Malaria main

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malaria

Malaria main

  1. 1. RAM NAIK. M 5th Sem AMC
  2. 2. INTRODUCTION¥ Otherwise known as AGUE¥ Derived from Italian: Mal’ aria= bad’ air (Horace Walpole in 1740)¥ Malaria continues to be most important cause o fever and morbidity in the Tropical world.
  3. 3. HISTORY
  4. 4. 2700 BC: China- Huang Di Nei Jing Described one form of intermittent fever recurring every one, two or three daysHippocratic corpus (400 B.C.) was the first to describe the manifestations of thedisease and to relate them to the time of the year and where the patient lived.
  5. 5. • The periodic fever episodes characteristic for malaria have been described by physician early on in human history. • People recognized a connection between malaria and swamps. • It was thought that swamps exude a miasma or poison which causes the disease Giovanni Maria Lancisi (1654-1720)☺He first described a characteristic black pigmentation ofthe brain and spleen in the victims of malaria.☺Lancisi linked malaria with poisonous vapors of swampsor stagnant water on the ground.
  6. 6. Discovery of the Malaria Parasite (1880)6th of November 1880.Charles Louis Alphonse Laveran, a French army surgeon concludedthat “Swamp fevers are due to a germ”Parasites in the blood of a patient suffering from malaria.Unable to identify the species.
  7. 7.  1883 - Methylene blue stain - Marchafava1891 - Polychrome stain- Romanowsky
  8. 8. Discovery that mosquitoes transmit malaria On august 20th, 1897, RONALD ROSS, a British officer in the Indian medical service, demonstrated that malaria parasites could be transmitted from infected patients to mosquitoes. In further work with bird malaria, Ross showed that mosquitoes could transmit malaria parasites from bird to bird. The mystery of malaria transmission was solved.
  9. 9. Discovery of the transmission of the human malaria parasites• In 1898, led by Giovanni Batista Grassi, a team of Italian investigators, collected Anopheles claviger mosquitoes and fed them on malaria patients.• The complete sporogonic cycle of Plasmodium falciparum, P. vivax, and P. malariae was demonstrated.• In 1899, mosquitoes infected by feeding on a patient in Rome were sent to London where they fed on two volunteers, both of whom developed malaria.
  10. 10. Camillo GolgiAn Italian neurophysiologist, established that there were at least two forms of the disease -one with tertian periodicity (fever every other day) and one with quartan periodicity (fever every third day).He prepared high quality micrographs anddescribed the asexual replication of theparasite within the RBC.He observed that fever coincided with therupture and release of merozoites into theblood stream.
  11. 11. 1948 - Site of Exoerythrocytic development in Liver by Shortt and Garnham
  12. 12. Major Developments in 20th Century • WHO 1955 • Malaria eradication programme using DDT • Resistance to DDT 1970 • Programme fails • Trager & Jensen 1976 • Invitro-cultivation of the parasite
  13. 13. PAUL ROSS MULLER • High efficient of• Oocyst of Plasmodium DDT as a contact in gut-wall of mosquito poison against• 1897-Aug-20 several arthropods• 1902 NOBLE LAVERAN LAURETES GOLGI• Noticed parasite • Asexual in the blood of a reproduction of patient Plasmodium in RBC• 1880-Nov-6• 1907
  14. 14. Why is it important…..?????Malaria remains the worlds most devastating human parasitic infection.Malaria affects over 40% of the worlds population.WHO, estimates that there are 350 - 500 million cases of malaria worldwide, of which 270 - 400 million are falciparum malaria, the most severe form of the disease.
  15. 15. MALARIA Kills more people than AIDSMalaria kills in one year what AIDS kills in 15 years.For every death due to HIV/AIDS there are about 50 deaths due to malaria.To add to the problem is the increasing drug resistance to the established drug.
  16. 16. TRANSMISSION• Mosquito Bite (Female Anopheles)• Blood – Maximum with fresh blood up to 5 days. – No infection - stored blood > 5 days. – No infection - Plasma Transfusion• Syringes – Drug Addict / Iatrogenic.• Congenital Malaria – Mother to Child ( Rare ) ( AIDS )
  17. 17. Factors affecting the transmission • Anopheles mosquito- species of the mosquito • Environment: Temperature between 16-33 oC Rainfall provides breeding site for mosquito. Humidity favors mosquito survival. At low altitudes • Vector resistance to insecticides • Parasitic resistance to drugs • Man-made: • War and migrations
  18. 18. Mosquito serves as a vector of human malaria because…… Susceptible to infection by malarial parasite. Repeatedly bite humans rather than animals for their blood- meal. Present in adequate number near human habitats. Live long enough for the development into sporozoits in the midgut
  19. 19. FACT FILESAffects >2400 million people, over 40% of the worlds population, in more than100 countries • About 1.5 million to 3 million people die of malaria every year (85% of these occur in Africa)One child dies of malaria somewhere in Africa every 20 sec., and one malarialdeath every 12 sec somewhere in the world • Estimated annual expenditure on malaria research, prevention and treatment: $ 84 million.Eradicated in Europe, USA, Korea, japan, Most of N&S AmericaIn India, Orissa constitutes 25% of cases
  20. 20. TAXONOMIC CLASSIFICATION Kingdom Protista Subkingdom Protozoa Phylum Apicomplexa Class Haematozoea Order Haemosporida Family Plasmodiidae Genus Plasmodium {sub genera- lavarania and plasmodium} Species falciparum, malariae, ovale, vivaxThere are 165 known species of Plasmodium- may infect reptiles, birds andmammalsOf these, 4 were known to infect humans.A new species- Plasmodium knowlesi- causes malaria in macaques but can also infecthumans.
  21. 21. Malaria 72 species of anopheles mosquito (♀) 90% casesPlasmodium Plasmodium Plasmodium PlasmodiumFalciparum vivax Ovale Malariae 95% malarial Death
  22. 22. Plasmodium falciparum:-Welch falx=cresent/sickle + parere=to bring forth. Malignant tertian or Estivo-autumnal or falciparum malariaPlasmodium vivax:-Grassi&Feletti,1890 vivax or tertian malaria. Occurrence of true relapses in characteristic. Described by Laveran- but not as a distinct species in 1880 Golgi described it as a distinct species.Plasmodium malariae:-Laveran,1881 malariae malaria or quartan malaria. Natural parasite of chimpanzee synonym= Pl.rodhainiPlasmodium ovale:-Stephans,1922 relatively restricted distribution. Ovale malaria
  23. 23. The morphological characteristics and features of the life cycle acts a major criteria in GARNHAM’S CLASSIFICATION. These include: Shape of the tropozoite Gametocyte Oocyst Number of nuclei in erythrocytic & exo-erythrocytic schizonts Aspect and distribution of pigment Nature of damage induced in host cell
  24. 24. General characteristics: Alternation of generation accompanied by alternation of hosts. Schizogony(asexual) takes place in humans Sporogony(sexual) takes place in mosquito Typically, pigment is produced during the developing stages parasite in RBC
  25. 25. PARASITE FORMSBlood forms: merozoites, Merozoite: invades erythrocytesrings, trophozoite, schizonts Sporozoite invades mosquito salivary glands and liver cells Mosquito forms: Ookinete invades mosquito gut epithelial cells Oocyst, ookinete, gametocytes, sporozoite
  26. 26. There is a Plant inside Malaria ! (secondary endosymbiosis)Plasmodium- contains a broken down old chloroplast (an Apicoplast)that doesnt do any photosynthesizing.The Apicoplast is however, needed for the parasite to invade new cells.Even more fascinating- common herbicides that are generally prettynon-toxic to humans seem to stop the Apicoplast from working. O =Apicoplast
  27. 27. Plasmodium blood forms: the ring stage 1st 14-16 hours spent as ring stage, or young trophozoite little to no Hb degradation only form seen in blood films of P. falciparum A ring stage of the cup-like form showing the nucleus (n), surrounded by ribosomes and some endoplasmic reticulum.
  28. 28. THE TROPHOZOITE• It is the form found inside the erythrocyte after 10-18 hours post-infection• It interact with the host cell in a very sophisticated way: •1) it takes up the red blood cell hemoglobin and digests it inside a food vacuole. Many of the drugs in use target this compartment; •2) it transports proteins from the parasite to the surface of the erythrocyte for its own benefit.
  29. 29. THE SCHIZONT• Schizogony: form of asexual reproduction in which multiple mitoses take place, followed by cytokinesis resulting in multiple daughter cells• multiple mitoses produce 20-24 nuclei• once nuclei & organelles replicated cytokinesis occurs• rupture of RBC membrane releases merozoites Schizont from Plasmodium falciparum
  30. 30. P.Falciparum Why is it important……????• Sticky knobs - obstruction to blood flow• Rosettes - clogs microcirculation• Secondary organ dysfunction• Pregnancy - adhere to placenta, so maternalanemia & low birth weight
  31. 31. Character P.falciparum P.vivax P.ovale P.malariaeRelative age of May infect cells of Only those are Only those are Only mature cellsinfected RBC all ages young &immature young &immatureAppearance of Normal size, no Enlarged, distorted Oval enlarged, Normal size, noinfected RBC distortion distorted with distortion ragged cell wallsStippling infected Maurer’s dots Schuffner James’s dots Ziemann’s dotsRBC dots
  32. 32. Character P.falciparum P.vivax P.ovale P.malariaeRing form Circle configuration/ head- Delicate cytoplasmic Similar to P.vivax Smaller than P.vivax phone configuration ring measuring 1/3 RBC Ring larger than Occupies 1/6th RBC Scanty cytoplasm&small Single chromatin dot P.vivax Heavy chromatin dot vacuole Ring surrounds a Often Pigment forms early Multiple rings common vacuole thick&amoeboid Accole forms are seen
  33. 33. Character P.falciparum P.vivax P.ovale P.malariaeTrophozoite Heavy rings common Irregular, Ring appearance Non-amoeboid with fine pigment amoeboid usually maintained solid cytoplasm granules Ring remnants until late In Coarse dark brown Mature forms seen only common development pigment that in severe infections Brown Amoeboid tendencies masks chromatin pigment not as evident as No vacuoles in P.vivax mature forms
  34. 34. Maurers clefts can be seen Maurers clefts resemble thein P. falciparum infections Schüffners dots seen in P.containing older ring-form vivax and P. ovale, but aretrophozoites and asexual usually larger and more coarse.stages.Visualization of these Like Schüffners dots,structures is dependent on the Maurers clefts appear toquality of the smear play a role in the metabolicpreparation and the pH of the pathways of the infectedGiemsa stain. RBCs.
  35. 35. Character P.falciparum P.vivax P.ovale P.malariaeImmature Multiple chromatin Mature Progressive Similar to P.vivax,schizont bodies surrounded chromatin bodies dividing only smaller and may by cytoplasm Brown pigment chromatin contain large dark Only detected in surrounded by peripheral granules severe infection cytoplasmic materialMature 8-36 merozoites. 12-24 merozoits Parasites occupy 6-12 merozoites inschizont in clusters Surrounded by ¾ RBC rosettes Only in severe cytoplasmic 8-12 merozoites Central arrangement infections material Rosettes of an of brown green average of pigment 8merozoites
  36. 36. Character P.falciparum P.vivax P.ovale P.malariaeMicro Sausage/cresent shaped Large pink to purple Similar to P.vivax, Similar to P.vivax,Gametocyte Dispersed central chromatin mass smaller in size smaller in size chromatin with nearly surrounded by colorless black pigment visible to pale halo. Brown pigment presentMacro Sausage/cresent shaped Round to oval cytoplasm Similar to P.vivax, Similar to P.vivax,gametocyte Compact chromatin Eccentric chromatin mass smaller in size smaller in size Black pigment visible Light brown pigment
  37. 37. schuffers amoeboid P. vivax Rings and accole maurersP. falciparum Band forms Undotted RBCP.malariae James dots P.ovale
  38. 38. THANK YOU

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