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Malaria and bebesia

Protozoan parasites characterized by the production of spore-like oocysts containing sporozoites were known as sporozoa.
They live intracellularly, at least during part of their life cycle

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Malaria and bebesia

  1. 1. Malaria parasite belongs to Phylum: Apicomplexa Class: Sporozoa Order: Haemosporida Genus: Plasmodium. Calassification of Malaria
  2. 2. Malaria remains the world's most devastating human parasitic infection. Malaria affects over 40% of the world's population. WHO, estimates that there are 350 - 500 million cases of malaria worldwide. In India 2 million cases and 1000 deaths annually Distribution of Malaria
  3. 3. Protozoan parasites characterized by the production of spore-like oocysts containing sporozoites were known as sporozoa. They live intracellularly, at least during part of their life cycle. At some stage in their life cycle, they possess a structure called the apical complex, by means of which they attach to and penetrate host cells. These protozoa are therefore grouped under the Phylum Apicomplexa. The medically important parasites in this group are the malaria parasites, Coccidia, and Babesia. The Phylum Apicomplexa includes 2 classes viz. haematozoa and coccidia and 3 orders—eimeriida, haemosporida, and piroplasmida. Characteristics of Malaria
  4. 4. Plamodium vivax: Benign Tertian Malaria. Plasmodium falciparum: Malignant Tertian Malaria. Plasmodium malariae: Benign Quartan Malaria. Plasmodium ovale: Benign Tertian Malaria. Causative Agents of Human Malaria
  5. 5. Malaria parasites—Erythrocytic stages of the four species (Giemsa stain. Magn × 2000)
  6. 6. The malaria life cycle is a complex system with both sexual and asexual aspects . cycle of all species that infect humans is basically the same. There is an exogenous sexual phase in the female Anopheles mosquito (the definitive host) called sporogony during which the parasite multiplies. There is also an endogenous asexual phase that takes place in the vertebrate or human(the intermediate host) host that is called schizogeny The malaria life cycle
  7. 7. life cycle of malaria
  8. 8. occurs due to enhanced phagocytosis of remnants of ruptured red cells and debris of schizont. Remnants Pathogenesis and Clinical Picture  Enlargement of liver and spleen.
  9. 9. The common first symptoms – fever, headache, chills and vomiting – usually appear 10 to 15 days after a person is infected. If not treated promptly with effective medicines, malaria can cause severe illness and is often fatal. Stage1 (cold stage): Chills for 15 mt to 1 hour Caused due to rupture from the host red cells escape into Blood Preset with nausea, vomitting,headache. Stage 2 (hotstage): Fever may reach upto 400c may last for several hours starts invading newer red cells. Early symptoms
  10. 10. Stage3: (sweating stage) Patent starts sweating, concludes the episode Cycles are frequently Asynchronous Paroxysms occur every 48 – 72 hours In P.malariae pyrexia may last for 8 hours or more and temperature my exceed 410c More commonly, the patient presents with a combination of the following symptoms Fever  Chills  Sweats  Headaches  Nausea and vomiting  Body aches  General malaise.
  11. 11. Complications • Vivax, ovale & malariae malaria Relatively benign. • Chronic malariae malaria Nephrotic syndrome. Parasite produces increased amount of antigens Immune system produces increased amount of antibodies. Antigens attach to antibodies producing immune-complex in blood. Immune-complexes are deposited on the glomerular walls activating the complement Child has nephrotic syndrome C1, 4, 2,3, 5, 7, 96, 8, MAC Kidney tissue damage.
  12. 12. Complications of falciparum malaria 1- Knobs develop on surface of infected RBCs Knobs are parasite antigens expressed on the surface of infected red cells containing trophozoites and schizont stages. They adhere to receptors found on endothelium of blood capillaries of blood supply internal organs anoxia and necrosis. Normal RBC Infected RBC Parasite antigens Blood capillary
  13. 13. In brain : cerebral malaria. Headache, drowsiness, convulsions & coma In GIT : ischaemia in capillary bed of intestinal wall. Diarrhoea, dysentery, gastrointestinal bleeding In liver : impaired glycogenolysis, Hypoglycaemia. In the kidney: acute renal failure. In the lung : Pulmonary oedema, difficulty in breathing. Hypotension, circulatory collapse & chock ,
  14. 14. Complications of falciparum malaria 2- Hyper-reactive malarial splenomegaly The spleen is markedly enlarged with increased IgM production. This is due to reduction of T-suppressor cells that control B-cell activation. 3- Black water fever Occurs: when? - Repeated attacks of P.falciparum infection. - Incomplete quinine therapy. Pathogenesis Massive intravascular haemolysis occurs producing Anaemia, haemoglobinuria, jaundice. Cause This is autoimmune with development of antibodies to infected red blood cells.
  15. 15. Pathogenesis of Black Water Fever Normal urine Haemoglobinuria Jaundiced patient Blood Vessel of the infected patient Normal RBCs Infected RBCs Auto-antibodies
  16. 16. 1- Thin and thick blood films to demonstrate the parasite. Thin blood film Thick blood film 5-Giemsa stained blood films Microscopic Diagnosis 3-One drop of blood spread on a slide 4- drops of blood spread in a small circle on a slide 1-Finger prick 2-put drop of blood on slide
  17. 17. Buffy Coat Method RBCs Plasma WBCs, platelets, parasite Patient’s blood Buffy coat Centrifugation of blood sample A technique used for collection of parasite from blood sample
  18. 18. P. vivax P. ovale P. malariae P. falciparum ♂♀ ♀ ♀♀ ♂ ♂♂ Schuffner’s dots Ziemann’s dots Maurer’s clefts Malaria pigments (Haemozoin) X X Enlarged, rounded Enlarged, oval Normal size & shape Ring 1/6 RBC size Ring 1/3 RBC size Ring 1/3 RBC size Ring 1/3 RBC size Multiple rings Not seen in peripheral blood Band- shaped
  19. 19. Diagnosis 2- Detection of circulating parasite antigen using monoclonal antibodies. 3- Detection of parasite DNA and RNA in patient’s blood using DNA and RNA probes. Malaria pigments = Haemozoin It is the remnants of haemoglobin that was digested by Plasmodium parasite Schuffner’s dots Ziemann’s dots Maurer’s clefts It is degeneration process occurring in Plasmodium infected RBCs Called: Stippling T C
  20. 20. Control • Treatment of cases. • Mosquito control. • Chemoprophylaxis. • Vaccination trials: The problem is antigenic variation. A synthetic vaccine with separation of the gene responsible for antigenic variation.
  21. 21. Chrooquine sulfadoxine, and pyrimethamine along with primaquine. In chlroquine resistance, quinine or artemesinin are used. Treatment
  22. 22. Babesia species causes Babesiosis Hard tick ‫القراد‬ Geographical Distribution: North and South America and Europe. Babesia is an animal parasite that causes Texas cattle fever. It affects humans in contact with animals.
  23. 23. Mode of Infection • Through the bite of hard ticks. • Through blood transfusion. budding merozoites Sporozoites infective stage Hard tick Rings diagnostic stage Rupture
  24. 24. Pathogenesis and Clinical Picture Asymptomatic. Malaria-like picture with haemolytic anaemia but NO periodicity. Fulminant disease that may end fatally in: Splenectomized OR Immunodefficient patients. Babesia is an opportunistic protozoan
  25. 25. Diagnosis 1- Blood film 2- Serology 3- PCR Prevention and Control Measures to control ticks Treatment Clindamycin + Quinine
  26. 26. Compare between Blood picture of falciparum malaria and babesia infected patient. Ring stage Gametocyte stage Ring stage P.falciparum Babesia Malaria pigments: present No malaria pigments

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Protozoan parasites characterized by the production of spore-like oocysts containing sporozoites were known as sporozoa. They live intracellularly, at least during part of their life cycle


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