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Pugud Samodro Bag/SMF Ilmu Penyakit Dalam  FKIK Unsoed/ RSUD Prof Margono Soekarjo Purwokerto
What is Malaria? ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Pictures of  P. falciparum
Etiology ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Plasmodium falciparum ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
P. vivax  and  P. ovale ,[object Object],[object Object],[object Object]
Etiology ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Epidemiology ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
What is the Malaria Vector? ,[object Object],[object Object],[object Object]
Pathogenesis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Malaria Lifecycle Sporogonous Cycle: Mosquito Stages Gametocytes P. falciparum P. vivax P. ovale P. malariae Human Liver Stages Exo-erythrocytic (hepatic) Cycle: Human Blood Stages Erythrocytic Cycle:
Pathology ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Symptoms of Malaria ,[object Object],[object Object],[object Object]
Clinical manifestation ,[object Object],[object Object],[object Object],[object Object]
Clinical manifestation ,[object Object],[object Object],[object Object],[object Object],[object Object]
Clinical manifestation ,[object Object],[object Object],[object Object],[object Object]
Clinical manifestation ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Clinical manifestation ,[object Object],[object Object],[object Object]
 
 
 
Complications ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Malaria Mortality ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Laboratory Findings ,[object Object],[object Object],[object Object],[object Object],[object Object]
 
 
Plasmodium vivax Ring stage Gametocyte Trophozoite Schizont
Plasmodium malariae Ring stage Gametocyte Trophozoite Schizont
Plasmodium ovale Ring Trophozoite Schizont Gametocyte
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Diagnosis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Differential Diagnosis ,[object Object],[object Object],[object Object],[object Object]
 
Roll Back Malaria (RBM) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Roll Back Malaria (RBM) ,[object Object],[object Object],[object Object],[object Object],[object Object]
Roll Back Malaria (RBM) Goals -  At least 60% ,[object Object],[object Object],[object Object]
Treatment ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Treatment ,[object Object],[object Object],[object Object],[object Object],[object Object]
Countries with at least one study indicating chloroquine total failure rate > 10 % No failure reported Chloroquine total failure rate < 10% No recent data available P- falciparum  resistance to chloroquine   Source: WHO global database on drug resistance 1996-2004
P. falciparum  resistance to sulfadoxine/pyrimethamine   Source: WHO global database on drug resistance 1996-2004 Countries with at least one study indicating pyrimethamine-sulfadoxine total failure rate > 10% No failure reported P yrimethamine-sulfadoxine   total failure rate < 10% No recent data available
P. falciparum  resistance to mefloquine Source: WHO global database on drug resistance 1996-2004 Countries with at least one study indicating mefloquine total failure rate  >  20% No failure reported Mefloquine total failure rate < 10% No recent data available Countries with at least one study indicating mefloquine total failure rate  >  10%
P.vivax  malaria distribution   and  Reported Treatment or Prophylaxis Failures or True Resistance, 2004 Source: WHO RBM Department, 2004 Vivax resistance to CQ confirmed in Guyana, Indonesia and Peru
Rationale for    antimalarial combination therapy ,[object Object],[object Object],[object Object],[object Object],[object Object]
The choice of    artemisinin combination therapy (ACT)   ,[object Object],Combinations which have been evaluated: piperaquine artemisinin + mefloquine artesunate + piperaquine dihydroartemisinin + mefloquine lumefantrine artemether + mefloquine naphthoquine chloroquine amodiaquine sulfadoxine-pyrimaethaminine mefloquine proguanil-dapsone chlorproguanil-dapsone atovaquone-proguanil clindamycin tetracycline doxycycline
Response to increasing resistance   Combination therapies  recommended by WHO ,[object Object],[object Object],[object Object],[object Object],WHO Technical Consultation on  “ Antimalarial Combination Therapy” – April 2001 ACTs FDC
Prevention ,[object Object],[object Object],[object Object],[object Object],[object Object]
 
 
 
 
 
 
[object Object],[object Object]

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Malaria

  • 1. Pugud Samodro Bag/SMF Ilmu Penyakit Dalam FKIK Unsoed/ RSUD Prof Margono Soekarjo Purwokerto
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  • 10. Malaria Lifecycle Sporogonous Cycle: Mosquito Stages Gametocytes P. falciparum P. vivax P. ovale P. malariae Human Liver Stages Exo-erythrocytic (hepatic) Cycle: Human Blood Stages Erythrocytic Cycle:
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  • 26. Plasmodium vivax Ring stage Gametocyte Trophozoite Schizont
  • 27. Plasmodium malariae Ring stage Gametocyte Trophozoite Schizont
  • 28. Plasmodium ovale Ring Trophozoite Schizont Gametocyte
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  • 54. Countries with at least one study indicating chloroquine total failure rate > 10 % No failure reported Chloroquine total failure rate < 10% No recent data available P- falciparum resistance to chloroquine Source: WHO global database on drug resistance 1996-2004
  • 55. P. falciparum resistance to sulfadoxine/pyrimethamine Source: WHO global database on drug resistance 1996-2004 Countries with at least one study indicating pyrimethamine-sulfadoxine total failure rate > 10% No failure reported P yrimethamine-sulfadoxine total failure rate < 10% No recent data available
  • 56. P. falciparum resistance to mefloquine Source: WHO global database on drug resistance 1996-2004 Countries with at least one study indicating mefloquine total failure rate > 20% No failure reported Mefloquine total failure rate < 10% No recent data available Countries with at least one study indicating mefloquine total failure rate > 10%
  • 57. P.vivax malaria distribution and Reported Treatment or Prophylaxis Failures or True Resistance, 2004 Source: WHO RBM Department, 2004 Vivax resistance to CQ confirmed in Guyana, Indonesia and Peru
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Hinweis der Redaktion

  1. What is the malaria vector? Malaria is spread by the bite of an infected female anopheline mosquito. In Africa, most malaria is spread by the A. gambiae. These mosquitoes bite at night, with a primary feeding time between 10:00 pm and 2:00 am. They are primarily an indoor biting mosquito. The picture on the left shows a number of Anopheles mosquitoes that were collected from a house in Kinshasa. If you look closely, you will notice some nice, fat mosquitoes that are quite well fed, presumably on the inhabitants of that house. The fat mosquitoes are the females. Female Anopheles mosquitoes require a blood meal to produce their eggs. You will also notice some very skinny mosquitoes. Those are the males. As a bloodmeal is needed for the female to produce her eggs, it is only the female that feeds on people. In the picture on the right, you can see several skinny larvae in their natural habitat. It takes about a week for larvae to develop and emerge as adult mosquitoes.
  2. There are four species of malaria that infect humans. All of them are transmitted in the same way, so I will explain the malaria lifecycle. Mosquito bites human Sporozoites injected into human host during blood meal Sporozoites infect liver cells, develop into schizonts, which release merozoites into the blood stream by rupturing the liver cells. Merozoites penetrate red blood cells and form schizonts; red blood cells release merozoites Some merozoites differentiate into male gametocytes or female gametocytes. Gametocytes are taken in by mosquito from a blood meal. Parasites undergo sexual reproduction, develop into oocysts which release sporozoites that invade the mosquito&apos;s salivary glands. And the cycle continues on……
  3. Once the parasite has entered the body, there are 2 main ways that malaria kills. Anemia. Malaria parasites destroy red blood cells, increasing anemia in populations that are already malnourished and anemic. Sustained moderate to severe anemia is associated with increased mortality. Cerebral malaria is the other major killer. It can kill very quickly. It is a type of complication of malaria in which the red blood cells obstruct the blood vessels in the brain. Other vital organs can also be damaged. has a fatality rate of 15% or more, even when treated and is extremely serious.
  4. Combining two or more antimalarial drugs with different modes of action (and thus drug targets) provides two main advantages. First cure rates are usually increased. Second, in the rare event that a mutant parasite which is resistant to one of the drugs arises de-novo during the course of the infection, it will be killed by the other drug. This mutual protection prevents the emergence of resistance. For both these advantages it is necessary that both partner drugs in a combination are independently effective. Balanced against these two advantages are the increased costs and the increased risks of adverse effects (although in some cases such as the combination of artesunate + mefloquine adverse effects such as vomiting are reduced).