-administered
ANSWER: E
Rationale:
Rifampicin is a potent inducer of CYP3A4, meaning it makes the liver produce much more of the enzyme that metabolizes praziquantel. As a result, praziquantel is broken down much faster, and its plasma levels fall by roughly 85 percent, which can cause treatment failure. For this reason rifampicin and praziquantel should not be co-administered; treatment must be timed or substituted to avoid the interaction.
Option A: Option A is incorrect: enzyme induction lowers, not raises, praziquantel levels, so reducing the dose would worsen the problem rather than fix it.
Option B: Option B is incorrect: praziquantel is in fact extensively metabolized by CYP3A4, which is exactly why a CYP3A4 inducer affects it.
Option C: Option C is incorrect: the interaction is metabolic (enzyme induction), not a physical binding in the gut, so spacing the doses by 2 hours does not solve it.
Option D: Option D is incorrect: rifampicin reduces praziquantel exposure through faster metabolism; it does not improve its effect, and the combination should be avoided.
21. A debilitated nursing-home resident is diagnosed with crusted scabies, with thick hyperkeratotic crusts on the hands and feet. Recalling why ordinary topical treatment is inadequate in this form, what is the correct management approach?
A) A single application of permethrin 5% cream alone, identical to the treatment of common scabies
B) Combination therapy with repeated oral ivermectin plus topical permethrin plus a keratolytic agent to remove the crust, because the thick crust blocks drug penetration and topical therapy alone fails
C) Oral metronidazole for 7 days as monotherapy
D) Reassurance only, since crusted scabies resolves without treatment
E) A topical corticosteroid alone, to reduce the crusting
ANSWER: B
Rationale:
In crusted (Norwegian) scabies, the thick hyperkeratotic crust contains enormous numbers of mites and physically prevents topical drug from reaching them, so topical permethrin alone is inadequate. Correct management combines repeated courses of oral ivermectin (which reaches the mites systemically) with topical permethrin and a keratolytic agent such as salicylic acid to break down the crust and allow drug penetration. Strict contact precautions and treatment of close contacts are also essential because these patients are highly contagious.
Option A: Option A is incorrect: a single permethrin application, adequate for common scabies, fails in crusted scabies because the crust blocks penetration and the mite burden is enormous.
Option C: Option C is incorrect: metronidazole does not treat the scabies mite and has no role here.
Option D: Option D is incorrect: crusted scabies does not self-resolve; untreated, it is severe, persistent, and a source of outbreaks.
Option E: Option E is incorrect: a corticosteroid is not scabicidal and could worsen the infestation by suppressing local immunity; it does not eradicate the mites.
22. Primaquine is used to achieve radical cure of Plasmodium vivax and Plasmodium ovale malaria. Which test must be performed before primaquine is given to any patient, and why?
A) Glucose-6-phosphate dehydrogenase (G6PD) testing, because primaquine can trigger severe breakdown of red blood cells (hemolysis) in patients who are deficient in this enzyme
B) A pregnancy test only, with no other screening needed
C) A complete cholesterol panel, because primaquine raises cholesterol
D) A bone density scan, because primaquine weakens bone
E) No testing is required before primaquine under any circumstances
ANSWER: A
Rationale:
Primaquine can cause acute hemolytic anemia in patients who are deficient in glucose-6-phosphate dehydrogenase (G6PD), an enzyme that protects red blood cells from oxidative stress. Because primaquine imposes an oxidative load, G6PD-deficient red cells are destroyed, sometimes severely. For this reason, G6PD testing is mandatory before primaquine is given to any patient, including children, so that deficient individuals can be identified and the risk managed.
Option B: Option B is incorrect: while pregnancy status matters for many antimalarials, the test specifically required before primaquine to prevent its characteristic toxicity is G6PD testing, not a pregnancy test alone.
Option C: Option C is incorrect: primaquine toxicity is hemolysis in G6PD deficiency, not a lipid effect, so a cholesterol panel is not the required screen.
Option D: Option D is incorrect: primaquine does not cause bone loss, so a bone density scan is not relevant.
Option E: Option E is incorrect: testing is required; giving primaquine without checking G6PD status risks severe hemolysis in a deficient patient.
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