A SICK TRAVELER Fatima Al Awadh

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.

EXAMINATION

Ill looking, slightly pale, not dehydrated, not jaundiced, nor dyspnoeic.

Hardly stands with fever of ().

Consciousness was normal.

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.

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)?

DIFFERENTIAL DIAGNOSIS

Travelling acquired infections : Meningitis. Dengue fever. Chikungunya. Malaria.

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.

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.

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.

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.

DIAGNOSIS

Most likely to be:

Malaria

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.

EPIDEMIOLOGY

300-500 million people are infected every year.

Over 1 million die annually.

25 000 international travelers per year are infected.

LIFE CYCLE

CLINICAL FEATURESP. 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.

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.

INVESTIGATIONS

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

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.

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.

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.

BLOOD SMEARP. 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.

BLOOD SMEARP. Vivax P. Ovale P. Malariae

P. Falciparu

m

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

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.

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.

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

THANK YOU