Microbiology 13 - Plasmodium.pdf

Microbiology Parasitology Plasmodium Microbiology| Plasmodium Contents : Protozoa 3 Plasmodium Species 4 Life Cycle 5 Pathogenicity and Symptoms 18 Diagnosis 23 Treatment 25 Microbiology| Plasmodium Protozoa (Sporozoa) : complex life cycle. sexual and asexual reproductive phases. Cryptosporidium, To...

Microbiology Parasitology Plasmodium Microbiology| Plasmodium Contents : Protozoa 3 Plasmodium Species 4 Life Cycle 5 Pathogenicity and Symptoms 18 Diagnosis 23 Treatment 25 Microbiology| Plasmodium Protozoa (Sporozoa) : complex life cycle. sexual and asexual reproductive phases. Cryptosporidium, Toxoplasma and malarial, (Plasmodium species) all are intracellular parasites. Microbiology| Plasmodium Plasmodium Species (Blood Sporozoa) : Phylum: Apicomplexa Class: Sporozoa MALARIA PARASITES four species are known to infect humans: P. falciparum, P. vivax, P. malariae, P. ovale It is vector-borne disease. P. vivax and P. falciparum account for 95% of infections. Microbiology| Plasmodium Life cycle : definitive host: female Anopheles mosquito. malaria parasites exhibit alternation of generations and alternation of hosts. Human cycle infective form: The sporozoites. The sporozoites: find in the salivary glands of the definitive host (Anopheles mosquito). When it bites it introduce the sporozoites directly to the human blood. Microbiology| Plasmodium The cycle in man comprises of following stages: 1. Primary exo-erythrocytic or pre-erythrocytic schizogony. 2. Erythrocytic schizogony. 3. Gametogony. 4. Secondary exo-erythrocytic or dormant schizogony. Microbiology| Plasmodium Primary exo-erythrocytic or pre-erythrocytic schizogony : 1. sporozoites leave the blood stream and enter into liver parenchyma cells. 2. sporozoites transform from The elongated, spindle-shaped bodies to rounded inside the liver cells. 3. multiple nuclear division. 4. followed by cytoplasmic division. Microbiology| Plasmodium Primary exo-erythrocytic or pre-erythrocytic schizogony : 5. develop into primary exoerythrocytic schizont or pre-erythrocytic schizont. 6. The duration of this cycle of P. falciparum, P. vivax, P. ovale and P. malariae is 6, 8, 9 and 13–16 days, respectively. 7. When this cycle complete, liver cell rupture and thousands of merozoites is in the blood. Microbiology| Plasmodium Erythrocytic schizogony : 1. merozoite enters the erythrocyte (specific receptors). 2. multiply and initiating erythrocytic schizogony. 3. pass through the stages of trophozoites (ring stage), schizonts and merozoites. 4. red cell ruptures to release the individual merozoites, which then infect fresh red blood cells. 5. multiplication in RBCs bringing on a clinical attack of malaria. Microbiology| Plasmodium Note: Erythrocytic schizogony may be continued for a considerable period, but in the course of time the infection tends to die out. P. falciparum differs from the other malaria parasites in that developing erythrocytic schizonts aggregate in the capillaries of the brain and other internal organs. Microbiology| Plasmodium Gametogony (gametocytogenesis) : 1. merozoites develop within red cells into male (microgametocytes) and female gametocytes (macrogametocytes). 2. Mature gametocytes of P. vivax, P. malariae and P. ovale are round, but the gametocytes of P. falciparum are elongated or crescent-shaped. 3. The host carrying gametocytes is known as carrier. 4. Although the longevity of mature gametocytes may exceed several weeks, their half-life in the blood stream may be only 2 or 3 days, while waiting for the mosquito to take them up. Microbiology| Plasmodium Secondary exo-erythrocytic or dormant schizogony : 1. hypnozoite or sleeping form: a resting (dormant) stage of sporozoites stays in the liver. It is rounded, uni-nucleate. 2. after 2 years hypnozoites are reactivated to become secondary exo-erythrocytic schizonts and release merozoites which infect red blood cells producing relapse of malaria. 3. P. falciparum and P. malariae: no hypnozoite, no relapse. Microbiology| Plasmodium Recrudescence: RBC infection is not eliminated by the immune system or by therapy and the numbers in the RBCs begin to increase again with subsequent clinical symptoms. All species of Plasmodium may cause a recrudescence. Without treatment, P. Malariae persist for more than 10 yrs. P. vivax and P. ovale persist as periodic relapses for up to 5 years. Microbiology| Plasmodium Microbiology| Plasmodium Mosquito cycle: Sporogony The gametocytes ingested by an Anopheles mosquito during a blood meal. Note: In the mosquito's stomach, from one The macrogametocyte does not show exflagellation, it developes into a macrogamete. microgametocye eight microgametes are formed by the process called exflagellation. Microbiology| Plasmodium Fertilization : occur when the microgametes penetrate the macrogametes generating zygotes. The zygotes in turn become motile and elongated (ookinetes). ookinetes invade the midgut wall of the mosquito where they develop into oocysts. The oocysts grow, rupture, and release millions of spindle-shaped sporozoites. sporozoites goes to mosquito's salivary glands. Inoculation of the sporozoites into cutaneous blood vessels in human and initiates infection. Microbiology| Plasmodium Microbiology| Plasmodium Pathogenicity and symptoms : 1. erythrocytic infection developes symptoms, exo- erythrocytic no symptoms. 2. RBCs destraction: A. Parasitized cells: Rupture and lysis. B. Non-parasitized: dibers and toxins of ruptured cells. Both of which lead to Anemia. Note: The number of RBCs in severe cases equal to half of normal number. Microbiology| Plasmodium 3. P. vivax and P. ovale infect youngest erythrocytes, while P. malariae infect oldest one. 4. P. falciparum invades erythrocytes of all ages, so produces extensive parasitemia and responsible for fatal infection. 5. In P. falciparum after 2-3 asexual cycles the number of infected RBCs reaches a dangerous threshold without production of typical chills and fever. Microbiology| Plasmodium 6. Erythrocytes containing P. falciparum adhere to one another and to lining of blood vessels causing blockage of blood capillaries in vital area such as brain, lung, and kidney. 7. Toxin production cause oxygen starvation of tissue followed by thrombosis in small blood vessels and decrease in the volume of circulating blood. 8. Spleen is typically enlarged and congested (splenomegaly), with dark color as amount of pigment increase and Liver is hard in chronic stage and soft and hemorrhagic in acute stage. Microbiology| Plasmodium 9. The liver hypertrophic and congested in acute malaria and contains deposits of pigments. 10. Bone marrow undergoes the same changes as spleen. Kidneys are congested. 11. Quarter malaria cause glomerulonephritis and pulmonary congestion. Microbiology| Plasmodium Malarial paroxysm : P. vivax, P. ovale or quarter malaria characterized by sudden develops with shaking chill followed by a fever of 40-40.6˚C with headache, muscular pain, malaise, nausea, vomiting, and increase in pulse and respiration rates. After several hours, the fever terminates and followed by drenching sweat and patient will be exhausted. The series of paroxysm constitute the primary attack complication and pernicious symptoms: coma, convulsion, and cardiac failure. Microbiology| Plasmodium Diagnosis : Microscopy: Thin and thick blood films taken at malarial paroxysm will detect number of parasites. 1. Thick blood film for rapid examination of a large volume of blood in small area on the slide (concentration of parasite). 2. Thin blood film for specific diagnosis of species. immunochromatographic methods: to detect the antigens in blood. other methods: as serology (detect antibodies) and PCR. Microbiology| Plasmodium Challenges in diagnosis 1. Low parasite density: Ex. P. vivax merozoites only invade immature red blood cells (reticulocytes), thus BM samples are needed. 2. Complex life cycle: P. vivax hypnozoite, undetectable with any currently available diagnostic methods. Microbiology| Plasmodium Treatment : Chloroquine and amodiaquine. P. falciparum showing drug resistant should treated with quinine alone or with combination with other drugs Control: requires community rather than individual reports 1. Antimosquito chemicals: like DDT (Dichloro Diphenyl Trichloroethane) and Malathion: preventing the breeding of Anopheles mosquito. 2. Avoiding exposure to mosquito bites. 3. Taking chemoprophylaxis: Chloroquine and the anti-folate drug