Malaria. benign (mild) malaria
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2 Malaria Caused by the plasmodium protozoa. Four species of plasmodium causes human malaria: Plasmodium falciparum responsible for nearly all serious complications and deaths. P. vivax P. malariae P. ovale seldom (rare) benign (mild) malaria Cause: the bite of an infected adult mosquito. Can also be transmitted by infected individuals via blood transfusion, congenitally (prior to birth), or via infected needles by drug abusers.
3 Malarial Parasite (plasmodium) Two Interdependent Life Cycles Sexual cycle: in the mosquito Asexual cycle: in the human Drugs are only effective during the asexual cycle.
4 Plasmodium Life Cycle Asexual cycle: two phases Erythrocytic phase: occurs inside the erythrocyte (RBCs) Exoerythrocytic phase: occurs outside the erythrocyte Erythrocytic phase drugs: chloroquine, hydroxychloroquine, quinine, mefloquine Exoerythrocytic phase drug: primaquine May be used together for synergistic or additive killing power.
5 Parasite Life Cycle I. Sexual stage in anopheles mosquito: Sexual stage gametocytes also develop in erythrocytes before being taken up by mosquitoes, where they develop into infective sporozoites. II. Asexual stage in human: 1 Primary exoerythrocytic stage: sporozoites invade liver cells schizonts incubation period 2 Asexual erythrocytic stage: merozoites invade erythrocytes, trophozoites schizonts, rupture host erythrocytes repeated cycles cause clinical illness 3 Secondary exoerythrocytic stage: In P vivax and P ovale infections, a dormant hepatic stage, hypnozoite relapses
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7 The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host. After initial replication in the liver (exoerythrocytic schizogony), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony). Multiplication of the blood stage parasites is responsible for the clinical manifestations of the disease. In the blood, some parasites differentiate into sexual erythrocytic stages (gametocytes). The gametocytes, after ingestion by an Anopheles mosquito during a blood meal, undergo a sporogonic cycle yielding sporozoites. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. Of note, in P. vivax and P. ovale, a dormant stage (hypnozoites) can persist in the liver and cause relapses by invading the bloodstream weeks, or even years later
8 Symptoms The symptomatology depends on parasitemia, the presence of the organism in different organs and the parasite burden. The incubation period varies generally between days. As the parasite load becomes significant, the patient develops headache, lassitude, vague pains in the bones and joints, chilly sensations and fever. As the disease progresses, the chills and fever become more prominent. The chill and fever follows a cyclic pattern with the symptomatic period lasting 8-12 hours. This interval is about hours in the case of P. vivax and P. ovale, and hours in the case of P. malariae.
9 The malarial paroxysm is most dramatic and frightening: it begins with chilly sensation which progresses to teeth chattering overtly shaking chill, peripheral vasoconstriction resulting in cyanotic lips and nails (cold stage) which lasts for about an hour. At the end of this period the body temperature begins to climb and reaches F (39-41 C). Fever is associated with severe headache, nausea (vomiting) and convulsions. Each paroxysm is due to the rupture of infected erythrocytes and release of parasites Chronic malaria results in spleenomegaly, hepatomegaly and nephritic syndromes.
10 Diagnosis: Diagnosis is based on symptoms and detection of parasite in blood smears. Treatment and Control: Treatment is effective with various quinine derivatives (quinine sulphate, chloroquine, meflaquine and primaquine, etc.). Drug resistance, particularly in P. falciparum and to some extent in P. vivax is a major problem. Control measures are eradication of infected anopheles mosquitoes. Vaccines are being developed and tried but none is available yet for routine use.
11 Drug Classification Classified by their selective actions on different phases of the parasite life cycle: 1. Blood schizonticides: act on erythrocytic parasites. E.g. Chloroquine, Quinine, Mefloquine, Halofantrine 2. Tissue schizonticides: eliminate developing or dormant liver forms. E.g. Pyrimethamine, Primaquine, Sulfonamides and Sulfone 3. Gametocides: kill sexual stages and prevent transmission to mosquitoes. E.g. Quinine, Primaquine
12 ANTIMALARIAL THERAPY IS GIVEN IN THE FOLLOWING FORMS CASUAL PROPHYLAXIS In this the pre-erythrocytic stage is the target. (a) PRIMAQUINE SUPPRESSIVE PROPHYLAXIS The schizontocides which suppress the erythrocytic phase and thus attacks of malarial fever can be used for this purpose. (a)chloroquine-300mg WEEKLY (b) MEFLOQUINE-250mg WEEKLY RADICAL CURE A radical curative is needed in relapsing malaria while in falciparum malaria adequate treatment of clinical attack leaves no parasite in the body. PRIMAQUINE-15mg DAILY FOR 2 WEAKS
13 CLINICAL CURE The erythrocytic schizontocides are used to terminate an episode of malarial fever THESE ARE:- (A) Fast Acting High Efficacy Drugs (a) CHLOROQUINE (b) MEFLOQUINE (c) HALOFANTRINE (B) Slow Acting Low Efficacy Drugs (a) PYRIMETHAMINE (b) SULFONAMIDES
14 Malignant malaria Malaria caused by P. falciparum is more severe than that caused by other plasmodia. The serious complication of P. falciparum involves cerebral malaria (involving the brain); massive haemoglobinuria (blackwater fever) in which the urine becomes dark in color, because of acute hemolysis of RBC; acute respiratory distress syndrome; severe gastrointestinal symptoms; shock and renal failure which may cause death.
15 Chloroquine A synthetic 4-aminoquinoline for oral use. Pharmacokinetics Rapidly and almost completely absorbed from the gastrointestinal tract. Concentrated in liver, spleen, kidney, lungs, and retina. Its accumulation in retina is responsible for its ocular toxicity. Slowly released from tissues and metabolized. Principally excreted in the urine.
16 Pharmacological Effects Highly effective blood schizonticide. Mechanism: 1 Plasmodium aggregates chloroquine, chloroquine incorporated into DNA chain of plasmodium inhibit proliferation. 2 chloroquine prevents the polymerization of the hemoglobin breakdown product, heme, into hemozoin and thus eliciting parasite toxicity due to the buildup of free heme. 3 ph By accumulating in acidic vesicles of parasite and because of its weakly basic nature it raises the vesicular ph and thereby interferes with degradation of haemoglobin by parasitic lysosomes. Resistance: very common among strains of P falciparum and uncommon but increasing for P vivax. The mechanism of resistance to chloroquine is associated with a decreased ability of parasite to accumulate chloroquine and resistant strains excretes drug more rapidly.
17 Adverse Effects and Cautions Usually very well tolerated, even with prolonged use. Pruritus is common. Nausea, vomiting, abdominal pain, headache, anorexia, blurring of vision, and urticaria are uncommon. Dosing after meals may reduce some adverse effects. Clinical Uses 1. Treatment: non-falciparum and sensitive falciparum malaria. 2. Chemoprophylaxis: for without resistant falciparum malaria in malarious regions.
18 Quinine Quinine and quinidine remain first-line therapies for falciparum malaria especially severe disease. Quinine is an alkaloid derived from the bark of the cinchona tree, a traditional remedy for intermittent fevers from South America. Quinine is the levorotatory stereoisomer of quinidine. Pharmacokinetic Rapidly absorbed after oral administration. Metabolized in the liver and excreted in the urine.
19 Pharmacological Effects Highly effective blood schizonticide against the four species of human malaria parasites. Gametocidal against P vivax and P ovale but not P falciparum. Not active against liver stage parasites. Mechanism of action It gets concentrated in the acidic vacuoles of the blood schizonts and causes pigment changes Also inhibits the polymerization of heme to hemozoin. Free heme or hemozoin complex damages parasite membrane and kills it.
20 Adverse Effects and Cautions 1. Cinchonism: tinnitus, headache, nausea, dizziness, flushing, visual disturbances 2. Cardiovascular effects: severe hypotension and arrhythmia. 3. Others: hypoglycemia, stimulate uterine contractions Clinical Uses: mainly for chloroquine-resistant falciparum malaria, especially for cerebral malaria. Malarial chemoprophylaxis Babesiosis (A disease of cattle and other livestock caused by protozoans of the genus Babesia, transmitted by the bite of ticks.) Nocturnal Muscle Cramps Spermicidal In Vaginal Creams
21 Mefloquine A synthetic 4-quinoline methanol that is chemically related to quinine. Pharmacokinetics Only be given orally because severe local irritation occurs with parenteral use, Well absorbed. Highly protein-bound, extensively distributed in tissues, and eliminated slowly. t 1/2 is 20 days. Extensive metabolism occurs in liver and is excreted in bile. Pharmacological Effects Strong blood schizonticidal activity against P falciparum and P vivax, but not active against hepatic stages or gametocytes.
22 MOA Like chloroquine it raises the intravascular ph. It binds to the haem and the complex damages membranes of the parasite. Resistant organisms accumulate less mefloquine Adverse Effects and Cautions Nausea, vomiting, diarrhea, abdominal pain dosedependent Neuropsychiatric toxicities: dizziness, headache, behavioral disturbances, psychosis, seizures. Clinical Uses Chemoprophylaxis: Treatment: mainly for chloroquine-resistant falciparum malaria.
23 Halofantrine Halofantrine HCl, a phenanthrene-methanol related to quinine, is effective against erythrocytic stages of all four human malaria species. It is not active against hepatic stages or gametocytes. Halofantrine is rapidly effective against most chloroquine-resistant strains of P falciparum, but its use is limited by irregular absorption and cardiac toxicity.
24 Artemisinin Artemesenin is the active principle of plant Artemesia annua, extracted from yellow flower. Kill trophozoites of erythrocytes. Through blood-brain barrier, treatment for cerebral malaria. ADVERSE EFFECTS Nausea, Vomiting, Abdominal pain, Itching Abnormal bleeding, Dark urine USES Acute attacks of severe falcifarum malaria Cerebral malaria Chloroquine/other multidrug resistant malaria
25 Malaridine (Pyronaridine) Developed by China. Blood schizonticidal activity. Treatment for all types malaria, including Chloroquine-resistant falciparum malaria. Mechanism: destroy parasite compound membrane and food vacuoles.
26 Pyrimethamine It is directly acting inhibitor of DHFRase inhibiting breeding of plasmodium. Pharmacokinetics Slowly but adequately absorbed from the GIT Concentrated in certain organs like liver, brain Slowly eliminated and excreted from urine. Pharmacological Effects Kill schizonts of primary exoerythrocytic stage. Act slowly against premature schizonts of erythrocytic stage. No action against gametocytes, but can inhibit development of plasmodium in mosquito.
27 Adverse Effects and Cautions Gastrointestinal symptoms, skin rashes Interfering folic acid metabolism in human megalocyte anemia, granulocytopenia Acute intoxication USES In combination with a sulfonamide, used in treatment of malaria.
28 Primaquine Synthetic 8-aminoquinoline. Drug of choice for the eradication of dormant liver forms of P vivax and P ovale. It is a poor erythrocytic schizontocide Pharmacokinetics Readily absorbed after oral absorption Oxidized in liver Plasma t 1/2 =3-6 hrs Excreted in urine within 24 hrs. Pharmacological Effects The only available agent active against the dormant hypnozoite stages of P vivax and P ovale. Also gametocidal against the four human malaria species.
29 Adverse Effects and Cautions Headache, nausea, epigastric pain, abdominal cramps. Clinical Uses Therapy (Radical Cure) of Acute Vivax and Ovale Malaria: chloroquine + primaquine Terminal Prophylaxis of Vivax and Ovale Malaria: prevent a relapse Chemoprophylaxis of Malaria: protection against falciparum and vivax malaria.
30 Sulfonamides and Sulfone Certain microbes require p-aminobenzoic acid (PABA) in order to synthesize dihydrofolic acid which is required to produce purines and ultimately nucleic acids. Sulfonamides, chemical analogs of PABA, are competitive inhibitors of dihydropteroate synthetase inhibiting to form dihydrofolic acid inhibiting production of purines and synthesis of nucleic acids. Only inhibiting plasmodial of exoerythrocytic stage Not used as single agents for the treatment. Combination with other agents.
31 Mechanism of Action
32 Rational Use of Antimalarial Drugs 1. Choice of Antimalarial Drugs: Control symptoms: Chloroquine Cerebral malaria: Chloroquine phosphate, Quinine, Artemisinin Chloroquine-resistant falciparum malaria: Quinine, Mefloquine, Artemisinin Prophylaxis: Pyrimethamine, Chloroquine Dormant hypnozoite stages : Pyrimethamine + Primaquine 2. Combination therapy: Chloroquine + primaquine: symptom stages Pyrimethamine + primaquine: dormant hypnozoite stages Combination of drugs with different mechanisms: therapeutic effect, resistance
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