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  1. 1. A SICK TRAVELER Fatima Al Awadh
  2. 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. 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. 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. 5. DIFFERENTIAL DIAGNOSIS Travelling acquired infections :  Meningitis.  Dengue fever.  Chikungunya.  Malaria.
  6. 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. 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. 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. 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. 10. DIAGNOSIS Most likely to be: Malaria
  11. 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. 12. EPIDEMIOLOGY  300-500 million people are infected every year.  Over 1 million die annually.  25 000 international travelers per year are infected.
  13. 13. LIFE CYCLE
  14. 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. 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. 16. INVESTIGATIONS  Complete blood count.  Blood chemistry.  Florescent microscopy.  Blood smear (thick and thin).  Imaging studies.
  17. 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. 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. 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. 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. 21. BLOOD SMEAR P. Vivax P. Ovale P. Malariae P. Falciparum
  22. 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. 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. 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. 25. REFERENCES Merck manuals Kumar and Clark Medical microbiology, Murray Basic pathology, Robbins Malaria journal
  26. 26. THANK YOU