Tropical diseases




  • Blood films
  • Must be made within 3-4 hours
    • Thick
      • Detection
      • Unfixed
      • Giemsa or modified field (rapid) stain
      • X100 objective
      • If negative despite strong clinical suspicion, examine larger area or repeat testing
    • Thin
      • Identification
      • Giemsa or leishman stain at pH 7.2
      • A rapid modified field stain will allow identification of P falciparum, but not the other species
      • If thin film negative
        • May be able to speciate on thick film
        • Treat as falciparum
        • Antigen testing to confirm falciparum



  • P. falciparum
    • Quantify percentage of parasitized cells
    • Examine 1000 red cells
    • Double infection, quantification applies only to falciparum
    • Exchange transfusion may be indicated if parasitaemia >10%
    • Should be repeated daily until no parastites (other than gametocytes)



  • Examined by two trained observers
  • All positive cases should be sent to a reference centre


  • Notifiable disease


  • Supplementary tests
  • Parasight F
    • Tests for soluble falciparum antigen in the blood
    • Sensitivity is equivalent to thick films
    • Useful to confirm falciparum esp. if mixed infection
      • Histidine rich protein2
        • May remain positive for 14 days even after treatment
        • False postivies with rheumatoid factor
      • Parasite LDH
        • Only produced by viable parasite, so becomes negative after 2-3 days
  • Quantitative buffy coat blood parasite detection
    • Fluorescence microscopy
    • Exposure of blood to acradine orange
    • Can be used as an initial screen
    • Disadvantages
      • Expensive
      • HJ bodies and reticulocytes also fluoresce with acridine orange
      • Speciation not possible
  • Ab tests
    • Not useful in acute attack, because stay after positive after successful treatment
    • Can be useful in excluding malaria in chronic PUO







Infected red cells

Normal size

Maurers cletfs


Schuffners dots

Enlarged and fimbriated

Schuffners dots


Ring forms


Multiply infected

Accolade forms

Small chromatin dot

Large and thick

Large chromatin dot

Thick compact rings

Small compact rings

Later trophozoites


2 chromatin dots


Smaller than p vivax

Band across cell


18-24 merozoites

Rare in peripheral blood

12-24 merozoites

8-12 merozoites

6-12 merozoites


Dark clumped mass

Fine granular, yellow-brown

Coarse light brown


At all stages







Life cycle

  • Injected sporozoites enter hepatocytes and divide
  • Rupture of hepatocyte releases merozoites, attach to red cell membrane
  • Digestion of Hb produces haemozoin = pigment
  • Asexual replication in red cell results in schizonts
  • Some form gametocytes, some rupture and reinfect other cells
  • Ovale and vivax have a dormant hypnozoite stage in the liver
  • Maximal immunity takes about 10 years and is lost over 1-5 years
  • In pregnancy, parasites are sequestered to placenta and can cause placental insufficiency
  • Falcip = SSA
  • Vivax = S Asia, India etc



  • Parasitized red cells are removed by spleen
  • Severe malarial anaemia
    • Also removal of non-parasatized cells
  • Reticulocyte suppression
  • Hyper reactive malarial splenomegaly
    • Hypersplenism
  • Blackwater fever
    • Intravascular haemolysis
    • Assoc with quinine and G6PD deficiency
  • Dyserythropoiesis in the marrow for weeks after acute infection


  • P vivax needs duffy antigen on red cells as a receptor
      • Often lacking in certain black races and thus protective



  • Falciparum:
    • Chlorquine if sensitive (mostly central/ S America)
    • Quinine if likely resistance
    • Alternatives include malarone, artesunate, mefloquine
  • Vivax/ ovale:
    • Primaquine for the hypnozoite stage
    • Chloroquine or quinine depending on likely resistance pattern
  • Malariae
    • Chloroquine


P. Falciparum – at different stages in thick and thin films – see the WHO website:




  • Not a tropical disease
  • Primarily a disease of animals, but rarely infects humans
  • Transmitted by tick bite
  • B. divergens  Europe
  • B. microti  N. America
  • Infect red blood cells and are confused with falciparum
  • Presenting features
    • Fever, prostration, hepatosplenomegaly, jaundice, haemolytic anaemia (usually DAT negative, despite being complement mediated), haemoglobinuria
    • May be fatal in splenectomised patients
    • Maltese cross forms on blood film
  • Parasitaemia does not correlate with severity
  • Treatment
    • Clindamycin and quinine
    • Exchange transfusion




Lymphatic filariasis

  • Wucheria bancrofti
      • Sheathed, nucei NOT to end of tail
      • Asia, Africa, America and pacific islands



  • Brugia malayi
    • Sheathed, more tightly coiled with a sub-terminal and terminal nuclei, often widely separated
    • China and far east 



  • Worms 4-10cm long and live in lymphatics
      • Microfilaria are produced by the female
      • Released into the blood after 3-8 months
      • Exhibit daily periodicity to coincide with mosquito activity
  • Presenting features
    • Lymphangitis (spreads distally), fever, redness and pain over lymphatic vessels
    • Chronic
      • Hydrocele, lymphoedema and elephantiasis, chyluria



    • Second commonest cause of infectious blindness in the world
    • Caused by oncocerca volvulus
    • Transmitted by black fly  simulium damnosum
    • Causes dermatitis and keratitis which leads to blindness if untreated
    • Simbiotic relationship with Wolbachia species (bacteria)
    • Treated with ivermectin or doxycycline (which kill the wolbachia)



Other filariae


Loa loa

  • Sheathed, nuclei to the end of the tail
  • Central Africa
  • Migrates through subcutaneous tissue, including the conjuctiva



Mansonella perstans

  • Unsheathed, nuclei to the end of the tail
  • Non-pathogenic, but frequently co-exist with W. bancrofti



Mansonella ozardi

  • Also probably non-pathogenic
  • West indies and S America


  • Eosinophilia
    • May develop tropical pulmonary eosinophilia (>10)
    • Immunological hyper responsiveness to microfilaria in the lungs
    • Microfilaria on lung biopsies
    • Visualise worms by USS in lymphatics
    • Rapid response to diethylcarbamazine
  • Diagnosis
    • Blood film
    • Best to take sample at midnight or midday
    • Wet preps
    • Thick and thin films
    • Antigen detection
      • ELISA or ICT for bancrofti
    • Antibody not helpful as most in endemic areas have Abs to crude filarial antigens



African trypanosomiasis

  • Trypanosoma brucei gambiense in west and central Africa
  • Trypanosoma brucie rhodesiense in East Africa
  • Transmitted by tsetse fly
  • Local multiplication of tryps at site of bite, followed by entry into blood stream
  • Clinical features
    • Lymphadenopathy esp. posterior cervical
    • Mild splenomegaly
    • Anaemia, haemorrhages and petechiae
    • Protracted febrile illness
    • Parasites invade CNS and death inevitable if untreated
  • Anaemia
    • Extravascular haemolysis
    • Failure to incorporate iron into red cell precursors
    • Mott morular cells in marrow
    • BM is hypercellular with areas of gelatinous degeneration
  • Diagnosis
    • Wet preps of fluid aspirated from LNs
    • QBC
    • Serological agglutination test
    • CSF examination to stage disease
  • Treatment
    • Pentamidine and suramin
      • Poor CNS penetration
    • Melarsoprol for late stage disease
      • Mortality 4-12%
    • Eflornithine


American trypanosomiasis

  • Trypanosome cruzi
  • Transmitted by triatome bugs
  • Americas
  • Clinical features
    • Chagoma at site of bite
    • Fever, hepatosplenomegaly, lymphadenopathy
    • Multiply intracellularly in muscle tissue
      • Heart, colon and oesophagus
  • Chronic disease is associated with heart disease in 30%
    • Arrythmias and cardiomegaly
  • Asymptomatic infection is common
    • Screened for in blood donations
  • Diagnosis
    • Serological
  • Treatment
    • Benznidazole



  • Transmitted by sand fly
  • Visceral form
    • L. donovani and L. infantum
  • Increasing with HIV infection
  • Clinical features
    • Diarrhoea, arthralgia, weight loss, bleeding gums
    • Muscle wasting, hepatosplenomegaly, fever, anaemia
    • Splenomegaly results in hypersplenism
  • Diagnosis
    • Intracellular amastigotes in macrophages
    • Splenic > BM aspirate
    • PCR
    • AB tests but may be negative in imunocompromised
  • Treatment
    • ambisome