From StudyingMed

< SH3‎ | Lectures
Jump to: navigation, search
  • See hand out: has additional information that is necessary
  • "Parasite" does not describe a
    • Used to classify "all the other" (e.g. not fungal, not bacteria, not viruses etc).
    • Parasites = protozoa + metazoa (worms)

Tropical Infections

  • Global impact of infectious diseases
  • Protozoa
  • Malaria
  • Gastrointestinal protozoal infections


  • Protozoa
    • single cell organisms
    • eukaryotic; separate nucleus and cytoplasm
    • variable morphology (complex lifecycles with different morphological forms in different hosts)
    • reproduce by asexual division or sexual reproduction
    • may involve more than one host


  • Protozoa - Plasmodium
  • 5 species infecting humans
    • P.falciparum - important (malignant)
    • P.vivax - important (benign; commonest imported to Aus)
    • P.ovale
    • P.malariae
    • P.knowlesi
  • Parasite transmitted to humans by mosquitoes
    • female Anopheles sp.
  • Mosquito-borne diseases: Malaria, dengue fever, ross river virus
  • Anopheles mosquito: dusk to dawn. Rural mosquito (not urban).
  • Dengue breeds in cities

Life cycle of plasmodium falciparum

  • Left = what happens in a mosquito. Right = what happens in the host
  1. Mosquito takes blood meal
  2. Injects saliva into host --> plasmodium in. Sporozoite goes into circulation
  3. In minutes, cleared out of circulation in the liver
  4. In the liver, it replicates, and changes morphological form. First stage of division is asexual. Does not elicit host response (no inflammation). Corresponds to the incubation period of malaria. Duration is variable (minimum 5 days, maximum is a month).
  5. Asexual division in RBCs --> inflammatory response
  6. Large number of parasites in RBCs --> lysis --> more malaria in blood
  • 48 hour cycle. Malariae = 72 hour cycle.
  • So the parasite cycles through RBCs causing a host immune response.
    • Death or remission
  • Gametocytes can form in the human. This are the sexual forms that are taken by the mosquito vector.
    • Inside the human, there are 2 forms of asexual reproduction (liver and blood).
    • Inside the mosquito, sexual reproduction occurs
      • Mosquito = definitive host.
      • Human = intermediate host.
  • Vivax + ovale: Malaria can recur because hynozoites can stay dormant in the liver and reactivate; start dividing years later and cause symptoms
    • Therefore vivax incubation period can be much longer (max 4 weeks iff division starts straight away)
  • Malariae + Falciparum: can persist for years; sitting on capillary endothelium of RBCs.
  • Female mosquito requires protein in blood to make eggs.

Malaria - global situation

  • 40% of world’s population (2,000 million) live in malarious areas
  • 300-500 million clinical cases annually
  • 90% of cases in Africa
  • 1-1.5 million deaths annually; children
  • Repeated attacks of malaria produce immunity; but specific to strain and location
    • Immunity is difficult and very easily lost (2 years in non-malarious area)
    • Australia is non-malarious - nothing to protect you
  • It's a tropical disease. Climate change increases distribution and intensity
  • Malaria receptive zone: above 20 degrees south in Australia. Sufficient Anopheles density for malaria transmission to occur

Malaria in Australia

  • Imported malaria; acquired outside Aust.
    • c800 cases/year
    • Vivax (70%); falciparum (20%) (falciparum is rarer but more severe)
  • Introduced malaria; local transmission from imported case
    • malaria receptive zone; airport (<1km flight zone of insect)
    • <10 cases/year
  • Induced malaria; from infected blood
    • transfusion, needle-sharing

Vivax malaria clinical features

  • febrile paroxysms (cold, rigors, then feel hot, sweating, headaches, aches, nonspecific)
  • tertian periodicity; may not be present early (fever corresponds to when the red cells lyse - classical feature = periodicity; doesn't always occur - only longterm infection)
  • splenomegaly (due to removal of parasitised RBCs; no lymphadenopathy or rash)
  • anaemia, thrombocytopenia (splenic hyperplasia causes thrombocytopenia -- innocent bystander; can be profound)
  • relapses due to hepatic hypnozoites

Falciparum malaria clinical features

  • paroxysms and periodicity less marked (often subacute; not instantaneous)
  • hyperparasitemia associated with complications:
    • cerebral malaria (blood cells are sticky - stick to cerebral endothelium and block blood flow; altered consciousness, focal neurological signs, convulsions, coma)
    • acute renal failure (blackwater fever) (lots of intravascular hemolysis, causes too much Hb in circulation --> saturates haptoglobin mechanism. This is a tubular poison --> affects renal tubular function --> HbUria --> black urine --> blackwater fever)
    • ARDS (severe sepsis; pro-inflammatory cytokines triggering multi-organ failure)
      • Once you trigger the process of multi-organ failure, the process doesn't stop (even if you remove the bug)
  • recrudescences (recurrences) due to persistent parasitemia
  • In endemic countries, it is children who are most at risk. But if we travel there, we are effectively children.

Diagnosis of Malaria

  • Consider in any febrile patient following travel to malaria area
  • Detection of malaria parasites on peripheral blood smears
    • Thick smear: screening (lyse cells, centrifuge down the parasite -- screening test to look at concentrated field)
    • Thin smear: determine species and intensity of infection (look at appearance of the parasite and the effect it has on RBCs). Intensity = see how many RBCs are parasitised.
  • Immunoassays
    • Reliable in diagnosis of faciparum malaria (not used for screening; important for diagnosis because people can die rapidly)
  • 1. Ring form: appearance of ring (chromatin - nuclear material). Early, when it first gets into RBC (vivax)
  • 2. Falciparum (two chromatin dots; many red cells in one field - must be falciparum)
  • 3. Thick smear: white cells weren't lysed. No RBCs (lysed). Blobs = malaria parasite. Next step is to do thin smear.
  • Child sleeping inside a tent: use of insecticide-impregnated nets = most effective way to prevent malaria. Night time is the problem.
  • No drug can stop malaria infection (biting)
  • No drug can stop the malaria replicating in the liver
  • Chemoprophylaxis is to stop symptoms (so that when the merozoites go into the bloodstream from the liver, then you're safe and don't get sick)

Malaria chemoprophylaxis

  • Degree of risk
    • local prevalence; seasonal variation
    • rural travel (use travel advisory service that tells you the drugs etc they need)
  • Occurrence of resistance to antimalarial drugs
  • Characteristics of traveller
    • age
    • pregnancy
    • drug allergies

We want people to start treatment before they leave (to detect adverse reactions to the drug, to make sure they tolerate it. It also takes time to develop a therapeutic dose). They have to continue to take prophylaxis while they're away, and when they get back (4 weeks after they get back because of incubation period).

Treatment of Malaria

  • Clinical cure
    • eradication of parasites from blood
    • results in resolution of clinical illness
    • chloroquine, quinine, doxycycline (an antibiotic), Malarone (combination), artemether (most potent)
    • do not work in the incubation period
  • Radical cure (P.vivax & P.ovale)
    • eradicates hepatic hypnozoites
    • prevents relapses
    • primaquine
    • toxic - GIT side effects (hence not used for prophylaxis)

Gastrointestinal Protozoa

  • Giardiasis
  • Cryptosporidiosis
  • Amoebiasis


Most common gut protozoa in Australia

  • Protozoa – Giardia lamblia (intestinalis)
  • Morphological forms:
    • Cyst – infective form excreted in stools
    • Trophozoite – adheres to small bowel (alters brush border enzymes)
  • Transmitted by oral-faecal route.
  • Worldwide distribution; occurs commonly in Australia.
  • Cysts that multiply, then cell wall breaks down, make trophozoite: either excreted or converted to cyst (which may replicate or be excreted).

Giardiasis – Clinical Features

  • Asymptomatic infection (most common)
  • Acute infection
    • Nausea, vomiting, watery diarrhoea (large volume, moderate frequency), abdominal pain. (Small bowel diarrhoea)
  • Chronic infection (1/3 patients)
    • Malabsorption syndrome

Giardiasis - Diagnosis

  • Stool tests
    • Microscopy
  • Cysts or trophozoites
    • Antigen detection
    • PCR


  • Transmitted by faecal-oral route; contaminated water
  • Small bowel infection
    • Normal host - watery diarrhoea (1-2 weeks)
    • Immunocompromised host (e.g. AIDS) - chronic diarrhoea
  • Diagnosis: stool microscopy (modified acid-fast stain)


  • Protozoa – Entamoeba histolytica
  • Morphological forms:
    • Cyst – infective form excreted in stools
    • Trophozoite – causes invasive infection in colon
  • Transmitted by oral-faecal route.
  • Worldwide distribution; common in developing countries

Amoebiasis – Clinical Features

  • Asymptomatic infection (most common)
  • Acute colitis (amoebic dysentery)
    • Abdominal pain, bloody diarrhoea, fever (very frequent, small volume)
  • Amoebic liver abscess (due to invasiveness of organism)
    • Right upper quadrant pain
    • Tender hepatomegaly
    • Fever

Amoebiasis - Diagnosis

  • Stool tests
    • Microscopy
  • Cysts or trophozoites
    • Antigen detection
  • Colonoscopy
    • Focal colitis; biopsy shows flask-shaped ulcers
  • Serology
    • Invasive infection (therefore we produce antibodies), especially liver abscess