slide1 l.
Skip this Video
Loading SlideShow in 5 Seconds..
Malaria: Epidemiology PowerPoint Presentation
Download Presentation
Malaria: Epidemiology

Loading in 2 Seconds...

play fullscreen
1 / 16

Malaria: Epidemiology - PowerPoint PPT Presentation

  • Uploaded on

Malaria: Epidemiology Four species: P. falciparum, P. vivax, P. ovale, P. malariae Majority of cases are P. falciparum or P. vivax Most deaths caused by falciparum; predominates in tropical Africa, SE Asia, Haiti, Amazon basin, Dominican Republic

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'Malaria: Epidemiology' - jaden

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
malaria epidemiology
Malaria: Epidemiology
  • Four species: P. falciparum, P. vivax, P. ovale, P. malariae
  • Majority of cases are P. falciparum or P. vivax
  • Most deaths caused by falciparum; predominates in tropical Africa, SE Asia, Haiti, Amazon basin, Dominican Republic
  • Vivax most prevalent in Central America, Middle East, India
life cycle
Life Cycle
  • Bite of the Female Anopheles mosquito
  • Sporozoites enter the bloodstream and travel to liver
  • Divide into mature tissue schizonts, containing thousands of daughter merozoites. (exoerythrocytic stage)
  • These rupture after 6-16 days and release merozoites into the bloodstream, where they invade RBC’s (erythrocytic stage)
life cycle6
Life Cycle
  • Within RBC matures from ring form to trophozoites to mature red cell schizonts (vivax, ovale, falciparum = 48 hours, falciparum = 72 hours); this is the asexual form.
  • Mature schizonts released from RBCs and can infect new red cells.
  • A few merozoites will differentiate into male or female gametocytes (the sexual form.)
life cycle7
Life cycle
  • Gametocytes do nothing but circulate in the bloodstream until they are ingested again by a mosquito to complete their life cycle in the gut of the Anopheles.
  • Vivax and ovale can remain dormant in the liver as hypnozoites and cause late relapse; falciparum and malariae have no dormant phase.
  • All malaria spp. digest red cell proteins and hemoglobin. They derive energy by anaerobic glycolysis; therefore patients are prone to hypoglycemia and lactic acidosis.
  • Parasites also deform the RBC membrane, causing hemolysis and accelerated splenic clearance.
  • Thrombocytopenia can occur due to increased splenic sequestration.
  • Release of proinflammatory cytokines during RBC lysis causes fever, chills, malaise.
  • P. falciparum causes additional pathology by forming sticky knobs on the surface of RBCs via an interaction with actin and spectrin.
  • Knobs bind to receptors on endothelial cells causing microvascular pathology and occlusion
clinical manifestations
Clinical manifestations
  • Fevers/chills that are cyclical
  • Sweats, headache, myalgias, fatigue, nausea, vomiting, abd pain, diarrhea, cough
  • Hepatosplenomegaly, jaundice, anemia
  • Vivax, ovale = invade young RBC’s, low level parasitemia, can have late relapse
  • Malariae = preferentially invades mature RBCs resulting in low grade parasitemia, mild symptoms
  • Falciparum = invades all ages RBCs
  • Renal failure: due to hypovolemia, microvascular occlusion, hemolysis
  • Pulmonary: sequestration of infected RBCs in the lung can cause pulmonary edema/ARDS
  • Hypoglycemia
  • Anemia, DIC
  • Splenic rupture
  • Travel history
  • Thick and thin smears: every 6 to 12 hours for 48 hours
  • Fluorescent microscopy
  • PCR
  • Antigen detection
  • Outpatient vs. inpatient
  • Supportive: antipyretics, glucose containing IVF
  • No drug acts on all stages of the life cycle
  • Quinoline derivatives: inhibit heme polymerase activity resulting in accumulation of free heme which is toxic to parasites. Chlorouqine, quinine, quinidine, mefloquine (intra-RBC); primaquine (intra-erythrocytic, intrahepatic, and gametocytes)
  • Antifolates (pyrimethamine, sulfonadmies, dapsone): kill intrahepatic forms (except hypnozoites) , gametocytes
  • Artemisinin derivatives: not available in the U.S. Bind iron, produce free radicals that damage parasites.
  • Antimicrobials: clinda, atovaquone, tetracycline—act synergistically to kill blood schizonts
  • Chloroquine: ovale, malariae = not observed. Falciparum = widespread with exception of Haiti, Mexico, Dominican Republic. Vivax = mainly Papua New Guinea
  • Primaquine: vivax from Thailand
  • Quinoline: falciparum from SE Asia
  • Antifolate resistance: prevalent in falciparum throughout the Amazone basin, SE Asia
  • Chloroquine (primaquine if vivax or ovale) or quinine plus antimicrobial for synergy
  • Parasitemia >5% = iv quinine
  • Exchange transfusion
  • Desferrioxamine