Malaria and Dengue

Microbiology — Tropical and Vector-borne Infection, NMC MBBS licence examination syllabus (Nepal Medical Council).

Malaria and dengue: the fever that must not wait

One kills in days if missed. The other kills as the fever settles.

A febrile patient with recent exposure to a malarious area is one of the few presentations in medicine where a single diagnosis must be excluded before anything else is considered. Falciparum malaria can progress from mild fever to cerebral involvement and death within a couple of days, and it is entirely treatable. Nothing else on the differential list carries that combination.

Dengue teaches the opposite lesson, and an equally uncomfortable one: its dangerous phase begins as the fever falls. A patient who looks better on day four, whose temperature has normalised and who is sent home, is the patient who returns in shock. Both diseases punish the reasonable assumption that an improving patient is a recovering one.

🩺 Where this lives: Dengue is no longer confined to the Terai. Outbreaks have extended into hill districts and the Kathmandu valley in recent years, which means the old heuristic — "no lowland travel, so not dengue" — is unreliable. Meanwhile malaria transmission in Nepal is concentrated in the lowland districts and among people who have travelled or worked across the border. Take a travel and residence history that includes internal movement, not just international travel.

💡 A note on regimens. Antimalarial treatment is set by national policy and shifts with local resistance patterns, so this chapter names drug classes and treatment principles rather than specific regimens or doses. Take the actual regimen from current national guidance — that is what an examiner in Nepal will expect, and it is what is correct at the bedside.

The febrile patient with exposure

The rule about repeating the films is the one most often broken. Parasitaemia in malaria fluctuates with the parasite's life cycle, so a single negative film taken at the wrong moment proves nothing. If clinical suspicion is real, repeat over 48 hours before abandoning the diagnosis — three negatives, not one.

Malaria: the parasite and the illness

THE LIFE CYCLE, IN THE FORM THAT MATTERS CLINICALLY Female Anopheles bite ↓ Sporozoites → LIVER ↓ Liver schizonts release merozoites into the blood ↓ BLOOD STAGE — invasion of red cells, cyclical rupture ↓ this is what causes the FEVER and the illness Some become gametocytes → taken up by the next mosquito P. VIVAX and P. OVALE additionally leave DORMANT HYPNOZOITES in the liver, which is why they RELAPSE weeks to months later — and why clearing the blood stage alone is not a cure in those species. INCUBATION is typically 1–4 weeks, but can be far longer, particularly with vivax or partial prophylaxis. A fever months after exposure does not exclude malaria.

💡 Exam angle: primaquine and G6PD is a reliably examined pairing. The drug that eradicates hypnozoites is an oxidant, and in G6PD deficiency it causes severe haemolysis — so G6PD status is checked before it is prescribed. This connects directly to the anaemia chapter, where the same enzyme defect appears from the haematological side.

Clinical features and severity

UNCOMPLICATED MALARIA Fever — the classic periodic pattern is often ABSENT, especially early and in falciparum. Do not require it. Rigors, sweats, headache, myalgia Nausea, vomiting, diarrhoea — frequently misread as gastroenteritis Anaemia, thrombocytopenia, mild jaundice Splenomegaly There is no reliable clinical feature that distinguishes malaria from other febrile illness. The diagnosis is made on the film or the rapid test, which is precisely why the threshold for testing must be low.

Two practical points about severe malaria. First, a drowsy patient with malaria may be hypoglycaemic rather than cerebral — check the glucose before concluding anything about the brain, and check it repeatedly. Second, severe malaria requires parenteral therapy: giving oral tablets to a vomiting, obtunded patient is not treatment, whatever the drug.

Dengue

THE VIRUS AND THE VECTOR Flavivirus, four serotypes, transmitted by AEDES mosquitoes — which bite by DAY, unlike the night-biting Anopheles of malaria. That difference matters for prevention advice. Infection with one serotype gives lasting immunity to THAT serotype only. A subsequent infection with a DIFFERENT serotype carries a higher risk of severe disease — which is why second infections are watched more carefully.

💡 Exam angle: the rising haematocrit with falling platelets is the classic laboratory signature of plasma leakage in dengue, and it is asked repeatedly. The haematocrit rises because plasma is leaving the circulation and the blood is concentrating — so a rising haematocrit in a dengue patient is not dehydration to be casually corrected, it is a warning of leakage requiring careful, monitored fluid management. Note also that aspirin and NSAIDs are avoided because of the bleeding risk.

Managing dengue

THERE IS NO ANTIVIRAL — MANAGEMENT IS FLUID AND TIMING MOST patients: oral fluids, paracetamol, rest, and clear advice about warning signs and when to return. WARNING SIGNS or SEVERE disease: admit, with careful INTRAVENOUS fluid guided by haematocrit, urine output and perfusion. THE BALANCE IS DELICATE Too little fluid during the critical phase → shock. Too much, especially into the RECOVERY phase when leaked fluid returns to the circulation → pulmonary oedema. This is why these patients are monitored rather than given a fixed regimen. AVOID aspirin and NSAIDs — bleeding risk. Platelet transfusion is NOT given for a low count alone; it is guided by bleeding, not by a number.

The rest of the differential

🔍 Other causes of fever worth holding in mind

Enteric feverTyphoid and paratyphoid. A stepwise fever with relative bradycardia, abdominal symptoms and constipation more often than diarrhoea. Blood culture is the diagnostic test; complications include intestinal perforation and haemorrhage in the later weeks.

LeptospirosisWater contact, especially after flooding. Fever with severe myalgia, conjunctival suffusion, and in severe disease jaundice with renal failure.

Scrub typhusRickettsial, transmitted by mites in scrub vegetation. Look for an eschar at the bite site — a painless black-crusted ulcer — which is easily missed unless the patient is fully undressed and examined.

Visceral leishmaniasis (kala-azar)Prolonged fever with marked splenomegaly, weight loss and pancytopenia. Endemic in parts of the Terai.

TuberculosisShould be in the differential for any prolonged fever — see the tuberculosis chapter.

And the ordinary onesPneumonia, urinary infection, and abscess remain common. An exotic exposure history does not make common infections uncommon.

Clinical reasoning: four presentations

🔍 Case 1 — the negative film

PresentationA 28-year-old returns from three months working in the Terai with five days of fever, rigors and headache. A single blood film is negative. He is sent home with paracetamol.

TrapOne negative film treated as exclusion.

ReasoningParasitaemia fluctuates with the parasite's cycle, so films can be negative at the wrong moment. With this exposure and this illness, malaria remains the leading diagnosis.

AnswerRepeat thick and thin films over 48 hours — three negatives before abandoning the diagnosis — and consider a rapid diagnostic test. Do not discharge a febrile patient with malarial exposure on a single negative result.

🔍 Case 2 — the drowsy patient

PresentationA patient with confirmed falciparum malaria becomes drowsy and difficult to rouse. The team prepares to manage cerebral malaria.

Key clueReduced consciousness in severe malaria has more than one cause.

ReasoningHypoglycaemia is common in severe malaria — driven by the parasite's glucose consumption, impaired gluconeogenesis, and quinine-induced insulin release where quinine is used. It is instantly reversible and easily missed.

AnswerCheck the glucose immediately and repeatedly, and treat hypoglycaemia if present. Then manage severe malaria with parenteral artesunate and supportive care. Both things can be true; only one of them is fixed in a minute.

🔍 Case 3 — better on day four

PresentationA 22-year-old with confirmed dengue has had four days of high fever. Today the temperature is normal and she says she feels better, though she has some abdominal pain and has vomited twice. Haematocrit has risen; platelets have fallen.

TrapDefervescence read as recovery.

ReasoningThe critical phase of dengue begins as the fever falls. Abdominal pain and persistent vomiting are warning signs, and a rising haematocrit with falling platelets indicates plasma leakage.

AnswerAdmit for monitoring and careful intravenous fluid guided by haematocrit and perfusion. Avoid NSAIDs. This is the moment she is most likely to deteriorate, not least.

🔍 Case 4 — the relapse

PresentationA patient treated for P. vivax malaria three months ago returns with an identical illness. He completed the blood-stage treatment he was given.

Key clueVivax, months later, after apparently complete treatment.

ReasoningVivax and ovale leave dormant hypnozoites in the liver. Blood-stage treatment clears the illness but not the liver reservoir, which reactivates weeks to months later.

AnswerTreat the acute episode, then give anti-relapse therapy directed at the liver stage — after checking G6PD status, since primaquine causes severe haemolysis in deficiency. Without that second drug, he will relapse again.

Commonly confused

Confusion	The distinction	Why it matters
One negative film vs no malaria	Parasitaemia fluctuates	Repeat over 48 hours before excluding it.
Falciparum vs vivax	Falciparum kills; vivax relapses	Different urgency and different treatment course.
Blood-stage cure vs radical cure	Hypnozoites need a separate drug	Otherwise the patient relapses months later.
Cerebral malaria vs hypoglycaemia	Both cause drowsiness in severe malaria	One reverses in minutes — check glucose first.
Defervescence vs recovery in dengue	The critical phase begins as fever falls	This is when patients are wrongly discharged.
Rising haematocrit vs dehydration	In dengue it signals plasma leakage	It guides monitored fluid, not casual rehydration.
Low platelets vs need for transfusion	Transfusion is guided by bleeding, not by a count	Prevents unnecessary and risky transfusion.
Anopheles vs Aedes	Anopheles bites at night; Aedes by day	Changes the prevention advice you give.

Rapid revision

MUST-KNOW FACTS 1. Fever + malarious exposure = MALARIA until proven otherwise. 2. Thick film detects; thin film speciates and quantifies. 3. ONE negative film does not exclude malaria — repeat over 48 hours. 4. Falciparum infects red cells of all ages and sequesters → severe disease. 5. Vivax and ovale leave LIVER HYPNOZOITES → relapse. 6. Radical cure needs a liver-stage drug in addition to blood-stage treatment. 7. Check G6PD before primaquine — it causes haemolysis in deficiency. 8. The classic periodic fever is often absent; do not require it. 9. Severe malaria: impaired consciousness, seizures, hypoglycaemia, acidosis, renal failure, severe anaemia, bleeding, high parasitaemia. 10. Severe malaria needs PARENTERAL artesunate, not oral therapy. 11. A drowsy malaria patient may be HYPOGLYCAEMIC — check the glucose. 12. Malaria regimens follow NATIONAL policy and local resistance. 13. Dengue is a flavivirus with four serotypes, spread by AEDES — a DAY biter. 14. Immunity is serotype-specific; a second, different infection is riskier. 15. Dengue phases: febrile → CRITICAL → recovery. 16. The critical phase begins as the FEVER FALLS. 17. Warning signs: abdominal pain, persistent vomiting, bleeding, lethargy, fluid accumulation, liver enlargement. 18. RISING HAEMATOCRIT with FALLING PLATELETS = plasma leakage. 19. No antiviral for dengue — management is careful fluid and monitoring. 20. Too little fluid → shock; too much in recovery → pulmonary oedema. 21. Avoid aspirin and NSAIDs in dengue. 22. Platelet transfusion is guided by bleeding, not by the count. 23. Also consider enteric fever, leptospirosis, scrub typhus (look for the ESCHAR), visceral leishmaniasis and tuberculosis. 24. Common infections remain common — exotic exposure does not exclude them.

💡 Exam angle: the reliable threads are (a) a single negative film not excluding malaria, (b) hypnozoites requiring a second drug and G6PD testing first, (c) hypoglycaemia mimicking cerebral malaria, (d) dengue deteriorating as the fever settles, and (e) the rising haematocrit with falling platelets. Both diseases in this chapter punish the assumption that a patient who looks or feels better is getting better.

Syllabus points

Fever with exposure: excluding malaria first
Thick and thin films, and why one negative is not enough
The malaria life cycle and hypnozoites
Falciparum versus vivax and ovale
Clinical features of uncomplicated malaria
Severe malaria and its defining features
Hypoglycaemia in severe malaria
Radical cure, primaquine and G6PD
Dengue: virus, vector and serotypes
The three phases and the critical phase warning signs
Fluid management in dengue
The wider differential: enteric fever, leptospirosis, scrub typhus

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