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Malaria
Malaria is caused by Plasmodium parasites transmitted via mosquito bites. P. falciparum causes the most severe disease. Symptoms include fever, chills, and flu-like illness. Without treatment, severe complications can occur including cerebral malaria, severe anemia, respiratory distress, and death. Diagnosis is by blood smear detecting parasites. Treatment depends on severity but involves fast-acting schizonticides like quinine or artemisinin-based combination therapies. Prevention focuses on mosquito bite avoidance, chemoprophylaxis, and emergency treatment for travelers in endemic areas.
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Malaria
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- 4. • Its mostlyEndemic but pandemics may also occur • In Southern Africa its endemic in Angola, Mozambique, Malawi, Northern Namibia, Northern Botswana, some areas of Zimbabwe and South Africa
- 5. Aetiology • Malaria isa vector borne protozoan infection caused by a parasite of genus Plasmodium. • Four sp known to cause Malaria: P. Vivax; P. Ovale; P. Malariae; P. Falciparum • All four species exist in southern Africa • Transmitted by the bite of Anopheles mosquitoes to nourish its developing eggs
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- 10. Effect on Treatment •P. Vivax ; P. Malariae; P. Ovale may re-enter the liver and continue to multiply long after the initial bloodstream invasion has ceased. • This may result in relapse of malaria e.g. P. Malariae can relapse as long as 40 yrs after the initial infection • P. Falciparum doesn’t have an exo-erythrocytic cycle
- 11. Clinical manifestations • Virulencedepends on the immune status of the host • Innate immunity occurs in people with G6PD, Sickle Cell Trait and absence of the DUFFY antigen in RBCs.
- 12. Resistance and immunity •The intraerythrocytic development of P. falciparum is inhibited in persons with various hemoglobinopathies. • Persons with G6PDD are more sensitive to certain antimalarials (quinine, 8-aminoquinoline). • Persons lacking the Duffy blood group antigen are resistant to P. vivax, but susceptible to P. ovale. • A milk diet partially inhibits the development of malarial parasites in the RBCs because of a resulting reduced supply of p- aminobenzoic acid (vitamin H1). This results in a milder malarial course, e.g., in infants.
- 13. Clinical manifestations • ThePlasmodium species with the most pronounced pathogenicity is Plasmodium falciparum, whereas the other Plasmodium species cause milder • Onset symptoms. Malaria begins with nonspecific initial symptoms that last several days: headache, muscle and joint pains, general fatigue, chills, occasionally nausea, intermittent fever, either continuous or at irregular intervals.
- 14. Classic malarial paroxysm •After an initial rise in temperature, peripheral vasoconstriction causes a period of chills (lasting for about 10 minutes to one hour), then the temperature once again rises to 40–41 °C, whereupon peripheral vasodilatation and an outbreak of sweating follow. • These bouts occur mainly in the afternoon and evening hours. • Once the paroxysm has abated and the fever has fallen, the patient feels well again until the next one begins. • In severe malaria tropica, however, circulatory disturbances, collapse, may occur without fever (algid malaria).
- 15. Complicated Malaria • Ifany of the symptoms is present, make a diagnosis of severe malaria and treat as an emergency: Cerebral malaria (unarousable coma) Severe anaemia (<5g/dl) High Parasitemia Renal failure (oliguria/anuria) Pulmonary edema Circulatory collapse Hypoglycemia DIC Severe metabolic acidosis Repeated generalized seizures
- 16. Nerological: Coma; Hypoglycaemia; Seizures; Opisthotonus; Cranialnerve palsies Respiratory: Pulmonary oedema; Secondary bacterial pneumonia CVS: Shock; Cardiac failure (algid malaria); Dysrhymias with quinine Renal: Acute renal failure; hemoglobinuria Abdomen: Hematological: Severe anaemia (<5g/dl); High parasitemia > 2%; DIC; Thrombocytopenia
- 17. Course of infectionand recurrence. • The malarial paroxysms are repeated at intervals until parasite multiplication in the erythrocytes is suppressed by chemotherapy or the host immune response. • Parasites that persist in the host can cause relapses for months or even years after the initial infection. • Recurrence results either from persistence of erythrocytic forms reactivation of hypnozoites (relapse).
- 18. Pathogenesis • The clinicalmanifestations of malaria are caused by the erythrocytic stages of the plasmodia and reflect multifactorial pathogenic process affecting many different organs.
- 19. The role ofcytokines • As a result of erythrocytic schizogony and the attendant rupture of erythrocytes, malarial antigens (phospholipids and glycolipids) are released that stimulate macrophages and monocytes to produce tumor necrosis factor alpha (TNFa) and other cytokines (IL-1, IL-6, IL-8). • Cytokine production is also initiated by IFNc produced in the immunological TH1 response. • TNFa plays a special role in pathogenicity, since the concentration of this cytokine in the blood correlates with the severity of a P. falciparum infection. • This substance also, at higher concentrations, induces fever, inhibits erythropoiesis, stimulates erythrophagocytosis, and causes various nonspecific symptoms such as nausea, vomiting, and diarrhea. • At lower concentrations, TNFa can contribute to the killing of the intracellular parasites. Various other cytokines either synergize with TNFa or induce different reactions.
- 20. Other processes • Dueto the destruction of RBCs and parasites and resulting production of TNFa, phagocytosing cells of the reticuloendothelial system are activated. • Signs of this include splenic swelling in the course of the infection and increased elimination of erythrocytes in the spleen. • Renal damage in acute malaria tropica is caused by capillary cytoadherence and tubular necrosis. In malaria quartana, such damage is due to deposition of immune complexes in the renal capillaries.
- 21. Pathological changes • Braincapillaries are clogged with infected RBCs (the pigment in the plasmodia is especially noticeable), hemorrhages, necrotic foci on obturated vessels surrounded by inflammatory reactions. • Further changes can be found in the spleen and liver (for instance swelling, hyperplasia of phagocytosing cells containing plasmodia and pigment), heart, lungs, kidneys, and other organs.
- 22. The Sickle celltrait
- 23. Diagnosis • Detection ofmalarial parasites in the blood. • Stages of P. falciparum, P. vivax, and P. ovale can be found in blood five to eight days after the infection at the earliest, P. malariae not until after 13– 16 days. • Rapid tests (ParaSight, MalaQuick, RDTs) have also been available for some years to diagnose P. falciparum infections. • Using a monoclonal antibody, these tests can detect a specific Plasmodium antigen (HRP2) in whole blood with a very high level of sensitivity and specificity. • Another rapid test (OptiMAL) for diagnosis of all Plasmodium species is based on detection of specific lactate dehydrogenase.
- 28. Therapy • Patients infectedfor the first time may suffer highly acute and severe courses of malaria. • Therapy and intensive clinical monitoring must therefore begin immediately, especially in acute malignant tertian malaria
- 29. Treatment of acutedisease • The clinical symptoms of malaria are caused by the asexual forms in the erythrocytic schizogonic cycle. A clinical cure is thus achieved by eliminating these forms or stages with so- called schizonticides. • The antimalarials preferred in this indication are fast-acting schizonticides such as quinine, mefloquine, and halofantrine (in most countries artemisinin based therapy ACT) as well as quinine combined with doxycycline (especially in complicated tropical malaria) and various combined preparations.
- 30. Treatment of uncomplicatedMalaria • Oral therapy: A combination of an atimalarial and artemenisinin. • CoArtem (artemether20/lumefantrine120) • 0 hrs, 8 hrs, 24hrs, 36hrs, 48hrs and 60 hrs • Artmether should be avoided in early pregnancy Weight Dose 5 - 14.9kg 1 tablet B.D *3 15 – 24.9kg 2 tablet B.D *3 25 – 34.9kg 3 tablet B.D *3 adult 4 tablets B.D *3
- 31. Treatment of ComplicatedMalaria tropica • IV quinine was a drug of choice • Loading dose of 20mg/kg in 5% DD over 4 hours • Followed by 10mg/kg every 8 hours until the patient can take oral quinine if they’re not vomiting • If IV access is not possible: give IM 10mg/kg at 0 hours, 4 hours and then 12 hourly • Give specific supportive treatment for complications
- 32. Quinine complications • QTprolongation dysarhythmias • Methemoglobinemia • Hemolysis in G6PDD • HYPOGLYCAEMIA • THROMBOCYTOPENIA
- 33. Artesunate • 2.4 MG/KGIV/IM AT 0, 12 HOURS, 24 HOURS then daily for 7 days • When patient has recovered, 2mg/kg of oral artesunate OD • Adverse effects (uncommon) • Cardiotoxicity in high doses • Drug induced fever • Skin rash
- 34. Prophylaxis • Malarone (Atovoquine250/proguanil hydrochloride100) taken once daily with food as prophylaxis. Should be started 2 days before travelling and continued for 7 days on return. • For paediatrics you give a dose Atovoquine 62.5mg/ proguanil hydrochloride 25mg
- 35. Prevention • mosquito biteprevention, • chemoprophylaxis, • emergency stand-by therapy.
- 36. References • https://www.sciencedaily.com/releases/2011/ 04/110428123931.htm • WittenbergD.F. (2009), Coovadia’s Paediatrics and Child Health. Oxford University Press Southern Africa (pty) Ltd • J. Alastair, 2016. Davidson’s Essentials of Medicine, 2nd ed. Churchill Livingstone Elsevier (pty) • 2016, WHO Malaria guidelines
Editor's Notes
- #3 Dr. Margaret Chan, Director-General of the World Health Organization for 2006–17
- #6 Transmitted mostly by a bite of a female anopheles mosquito Rarely blood transfusions and from mother to child
- #10 Asexual (schizogony) Phase in Humans-Erythrocytic and exoerythrocytic cycles Sexual phase (sporogony) in mosquitos
- #12 Duffy antigen/chemokine receptor (DARC), also known as Fy glycoprotein (FY) or CD234 (Cluster of Differentiation 234), is a protein that in humans is encoded by the DARC gene. The Duffy antigen is located on the surface of red blood cells, and is named after the patient in which it was discovered.
- #24 Malaria smears should be used in treatment monitoring to assess the parasitemic count RDTs will remain positive even if the pt has been cured, so they should only be used as screening tests
- #34 According to Dr. Sega, no need to change to oral route… so give IV artesunate until the malaria smear are negative Also give primaquine in addition to artesunate to clear the gametocytes. Primaquine is effective in treating the hypnozoints (sp), esp in p.malariae..
- #35 Other options: Patients can be initiated on full antimalarial course Tetracyclines and fluoroquinolones can be used as prophyaxis