Core Revision
Revision aid, not clinical advice. This page is educational material written for exam preparation. It is not a substitute for the current guideline or for clinical judgement, and must not be relied on for the care of any individual. Always check up-to-date national guidance and verify independently before acting on anything here.
Diplomas · Core Tools
DTM&H Core Tools
Two ways to train, both of them active. Reason makes you commit to an answer before anything is revealed — then shows you why every other option fails. Recall drills the highest-yield facts on a spaced schedule. No skimming, no fooling yourself.
Choose an option in each scenario. Nothing is revealed until you commit — that is the point.
1 · Fever in the returning traveller
Malaria first, always. Then let the incubation period and the exposure history narrow the field.
Scenario 1 of 6
A 34-year-old returns from three weeks in Lagos, Nigeria. He took no chemoprophylaxis. Nine days after arriving home he develops fever to 38.9°C, headache and myalgia. There are no localising signs. He is alert, BP 118/70, HR 96.
What is the single most important first investigation?
Commit to one answer.
Why
Falciparum malaria is the one imported fever that kills a previously well adult within days, and West Africa is the highest-risk exposure there is. Nine days is entirely compatible: the minimum incubation for falciparum is about 7 days, so any fever from day 7 onwards after entering an endemic area is malaria until proven otherwise. Films plus an antigen test are quick, cheap and definitive — and a single negative set does not exclude it, so repeat at 12–24 hour intervals up to three sets.
Why not the others
- B — Chest X-ray: reasonable as part of a fever screen, but it will not diagnose the thing that can kill him tonight; it treats a normal film as reassurance when it is not.
- C — Blood cultures alone with a 48-hour review: cultures are needed (typhoid, invasive Salmonella), but a 48-hour wait in untreated falciparum is how non-immune travellers progress to cerebral malaria.
- D — Dengue testing: a sensible parallel test, never the first one. Dengue rarely kills a well-hydrated adult in the first days; falciparum can.
- E — Stool studies: he has no diarrhoea, and enteric parasites do not explain an undifferentiated fever of this speed.
Scenario 2 of 6
A woman presents with fever and rigors that began five weeks after returning from a six-week trip to Thailand and Laos. She is otherwise well between spikes.
Which diagnosis can you now reasonably move to the bottom of the list on incubation grounds alone?
Commit to one answer.
Why
Incubation period is the cheapest diagnostic test you own. The arboviruses — dengue, chikungunya, Zika — and the rickettsioses all have short incubations, essentially always under 14 days. A fever that begins more than 21 days after the last possible exposure effectively excludes them. What remains are the long-incubation imports: malaria (especially vivax, which can relapse months later), enteric fever, TB, viral hepatitis, amoebic liver abscess, visceral leishmaniasis, acute HIV.
Why not the others
- A — Vivax malaria: the archetypal late presenter. Hypnozoites relapse weeks to months after return, so late fever makes vivax more likely, not less.
- C — Enteric fever: usual incubation 7–21 days but can extend well beyond; it stays firmly on the list at five weeks.
- D — Amoebic liver abscess: classically presents months to years after exposure, often with no history of dysentery at all.
- E — Tuberculosis: has no meaningful upper incubation limit; late fever, sweats and weight loss are exactly its pattern.
Scenario 3 of 6
A backpacker returns from two weeks in Bangkok. Four days later he has abrupt fever 39.5°C, severe retro-orbital headache, myalgia and a fine erythematous rash. Platelets 96, WCC 3.1, ALT 88. Malaria films are negative.
Which is the most likely diagnosis, and what most concerns you?
Commit to one answer.
Why
Fever four days after returning from a two-week trip is not too fast for malaria: the incubation clock runs from first exposure, so he could have been infected up to 18 days before onset. What points away from malaria is Bangkok’s negligible urban risk plus negative films — not the timing. What points to an arbovirus is the clinical picture. The triad of retro-orbital pain, myalgia and rash with leucopenia, thrombocytopenia and a raised ALT is dengue until proven otherwise. The trap is that patients deteriorate as the fever falls, around days 4–6: that defervescence marks the critical phase when capillary leak causes a rising haematocrit, falling platelets, effusions and shock. Manage with careful fluids and serial haematocrit, and avoid NSAIDs and aspirin.
Why not the others
- A — Falciparum: the timing does not rule it out — he could have been bitten up to 18 days before the fever began. What argues against it is Bangkok’s negligible urban malaria risk and the negative films. Keep repeating films if the story shifts, but do not anchor here.
- B — Enteric fever: too early, and typhoid usually gives a stepwise fever with relative bradycardia and few rashes beyond sparse rose spots.
- D — Leptospirosis: a genuine differential, but it needs a freshwater or rodent-urine exposure and typically brings conjunctival suffusion, calf tenderness and renal impairment.
- E — Acute HIV: always worth testing in any returning traveller with fever and rash, but it does not explain this specific triad, and testing alone is not a management plan.
Scenario 4 of 6
A 26-year-old spent a month in Malawi and swam several times in Lake Malawi. Six weeks later she develops fever, dry cough, urticarial rash and malaise. Eosinophils 2.4 x10⁹/L. Malaria films are negative.
What is the most likely diagnosis?
Commit to one answer.
Why
Freshwater contact in sub-Saharan Africa plus fever, urticaria and marked eosinophilia 3–8 weeks later is Katayama syndrome — an immune-complex hypersensitivity reaction to migrating schistosomes. It occurs in non-immune travellers, which is exactly this group. Eggs are often not yet excreted and serology may still be negative this early, so treat on clinical grounds; praziquantel is given but does not kill immature schistosomulae, so a repeat course after 6–12 weeks is standard, with steroids if the illness is severe.
Why not the others
- A — Loeffler syndrome: also causes cough and eosinophilia, but it follows soil or faecal-oral exposure, not swimming, and lacks the urticarial, systemic Katayama picture.
- B — Vivax relapse: the timing fits but the film does not, and vivax does not cause urticaria or eosinophilia — malaria typically suppresses the eosinophil count.
- C — Visceral leishmaniasis: presents with months of fever, massive splenomegaly and pancytopenia, and eosinophilia is not a feature.
- E — Strongyloides hyperinfection: occurs in the immunosuppressed (especially on corticosteroids) with sepsis and Gram-negative bacteraemia — not in a well young traveller weeks after a swim.
Scenario 5 of 6
A 41-year-old returned from Ghana 10 days ago. He is febrile, drowsy and confused (GCS 13). Blood film shows P. falciparum with 6% parasitaemia. Lactate 5.2 mmol/L, glucose 3.0 mmol/L, creatinine 168.
What is the correct immediate management?
Commit to one answer.
Why
He has severe malaria on two WHO criteria: impaired consciousness and acidosis with a lactate above 5 — any one is enough. His glucose of 3.0 and creatinine of 168 do not meet the WHO thresholds (hypoglycaemia is below 2.2 mmol/L; renal impairment is creatinine above 265 micromol/L), though both need watching. Parasitaemia above 10% is severe in its own right, so his 6% is not severe by that criterion (in the UK, though, a parasitaemia over 2% would itself mandate IV artesunate). WHO recommends intravenous artesunate for severe malaria in adults and children; it outperformed quinine on mortality in the SEAQUAMAT and AQUAMAT trials and needs no cardiac monitoring. Watch glucose closely, treat with a full oral ACT course once he can swallow, and remember the delayed post-artesunate haemolysis that can appear 1–3 weeks later.
Why not the others
- A — Oral ACT on a ward: a drowsy, vomiting, acidotic patient cannot be relied on to absorb an oral drug, and this is a critical-care illness, not a ward one.
- B — Quinine plus doxycycline: quinine is now second line for severe disease (used only if artesunate is unavailable) and brings hypoglycaemia, QT prolongation and cinchonism; oral quinine here is doubly wrong.
- C — Exchange transfusion: no longer routinely recommended; the evidence never showed a mortality benefit and it must never delay artesunate.
- D — Dexamethasone: actively harmful in cerebral malaria — steroids prolong coma and increase complications without improving survival.
Scenario 6 of 6
A nurse returns from Sierra Leone 8 days ago, where she worked in a rural clinic and attended a funeral. She now has fever 39°C, sore throat, myalgia and vomiting. She telephones your practice.
What is the correct approach?
Commit to one answer.
Why
Fever within 21 days of leaving a VHF-endemic area, with a healthcare or funeral exposure, places her in the “at risk of VHF” category of the current UKHSA/ACDP algorithm — the older “high possibility of VHF” wording has been retired. That does not mean abandoning malaria — malaria remains by far the likeliest diagnosis and must still be tested for — but the sample handling, transport and patient isolation all change. Isolate, avoid unnecessary sharps and aerosols, use appropriate PPE, and speak to the Imported Fever Service and your local infection team before taking blood, so that testing happens under the correct containment.
Why not the others
- B — Routine bloods in the surgery: exposes staff and the laboratory to an unrecognised high-risk sample; the sequence, not the test, is what is wrong.
- C — Empirical treatment at home: treats a presumed diagnosis without confirmation and leaves a possible VHF case unisolated in the community.
- D — No bleeding, no VHF: a dangerous myth. Early VHF is a non-specific febrile illness; haemorrhage is late, inconsistent and no part of the initial risk assessment.
- E — Public transport to ED: an unannounced, unisolated arrival is exactly the scenario the pathway exists to prevent. Transfers are pre-arranged and notified.
2 · Malaria decoder
Which species, how sick, which drug — and why the answers to those three questions are not independent.
Scenario 1 of 6
A patient treated for P. vivax malaria with a full course of chloroquine returns four months later with an identical illness. He never left the UK in the interim.
What explains this, and what was missing from his first treatment?
Commit to one answer.
Why
P. vivax and P. ovale form hypnozoites — dormant liver stages that no blood-stage drug touches. Chloroquine (or an ACT) clears the parasitaemia and the patient gets better, but weeks to months later the hypnozoites reactivate and the illness returns. Preventing that requires radical cure with a 14-day course of primaquine, and primaquine causes haemolysis in G6PD deficiency, so you must check G6PD status before prescribing. Tafenoquine is a single-dose alternative where available, with the same G6PD caveat.
Why not the others
- A — Chloroquine resistance: exists in vivax (notably Oceania and parts of Indonesia) but it causes early treatment failure, not a clean recovery followed by relapse four months later.
- C — Reinfection: impossible — he has not left the UK, and there is no local transmission.
- D — Recrudescence: that is failure of blood-stage clearance and shows up within days to weeks, not after a symptom-free four months.
- E — Prophylaxis at home: prophylaxis prevents new infection from mosquito bites; it does nothing about hypnozoites already sitting in the liver.
Scenario 2 of 6
Four adults with confirmed falciparum malaria are on the acute take.
Which single finding defines severe malaria and mandates parenteral treatment?
Commit to one answer.
Why
Hypoglycaemia below 2.2 mmol/L is a WHO severity criterion in its own right — it reflects parasite glucose consumption and impaired gluconeogenesis, it is worsened by quinine, and it is a common, reversible cause of coma and death. The other WHO criteria worth knowing cold are: impaired consciousness, prostration, seizures, respiratory distress or acidosis, shock, pulmonary oedema, acute kidney injury, jaundice with another organ dysfunction, severe anaemia, abnormal bleeding, haemoglobinuria, and hyperparasitaemia.
Why not the others
- A — High fever and rigors: universal in malaria and carries no prognostic weight; severity is about organ dysfunction, not temperature.
- B — Splenomegaly: an expected finding in malaria of any severity and not a criterion at all.
- D — Platelets 84: thrombocytopenia is almost the rule in malaria and, in isolation without bleeding, does not define severe disease.
- E — Parasitaemia 1.5%: below the threshold. Hyperparasitaemia is over 10% in WHO criteria. In UK practice a parasitaemia above 2% is treated with intravenous artesunate, even with no other severity feature, until the patient can complete an oral ACT; 1.5% with no severity features is uncomplicated.
Scenario 3 of 6
A well 30-year-old, fully alert, tolerating oral fluids, has uncomplicated P. falciparum malaria acquired in Uganda. Parasitaemia 0.8%. No severity features. She is not pregnant.
What is the standard first-line treatment?
Commit to one answer.
Why
WHO recommends an ACT for all uncomplicated falciparum malaria. Artemether-lumefantrine is the usual UK choice; it must be taken with fatty food or milk, because lumefantrine absorption is poor otherwise and under-absorption is a genuine cause of treatment failure. The artemisinin component clears parasites rapidly; the long-acting partner drug eliminates the residual parasites and protects the artemisinin from resistance.
Why not the others
- A — Chloroquine: falciparum is widely chloroquine-resistant; chloroquine has a role in sensitive vivax and in some non-falciparum species, not here.
- B — Artemisinin monotherapy: the fastest route to artemisinin resistance and the reason WHO explicitly prohibits oral monotherapy. Always combine.
- C — Primaquine 14 days: aimed at liver hypnozoites, which falciparum does not form; it is not a blood-stage cure. (A single low dose is used as a transmission-blocking gametocytocide in endemic settings.)
- E — IV artesunate for everyone: over-treatment. Parenteral therapy is for severe disease or those who cannot take or retain oral drugs.
Scenario 4 of 6
A traveller returns from forested Borneo. The film is reported as “P. malariae — band forms seen”, but parasitaemia has risen from 0.3% to 4% in 24 hours and he is becoming breathless.
What is the most likely species, and what does that mean?
Commit to one answer.
Why
P. knowlesi is a macaque parasite transmitted to humans in the forested parts of Southeast Asia, especially Malaysian Borneo. Its early trophozoites resemble falciparum rings and its mature forms resemble the band forms of P. malariae, so microscopy routinely mis-reports it — PCR is the reliable test. The clinical difference is decisive: knowlesi has a 24-hour erythrocytic cycle, so parasitaemia can climb explosively and cause severe disease with respiratory distress, AKI and shock. A rapidly rising “malariae” from Borneo is knowlesi until proven otherwise, and should be treated as severe malaria.
Why not the others
- A — Benign quartan malariae: true P. malariae has a 72-hour cycle and characteristically low parasitaemia; it does not quadruple overnight or cause respiratory distress.
- B — P. ovale: gives enlarged, oval, fimbriated red cells with Schuffner dots, not band forms, and does not behave aggressively.
- C — Mixed infection treated with ACT alone: even if mixed, ignoring the severity features and the geography would leave a rapidly deteriorating patient on oral therapy.
- D — Wait 48 hours: the trajectory is the diagnosis. Delay in a knowlesi infection doubling daily is exactly how these patients die.
Scenario 5 of 6
A traveller took atovaquone-proguanil (Malarone) faithfully throughout a trip to Ghana and for seven days afterwards. Twelve days after returning he develops falciparum malaria, uncomplicated, and is fit for oral therapy.
What is the most appropriate treatment?
Commit to one answer.
Why
Two principles collide here, and both matter. First, no chemoprophylaxis is 100% effective — breakthrough malaria happens even with perfect adherence, which is why bite avoidance and prompt testing of any fever still matter. Second, if a patient develops malaria while taking a drug, you must assume that drug has failed and treat with an agent from a different class. Here that means an ACT such as artemether-lumefantrine.
Why not the others
- B — Repeat the same drug: the drug was present in his blood and the parasite grew anyway; giving more of it risks a second failure in someone who has already proved susceptible.
- C — Extend prophylaxis: a prophylactic dose cannot treat established, symptomatic infection.
- D — Primaquine for falciparum hypnozoites: falciparum does not form hypnozoites — there is nothing dormant in the liver to eradicate.
- E — Watchful waiting: untreated falciparum in a non-immune adult can become severe within 24 hours. There is no observation option.
Scenario 6 of 6
A febrile traveller back from Kenya has a negative malaria rapid diagnostic test and one negative thick film. He remains febrile at 39°C with no alternative diagnosis.
What do you do next?
Commit to one answer.
Why
Parasitaemia fluctuates with the schizogony cycle, so a single film can genuinely be negative in symptomatic malaria — particularly at low parasite density or early in the illness. The standard is three negative films taken over 48 hours, ideally at different times, before malaria is excluded in a febrile returning traveller. Rapid tests add speed but do not replace this: HRP2-based tests can be falsely negative with pfhrp2 gene deletions, and they are poor at detecting low-density non-falciparum species.
Why not the others
- A — Excluded: a single negative film is the classic missed-malaria trap; the diagnosis is excluded by a protocol, not by one test.
- C — Blind empirical treatment: only justified where testing is unavailable or the patient is critically ill and deteriorating; it also removes your ability to confirm species and severity.
- D — RDT alone: RDTs miss low parasitaemias, can be falsely negative in HRP2-deleted falciparum, and are unreliable for ovale and malariae. Microscopy also gives you the parasite count you need for severity.
- E — Serology: shows past exposure, takes days, and cannot diagnose acute malaria. It has no place in the acute workup.
3 · Parasite and vector recognition
For the specimen paper. Each specimen is described in words — train yourself to reason from the one discriminating feature, not the general impression.
Scenario 1 of 6
A Giemsa-stained thin film shows red cells of normal size containing multiple delicate ring forms, some rings with double chromatin dots and some applied to the cell margin. Parasitaemia is high. A single banana-shaped (crescentic) gametocyte is seen. No mature trophozoites or schizonts are present.
Which species?
Commit to one answer.
Why
The banana-shaped gametocyte is pathognomonic of P. falciparum — no other Plasmodium makes one. The supporting features all point the same way: normal-sized red cells (falciparum invades cells of any age and does not enlarge them), high parasitaemia, multiply-infected cells, appliqué forms and double chromatin dots, and an absence of later stages, because mature falciparum parasites sequester in the deep microvasculature and are not seen in peripheral blood.
Why not the others
- A — P. vivax: infects reticulocytes, so red cells are enlarged, with Schuffner dots and amoeboid trophozoites; gametocytes are round.
- B — P. ovale: enlarged, often oval red cells with a fimbriated (ragged) edge and Schuffner dots — never crescentic gametocytes.
- D — P. malariae: normal-sized cells but with characteristic band-form trophozoites, a low parasitaemia, and rosette schizonts — all stages visible, not just rings.
- E — Babesia: mimics falciparum rings but shows the tetrad “Maltese cross”, no gametocytes and no pigment, and comes with a tick exposure in temperate regions, not the tropics.
Scenario 2 of 6
A terminal urine specimen from a boy who has swum in the Nile shows a large ovoid egg, roughly 140 micrometres long, with a prominent terminal spine. He reports painless haematuria at the end of micturition.
Which organism, and what is the long-term risk?
Commit to one answer.
Why
Terminal spine plus urine plus Africa equals S. haematobium. The adult worms live in the vesical venous plexus; eggs traverse the bladder wall, causing the classic terminal haematuria of a child in an endemic area. Chronic infection produces bladder wall fibrosis and calcification, ureteric obstruction with hydronephrosis, and — uniquely among the schistosomes — squamous cell carcinoma of the bladder. It is also a recognised co-factor for HIV acquisition in female genital schistosomiasis. Treatment is praziquantel.
Why not the others
- A — S. mansoni: a lateral spine, found in stool, causing intestinal disease and periportal (Symmers pipe-stem) fibrosis with portal hypertension — not bladder disease.
- B — S. japonicum: a small, rounder egg with only a rudimentary lateral knob, found in stool in East Asia; it is the species most associated with CNS disease, but not with a large terminal spine in urine.
- C — Fasciola hepatica: a large operculate egg, seen in stool or bile, with no spine, acquired from watercress rather than swimming.
- E — Enterobius: a tiny flattened egg recovered on perianal adhesive tape, never in urine, and never spined.
Scenario 3 of 6
A specimen jar contains a robust brown fly, roughly the size of a housefly, with wings folded scissor-like over the abdomen at rest, a distinctive hatchet cell in the wing venation, and a rigid forward-projecting proboscis. Both sexes bite by day, and the bite is painful.
Which vector and which disease?
Commit to one answer.
Why
Glossina is unmistakable once you know the three features: scissor-folded wings with the hatchet cell, a forward-projecting rigid proboscis, and painful day-time biting by both sexes (most vectors are female-only blood feeders). It transmits Trypanosoma brucei — gambiense in West and Central Africa (chronic, slowly progressive) and rhodesiense in East and Southern Africa (acute, often with a trypanosomal chancre at the bite, and the form travellers on safari acquire).
Why not the others
- A — Anopheles: a slender mosquito that rests at a characteristic angle to the surface and bites at night; the description is nothing like a fly of this build.
- B — Sandfly: tiny, hairy, silent, hops rather than flies, and bites at dusk and night — far smaller than a housefly.
- C — Triatomine bug: a true bug, not a fly. It bites at night, painlessly, and transmits by rubbing infected faeces into the wound or the conjunctiva; found in the Americas.
- D — Blackfly: small, humpbacked, breeds in fast-flowing rivers (“river blindness”), and does not have the tsetse’s proboscis or wing pattern.
Scenario 4 of 6
A fresh warm stool from a patient with bloody diarrhoea shows a motile amoeboid trophozoite, roughly 25 micrometres, with a single nucleus bearing a small central karyosome, and ingested red blood cells within its cytoplasm.
What is the significance of the ingested red cells?
Commit to one answer.
Why
E. histolytica and E. dispar are indistinguishable under the microscope, and E. dispar is by far the more common and is non-pathogenic — so “cysts seen” on a stool report means very little on its own. The one morphological feature that proves invasion is a trophozoite that has eaten red blood cells. That, or antigen detection / PCR, is what justifies treatment: metronidazole or tinidazole for the invasive disease, followed by a luminal amoebicide such as paromomycin or diloxanide furoate to clear residual cysts from the gut.
Why not the others
- B — E. coli (the amoeba): a genuine commensal, but it has a larger, eccentric karyosome and coarse peripheral chromatin, and it does not ingest red cells.
- C — Giardia: a pear-shaped flagellate with two nuclei and a “falling leaf” motility; it causes watery, not bloody, diarrhoea and never phagocytoses red cells.
- D — Contamination: the finding is the diagnosis, not an artefact — and a warm fresh stool is precisely how you catch motile trophozoites.
- E — Balantidium coli: a large ciliated protozoan (over 50 micrometres) with a kidney-shaped macronucleus, associated with pig contact — quite different in appearance.
Scenario 5 of 6
A skin snip taken from an itchy patient in West Africa is incubated in saline. Motile microfilariae emerge. They are unsheathed, and the nuclei do not extend to the tip of the tail. No microfilariae are found in a daytime or a midnight blood film.
Which parasite, and what must you check before treating?
Commit to one answer.
Why
Onchocerca microfilariae live in the skin, not the blood, so a skin snip is diagnostic and blood films are negative — that alone makes the answer. They are unsheathed with tail nuclei stopping short of the tip. Onchocerciasis (river blindness) is transmitted by Simulium blackflies near fast-flowing rivers and causes intense itch, a papular dermatitis, hanging groin and keratitis. Ivermectin is the treatment, but in Central/West Africa you must first exclude a heavy Loa loa co-infection, because microfilarial death in high Loa loa loads can precipitate fatal encephalopathy. Doxycycline, which kills the Wolbachia endosymbiont, is used as an adjunct.
Why not the others
- A — Loa loa: its microfilariae are sheathed, with nuclei running right to the tail tip, and circulate in blood with a daytime periodicity — they are not found in a skin snip.
- C — Wuchereria bancrofti: sheathed, nocturnally periodic in blood, causing lymphoedema; and praziquantel is a fluke and cestode drug, not a filaricide.
- D — Mansonella perstans: unsheathed but blood-dwelling and non-periodic; it is largely asymptomatic and notoriously poorly responsive to standard therapy — not an urgent treat.
- E — Dracunculus: a metre-long adult worm emerging through a skin blister; there are no microfilariae in a snip, and the disease is nearly eradicated.
Scenario 6 of 6
A patient from Bihar, India, has four months of fever, weight loss, massive splenomegaly and darkened skin. Hb 76, WCC 2.1, platelets 68. A splenic or bone-marrow aspirate shows small oval intracellular bodies within macrophages, each with a nucleus and a small rod-shaped kinetoplast.
What are these bodies?
Commit to one answer.
Why
The kinetoplast — a rod of mitochondrial DNA sitting beside the nucleus — is the identifying feature of the amastigote and is what separates Leishmania from every other small intracellular body. Bihar is the classic hyperendemic focus for L. donovani. The clinical picture is unmistakable: months of fever, gross splenomegaly, pancytopenia, hypergammaglobulinaemia, wasting and darkened skin (hence kala-azar, “black fever”). It is transmitted by the sandfly and is fatal untreated; liposomal amphotericin B is the standard treatment in the UK and in South Asia.
Why not the others
- A — Histoplasma: also small and intracellular in macrophages, but it has no kinetoplast — that single feature is the discriminator; it stains with silver stains and grows on fungal culture.
- B — Toxoplasma tachyzoites: crescentic, no kinetoplast, and clinically give lymphadenopathy or encephalitis in the immunosuppressed, not kala-azar.
- D — Trypanosomes: extracellular, flagellated and free in the blood or CSF, with an undulating membrane — never packed inside marrow macrophages.
- E — Falciparum schizonts: sit inside red cells and contain malaria pigment; they do not reside in macrophages and have no kinetoplast.
4 · Tropical diarrhoea
Watery or bloody. Acute or persistent. Answer those two questions first and the organism, and the decision to treat, usually follow.
Scenario 1 of 6
During a cholera outbreak in a refugee camp, a man passes torrential painless watery stool described as “rice water”, with vomiting and no fever. He is sunken-eyed, has no radial pulse and is barely conscious.
What is the single priority?
Commit to one answer.
Why
Cholera kills by dehydration, not by infection, and losses can exceed a litre an hour. Severe dehydration means immediate intravenous Ringer’s lactate (the isotonic, potassium- and base-containing fluid of choice), transitioning to ORS as soon as the patient can drink. Untreated severe cholera can kill within hours; with prompt rehydration, WHO expects case fatality in treatment centres to stay below 1%. Antibiotics — doxycycline or azithromycin depending on local resistance — shorten the illness, reduce fluid requirements and shorten shedding, but they are an adjunct and never the priority.
Why not the others
- A — Await the culture: he will be dead long before it grows. Cholera is a clinical and epidemiological diagnosis in an outbreak.
- B — Doxycycline as primary treatment: right drug, wrong priority — it does nothing about the circulating volume he has already lost.
- C — Loperamide: does not reduce the true fluid loss (it pools it in the bowel), masks deterioration, and is contraindicated in this setting.
- E — 5% dextrose: supplies almost no sodium; it will not restore intravascular volume and risks hyponatraemia in a patient losing salt torrentially.
Scenario 2 of 6
A traveller in India develops abrupt fever 39°C, cramping abdominal pain, tenesmus and small-volume bloody stools with mucus, up to twelve times a day. He is systemically unwell. WCC 15.
Which is the most likely organism, and how would you manage it?
Commit to one answer.
Why
Fever, tenesmus, small-volume bloody mucoid stool and a systemic inflammatory response is the classic invasive colitic (dysenteric) picture. Shigella is the prototype, with Campylobacter, invasive Salmonella and EIEC as the other main candidates — and Shigella needs a strikingly small infectious dose, so person-to-person spread is common. Antibiotics shorten illness and reduce transmission but resistance in South Asia is now substantial, so treatment is guided by local patterns and culture. Antimotility agents should be avoided in fever-plus-blood dysentery.
Why not the others
- A — ETEC: the commonest cause of travellers’ diarrhoea, but it is a toxin-mediated, watery, non-febrile illness with no blood and no tenesmus.
- B — Giardia: a non-invasive small-bowel protozoan causing bloating, foul stools and steatorrhoea over weeks — never fever with bloody colitis.
- C — Cholera: profuse painless watery “rice-water” stool, no blood, no fever — the exact opposite pattern.
- D — Norovirus: vomiting-predominant, short-lived and watery; it does not produce blood, tenesmus or a WCC of 15.
Scenario 3 of 6
Six weeks after trekking in Nepal, a woman still has intermittent loose, pale, greasy, foul-smelling stools with marked bloating, flatulence, upper abdominal cramps and 4 kg of weight loss. No fever, no blood.
What is the most likely diagnosis and treatment?
Commit to one answer.
Why
Giardia is the classic cause of persistent (over 14 days) non-bloody travellers’ diarrhoea, particularly from South Asia, Russia and mountain freshwater. It parasitises the duodenum and jejunum, causing partial villous atrophy and malabsorption — hence steatorrhoea, bloating, sulphurous belching and weight loss without fever or blood. Stool microscopy is insensitive (cysts are shed intermittently), so use faecal antigen or PCR, and treat empirically where suspicion is high. Nitroimidazoles are first line. Secondary lactose intolerance may persist for weeks afterwards and is not treatment failure.
Why not the others
- B — Amoebic dysentery: presents with bloody, mucoid stools and colitis, not fatty malabsorptive stools with bloating.
- C — Post-infectious IBS: a real entity and a common sequel, but it is a diagnosis of exclusion — you must exclude a treatable persisting parasite (and coeliac disease) first.
- D — Coeliac disease: can certainly be unmasked after an enteric infection and deserves testing, but a duodenal biopsy before a simple, treatable, geographically typical parasite is the wrong order.
- E — Chronic cholera carriage: not a real clinical syndrome; cholera is acute and does not cause chronic malabsorption.
Scenario 4 of 6
A healthy 28-year-old on day 3 of a fortnight in Mexico has three or four loose watery stools a day with mild cramps. No fever, no blood. He is eating and drinking normally and asks what to take.
What is the most appropriate advice?
Commit to one answer.
Why
Most travellers’ diarrhoea is mild, bacterial (enterotoxigenic E. coli is the single commonest cause) and resolves in 1–5 days without any specific therapy. The mainstay is fluid and salt replacement, and loperamide is acceptable for symptom control in mild non-dysenteric illness. Antibiotics — increasingly azithromycin rather than a fluoroquinolone, given resistance and the association between quinolones and acquiring multi-drug-resistant Enterobacterales while travelling — are reserved for moderate to severe or disabling illness. Watch instead for the red flags: fever, blood, or persistence beyond two weeks.
Why not the others
- A — Antibiotics for everyone: over-treats a self-limiting illness, drives resistance, and there is good evidence that travellers taking quinolones return colonised with resistant organisms.
- C — Nil by mouth: the opposite of what is needed; withholding fluid causes the dehydration you are trying to prevent, and early feeding is safe.
- D — Empirical metronidazole: Giardia causes persistent, not day-3, diarrhoea; treating this early is guesswork against the wrong organism.
- E — Fly home: a wild over-reaction to a benign, self-limiting illness in a well young adult.
Scenario 5 of 6
A man who lived in Bangladesh two years ago presents with three weeks of fever, sweats, weight loss and constant right upper quadrant pain that is worse on movement. He has no diarrhoea. Tender hepatomegaly; ultrasound shows a single 7 cm cystic lesion in the right lobe. Amoebic serology is positive.
What is the correct treatment?
Commit to one answer.
Why
Amoebic liver abscess is characteristically a solitary right-lobe lesion appearing months to years after exposure, and — the exam’s favourite point — fewer than a third of patients have any history of dysentery at all. Serology is positive in the great majority of extraintestinal disease. Metronidazole or tinidazole rapidly treats the invasive tissue infection, but it does not reliably clear cysts from the gut lumen, so a luminal amoebicide must follow or the patient will relapse and continue to shed. Aspiration is reserved for large or left-lobe lesions at risk of rupture, uncertain diagnosis, or failure to improve after around 5–7 days.
Why not the others
- A — Surgery: almost never indicated; amoebic abscesses respond dramatically to medical therapy, and surgery adds risk for no benefit.
- B — Metronidazole alone: the single commonest error. Tissue amoebicides do not clear luminal cysts — always follow with a luminal agent.
- D — Albendazole: that is the drug for hydatid disease, which would give a calcified, daughter-cyst-containing lesion, usually without a septic picture — and blind aspiration of a hydatid cyst risks anaphylaxis.
- E — Pyogenic abscess cover: a real differential, but the serology, the single right-lobe lesion and the epidemiology point to amoeba; treat that, and reconsider only if he fails to respond.
Scenario 6 of 6
A man who worked barefoot in rural Cambodia twenty years ago has intermittent loose stools, epigastric discomfort and a migratory serpiginous urticarial rash on his buttocks. Eosinophils 1.8 x10⁹/L. His rheumatologist is about to start high-dose corticosteroids.
What is the diagnosis, and why does the steroid plan matter?
Commit to one answer.
Why
Strongyloides stercoralis is the only common helminth that completes its life cycle inside the host by autoinfection, so it can persist for decades after a single exposure — a classic in ex-servicemen and long-ago expatriates. The migratory serpiginous rash (larva currens, which moves centimetres per hour) plus eosinophilia plus vague gut symptoms is the signature. Corticosteroids, HTLV-1 and other T-cell immunosuppression accelerate autoinfection into hyperinfection and disseminated strongyloidiasis, with larvae carrying gut bacteria into the blood and meninges — mortality is very high. Screen (serology, ideally with stool studies) and treat with ivermectin before immunosuppression.
Why not the others
- A — Giardia: does not cause eosinophilia (it is a protozoan, not a helminth), does not cause a migratory rash, and carries no hyperinfection risk.
- B — Hookworm: causes eosinophilia and iron-deficiency anaemia, but it cannot autoinfect, so it dies out within a few years and poses no steroid-related danger.
- C — Cutaneous larva migrans: the animal hookworm rash — slow-moving (millimetres per day), on the feet, and it does not persist for twenty years or disseminate.
- E — Post-infectious IBS: would leave a treatable, potentially lethal parasite unscreened in a patient about to be immunosuppressed. Eosinophilia is never IBS.
5 · Public health and epidemiology in the tropics
The Society of Apothecaries’ 2026 Regulations and Syllabus give public health and preventive medicine about a quarter of the DTM&H, including a one-hour preventive medicine short structured question paper. Think in populations, definitions and denominators.
Scenario 1 of 7
Over three days, the clinic in a camp for displaced people sees 14 adults with acute watery diarrhoea; two have died. Stool samples have gone to the reference laboratory and results will take several days. You are asked to lead the response.
Which approach reflects standard outbreak investigation practice?
Commit to one answer.
Why
UKHSA’s Communicable disease outbreak management guidance (updated July 2026) defines an outbreak as two or more people with the same infection linked by time, place or common exposure. The core work is: agree an initial case definition as early as possible and revise it as information arrives; find cases; describe them by time and place and by characteristics such as age, sex and severity; form a provisional hypothesis about cause, vehicle and source; test it with an analytical study; and communicate throughout. The guidance is explicit that control measures are implemented promptly alongside the initial investigation, not after it. In a camp with deaths from watery diarrhoea, the expected answer does not wait for a culture result.
Why not the others
- A — Wait for the lab: confirmation matters, but the guidance says control measures run alongside the investigation; a delay of several days in a camp costs lives.
- B — Analytical study first: a case-control study tests a hypothesis. Without a case definition you cannot say who is a case, and without descriptive epidemiology you have no hypothesis to test.
- D — Split off the deaths: deaths with the same syndrome in the same place over the same days belong to the cluster until shown otherwise; excluding them biases the description and hides severity.
- E — Fixed threshold: UKHSA defines an outbreak as two or more linked cases. Thresholds are a surveillance alarm, not a reason to delay acting on a cluster you can already see.
Scenario 2 of 7
A district that has had no cholera for years reports one locally acquired case of Vibrio cholerae O1, confirmed by culture. The following week, health workers ask how they should now count new patients.
Under the Global Task Force on Cholera Control (GTFCC) surveillance guidance (2024), which suspected-case definition now applies in that district?
Commit to one answer.
Why
The GTFCC’s Public health surveillance for cholera (2024) uses two suspected-case definitions. Where there is no outbreak, it is narrow — a person aged 2 years or older with acute watery diarrhoea and severe dehydration, or who died from it with no other known cause — so that sporadic diarrhoea does not raise false alarms. In a previously unaffected area, one locally acquired confirmed case is a confirmed outbreak, and the definition then widens to any person with, or dying from, acute watery diarrhoea, so that cases are captured fast and managed on dehydration status rather than on test results. This is the general trade-off for any case definition: specificity when false alarms are the risk, sensitivity when missed cases are.
Why not the others
- A — Confirmed cases only: culture or PCR confirms cases and tracks the outbreak, but counting only confirmed cases would miss most patients during an outbreak.
- B — The narrow definition: that is the definition for areas without an outbreak; keeping it now would undercount.
- C — RDT-positive only: GTFCC treats rapid tests as screening tools — good negative predictive value, but not enough positive predictive value to confirm an individual case. They are not the case definition.
- D — Under-5 loose stools: a generic childhood diarrhoea measure, not the cholera definition; cholera affects all ages.
Scenario 3 of 7
A camp of 20,000 people records 400 new cholera cases over four weeks. Twelve of those patients die. On a single survey day, 150 people are currently ill.
What is the case-fatality rate, and what does it suggest?
Commit to one answer.
Why
Case-fatality rate is the proportion of cases who die of the condition: 12 deaths ÷ 400 cases = 3%. (Strictly it is a proportion, not a rate — CDC’s Principles of Epidemiology notes some prefer “case-fatality ratio”.) The other figures are different measures: 400 ÷ 20,000 = 2% is the attack rate (incidence proportion) over four weeks; 150 ÷ 20,000 = 0.75% is point prevalence on the survey day; 12 ÷ 20,000 = 0.06% is mortality across the whole population. The WHO cholera fact sheet states that, with proper treatment, the case-fatality rate should remain below 1% — so 3% is a signal to look at late presentation, access to oral rehydration and treatment-centre capacity.
Why not the others
- A — 0.06%: that is deaths over the whole population — a mortality figure, not deaths over cases. It hides how lethal the disease is for those infected.
- C — 8%: the people ill on one day are a prevalence count. The deaths came from all 400 cases over four weeks, so numerator and denominator do not match.
- D — 2%: this is the attack rate — the proportion of the population who became cases — not the proportion of cases who died.
- E — 0.75%: point prevalence describes the burden on one day; it is not a fatality measure at all.
Scenario 4 of 7
A donor offers a cheap, accurate point-of-care test so that a rural district can screen every adult for a common chronic infection. The district hospital has no supply of the treatment, no staff to follow people up, and no plan to add either.
Judged against the classic screening principles (Wilson and Jungner, WHO 1968) as built on by the UK National Screening Committee criteria, what is the strongest objection?
Commit to one answer.
Why
Wilson and Jungner’s principles (WHO Public Health Paper 34, 1968), and the UK NSC criteria that build on them (updated September 2022), judge the programme, not just the test. The UK NSC criteria ask for an important health problem judged by frequency and/or severity; a simple, safe, precise and validated test; an effective intervention, with evidence that intervening early leads to better outcomes; benefit that outweighs harm; and adequate staffing and facilities for testing, diagnosis, treatment and programme management before the programme starts. Finding people with a treatable condition you cannot treat brings the harms of screening — anxiety, labelling, cost — without the benefit.
Why not the others
- A — Test-first thinking: a simple, safe, precise test is only one criterion; the programme also needs an effective intervention and the facilities to deliver it.
- B — Rarity: the criteria ask for an important health problem judged by frequency and/or severity — a common condition is often a strong candidate.
- C — Perfect test: no test is perfect; the criteria ask for a simple, safe, precise and validated test, not 100% accuracy.
- E — Never in low-income settings: the principles apply everywhere; what fails here is this programme’s missing treatment pathway, not the setting.
Scenario 5 of 7
In a community nutrition screening round, a 2-year-old has a mid-upper arm circumference (MUAC) of 112 mm. There is no oedema. He is alert, has no medical complications and passes the appetite test. Weight-for-height has not yet been measured.
How is he classified, and where does WHO guidance place his care?
Commit to one answer.
Why
WHO (eLENA, updated August 2023, from the 2013 guideline on severe acute malnutrition) defines SAM in children aged 6–59 months as any one of: MUAC below 115 mm; weight-for-height below −3 Z-scores of the WHO Child Growth Standards; or bilateral pitting oedema. One criterion is enough, so 112 mm is SAM without waiting for weight-for-height. WHO advises referral for full assessment at a treatment centre, and children who pass the appetite test and are clinically well and alert are treated as outpatients. Moderate wasting is weight-for-height between −3 and −2 Z-scores and/or MUAC from 115 mm to below 125 mm.
Why not the others
- B — Moderate: the moderate band starts at 115 mm; 112 mm is below it.
- C — Wait for weight-for-height: the WHO criteria are alternatives — MUAC below 115 mm on its own defines SAM.
- D — Admit everyone: WHO advises outpatient treatment for children with SAM who pass the appetite test and are clinically well and alert.
- E — Normal: no oedema removes one criterion, not the others; the MUAC alone defines SAM.
Scenario 6 of 7
A coastal city reports a rising number of dengue cases. Inspectors find mosquito larvae in household water-storage drums, discarded tyres and flower-pot saucers. The council proposes free bed nets for every household as its main response.
Which response best fits WHO guidance on the dengue vector?
Commit to one answer.
Why
Dengue is spread by the bite of infected Aedes mosquitoes, mainly Aedes aegypti, which WHO notes are active during the day (WHO dengue fact sheet, August 2025). WHO’s prevention advice centres on the vector’s breeding: environmental management to stop mosquitoes reaching egg-laying habitats; covering, emptying and cleaning domestic water-storage containers weekly; appropriate insecticides for outdoor water containers; and personal protection — window screens, repellents and nets. Routine vector surveillance and targeted community engagement greatly strengthen control. Contrast malaria, where WHO names insecticide-treated nets and indoor residual spraying as the two core vector-control interventions (WHO malaria fact sheet, December 2025).
Why not the others
- A — Nets as the main response: WHO does list nets among personal protection, but the dengue vector is active during the day, so night-time nets cannot be the main answer; the breeding sites are the target.
- B — Drain the marshes: the larvae here are in containers around homes, and WHO’s dengue advice targets those domestic water containers and egg-laying habitats.
- D — Chemoprophylaxis: WHO states there is no specific treatment for dengue; prevention rests on vector control and personal protection, not mass medication.
- E — Isolation: dengue is transmitted by mosquito bites, so isolating patients in hospital does not address the route of spread.
Scenario 7 of 7
A novel respiratory virus was declared a public health emergency of international concern (PHEIC) a month ago. It is now spreading within many countries on several continents, hospitals in several of them are overwhelmed, and schools, travel and trade are badly disrupted. A colleague asks what the International Health Regulations now allow the WHO Director-General to do.
Under the 2024 amendments to the IHR (in force since 19 September 2025), which statement is correct?
Commit to one answer.
Why
The amendments to the IHR (2005) were adopted by the Seventy-seventh World Health Assembly on 1 June 2024 (resolution WHA77.17) and came into force on 19 September 2025 (WHO IHR amendments Q&A). They add a pandemic emergency: the highest level of global alert the Director-General may issue. It is a PHEIC caused by a communicable disease that has, or is at high risk of having, wide geographical spread to and within multiple States; is exceeding, or is at high risk of exceeding, the capacity of health systems; is causing, or is at high risk of causing, substantial social and/or economic disruption; and requires rapid, equitable and enhanced coordinated international action. Here all four are met. The same package asks each State Party to designate a National IHR Authority to coordinate implementation, and adds equity provisions: WHO is to facilitate timely and equitable access to relevant health products, and a Coordinating Financial Mechanism is established (IHR (2005) as amended in 2024, Articles 4, 13 and 44bis).
Why not the others
- A — PHEIC is the ceiling: no longer. Since 19 September 2025 the pandemic emergency sits above a PHEIC as the highest alert.
- B — Binding lockdowns: WHO’s temporary recommendations are not legally binding, and WHO has no ability to impose lockdowns or travel restrictions on populations (WHO IHR amendments Q&A).
- C — An Assembly vote: the Director-General determines a pandemic emergency, as with a PHEIC; it does not wait for a World Health Assembly vote.
- E — Spread alone: wide geographical spread is only one of four criteria; all four must be met, including health systems exceeded or at high risk of being exceeded.
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Fever in the returning traveller
How many negative blood films, over what period, are needed to exclude malaria?
Three negative films over 48 hours, taken 12–24 hours apart. Parasitaemia fluctuates with the schizogony cycle, so a single negative film — or a single negative rapid test — never excludes malaria in a febrile returning traveller.
Fever in the returning traveller
A fever begins more than 21 days after leaving the tropics. Which broad group of diagnoses does that effectively exclude, and what remains?
It effectively excludes the short-incubation infections: dengue, chikungunya, Zika and the rickettsioses (all under about 14 days). What remains: malaria (especially vivax and ovale relapse), enteric fever, TB, viral hepatitis, amoebic liver abscess, visceral leishmaniasis, acute HIV.
Fever in the returning traveller
What is the minimum incubation period of falciparum malaria, and why does that number matter?
About 7 days. A fever that begins fewer than 7 days after first entering an endemic area is essentially never malaria — it points to an arbovirus (dengue, chikungunya) or another short-incubation cause. Conversely, any fever from day 7 onwards is malaria until excluded.
Fever in the returning traveller
In dengue, when is the patient most at risk of deterioration?
At defervescence — as the fever falls, usually days 4–6. This is the critical phase of plasma leakage: rising haematocrit, falling platelets, effusions and shock. Monitor serial haematocrit and platelets, give careful fluids, and avoid NSAIDs and aspirin.
Fever in the returning traveller
Fever, urticaria and marked eosinophilia 3–8 weeks after freshwater swimming in Africa. What is it, and what is the catch with testing?
Katayama syndrome — acute schistosomiasis, a hypersensitivity response to migrating schistosomulae. The catch: eggs are often not yet being excreted and serology may still be negative this early, so treat clinically. Praziquantel does not kill immature worms, so a repeat course after 6–12 weeks is standard; steroids if severe.
Fever in the returning traveller
A febrile patient returned 8 days ago from a VHF-endemic country with a healthcare exposure. What changes about your approach?
Fever within 21 days of leaving a VHF-endemic area with a relevant exposure triggers a VHF risk assessment: isolate the patient, use appropriate PPE, avoid unnecessary venepuncture and aerosols, and speak to the Imported Fever Service and local infection team before sampling, so that malaria testing happens under the right containment. You still exclude malaria — it remains the likeliest diagnosis.
Fever in the returning traveller
Eosinophilia in a febrile returning traveller — what does it tell you, and what does it argue against?
It points to a helminth (schistosomiasis, strongyloides, filariasis, hookworm) — or to a drug reaction. It argues against malaria and most bacterial infections, which typically suppress or do not raise the eosinophil count. Protozoa (giardia, amoeba) do not cause eosinophilia either.
Malaria decoder
Which malaria species form hypnozoites, and what follows from that?
P. vivax and P. ovale. Dormant liver hypnozoites cause relapse weeks to months later, so blood-stage treatment alone is not a cure. Radical cure needs primaquine for 14 days (or single-dose tafenoquine), and G6PD status must be checked first because both cause haemolysis in G6PD deficiency.
Malaria decoder
Name the WHO features of severe falciparum malaria.
Impaired consciousness, prostration, multiple seizures, respiratory distress or metabolic acidosis, shock, pulmonary oedema, acute kidney injury, jaundice with other organ dysfunction, severe anaemia, abnormal bleeding, haemoglobinuria, hypoglycaemia (under 2.2 mmol/L), and hyperparasitaemia (over 10%). Any one is enough. In UK practice, a parasitaemia over 2% is treated with intravenous artesunate, even without other severe features.
Malaria decoder
First-line treatment for (a) severe falciparum and (b) uncomplicated falciparum?
(a) Intravenous artesunate — superior to quinine on mortality (SEAQUAMAT, AQUAMAT); follow with a full oral ACT course once the patient can swallow, and warn about delayed post-artesunate haemolysis at 1–3 weeks. (b) An oral ACT such as artemether-lumefantrine, taken with fatty food to ensure absorption.
Malaria decoder
Why does P. knowlesi matter, and how is it misread?
A macaque parasite of forested Southeast Asia (especially Malaysian Borneo). It is routinely misreported as P. malariae (band forms) or falciparum (rings), but it has a 24-hour erythrocytic cycle, so parasitaemia rises explosively and severe disease is common. PCR confirms. Manage a rapidly rising “malariae” from Borneo as severe malaria.
Malaria decoder
A patient develops malaria despite taking chemoprophylaxis correctly. What are the two lessons?
1. No prophylaxis is 100% effective — bite avoidance and prompt testing of any fever remain essential. 2. Treat with a different drug class from the one used for prophylaxis, since the parasite grew in its presence. Never simply repeat the failed agent at treatment dose.
Malaria decoder
Define relapse, recrudescence and reinfection in malaria.
Relapse — reactivation of liver hypnozoites (vivax, ovale only), weeks to months later. Recrudescence — regrowth of persisting blood-stage parasites after inadequate treatment or resistance, within days to weeks. Reinfection — a new mosquito bite, requiring fresh exposure.
Malaria decoder
Why is artemisinin monotherapy never acceptable?
Artemisinins clear parasites fast but have a very short half-life, so used alone they leave residual parasites and select for resistance — which has emerged in the Greater Mekong and is now reported in parts of East Africa. WHO therefore mandates a combination: the artemisinin for rapid kill, a long-acting partner drug to eliminate the remainder and protect the artemisinin.
Parasite and vector recognition
Which blood-film features identify P. falciparum?
Banana-shaped (crescentic) gametocytes — pathognomonic. Plus: normal-sized red cells, high parasitaemia, multiply-infected cells, appliqué (marginal) forms, double chromatin dots, and only ring forms visible, because mature stages sequester in the microvasculature.
Parasite and vector recognition
Distinguish vivax, ovale and malariae on a film.
Vivax — enlarged red cells, Schuffner dots, amoeboid trophozoites (infects reticulocytes). Ovale — enlarged, oval, fimbriated (ragged-edged) cells, Schuffner dots. Malariae — normal-sized cells, band-form trophozoites, rosette schizonts, low parasitaemia, 72-hour cycle.
Parasite and vector recognition
Schistosome eggs: how do you tell haematobium, mansoni and japonicum apart?
S. haematobium — terminal spine, found in urine; bladder disease, obstructive uropathy, squamous cell bladder carcinoma. S. mansoni — lateral spine, found in stool; intestinal disease and periportal (pipe-stem) fibrosis with portal hypertension. S. japonicum — small, round, rudimentary knob, in stool; East Asia; most associated with CNS disease.
Parasite and vector recognition
Match the vector to the disease: Anopheles, Aedes aegypti, Glossina, Phlebotomus, Triatomine, Simulium.
Anopheles (night-biting) — malaria. Aedes aegypti (day-biting, urban) — dengue, yellow fever, Zika, chikungunya. Glossina, the tsetse (painful day bite, scissor wings, forward proboscis) — African trypanosomiasis. Phlebotomus, the sandfly — leishmaniasis. Triatomine bug (night, painless, infected faeces) — Chagas disease. Simulium, the blackfly (fast rivers) — onchocerciasis.
Parasite and vector recognition
On stool microscopy, what single feature proves invasive Entamoeba histolytica?
Erythrophagocytosis — a trophozoite containing ingested red blood cells. E. histolytica is morphologically identical to the far commoner non-pathogenic E. dispar, so cysts alone mean little; antigen detection or PCR is the alternative discriminator. Treat invasive disease with metronidazole or tinidazole, then a luminal amoebicide.
Parasite and vector recognition
How do you tell Onchocerca, Loa loa and Wuchereria microfilariae apart?
Onchocerca — in skin (skin snip), unsheathed, nuclei stop short of the tail tip; blackfly-borne; river blindness. Loa loa — in blood, sheathed, nuclei run to the tail tip, daytime periodicity. Wuchereria bancrofti — in blood, sheathed, nuclei not to the tip, nocturnal periodicity; lymphatic filariasis. Exclude heavy Loa loa before giving ivermectin: risk of fatal encephalopathy.
Parasite and vector recognition
What are Leishman-Donovan bodies, and what is the discriminating microscopic feature?
Leishmania amastigotes inside macrophages, seen in splenic or bone-marrow aspirate in visceral leishmaniasis (kala-azar). The discriminator is the kinetoplast — a rod of mitochondrial DNA beside the nucleus — which separates them from Histoplasma and other small intracellular bodies. Sandfly-borne; treat with liposomal amphotericin B.
Tropical diarrhoea
What is the priority in severe cholera, and which intravenous fluid?
Rehydration, not antibiotics. Severe dehydration: intravenous Ringer’s lactate (isotonic, contains potassium and base), moving to ORS as soon as the patient can drink. Untreated severe cholera can kill within hours; with prompt rehydration, WHO expects case fatality in treatment centres to stay below 1%. Doxycycline or azithromycin shortens illness and shedding but is an adjunct.
Tropical diarrhoea
Bloody diarrhoea with fever in a traveller — which organisms, and what must you avoid?
Invasive colitis: Shigella, Campylobacter, non-typhoidal Salmonella, EIEC (and amoebic colitis, usually with less fever and a more gradual onset). Culture the stool, rehydrate, and treat with an antibiotic guided by local resistance if severe. Avoid loperamide in fever-plus-blood dysentery.
Tropical diarrhoea
Persistent (over 14 days) non-bloody diarrhoea with bloating and greasy stools after travel. Diagnosis and treatment?
Giardiasis. Duodenal/jejunal infection causing partial villous atrophy and malabsorption — steatorrhoea, flatulence, weight loss, no fever, no blood. Stool microscopy is insensitive (intermittent shedding): use faecal antigen or PCR. Treat with metronidazole or single-dose tinidazole. Secondary lactose intolerance may persist afterwards and is not treatment failure.
Tropical diarrhoea
Commonest cause of travellers’ diarrhoea, and when do you actually give an antibiotic?
Enterotoxigenic E. coli (ETEC) — watery, afebrile, self-limiting in 1–5 days. Mainstay is oral rehydration; loperamide is acceptable in mild non-dysenteric illness. Reserve antibiotics (increasingly azithromycin over fluoroquinolones, given resistance and the risk of returning colonised with resistant Enterobacterales) for moderate to severe or disabling illness.
Tropical diarrhoea
Amoebic liver abscess: the classic picture, and the treatment error people make.
Typically a solitary right-lobe abscess presenting months to years after exposure, with fever, weight loss and RUQ pain — and fewer than a third have any history of dysentery. Serology is usually positive. The error: giving metronidazole alone. It does not clear luminal cysts, so always follow with a luminal amoebicide (paromomycin or diloxanide furoate). Aspirate only if large, at risk of rupture, diagnostically uncertain, or failing to respond.
Tropical diarrhoea
Why is Strongyloides different from every other helminth, and what is the practical consequence?
It autoinfects, completing its life cycle within the host, so it persists for decades after a single exposure. Larva currens (a fast, migratory serpiginous rash) plus eosinophilia is the signature. Corticosteroids, HTLV-1 or other T-cell immunosuppression trigger hyperinfection and dissemination, with Gram-negative sepsis and meningitis and very high mortality. Screen and treat with ivermectin before immunosuppressing anyone who has lived in the tropics.
Tropical diarrhoea
Give the two questions that should organise your thinking about any tropical diarrhoea.
1. Watery or bloody? Watery equals toxin-mediated or small-bowel (ETEC, cholera, viruses, giardia); bloody equals invasive colitis (Shigella, Campylobacter, Salmonella, EIEC, amoeba). 2. Acute or persistent (over 14 days)? Persistent shifts you towards parasites (giardia, cryptosporidium, cyclospora, strongyloides), post-infectious IBS and secondary lactose intolerance.
Public health in the tropics
Under the International Health Regulations (2005), which four diseases must always be notified to WHO, and how fast?
Smallpox, poliomyelitis due to wild-type poliovirus, human influenza caused by a new subtype, and SARS — a single case is always notifiable. The State Party notifies WHO through its National IHR Focal Point within 24 hours of assessment (WHO guidance on the use of Annex 2 of the IHR).
Public health in the tropics
What are the four questions of the IHR (2005) Annex 2 decision instrument, and how many must be met for an event to be notifiable?
Is the public health impact serious? Is the event unusual or unexpected? Is there a significant risk of international spread? Is there a significant risk of international travel or trade restrictions? Any two of the four make it notifiable. Events involving diseases such as cholera, pneumonic plague, yellow fever and the viral haemorrhagic fevers must always be assessed with the instrument.
Public health in the tropics
What does WHO describe as the long-term solution for cholera, and where do vaccines and antibiotics fit?
Safe drinking water, basic sanitation and good hygiene (WASH) — WHO cholera fact sheet. There are three WHO-approved oral cholera vaccines; because of supply constraints since 2022, only one-dose regimens are being used. Mass antibiotic chemoprophylaxis is not recommended: it has no proven effect on spread and may contribute to antimicrobial resistance. With proper treatment, the case-fatality rate should remain below 1%.
Public health in the tropics
What MUAC and weight-for-height thresholds define moderate wasting in children aged 6–59 months?
Weight-for-height between −3 and −2 Z-scores of the WHO Child Growth Standards and/or MUAC from 115 mm to below 125 mm (WHO eLENA, 2023). MUAC below 115 mm, weight-for-height below −3 Z, or bilateral pitting oedema is severe acute malnutrition.
Public health in the tropics
How do incidence and prevalence differ, and how are they linked?
Incidence counts new cases in a population at risk over a period — as a proportion (the attack rate) or per unit of person-time. Prevalence is the proportion who have the condition at a point in time or over a period. Prevalence depends on both incidence and duration: a high prevalence may reflect high incidence, prolonged survival without cure, or both (CDC, Principles of Epidemiology).
Public health in the tropics
Name WHO’s two core malaria vector-control interventions, and the main control approach for the dengue vector.
Malaria: insecticide-treated nets and indoor residual spraying (WHO malaria fact sheet, December 2025); new-generation nets give better protection than pyrethroid-only nets. Dengue: Aedes is active during the day, so control centres on removing egg-laying habitats — cover, empty and clean water-storage containers weekly — with community engagement (WHO dengue fact sheet, August 2025).
Public health in the tropics
What did the 2024 amendments to the International Health Regulations add, and when did they come into force?
Adopted by the World Health Assembly on 1 June 2024 (WHA77.17); in force from 19 September 2025 (11 of the 196 States Parties rejected them, and previous versions still apply to those). Key additions: a pandemic emergency — the highest alert the Director-General can issue, for a PHEIC with wide spread to and within multiple States, health-system capacity exceeded or at high risk, substantial social or economic disruption, and a need for rapid, equitable, coordinated action; a National IHR Authority in each State Party to coordinate implementation; and equity and solidarity provisions — WHO to facilitate equitable access to relevant health products, and a Coordinating Financial Mechanism (WHO IHR amendments Q&A, 2025; IHR (2005) as amended in 2024).
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This tool is free. If you are preparing for the DTM&H, the full course puts the same reasoning into exam-style questions: a question bank with Core Lens and Deep Dive explanations, a Core Calendar revision plan built around your exam date, and Core Compass to show you which topics need you next.
Core Revision is an independent revision resource, not affiliated with the Worshipful Society of Apothecaries. Always confirm with current guidance.
The rest of the DTM&H toolkit
Every part of the DTM&H track, one click away. Work across them rather than through them — the guide explains it, the tools drill the decision, the bank tests it and the Compass tells you what is left.