PARASITOLOGY - CHAPTER   TWO  

BLOOD AND TISSUE PROTOZOA 

PART 2  

MALARIA

Dr Abdul Ghaffar 
Professor Emeritus
University of South Carolina

 

• Part 1: Trypanosomiasis and Leishmaniasis

• Part 2: Malaria

• Part 3: Other blood and tissue protozoa

Distribution of malaria, 2014
CDC

MALARIA

Etiology
Four Plasmodium species are responsible for human malaria These are P. falciparum, P. vivax, P. ovale and P. malariae.

Epidemiology
There were an estimated 207 million global cases of malaria in 2012 and at least 627,000 people died of malaria, mostly (over 90%) young children in sub-Saharan Africa. This makes malaria the leading cause of mortality in this region. A decade ago, malaria led to the deaths of more than one million people per year. This drop in mortality, largely as a result of mosquito control efforts and the use of insecticides within the home, has cut malaria cases by 45% and saved the lives of 3.3 million people around the world.

Malaria has been eradicated in North America and Europe as a result of mosquito control. Yet travel-associated cases are malaria are still encountered in these regions. Each year around 2,000 cases of malaria are reported in the United States with a high of 1,925 in 2011. These are mainly in  immigrants who travel to endemic areas and do not take proper prophylactic measures. These malaria infections have led to localized outbreaks in the United States as local mosquitoes acquire the parasite from infected people. In addition, malaria can be spread as a result of blood transfusions from infected donors. Between 1863 and 2011, there were 97 such cases.

In the United Kingdom in 2012 there were 1,400 travel-associated cases and two deaths.

P. falciparum (malignant tertian malaria) and P. malariae (quartan malaria) are the most common species of malarial parasite and are found in Asia and Africa. P. vivax (benign tertian malaria) predominates in Latin America, India and Pakistan, whereas, P. ovale (ovale tertian malaria) is almost exclusively found in Africa (figure 12G).

Places where malaria is endemic:

• Much of Africa and southern Asia

• Central and South America

• Some areas of the Caribbean (Haiti and Dominican Republic)

• Middle East

• Some Pacific Island

Morphology
Malarial parasite trophozoites are generally ring shaped, 1-2 microns in size, although other forms (ameboid and band) may also exist. The sexual forms of the parasite (gametocytes) are much larger and 7-14 microns in size. P. falciparum is the largest and is banana shaped while others are smaller and round. P. vivax causes stippling of infected red cells (figure 13-17).

Plasmodium falciparum: Blood Stage Parasites: Thin Blood Smears  Fig. 1: Normal red cell; Figs. 2-18: Trophozoites (among these, Figs. 2-10 correspond to ring-stage trophozoites); Figs. 19-26: Schizonts (Fig. 26 is a ruptured schizont); Figs. 27, 28: Mature macrogametocytes (female); Figs. 29, 30: Mature microgametocytes (male)  CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971	Plasmodium falciparum: Blood Stage Parasites: Thick Blood Smears Illustrations from: Wilcox A. Manual for the Microscopical Diagnosis of Malaria in Man. U.S. Department of Health, Education and Welfare, Washington, 1960.  CDC
Plasmodium malariae: Blood Stage Parasites: Thin Blood Smears Fig. 1: Normal red cell; Figs. 2-5: Young trophozoites (rings); Figs. 6-13: Trophozoites; Figs. 14-22: Schizonts; Fig. 23: Developing gametocyte; Fig. 24: Macrogametocyte (female); Fig. 25: Microgametocyte (male)   CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971	Plasmodium malariae: Blood Stage Parasites: Thick Blood Smears Illustrations from: Wilcox A. Manual for the Microscopical Diagnosis of Malaria in Man. U.S. Department of Health, Education and Welfare, Washington, 1960.  CDC
Plasmodium ovale: Blood Stage Parasites: Thin Blood Smears Fig. 1: Normal red cell; Figs. 2-5: Young trophozoites (Rings); Figs. 6-15: Trophozoites; Figs. 16-23: Schizonts; Fig. 24:  Macrogametocytes (female); Fig. 25: Microgametocyte (male)   CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971	Plasmodium vivax: Blood Stage Parasites: Thin Blood Smears  Fig. 1: Normal red cell; Figs. 2-6: Young trophozoites (ring stage parasites); Figs. 7-18: Trophozoites; Figs. 19-27: Schizonts; Figs. 28 and 29: Macrogametocytes (female); Fig. 30: Microgametocyte (male)   CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971
Figure  13  Trophozoites: Blood stages malarial parasites  DPDx Parasite Image Library

Plasmodium falciparum: Gametocytes Figs. 27, 28: Mature macrogametocytes (female); Fig. 29, 30: Mature microgametocytes (male) CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971		Plasmodium malariae: Gametocytes Fig. 23: Developing gametocyte; Fig. 24: Macrogametocyte (female); Fig. 25: Microgametocyte (male) CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971
Plasmodium falciparum: Gametocytes: An asplenic, 41 y.o. woman, immigrant from Haiti, who returned to the US 2 days ago; high P. falciparum parasitemia; the presence of such young gametocytes in the peripheral blood is exceptional (specimen contributed by Florida SHD) CDC	Plasmodium falciparum: Gametocytes: A patient from Haiti; mature gametocytes (specimen contributed by Florida SHD) CDC	Plasmodium malariae: Gametocytes: Smear from patient:  56 y.o. man who had traveled to Kenya (specimen contributed by Wisconsin SHD) CDC	Plasmodium malariae: Gametocytes: Smear from patient:  56 y.o. man who had traveled to Kenya (specimen contributed by Wisconsin SHD) CDC
Plasmodium ovale: Gametocytes Fig. 24: Macrogametocyte (female); Fig. 25: Microgametocyte (male). CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971		Plasmodium vivax: Gametocytes Fig. 28 and 29: Nearly mature and mature macrogametocyte (female); Fig. 30: Microgametocyte (male) CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971
A B Plasmodium ovale: Gametocytes Smears from patients: Note the Schüffner's dots in A, and the fimbriation of the erythrocyte in B. The erythrocytes in P. ovale infections are less enlarged than with P. vivax, and are not as deformed. A, B: Male patient born in Nigeria, who came to the US 5 days ago (specimen contributed by Michigan SHD) CDC		A  B C Plasmodium vivax: Gametocytes Smears from patients: Note the variability in Schüffner's dots. A: A pregnant woman who visited India 6 months ago (specimen contributed by New Jersey SHD) B,C: 50 y.o. woman 3 months ago from a 1-month visit to India (specimen contributed by Indiana SHD) CDC
Figure 14  Gametocytes DPDx Parasite Image Library

Plasmodium falciparum: Ring Stage Parasites. Fig. 1: Normal red cell; Figs. 2-10: Increasingly mature ring stage parasites. CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971	Plasmodium malariae: Ring Stage Parasites Fig. 1: Normal red cell; Figs. 2-5: Rings CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971
Appliqué form   Ring with double chromatin dot   Older ring stage parasite   Doubly infected erythrocyte   Multiple infections, 6 rings in 2 erythrocytes An asplenic, 41 y.o. woman, immigrant from Haiti, who returned to the US 2 days ago; high P. falciparum parasitemia (specimen contributed by Florida SHD). CDC	Plasmodium malariae: Ring Stage Parasites  Smears from patients:  56 y.o. man who had traveled to Kenya (specimen contributed by Wisconsin SHD) CDC
Plasmodium ovale: Ring Stage Parasites Fig. 1: Normal red cell; Figs. 2-5: Ring stage parasites CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971	Plasmodium vivax: Ring Stage Parasites Fig. 1: Normal red cell; Figs. 2-6: Ring stage parasites (young trophozoites) CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971
A  B C   Plasmodium ovale: Ring Stage Parasites Smears from patients: Note the relatively large chromatin dots. A, C: 54 y.o. man who returned the previous month from a visit to Kenya and Malawi. P. ovale, confirmed by PCR (specimen contributed by New Mexico SHD). B: 20 y.o. man who returned 10 months ago from a visit to Mozambique, Zimbabwe and Swaziland; this attack is thus a relapse (specimen contributed by New York SHD). CDC	Plasmodium vivax: Ring Stage Parasites Smears from patients: A: Rings in 2 slightly enlarged RBCs; 17 y.o. man with a relapse due to P. vivax (PCR confirmed), 6 months after returning from a visit to Papua New Guinea (specimen contributed by Virginia SHD) B: Double infection with rings, RBC enlarged and deformed, Schüffner's dots beginning to become visible; 69 y.o. woman born in India who was symptomatic on the day of arrival to the US (specimen contributed by Pennsylvania SHD)  C: Late ring in a RBC with Schüffner's dots; 60 y.o. man who returned 2 months ago from a 3 month trip to Laos and North Korea (specimen contributed by Hawaii SHD) CDC
Figure 15  Ring stage parasites DPDx Parasite Image Library

Plasmodium falciparum: Schizonts Figs. 19-25: Increasingly mature schizonts; Fig. 26: Ruptured schizont CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971	Plasmodium malariae: Schizonts.  Increasingly mature schizonts CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971
A B Plasmodium falciparum: Schizonts. Smears from patients: Schizonts are seen only rarely in P. falciparum malaria. An asplenic, 41 y.o. woman, immigrant from Haiti, who returned to the US 2 days ago; high P. falciparum parasitemia A: Young schizont with 10 nuclei; B: Mature schizont with 24 nuclei, ready to rupture (“segmenter”)   (specimen contributed by Florida SHD) CDC	A B C   D Plasmodium malariae: Schizonts.Smears from patients: The parasites are compact and the infected erythrocytes are not enlarged. In C and D, the merozoites are arranged in a rosette pattern.  A, B, C, D: 56 y.o. man who had traveled to Kenya (specimen contributed by Wisconsin SHD) CDC
Plasmodium ovale: Schizonts  Increasingly mature schizonts CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971	Plasmodium vivax: Schizonts Figs. 19-27: Increasingly mature schizonts  CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971
A B Plasmodium ovale: Schizonts Smears from patients: A, B: 54 y.o. man who returned the previous month from a visit to Kenya and Malawi. Infection with P. ovale, confirmed by PCR   Note the fimbriation of the erythrocyte in A. (specimen contributed by New Mexico SHD). CDC	A B C D E Plasmodium vivax: Schizonts Smears from patients: Note that in these patients, the Schüffner's dots are not conspicuous. (This happens in many of the smears received at CDC; it is probably related to variability in staining.)  A, C, D, E: A pregnant woman who visited India 6 months ago (specimen contributed by New Jersey SHD) B: 17 y.o. man with a relapse due to P. vivax (PCR confirmed) (specimen contributed by Virginia SHD) CDC
Figure 16  Schizonts DPDx Parasite Image Library

Plasmodium falciparum: Trophozoites Figs. 11-18: Increasingly mature trophozoites CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971	Plasmodium malariae: Trophozoites Figs. 6-13: Increasingly mature trophozoites; Fig. 13 is a "band form". CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971
A B Thin smears from two patients with high parasitemias: A: An asplenic, 41 y.o. woman, immigrant from Haiti, who returned to the US 2 days ago; high P. falciparum parasitemia (specimen contributed by Florida SHD) CDC B: A patient who acquired malaria by blood transfusion and died with extremely high parasitemia; PCR confirmed P. falciparum; one of the 2 RBCs contains 3 young trophozoites, which have begun to accumulate pigment (specimen contributed by Missouri SHD); CDC	A B C Plasmodium malariae: Trophozoites  Smears from patients:  The infected erythrocytes are not enlarged (sometime they even appear smaller than non-infected ones). C is a "band form" trophozoite. A, B, C: 56 y.o. man who had traveled to Kenya (specimen contributed by Wisconsin SHD) CDC
Plasmodium ovale: Trophozoites Increasingly mature trophozoites. Note the fimbriated red cells (Figs. 8, 13) CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971	Plasmodium vivax: Trophozoites Figs. 8-18: Increasingly mature trophozoites of P. vivax CDC  Illustrations from: Coatney GR, Collins WE, Warren M, Contacos PG. The Primate Malarias. U.S. Department of Health, Education and Welfare, Bethesda, 1971
Plasmodium ovale: Trophozoites   Smears from patients: Note the lack of ameboidicity in the older trophozoites (B,C) and the fimbriation of the erythrocyte in C. The erythrocytes in P. ovale infections are less enlarged than with P. vivax, and are not as deformed. The Schüffner's dots are visible in A, but not B and C.  A: 20 y.o. man who returned 10 months ago from a visit to Mozambique, Zimbabwe and Swaziland (specimen contributed by New York SHD). CDC B, C: 23 y.o. man who arrived to the US 5 months ago after having been in Liberia and Ivory Coast (specimen contributed by Kentucky SHD) CDC	A B C   D  E Plasmodium vivax: Trophozoites Smears from patients: Increasingly mature trophozoites. The RBCs are enlarged and deformed, the parasites are ameboid, and the Schüffner's dots vary in intensity. A, B: 26 y.o. woman who spent 2 weeks in Papua New Guinea 5 months ago (specimen contributed by Pennsylvania SHD)  CDC C, E: 60 y.o. man who returned 2 months ago from a 3-month visit to Laos and North Korea (specimen contributed by Hawaii SHD) D: 28 y.o. woman who returned 3 months ago from a 2 weeks visit to Kenya (specimen contributed by Texas SHD) CDC
Figure  17  Trophozoites DPDx Parasite Image Library

 

Life cycle
Malarial parasites are transmitted by the infected female anopheline mosquito which injects sporozoites present in the saliva of the insect (Figure 18). Sporozoites infect the liver parenchymal cells where they may remain dormant (hypnozoites) or undergo stages of schizogony to produce schizonts and merogony to produce merozoites (meronts). When parenchymal cells rupture, thousands of meronts are released into blood and infect the red cells. P. ovale and P. vivax infect immature red blood cells whereas P. malariae infects mature red cells. P. falciparum infects both. In red cells, the parasites mature into trophozoites. These trophozoites undergo schizogony and merogony in red cells which ultimately burst and release daughter merozoites. Some of the merozoites transform into male and female gametocytes (figure 19) while others enter red cells to continue the erythrocytic cycle. The gametocytes are ingested by the female mosquito, the female gametocyte transforms into ookinete, is fertilized, and forms an oocyst (figure 20) in the gut. The oocyte produces sporozoites (sporogony) (figure 20) which migrate to the salivary gland and are ready to infect another host. The liver (extraerythrocytic) cycle takes 5-15 days whereas the erythrocytic cycle takes 48 hours or 72 hours (P. malariae). Malaria can be transmitted by transfusion and transplacentally.
 

How does the plasmodium-infected red cell escape destruction?

Stage II (central) and stage III (bottom right) immature gametocytes (blood film, wet mount, x1000 magnification under oil immersion) Image courtesy of Dr Andrew Taylor-Robinson, University of Leeds, UK  © Dr Andrew Taylor-Robinson	Stage IV immature gametocyte, located centrally (blood film, wet mount, x400 magnification) Image courtesy of Dr Andrew Taylor-Robinson, University of Leeds, UK  © Dr Andrew Taylor-Robinson
Stage V mature gametocyte, showing characteristic sausage-shaped morphology, located centrally (blood film, wet mount, x1000 magnification under oil immersion) Image courtesy of Dr Andrew Taylor-Robinson, University of Leeds, UK  © Dr Andrew Taylor-Robinson	Male (micro)gametocyte exflagellation - extrusion of motile, flagella-like microgametes with vigorous movement (blood film, wet mount, x1000 magnification under oil immersion) (an unusually clear picture of this metabolically dynamic and visually striking event)  Image courtesy of Dr Andrew Taylor-Robinson, University of Leeds, UK  © Dr Andrew Taylor-Robinson
Figure 19  Sexual stages of the malaria parasite Plasmodium falciparum

Two oocysts, dissected from the outer wall of the Anopheles stephensi midgut, 10 days post infection of the mosquito (wet mount, x400 magnification) Image courtesy of Dr Andrew Taylor-Robinson, University of Leeds, UK  © Dr Andrew Taylor-Robinson	Single oocyst, dissected from the outer wall of the Anopheles stephensi midgut, 10 days post infection of the mosquito (wet mount, x400 magnification) Image courtesy of Dr Andrew Taylor-Robinson, University of Leeds, UK  © Dr Andrew Taylor-Robinson
Single oocyst, dissected from the outer wall of the Anopheles stephensi midgut, 10 days post infection of the mosquito (wet mount, x1000 magnification under oil immersion) Image courtesy of Dr Andrew Taylor-Robinson, University of Leeds, UK  © Dr Andrew Taylor-Robinson	Isolated bow-shaped sporozoite, dissected from the salivary glands of Anopheles stephensi, 17 days post infection of the mosquito (wet mount, x1000 magnification under oil immersion)   Image courtesy of Dr Andrew Taylor-Robinson, University of Leeds, UK  © Dr Andrew Taylor-Robinson
Figure 20  Developmental stages of Plasmodium falciparum in the Anopheles mosquito vector

Symptoms
The symptomatology of malaria depends on the parasitemia, the presence of the organism in different organs and the parasite burden. The incubation period varies generally between 10 to 30 days. As the parasite load becomes significant, the patient develops headache, lassitude, vague pains in the bones and joints, chilly sensations and fever. As the disease progresses, the chills and fever become more prominent. The chill and fever follow a cyclic pattern (paroxysm) with the symptomatic period lasting 8 to 12 hours. In between the symptomatic periods, there is a period of relative normalcy, the duration of which depends upon the species of the infecting parasite. This interval is about 34 to 36 hours in the case of P. vivax and P. ovale (tertian malaria), and 58 to 60 hours in the case of P. malariae (quartan malaria). Classical tertian paroxysm is rarely seen in P. falciparum and persistent spiking or a daily paroxysm is more usual.

The malarial paroxysm is most dramatic and frightening. It begins with a chilly sensation that progresses to teeth chattering, overtly shaking chill and peripheral vasoconstriction resulting in cyanotic lips and nails (cold stage). This lasts for about an hour. At the end of this period, the body temperature begins to climb and reaches 103 to 106 degrees F (39 to 41degrees C). Fever is associated with severe headache, nausea (vomiting) and convulsions. The patient experiences euphoria, and profuse perspiration and the temperature begins to drop. Within a few hours the patient feels exhausted but symptom-less and remains asymptomatic until the next paroxysm. Each paroxysm is due to the rupture of infected erythrocytes and release of parasites.

Without treatment, all species of human malaria may ultimately result in spontaneous cure except with P. falciparum which becomes more severe progressively and results in death. This organism causes sequestration of capillary vasculature in the brain, gastrointestinal and renal tissues. Chronic malaria results in splenomegaly, hepatomegaly and nephritic syndromes. Nevertheless, malaria is treatable if caught early enough.

Patients infected with P. ovale and P. vivax may experience relapses over a period of months or years. During remission periods, the parasite (hypnozoite) lies dormant in the liver.

Summary of symptoms

In the first 8 to 12 hours of overt disease, the following symptoms are experienced:

• Chills: Feeling cold and shivering

• Fever: Feeling hot with headache and nausea. There may be seizures in children

• Sweats: The patient's fever subsides and temperature falls. The patient feels weary with general malaise and aches

This is then followed by a cyclic pattern of similar symptoms, the intervals between cycles depending on the type of infection.

This may be followed by a more severe disease in which organ collapse occurs and many erythrocytes contain parasites:

• Infection of the brain leading to seizures, coma and behavioral changes

• Anemia resulting from erythrocyte lysis

• Hemoglobin in the urine (hemoglobinurea)

• Lung inflammation resulting in respiratory distress

• Cardiovascular collapse from low blood pressure

• Kidney failure

• Acidosis and hypoglycemia

Pathology and immunology
Symptoms of malaria are due to the release of massive number of merozoites into the circulation. Infection results in the production of antibodies which are effective in containing the parasite load. These antibodies are against merozoites and schizonts. The infection also results in the activation of the reticuloendothelial system (phagocytes). The activated macrophages help in the destruction of infected (modified) erythrocytes and antibody-coated merozoites. Cell mediated immunity also may develop and help in the elimination of infected erythrocytes. Malarial infection is associated with immunosuppression.

Diagnosis
Diagnosis is based on symptoms and detection of parasite in Giemsa stained blood smears. There are also antibody tests (Figure 20B). Other laboratory findings may include: thrombocytopenia, high bilirubin, high aminotransferases.

Treatment and Control
Treatment is effective with various quinine derivatives (quinine sulphate, chloroquine, meflaquine and primaquine, etc.). Drug resistance, particularly in P. falciparum and to some extent in P. vivax is a major problem. Control measures are eradication of infected anopheline mosquitos. Vaccines are being developed and tried but none is available yet for routine use.

An infection (particularly with P. falciparum ) may be treated with a variety of drugs among which are:

• Chloroquine
  This binds to heme, released from hemoglobin in the parasitized erythrocyte, to form a complex that is toxic to and lyzes the erythrocyte.

• Atovaquone-proguanil (Malarone)
  Atovaquone is a mitochondrial electron transfer blocker. Proguanil is a prodrug that is metabolized to cycloguanil that blocks dihydrofolate reductase and also enzymes involved in DNA production.

• Mefloquine (Lariam)
  This drug is widely used as a prophylactic, especially where chloroquine-resistant plasmodia occur. It can have serious side effects in some people. It has been proposed to interact with an erythrocyte membrane protein called stomatin and is then transferred to the parasite's membrane.

• Artemether-lumefrantine (Coartem). Artemether is a semi-synthetic derivative of artemisinin and is metabolized to dihydroartemisinin which may act via an endoperoxide moiety. The mechanism of action of lumefrantine, which is a synthetic compound, is unknown. This drug combination is used to treat acute uncomplicated P. falciparum malaria.

• Quinine
  This drug has been around since the 17th century and was the first effective anti-malarial in western medicine.  It comes from the bark of the cinchona tree. The mechanism of action is not known but is proposed to be similar to choroquine. Quinidine is a stero isomer of quinine

• Doxycycline (combined with quinine)
  In addition to be an anti-bacterial agent, doxycyline is anti-protozoal and is used in malaria prophylaxis. It may alter the division of a plastid found in protozoan cells called the apicoplast.

• Clindamycin  (combined with quinine)
  This is also an anti-bacterial but has action against some protozoans. It probably acts on the ribosome.

• Artesunate
  This is not license for use in the United States. Like artemether, this is a semi-synthetic derivative of artemisinin.

Prophylaxis treatment often includes: Atovaquone-proguanil or Mefloquine as chloroqine-resistance is becoming increasingly common.
 

 

CASE REPORT
One Traveler’s Ordeal with Severe Malaria: A Cautionary Tale
CDC

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