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Malaria
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Malaria

  1. 1. MALARIA NURUL HIDAYU | NASHRIQ AIMAN | AUDI ADIBAH
  2. 2.  Malaria is a life-threatening disease caused by parasites that are transmitted to people through the bites of infected female Anopheles mosquitoes.  It is widespread in tropical and subtropical regions  350 – 500 million cases per year INTRODUCTION
  3. 3. Parasite : I. P. vivax II. P. falciparum III. P. malariae IV. P. ovale ETIOLOGY Vectors : INCUBATION PERIOD  P. falciparum: 9 – 14 days  P. vivax: 12-17 days  P. ovale: 16 – 18 days  P. malariae: 18 – 40 days
  4. 4. Life cycle of malarial parasite  Hepatic phase / Tissue phase  Erythrocytic phase  Sexual reproduction 2 HOSTS–  DEFINITE HOST– Anopheles Mosquito  INTERMEDIATE HOST– Human
  5. 5. CLASSIFICATION UNCOMPLICATED MALARIA SEVERE MALARIA  Symptomatic malaria without signs of severity or evidence (clinical or laboratory) of vital organ dysfunction.  The sign and symptoms are nonspecific  Evidence (clinical or laboratory) of vital organ dysfunction.  Usually due to Falciparum or mixed infections.
  6. 6. All four species can exhibit non- specific prodromal symptoms few days before the first febrile attack. Prodromal symptoms are generally described as 'flu-like' and include: headache, slight fever, muscle pain, anorexia and nausea. Other symptoms : anemia, splenomegaly, jaundice and dehydration CLINICAL MANIFESTATIONS
  7. 7. FEBRILE PAROXYSMS COLD STAGE 1. CHILLS 2. RIGORS 3. NAUSEA 4. MALAISE 5. ANOREXIA 6. 20mins – 1 hr. HOT STAGE 1. DRY & FLUSHED SKIN 2. RAPID RESPIRATION 3. MARKED THIRST 4. 1 – 4 hrs. SWEATING STAGE 1. TEMPERATURE FALLS BY CRISIS 2. 2 – 3 hrs. 3. NO FEVER – 24-48 HOURS CLINICAL MANIFESTATIONS
  8. 8. DIFFERENTIAL DIAGNOSIS 1. Dengue 2. Typhoid fever 3. Leptospirosis 4. Septicemia
  9. 9. COMPLICATIONS Cerebral malaria Anemia Gastrointestinal illness Algid malaria Blackwater fever Renal lesions Splenic rupture Hypoglycemia Hyperpyrexia Convulsions Spontaneous bleeding & coagulopathy Aspiration pneumonia COMPLICATIONS
  10. 10. CEREBRAL MALARIA
  11. 11. Severe form of malaria Caused by P. Falciparum Most common non-traumatic encephalopathy Common in children and non- immune adults Adhering of P. falciparum infected erythrocytes to brain capillaries causing coma & death. Manifested with: — Coma — Convulsion — Hemoglobinuria on investigation : CSF is normal on examination : Splenomegaly
  12. 12. BLACKWATER FEVER
  13. 13. also known as malarial hemoglobinuria , one of the less common yet most dangerous complications of malaria. Sudden hemolysis caused by P. falciparum Leads to Hemoglobinemia & Hemoglobinuria (‘cola-coloured urine’) Other clinical features: — Rapid pulse — High fever and chills — Extreme prostration — Rapidly developing anemia Causes jaundice and eventually renal failure High mortality
  14. 14. 1. Blood Film Examination for Malaria Parasite (BFMP) • Thick blood film : detection of even low levels of parasitaemia • Thin blood film : to identify parasite morphology 2. Quantitative Buffy coat test • It involves staining of the centrifuged & compressed red cell layer with acridine orange & its examination under UV light source 3. Rapid diagnostic tests • Detects malarial antigens (PfHRP2/PMA/pLDH) from asexual &/or sexual forms of the parasite. 4. Polymerase chain reaction:- • specific test for detecting all species of malaria INVESTIGATIONS
  15. 15. 5. Other investigations: Complete blood counts Blood levels of glucose Renal Profile Urine Analysis Liver Function Test Other’s rapid test to rule out dengue or leptospirosis
  16. 16. THIN AND THICK SMEAR
  17. 17. Treatment of malaria depends on the number of different factors that include disease severity, the particular species of Plasmodium infecting the patient and the potential for drug resistance of the various species and strains of Plasmodium. In general, it takes about two weeks of treatment to be cured of malaria. How long will it take to recover from malaria?
  18. 18. TREATMENT  ANTI-MALARIAL THERAPY 1. Cinchona alkaloids : Quinine, Quinidine 2. Artemisinin derivatives : Artemether & Artesunate 3. Other antimalarials : halofantrine, Mefloquine, atavaquone, doxycycline and tetracycline  SUPPORTIVE TREATMENT : to manage the complications
  19. 19. Clinical diagnosis/ plasmodium species Recommended drugs Uncomplicated malaria/ p.falciparum Chloroquine sensitive Chloroquine phosphate Chloroquine resistant A)Quinine sulphate+ doxycycline, or tetracycline, or Clindamycin B).Atovaquone-Proguanil C) Mefloquine
  20. 20. Clinical diagnosis/ plasmodium species Recommended drugs Uncomplicated malaria/ p.malariae Chloroquine phosphate Uncomplicated malaria/ p.vivax or p.ovale Chloroquine phosphate + primaquine phosphate Uncomplicated malaria/ p.vivax  chloroquine resistant A). Quinine sulphate + (doxycycline or tatracycline) + primaquine phosphate B). Mefloquine + primaquine sulphate
  21. 21. Clinical diagnosis Recommended drugs SEVERE MALARIA Artesunate IV or IM Quinine IV Artemether IM  give parenteral antimalarial for min of 24hrs once started & there after complete treatment by giving a complete course of artesunate + clindamycin or doxycycline quinine + clindamycin or doxycycline
  22. 22. IMMUNITY  Sickle cell and malaria Sickling of the RBC causes a disruption in the reproductive cycle of Plasmodium, resulting in lower parasite levels and less severe symptoms  G6PD deficiency and malaria Plasmodium oxidizes RBC NADPH from the Pentose Phosphate pathway for its metabolism  deficiency of RBC GSH  peroxide-induced hemolysis curtails the development of Plasmodium

Notas do Editor

  • Drug resistance : Resistance is now common against all classes of antimalarial drugs apart from artemisinins.
    Chloroquine resistance has spread to nearly all areas of the world where falciparum malaria is transmitted

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