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20 Cards in this Set
- Front
- Back
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The malarias
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Plasmodium falciparum
Plasmodium vivax Plasmodium malariae Plasmodium ovale |
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Malaria parasite
Infection |
There are two distinct phases of the life cycle of the malaria parasite, one in the mosquito (sexual), and one in the human (asexual).
The female anopheline mosquito transmits the infection from person to person through the injection of the sporozoite stage of the parasite |
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Malaria parasite
Asexual Infection Exoerythrocytic stage |
An infected female Anopheles mosquito takes a blood meal and infects salivary fluids into the wound. These fluids contain sporozoites, small, spindle-shaped, motile forms of the parasite, which initiate the infection. They are cleared from the circulation within an hour and eventually reach parenchymal cells of the liver. Once inside the liver cell, the parasites undergo asexual division.
These stages of the infection occur intracellularly in the parenchymal cells of the liver and give rise to the erythrocytic stages |
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Malaria parasite
Asexual Infection Erythrocytic stage - Immature trophozoite |
When merozoites are released from the liver schizonts, they invade RBCs and initiate the erythrocytic phase of infection. Attachment of the merozoite to the erythrocyte membranes involved interaction with specific receptor sites. The parasite enters by localized endocytic invagination of the RBC membrane.
A. Signet ring stage (immature trophozoite) - Named for its resemblence to a signet ring, Once inside the cell, the parasite begins to grow, first forming the ring-like early trophozoite and usually occurs as a single parasite |
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Malaria parasite
Asexual Infection Erythrocytic stage - Mature trophozoite |
B. Mature trophozoite stage - This stage of development is characterized by an enlargement of the malaria parasite's cytoplasm within the red cell
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Malaria parasite
Asexual Infection Erythrocytic stage - Schizont stage |
C. Schizont stage - The schizont stage of the red cell infection is the final step in the division cycle. The ogranism undergoes asexual division to become schizont composed of merozoites. The parasites are nourished by the hemoglobin within the erythrocytes and produce a characterisitic pigment called hemazoin. Merozoites are released when the infected red cell ruptures and releases meozoites that proceed to invade other erythrocytes. P. falciparum schizonts are extremely rare in peripheral blood.
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Malaria parasite
Asexual Infection Erythrocytic stage - Gametocytes |
D, Gametocytes - The precursors of sex cells of Plasmodium spp. are the microgametocyte (male) and the macrogametocyte (female). This stage of infection is difficult to locate, especially P. vivax and P. malariae. However, gametocytes of P. falciparum are so characteristic in their shape that a definitive diagnosis can be made if only one is seen. Gametocytes are best seen on the "thick smear" portion of each slide.
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Malaria parasite
Sexual stage |
Occurs in the mosquito
Not all merozoites develop asexually. Some differentiate into the sexual forms - macrogametocytes (female) and microgametocytes (male) - which can complete their development only within the gut of an appropriate mosquito vector. On ingestion by the mosquito in the blood meal, the gametocytes shed their protective erythrocyte membrane in the gut of the vector. male gametocytes initiate exflaggleation, a rapid process that produces up to eight active, sperm-like microgametes, each of which can eventually fertilize the macrogametes. The resulting zygotes elongate into diploid vermiform ookinetes, which penetrate the gut wall and come to lie under the basement membrane. The parasites then transform into oocysts within 24 hours of ingestion of the blood meal. Development of sporozoites follows, leading to production of more than 1k of these now-haploid forms in each oocyst. They mature within 10-14 days, escape from the oocyst and invade the salivary glands. When the mosquito bites another human host, a new cycle begins. |
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Malaria parasite
Pathology |
Malaria is characterized by 4 clinical features: periodic chills (lack of O2 due to destruction of RBC), fevers (pyrogenic material when RBC burst) and sweat (after effects of fever), splenomegaly, anemia, and in severe P. falciparum infection, coma (induce TNF in brain leading to NO in brain and cause sleep and possibly coma)
1. Anemia arises from the destrcution of erythrocytes when the merozoites burst out of the infected RBC, which is greater than can be accounted for by this mechanism. The rise in temperature is also correlated with the synchronous release of merozoites. 2. The liver and spleen also harbor numerous paraistized RBCs. Abundant malarial pigment is seen. Giemsa stain allows better visualization. 3. The central nervous system complications of falciparum malaria infection are due to anoxia caused by plugging of the capillaries by parasitized RBCs. 4. The placenta infected with malaria may have many parasites. 5. Liberation of parasite and erythrocyte material into circulation 6. Host reaction to these events (multiple organ system disease, 7. P. falciparum has unique sequestration in micro-circulation of vital organs interfering with flow and tissue metabolism (metabolic acidosisin acute disease) 8. Long-term effects of repeated infections - learning deficit, reduced growth rate, spontaneous abortion; all may be due to prolonged metabolic acidosis |
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Malaria parasite
Diagnosis |
Thick and thin blood smears stained with either Wrights or Giemsa. The lab tech is required by the CDC regulations to scan a thin blood smear under oil immersion for malaria for at least 20 min before deciding "no parasites seen". Take a blood sample every 6 hours until detect the parasite.
A PCR test can also be useful, especially in transfusion malaria cases where a portion of the transfused blood is still available. |
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Malaria
Differential Diagnosis in Blood P. vivax |
Size of infected cell: Many are enlarged
Color of infected cell: may be pale RBC: May have Schuffner's dots Stage in peripheral blood: All Small trophozoite (early rings): Heavy chromatin dot, and cytoplasmic ring; pseudopodia Large trophozoite: Large single mass chromatin, irregular cytoplasm. Brown pigment. Parasite fills cells Schizont: 12-24 merozoites Gametocytes: Large; circular or oval |
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Malaria
Differential Diagnosis in Blood P. falciparum |
Size of infected cell: Normal
Color of infected cell: Normal RBC: Maurer's dots (rare) Stage in peripheral blood: Rings and crescents Small trophozoite (early rings): Delicate cytoplasm; small chromatin dot; double dots and infection; "applique" forms Large trophozoite: Seen in peripheral blood in heavy infections only Schizont: 8-24 merozoites. In peripheral blood in heavy infections, only Gametocytes: Crescent |
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Malaria
Differential Diagnosis in Blood P. Malariae |
Size of infected cell: Normal or small
Color of infected cell: Dark RBC: Ziemann's dots (rare) Stage in peripheral blood: All Small trophozoite (early rings): Thick, heavy cytoplasm and chromatin dot Large trophozoite: Elongate chromatin. Cytoplasm dense. "Band forms" Pigment dark and coarse Schizont: 6-12 merozoites. "Rosette" Gametocytes: Large; circular or oval. Dark pigment |
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Malaria parasite
Clinical signs & symptoms |
• Fever, paroxysms of shaking chills
• Tertian vs quartan fever pattern • Symptoms when other organs involved • Hemolysis: icterus, jaundice, enlarged spleen. Liver does not enlarge • Retinopathy and loss of vision |
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Plasmodium vivex
Latent stage |
Plasmodium vivex may undergo an extra stage where some merozoites become latent and become hypnozoid stage. Causes relapsing malaria. Can wait up to 5 years. Treatment may not get the latent parasites, and when become activated, malaria may be transmitted to other individuals by mosquito bites (in summer when mosquitos are out)
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Malaria parasite
Treatment |
Dependent on:
• Type of malaria • Knowledge of regional resistance • Severity of illness (oral vs intravenous) • Age of patient Resistance to chloroquine is in many countries. In cases of infection with chloroquine-resistant P. falciparum or with a paraiste whose resistance cannot be determined, the treatment consists of quinine sulfate and a 2nd agent that often includes pyrimethamine-sulfadoxine, tetracycline or clindamycin. Artemisinin derivates are now recommended as primary therapy in areas of high drug reesistance and must be used in combination with a second agent to prevent recrudescence. If a patient has P. falciparum infection and is from anywhere in Central America, chloroquine can be used as little resistance to the drug there. In the rest of the world, resistance to chloroquine is so frequently reported that every patient must be assumed to have this form of P. falciparum,.If the origin of infection is unknown, as may be the case with induced malaria, one must treat the infection as if the organisms were resistant. For patients who are too ill to take drugs orally, chloroquine HCl can be administered IM. For resistant falciparum malaria, IV quinidine or quinine dihydrochloride must be used. IV administration is dangerous because the drug can cause fatal arrhythmias. It is mandatory to administer it slowly over a period of one hour and to monitor the patient's vital signs. Relapses due to P. vivax can be prevented by treatment with primaquine to eradicate the hynozoites. It does not have to be started immediately, but can be deferred until the acute attack is over. |
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Malaria parasite
Drugs of choice |
Parent compound: Quinine
Older derivative with extensive resistance: Chloroquine Newer derivative: Mefloquine Drugs of choice (given as a combo): Atovaquon (ubiquinone analogue) and Proguanil (dihyrdate folate reductase inhibitor, anti-folate) |
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Malaria drug
Artemesinin |
From wikipedia:
At present it is strictly controlled under WHO guidelines as it has proven to be effective against all forms of multi-drug resistant P. falciparum, thus every care is taken to ensure compliance and adherence together with other behaviours associated with the development of resistance. It is also only given in combination with other anti-malarials. |
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Antimalarial Prophylaxis
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• North American travelers lack immunity to malaria
• Risk of acquiring malaria depends on rural travel, altitude, season of travel. • Highest risk in low lying areas during rainy season • Personal protection measures against mosquitoes as important as drugs. • Insect repellants, mosquito nets, clothing covering body • Antimalarial drugs do not prevent infection and initial liver stage |
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Antimalarial Prophylaxis
Drugs |
• Prophylaxis with medications based on knowledge of geographic resistance patterns
• Mefloquine, Doxycycline, Atovaquone-Proguanil • Self treatment: Fansidar, Quinine • Combination of both: Chloroquine chemoprophylaxis with standby Rx (Not Recommended!) • MDR resistance a problem in Thailand, Cambodia and Increasingly E. Africa |
