Imagine: you are the single provider manning a rural clinic in Northern Tanzania along the shore of Lake Victoria. You are one of only a handful of physicians in the entire region and you have minimal access to diagnostics or therapeutics. Your clinic does not have any power. Your diagnostics include: urinalysis, urine pregnancy, CBC and rapid tests for HIV, syphilis, and malaria. You have 2 nurses, one of whom acts as a translator (from Swahili to English). You are armed primarily with your intellect, knowledge of local disease processes, and your keen sense of intuition.
13 year old male with no significant PMH presents with 3 days of fever, cough, chest pain, and intermittent nose bleeds. He denies nausea, vomiting, diarrhea, or abdominal pain. His cough is non-productive. No sick contacts.
T 39.1C HR 98 BP 110/70 RR 16 weight 40kg
Gen: Mildly ill-appearing; skin warm to touch
HEENT: PERRL, EOMI, Mild conjunctival pallor; Oropharynx clear, no erythema or lesions
C/V: S1S2 present, borderline tachycardia, regular rhythm, no murmurs
Resp: No resp distress, good air movement. Diffuse mild expiratory wheezing.
Abd: Soft, nt/nd. +Splenomegaly. Lower spleen edge palpated 2-3 finger-breadths below L costal margin
Skin/Ext: No edema or rash.
What’s the most likely diagnosis?
28 year old female G4P3 at approximately 14 weeks gestational age who presents with several weeks of dysuria, lower abdominal pain, and fever. No hematuria. No diarrhea or blood/mucus in stool. Reports feeling weak but denies dizziness or syncope.
T 39.3C HR 110 BP 120/80 RR 12 weight 55kg
Gen: Appears uncomfortable but not in acute distress.
HEENT: PERRL, EOMI. Significant conjunctival pallor. Oropharynx clear.
C/V: S1S2 present, tachycardic, no murmurs.
Resp: CTAB, no crackles/wheezes
Abd: Mild periumbilical tenderness. No rebound/guarding. No masses palpated.
+FHT (~140 bpm)
What’s the most likely diagnosis?
57 year old female with PMH HIV & currently active TB presents with 3 days of dizziness and palpitations and discovered to be febrile with splenomegaly and significant anemia (Hb<3.0). What’s the diagnosis?
14 month old male with no significant PMH presents in acute distress w/ fever, lethargy, poor feeding, tachycardia, tachypnea (RR>60), and anemia (Hb 5.5) whom you immediately refer to the main hospital but dies en route. What’s the diagnosis?
“If you think you are too small to make a difference, you have not spent a night with a mosquito.”
-- African Proverb
Dx = Malaria, Plasmodium falciparum (for all 4 cases)
Malaria is a mosquito-borne infectious disease commonly transmitted via a bite from an infected female Anopheles mosquito. The disease is widespread in tropical regions surrounding the equator. There are five species of Plasmodium and the vast majorities of deaths are caused by P. falciparum. There were 198 million documented cases of malaria in 2013 and as many as 1.2 million people died (WHO). Most deaths occur in children under the age of 5, and it is estimated that a child dies of malaria every 30 seconds. Other high risk groups include pregnant women and non-immune travelers. Malaria is commonly associated with poverty and is a potential barrier to economic growth, accounting for nearly 40% of public health expenditure in Africa.
Signs/symptoms of malaria typically begin 8-25 days following infection. Patients often initially develop flu-like symptoms. Presentation may include fever (often cyclical), headache, rigors, arthralgias, nausea/vomiting. Findings include hemolytic anemia (sometimes severe), splenomegaly, jaundice, hemoglobinuria (aka “Blackwater Fever with renal failure), and jaundice. Cerebral malaria is defined as severe P. falciparum-malaria presenting with neurologic symptoms, including coma or seizure, and is often fatal. Severe malaria can progress rapidly and mortality is as high as 20% despite aggressive management.
There are no pathognomonic clinical signs or symptoms for the diagnosis of malaria. The gold standard is visualization of parasites in stained samples—3 sets of Giemsa thick & thin blood smears. In resource-limited settings Rapid diagnostic tests (RDTs), detecting antigens or antibodies, are more common and very useful.
Most effective treatment is with use of artemisinins in combination with other antimalarials (amodiaquine, lumefantrine, mefloquine, or sulfadoxine/pyrimethamine). We commonly used artemisinin-lumefantrine for outpatient treatment in Tanzania. For severe cases and inpatient management we used IV quinine therapy as well. For U.S. guidelines please see UCMC’s Emergency Knowledge Translation protocol for Malaria diagnosis and treatment below.
Multiple regimens including chloroquine (extensive resistance), mefloquine, doxycycline, and Malarone (atovaquone-proguanil HCl) can be used.
CDC Guideline for Treatment of Malaria in the United States: http://www.cdc.gov/malaria/resources/pdf/treatmenttable.pdf
White NJ, Pukrittayakamee S, Hien TT, et al. Malaria. The Lancet 2014; 723-735.
Agarwal A, McMorrow M, Onyango P, et al. A randomized trial of artemether-lumefantrine and dihydroartemisinin-piperaquine in the treatment of uncomplicated malaria among children in western Kenya. Malaria Journal 2013; 12:254.
Rosenthal PJ. Artesunate for the Treatment of Severe Falciparum Malaria. N Engl J Med. 2008; 388:1829-36.
Breman, JG. Conquering Malaria. Improving Population Health Workshop. Fogarty International Center. Cuernavaca, Mexico. 2003.
Trampuz A, Jereb M, Muzlovic I, et al. Clinical Review: Severe Malaria. Critical Care. 2003, 7:315-323.