A returning traveller with fever needs rapid triage, not a reflex “tropical infection” label. First identify physiological instability and infection-control/public-health risk; then urgently exclude malaria after travel to an endemic area and obtain cultures for treatable invasive infection such as enteric fever. Exact itinerary, dates, exposures, host factors and incubation periods turn a huge list into a workable differential.

1. Understand the spectrum of health risks associated with international travel.
2. Know how to take a structured travel history for a febrile returning traveller.
3. Match exposure types to likely pathogens.
4. Construct a differential diagnosis using geography, incubation period, activities, and clinical features.
5. Recognise infectious disease emergencies — especially severe/falciparum malaria, sepsis, meningitis/encephalitis, and suspected high-consequence transmissible infection.
6. Know the principles of malaria diagnosis, treatment, and chemoprophylaxis.
7. Understand travellers' diarrhoea: epidemiology, risk factors, prevention, and management.
8. Appreciate epidemic/pandemic-prone infections and antibiotic-resistant organisms as considerations in returned travellers.

Historical surveillance result: in the cited EuroTravNet cohort, patients with malaria had a 2.5:1 mortality risk ratio compared with all other diagnoses. This is not a timeless individual risk estimate. ^[1]

The durable lesson is to recognise emergencies early. The lecture's arrival-count, cause-of-death and illness-frequency graphics describe their stated study periods; they should not be read as current global incidence.

• The World Bank line graph shows a long rise in international arrivals through 2019; it is an exposure-volume graphic, not a disease-incidence graph.
• The UNWTO bars make the pandemic interruption visible: roughly 1.46 billion arrivals in 2019, 407 million in 2020, 458 million in 2021, then 969 million in 2022. The message is disruption followed by rebound, not that travel-associated infection moved in the same proportion.
• The older tourist-death charts show cardiovascular disease and injury dominating recorded deaths, with infection a smaller category. They counter availability bias (“travel death = exotic infection”) but do not reduce the urgency of treatable infections in a febrile patient.

This table is extremely high yield and directly from the lecture. Expect MCQ/SAQ stems that give an exposure and ask you to identify the pathogen.

General: Skin lesions (rash, eschar, bite marks, needle marks), jaundice, bleeding tendencies. Systemic: Lymphadenopathy, organomegaly, localizing signs (e.g. meningism). ^[1]

Why each sign matters:

• Eschar → Scrub typhus or other rickettsioses (look in axillae, groin, behind ears).
• Jaundice → Malaria (haemolysis), viral hepatitis, leptospirosis.
• Bleeding tendencies → Viral haemorrhagic fevers (Ebola, dengue haemorrhagic fever) — triggers isolation consideration.
• Rash → Rose spots (typhoid), maculopapular (dengue, chikungunya, rickettsial), petechial/purpuric (meningococcaemia, VHF).
• Hepatosplenomegaly → Malaria, enteric fever, visceral leishmaniasis, brucellosis.
• Meningism → Bacterial meningitis, viral encephalitis (Japanese encephalitis if travel to endemic areas).

Malaria, respiratory tract infections, diarrhoeal disease, enteric fevers, genitourinary infections, arboviruses (e.g. dengue, chikungunya), and viral syndromes. ^[1]

The slide's timeline (SARS 2003, pandemic influenza 2009, Ebola 2014, Zika 2015, COVID-19 2020, mpox 2022) is historical orientation, not a current outbreak list. Always check current destination-specific alerts; distributions and transmission change. ^[7]

Potential for local transmission: malaria, dengue, chikungunya, VHFs, Zika. ^[1]

Travel and overseas healthcare can lead to colonisation or infection with ESBL- or carbapenemase-producing Enterobacterales, MRSA, VRE and other resistant organisms. The slide's fixed “highest-risk” regions can date quickly; record healthcare and antibiotic exposure and use current surveillance rather than geography alone. [1,7]

Re-emerging infectious diseases: e.g. measles in adults. ^[1]

Understanding incubation periods lets you include or exclude diagnoses based on the timeline between exposure and symptom onset.

"Malaria must be suspected in the differential diagnosis of any acute febrile illness in a patient who could have been exposed to malaria." — DA Warrell ^[1]

Fever pattern: Usually not helpful. ^[1]

The initial smear must not be delayed while waiting for a “classic” periodic fever or for 7 days to elapse.

Severe malaria is defined by any major organ dysfunction (e.g. impaired consciousness/coma, acidosis, hypoglycaemia, Hb < 7 g/dL, acute kidney injury, ARDS/pulmonary oedema, shock, DIC/significant bleeding, or jaundice with other severe features) or high parasite density. The deck uses a historical > 10% falciparum parasitaemia threshold; current CDC imported-malaria guidance uses ≥5% parasitaemia, and severe disease from any species warrants parenteral treatment. ^[8]

Why each feature occurs:

• Impaired consciousness — Sequestration of parasitized RBCs in cerebral microvasculature → cerebral malaria.
• Acidosis — Tissue hypoxia from anaemia + microvascular obstruction → lactic acidosis.
• Hypoglycaemia — Parasite glucose consumption + quinine-induced insulin secretion.
• Severe anaemia — Haemolysis of parasitized RBCs + suppressed erythropoiesis + splenic clearance.
• Renal impairment — Acute tubular necrosis from haemoglobinuria, hypovolaemia, sequestration.
• Jaundice — Haemolysis + hepatocyte dysfunction.
• Pulmonary oedema — Increased capillary permeability (non-cardiogenic) or fluid overload.
• Hyperparasitaemia — High parasite burden is a severity marker; apply the threshold used by the current local guideline rather than memorising the slide's old > 10% figure.

Falciparum malaria is a medical emergency. Accounts for most of the mortality due to malaria. Prompt initiation of treatment ± ICU monitoring. ^[1]

Diagnosis is normally made from urgent peripheral blood thick and thin films. Bone-marrow and post-mortem examples on the slide are possible specimen sources, not routine diagnostic steps. RDTs can accelerate detection but do not replace microscopy for species identification and parasitaemia; PCR is useful for confirmation or difficult low-density/mixed infections but is often too slow for the first decision. ^[9]

One negative film does not exclude malaria. If suspicion remains, repeat thick and thin films every 12–24 hours until positive or until three sets are negative. Obtain expert/parasitology advice if the clinical picture remains concerning. ^[9]

Why primaquine/tafenoquine for P. vivax/ovale? These species form hypnozoites—dormant hepatic forms that can reactivate months to years later. Both 8-aminoquinolines can cause severe haemolysis in G6PD deficiency, so use a quantitative G6PD test and check pregnancy/breastfeeding and drug-specific eligibility. After IV artesunate, monitor for post-artesunate delayed haemolysis during follow-up. [8,10]

The handout's image connects biology to prevention, symptoms and transmission: ^[2]

1. An infected Anopheles mosquito inoculates sporozoites, which reach hepatocytes rapidly.
2. All species first replicate in the liver and release merozoites. P. vivax and P. ovale can additionally leave dormant hypnozoites, explaining relapse and the need for radical cure.
3. Merozoites invade red cells and cycle through ring → trophozoite → schizont → rupture. This asexual blood stage produces symptoms and is what films quantify.
4. Some parasites become gametocytes; a mosquito ingests them, sexual reproduction occurs in the vector, and sporozoites return to the salivary glands.
5. The green treatment boxes map to different targets: chemoprophylaxis suppresses/prevents clinical infection, treatment clears symptomatic blood stages, radical cure targets hypnozoites, and effective therapy can reduce onward transmission. No single drug should be assumed to cover every stage.

The lecture graph is a historical surveillance figure to August 2023, including the marked 2022 spike. Do not infer current incidence from it. The CHP 2014–2023 summary classifies most cases as imported but records three 2022 local recrudescence cases, so “all Hong Kong cases are imported” is too absolute. ^[12]

Enteric fever is systemic infection caused by Salmonella enterica serovars Typhi (typhoid) or Paratyphi A, B or C (paratyphoid). The slide places Yersinia, Brucella and Campylobacter fetus beside them; these are different causes of invasive febrile/bacteraemic illness, not causes of enteric fever. ^[13]

The 2019 minicase is a near-perfect case study of this lecture ^[4]:

• 23-year-old female, returned from Bangladesh
• Recurrent fever for 2 weeks
• Constipation in week 1 → non-bloody diarrhoea in week 2 (classic biphasic GI pattern of typhoid)
• Did not drink exclusively bottled water (faecal-oral transmission)
• Multiple mosquito bites (must also consider malaria/dengue)

Physical examination clues:

• High fever of 40°C with pulse rate 50 bpm → relative bradycardia ^[4]. This and “rose spots” are classic clues but neither is sufficiently sensitive or specific to establish the diagnosis.
• Rose spots: “A few rashes found on the lower chest and abdomen” ^[4] — faint salmon-pink blanching macules/papules may occur on the trunk but are often absent.
• Abdominal distension, RLQ tenderness — the terminal ileum has Peyer's patches, the primary site of S. Typhi invasion and ulceration.

From the 2019 minicase (Q5: "Name five investigations to confirm your diagnosis"):

1. Blood cultures before antibiotics — the principal diagnostic test; take multiple sets in undifferentiated fever. A negative result does not exclude disease, especially after antibiotics. [7,13]
2. Stool culture — less sensitive for acute diagnosis; can support diagnosis and public-health follow-up.
3. Bone-marrow culture — more sensitive but invasive and not routine; reserve for selected culture-negative cases with specialist input.
4. Do not rely on the Widal test — inadequate sensitivity/specificity and difficult interpretation make it unsuitable for confirming acute disease in most settings. ^[13]
5. CBC/LFT/renal profile — assess severity and complications; leukopenia is possible but not obligatory.
6. Urgent malaria films — if the itinerary permits malaria exposure; mosquito bites do not specifically distinguish malaria from arbovirus infection.

Start empiric antibiotics after cultures when illness is clinically suspected, then tailor to susceptibility. Travel history changes the empiric choice: current CDC guidance uses ceftriaxone or azithromycin for most returning travellers, but suspected uncomplicated infection after travel to Pakistan or Iraq is treated empirically with azithromycin and complicated disease with a carbapenem because of XDR/ceftriaxone-resistant strains. Resistance now also affects azithromycin in some locations, so current local guidance, microbiology and public-health advice are essential. ^[13]

From the 2019 minicase Section 4: Patient developed shock and severe diffuse abdominal pain on day 2 of antibiotics → emergency laparotomy ^[4]. This is intestinal perforation — the most feared complication.

From the 2019 minicase Section 3: "Gram smear demonstrated bacteria stained in red colour" → Gram-negative bacilli (rods). ^[4] Salmonella Typhi is a Gram-negative, facultative anaerobic rod of the family Enterobacteriaceae.

Historical lecture figures: 30–50% of travellers from “industrialized to developing countries,” mostly in the first 2 weeks, with mean duration 3–4 days. The terminology and percentages are dated; individual risk varies with destination, season, food/water exposure and host factors. ^[1]

Why so common? Travellers lack local enteric immunity and are suddenly exposed to new enteropathogenic strains via contaminated food/water.

Destination, country of origin, travel behaviour (accommodation, food, standard of hygiene, food habits), and at-risk populations: hypo- or achlorhydria (e.g. PPI users), extremes of age, immunosuppressed (HIV/AIDS, steroids, transplant recipients). ^[1]

Why achlorhydria matters: Gastric acid is a key defence against ingested pathogens. PPIs remove this barrier → lower infectious dose needed.

The deck's multi-region chart is historical and study-dependent, but it teaches two useful points: no pathogen was identified in about 39–50% of episodes, and the leading isolate varied by destination (ETEC prominent in several Latin American/African/South Asian datasets; Campylobacter relatively prominent in Southeast Asia). Do not turn those bars into fixed geography rules—current resistance, outbreak data and the clinical syndrome matter more than a memorised ranking.

Pre-travel counselling and education, behavioural modification/precautions, vaccination, pharmacological (antimicrobial) prophylaxis. ^[1]

• "Boil it, cook it, peel it, or forget it" — the traveller's food-safety mantra.
• Antimicrobial prophylaxis is generally NOT recommended for most travellers (risk of resistance, side effects) but may be considered for high-risk individuals (immunocompromised, short critical trips).

ORS and fluid/electrolyte replacement are the foundation. Modern guidance uses impact on activities rather than stool count: ^[14]

Do not use loperamide alone with bloody diarrhoea or diarrhoea plus fever. Rifaximin/rifamycin are only for non-invasive disease. Fluoroquinolone resistance and adverse-effect profile limit empiric use; choose treatment by destination and patient factors. Routine antibiotic prophylaxis is generally avoided because harms include adverse events, C. difficile and carriage of resistant organisms. ^[14]

1. Enteric infections — travellers' diarrhoea, enteric fever, dysentery (bacillary and amoebic).
2. Arthropod-borne infections — malaria, dengue, chikungunya, Zika, rickettsioses.
3. STIs and blood-borne infection including HIV, viral hepatitis, syphilis and mpox where exposure is compatible.
4. Leptospirosis — freshwater exposure; Weil's disease (severe form with jaundice, renal failure, haemorrhage).
5. Viral hepatitis — HAV/HEV (food), HBV/HCV (parenteral/sexual).
6. Others — cholera, giardiasis, VHFs, hantavirus, Japanese encephalitis, rabies — relatively uncommon.
7. Acquisition of antibiotic-resistant bacteria — carbapenem-resistant Enterobacterales, extensively drug-resistant S. Typhi, MDR-TB, Candida auris.
8. Re-emerging infectious diseases — measles in adults.
9. Don't forget common ubiquitous infections (RTI, UTI) which may not be related to travel. Some RTIs are geographically restricted — e.g., MERS-CoV associated with travel to the Middle East, especially camel contact. ^[2]

From the 2018 minicase (Q11): "Name two suspected conditions that should be admitted to the isolation ward in returning travellers presenting with pneumonia." ^[5]

Potential answers depend on the stem's destination, timing and exposure: pulmonary TB, MERS after a compatible Arabian Peninsula/camel exposure, or novel/avian influenza after relevant animal or outbreak exposure. Apply syndrome-appropriate precautions immediately and contact infection control/public health rather than waiting for a final diagnosis. COVID-19 is now assessed using current local respiratory-virus policy, not travel history alone. A viral haemorrhagic fever is not a generic cause of pneumonia: suspicion requires a compatible exposure, geography and incubation window (usually no more than 21 days). [7,15]

These are all mosquito-borne (Aedes aegypti/albopictus) and present similarly but with distinguishing features:

The handout describes a “biphasic” illness; the safer modern model is febrile → critical → recovery. The critical phase often begins at defervescence and lasts about 24–48 hours, so falling temperature does not necessarily mean recovery. Watch for severe abdominal pain, persistent vomiting, fluid accumulation, mucosal bleeding, altered mental state, hepatomegaly and a rising haematocrit. Severe dengue means severe plasma leakage causing shock/respiratory distress, severe bleeding, or severe organ involvement. ^[16]

• Testing in days 0–7: serum NAAT (RT-PCR) plus IgM, or NS1 antigen plus IgM. A negative NAAT/NS1 alone does not exclude dengue; after day 7, IgM becomes more useful. A single IgG result should not diagnose acute dengue. ^[17]
• Treatment: supportive, with careful oral/IV fluid titration and repeated review. Use paracetamol for fever; avoid aspirin and NSAIDs until dengue is excluded. Do not give routine prophylactic platelets or corticosteroids. ^[16]
• Transmission prevention: patients should avoid further mosquito exposure while viraemic to reduce the chance of local onward transmission.

The handout-only section distinguishes intestinal Entamoeba histolytica infection (asymptomatic colonisation, diarrhoea or dysentery; rarely fulminant colitis) from extra-intestinal disease, most often an amoebic liver abscess. A liver abscess may occur without concurrent diarrhoea or a positive stool microscopy result.

• Stool PCR or species-specific antigen is preferable when available because microscopy cannot reliably distinguish pathogenic E. histolytica from non-pathogenic E. dispar. Serology is mainly helpful for extra-intestinal disease. ^[18]
• Invasive intestinal or extra-intestinal amoebiasis needs a tissue-active nitroimidazole (metronidazole or tinidazole), followed by a luminal agent such as paromomycin or iodoquinol. Metronidazole alone does not reliably eradicate luminal colonisation. [14,18]