Malaria

1. A SICK TRAVELER Fatima Al Awadh

2. CASE
 30 year old man.
 Recently ill.
 Travelled from Syria to Netherlands, also to Kenya, Gambia,
Italy, Turkey, and Thailand. He left his last journey, which was to
Gambia, weeks ago.
 Headache, weakness, chills and malaise since three days.
 Fever, fallen ill while travelling.

3. EXAMINATION
 Ill looking, slightly pale, not dehydrated, not jaundiced, nor dyspnoeic.
 Hardly stands with fever of (39.7°∁).
 Consciousness was normal.
 𝑅𝑅 = 20 𝑐𝑦𝑐𝑙𝑒𝑠
𝑚𝑖𝑛 .
 𝑃𝑢𝑙𝑠𝑒 = 130 𝑏𝑒𝑎𝑡𝑠
𝑚𝑖𝑛 but regular.
 No neck rigidity and no lymph nodes palpable.
 Clear chest with normal breath sounds, HS normal with no murmur.
 Abdomen slightly tender on LUQ, no hepato-splenomegaly.
 No skin abnormality.

4. LEARNING QUESTIONS
 What is the differential diagnosis?
 Which initial laboratory tests to order and
why?
 Do you expect any abnormality in blood
indices ( Hb, WBC, and platlets) and blood
chemistry ( electrolytes, liver enzymes, RFT,
serum albumin)?

5. DIFFERENTIAL DIAGNOSIS
Travelling acquired infections :
 Meningitis.
 Dengue fever.
 Chikungunya.
 Malaria.

6. BACTERIAL MENINGITIS
Supporting the diagnosis :
 Malaise, fever, headache
 Tachycardia,
 Travelling history.
Against the diagnosis :
 No risk factors (previous infection,
wound or immune def.)
 Begins with 3 to 5 days.
 No irritability or vomiting.
 No neck stiffness, photophobia or
change in mental status.
Is a rapidly progressive bacterial infection of the
meninges and subarachnoid space.

7. DENGUE FEVER
Supporting the diagnosis :
 Travelling to endemic country.
 Incubated for 3 to 15 days.
 High fever and headache.
Against the diagnosis :
 Tachycardia.
 No arthralgias or myalgias.
 No respiratory symptoms.
 No Petechia, retro-orbital pain or
lymphadenopathy.
Is a mosquito-borne disease caused by a
flavivirus.

8. CHIKUNGUNYA
Supporting the diagnosis :
 Travelling to endemic country.
 Fever and headache
 Fatigue.
Against the diagnosis :
 Incubated for 2-4 days.
 No arthralgia or backache.
 No rash, nausea, vomiting, or myalgias.
 Fever lasted > two days.
 No insomnia.
Is an acute febrile illness followed by more chronic
polyarthritis. Caused by CHIKV transmitted by mosquitoes.

9. MALARIA
Supporting the diagnosis :
 Travelling to endemic country.
 Incubation period is > 10 days.
 Fever, chills, malaise and headache.
 Pale, RUQ tenderness.
Against the diagnosis :
 No hepato-spleenomegaly.
 No jaundice.
Is a febrile parasitic infection transmitted by
mosquitos.

10. DIAGNOSIS
Most likely to be:
Malaria

11. MALARIA
 Caused by one of four species of the genus Plasmodium:
P. falciparum, P. vivax, P. ovale, P. malariae.
 Transmitted by the bite of female anopheline
mosquitoes.
 Symptoms and signs include fever, chills, sweating,
hemolytic anemia, and splenomegaly.
 Endemic in Africa, South Asia, Korea, Mexico, Haiti, the
Dominican Republic, South America, the Middle East,
and Central Asia.

12. EPIDEMIOLOGY
 300-500 million
people are infected
every year.
 Over 1 million die
annually.
 25 000 international
travelers per year are
infected.

13. LIFE CYCLE

14. CLINICAL FEATURES
P. Vivax
• “Bengin and tertian
malaria”.
• Most prevalent.
• Incubated for 10-
17 days.
• Vague influenza
like symptoms,
followed by
malarial paroxysms
(every 48 hr).
• Untreated lats
years.
• Relapses.
P. Ovale
• “benign or ovale
tertian malaria”.
• Similar to vivax.
• Untreated lasts 1
yr.
• Relapses.
P. Malariae
• “Quartan malaria”.
• Incubation is the
longest (18-40
days or months to
year.
• Early influenza
like symptoms, with
72 hr pattern
fever.
• Moderate to sever.
• Untreated lasts 20
yrs.
P. Falciparum
•“Malignant tertian
malaria”.
•Shortest incubation
(7-10 days).
•Early influenza
like symptoms,
rapidly progressing
to malaria
paroxysms (every
36-48 hr).
• Most likely to
result in death if
not treated.

15. P. FALCIPARUM COMPLICATIONS
 Unlike other forms of malaria, it causes microvascular obstruction because infected
RBCs adhere to vascular endothelial cells.
 Ischemia develops with resultant tissue hypoxia, particularly in the brain, kidneys,
lungs, and GI tract.
 Hypoglycemia and lactic acidosis.
 Cerebral malaria is marked by diminished consciousness, confusion and convulsions,
often progressing to coma and death
 Blackwater fever is due to widespread intravascular haemolysis, affecting both
parasitized and unparasitized red cells, giving rise to dark urine.

16. INVESTIGATIONS
 Complete blood count.
 Blood chemistry.
 Florescent microscopy.
 Blood smear (thick and thin).
 Imaging studies.

17. COMPLETE BLOOD COUNT
 Hemoglobin (decreased in 25% of patients).
 Platelet counts (thrombocytopenia in 50-68% of patients).
 Leucocytes (fewer than 5% of patients with malaria have an elevated white
blood cell count). This should broaden the DDx.
 Reticulocytosis due to hemolytic anemia.

18. BLOOD CHEMISTRY
 Liver function (results abnormal in 50% of patients).
 Renal function may be abnormal.
 Electrolytes may be abnormal especially hypernatremia.
 Hepatoglobin and LDH increase due to hemolysis.
 Heamoglubinemia due to intravascular hemolysis.
 Blood glucose levels may decrease.
 Albumin may decrease because malaria parasite degrade it.

19. BLOOD SMEAR
 Types of Films
 Giemsa-stained THICK films :
RBCs are lysed before staining.
More sensitive.
More difficult to prepare and interpret.
 Giemsa-stained THIN films :
Assessment of parasite morphology within RBCs.
Often speciation.
Determination of percentage parasitemia.
 Blood smears should be repeated at 4- to 6-h intervals if the initial smear is
negative.
 Sensitivity and accuracy of the results depend on the examiner's experience.

20. BLOOD SMEAR
P. Vivax
• Selective,
invades only
immature RBCs.
• Infected cells
are enlarged.
• Round
gametocytes.
• Schüffner dots.
• 24 merozoites
/schizont.
P. Ovale
• Selective for
immature RBCs.
• Host cells
enlarge and
distorted (oval).
• Schüffner dots.
• Cell border is
ragged.
• 12 merozoites
/schizont.
P. Malariae
• Infect only
mature RBCs.
• No enlargement
or distortion.
• Band
trophozoites.
• Ziemann dots.
• 8 merozoites/
schizont.
P. Falciparum
•No selectivity.
•Not enlarged.
•Multiple rings in
infected cell.
•Accolé position.
•Crescentic
gametocytes.
•Maurer dots.
•24 merozoites
/schizont.

21. BLOOD SMEAR
P. Vivax P. Ovale P. Malariae P. Falciparum

22. OTHER TESTS
 Rapid diagnostic tests (RDT) Immunochromatographic
tests based on antibody to histidine-rich protein-2
(PfHRP2), parasite LDH (pLDH).
RDTs are less effective when parasite levels are below
100 parasites/mL of blood.
 PCR assay testing and Nucleic acid sequence-based
amplification (NASBA), are very specific and sensitive
but expensive and unavailable in most developing
countries

23. IMAGING STUDIES
 Chest radiography may be helpful if respiratory
symptoms are present.
 If CNS symptoms are present, a computed tomography
(CT) scan of the head may be obtained to evaluate
evidence of cerebral edema or hemorrhage.

24. SUMMARY
 There are 300 to 500 million people infected with malaria worldwide; about
660,000 deaths occur yearly, mostly in children < 5 yr in Africa.
 P. falciparum causes microvascular obstruction and tissue ischemia, particularly in
the brain, kidneys, lungs, and GI tract of nonimmune infants and adults; patients
may die within days of their initial symptoms.
 P. vivax, P. ovale, and P. malariae typically do not compromise vital organs;
mortality is rare.
 Manifestations include recurrent fever and rigor, headache, myalgia, and nausea;
hemolytic anemia and splenomegaly are common.
 Diagnose using light microscopy of blood (thin and thick smears) and/or rapid
blood assays.

25. REFERENCES
Merck manuals
Kumar and Clark
Medical microbiology, Murray
Basic pathology, Robbins
Malaria journal
http://www.medscape.com/viewarticle/730561_4
http://emedicine.medscape.com/article/221134-workup#a0756

26. THANK YOU