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Slide 1 - Malaria H2012 Protozoan Disease 108 countries 3 billion people 1 million deaths each year
Slide 2 - In the late twentieth : Eliminated United States, Canada, Europe, Russia Prevalence rose in many parts of the tropics
Slide 3 - Resurgence Increases in the drug resistance of the parasite Insecticide resistance of its vectors Human travel and migration
Slide 4 - Etiology Five species of the genus Plasmodium cause nearly all malarial infections in humans. Falciparum Vivax Ovale Malariae Knowlesi (in Southeast Asia—the monkey malaria parasite )
Slide 5 - Almost all Deaths Falciparum
Slide 6 - Female Anopheline Mosquito Sporozoites Liver Asexual Reproduction Single Sporozoite eventually 10,000 to >30,000 Daughter Merozoites Liver cell eventually bursts 100 million parasites in the blood of an adult, the symptomatic stage of the infection begins
Slide 7 - Vivax and Ovale Intrahepatic forms Dormant(Hypnozoites) for a period ranging from 3 weeks to a year or longer before reproduction begins Relapses
Slide 8 - Duration of Erythrocytic Cycle (hours) Falciparum 48 h Vivax 48 h Ovale 50 h Malariae 72 h
Slide 9 - Red Cell Preference Falciparum Younger cells (but can invade cells of all ages) Vivax Reticulocytes and cells up to 2 weeks old Ovale Reticulocytes Malariae Older cells
Slide 10 - Morphology Falciparum Usually only ring forms; Banana-shaped gametocytes Vivax Irregularly shaped large rings and trophozoites; enlarged erythrocytes; Schüffner's dots Ovale Infected erythrocytes, enlarged and oval with tufted ends; Schüffner's dots Malariae Band or rectangular forms of trophozoites common
Slide 11 - Relapses Vivax , Ovale :Yes Falciparum , Malariae : No
Slide 12 - Parasitemias of >2% are suggestive of Falciparum infection
Slide 13 - Vivax Duffy blood-group antigen Fya or Fyb Most West Africans and people with origins in that region carry the Duffy-negative FyFy phenotype and are therefore resistant to P. vivax
Slide 14 - Disease Direct effects of RBC invasion and destruction by the asexual parasite and the host's reaction
Slide 15 - Epidemiology Falciparum predominates in Africa, New Guinea, and Hispaniola (i.e., the Dominican Republic and Haiti) Vivax is more common in Central America Malariae is found in most endemic areas Ovale is relatively unusual outside of Africa
Slide 16 - Endemicity Parasitemia rates or palpable-Spleen rates in children 2–9 years Hypoendemic (<10%) Mesoendemic (11–50%) Hyperendemic (51–75%) Holoendemic (>75%)
Slide 17 - Holo- and Hyperendemic areas (e.g., certain regions of tropical Africa or coastal New Guinea) where there is intense Falciparum transmission, people may sustain more than one infectious mosquito bite per day and are infected repeatedly throughout their lives Morbidity and Mortality during early Childhood Adulthood, most infections are Asymptomatic
Slide 18 - Stable Transmission Constant Frequent Year-round infection
Slide 19 - Unstable Transmission Transmission is low, Erratic, or Focal, full protective immunity is not acquired, and symptomatic disease may occur at All Ages Usually exists in Hypoendemic
Slide 20 - An Epidemic Changes in Environmental, Economic, or Social conditions, such as heavy rains or migrations (usually of Refugees or Workers) from a nonmalarious region to an area of high transmission; a breakdown in malaria control and prevention service All Age Groups
Slide 21 - Anophelines >400 can transmit malaria, and the 40 considerably in their efficiency as malaria vectors Life cycle within the mosquito—from gametocyte ingestion to subsequent inoculation (sporogony)—lasts 8–30 days mosquito must survive for >7
Slide 22 - Sporogony Is not completed at cooler temperatures <16°C for P. vivax and < 21°C for Falciparum; transmission does not occur below
Slide 23 - The most effective mosquito vectors such as Anopheles gambiae in Africa, which are long-lived, occur in high densities in tropical climates, breed readily, and bite humans in preference to other animals
Slide 24 - Entomologic Inoculation Rate (EIR) the number of sporozoite-positive mosquito bites per person per year is the most common measure of malaria transmission and varies from <1 in some parts of Latin America and Southeast Asia to >300 in parts of tropical Africa.
Slide 25 - Erythrocyte Changes Consumes and degrades intracellular proteins principally hemoglobin Alters the RBC membrane by changing its transport properties, exposing cryptic surface antigens, and inserting new parasite-derived proteins. The RBC becomes more irregular in shape, more antigenic, and less deformable.
Slide 26 - Severe malaria is also associated with reduced deformability of the uninfected erythrocytes, which compromises their passage through the partially obstructed capillaries and venules and shortens RBC survival.
Slide 27 - In the other three ("benign") human malarias, sequestration does not occur, and all stages of the parasite's development are evident on peripheral-blood smears. Whereas Vivax, Ovale, and Malariae show a marked predilection for either young RBCs (Vivax, Ovale) or old cells (Malariae) and produce a level of parasitemia that is seldom >2%, Falciparum can invade erythrocytes of all ages and may be associated with very high levels of parasitemia.
Slide 28 - Host Response Initially, nonspecific defense mechanisms Splenic immunologic and filtrative clearance Removal of both parasitized and uninfected erythrocytes Strain-specific immune response then controls the infection
Slide 29 - Exposure to sufficient strains confers protection from high-level parasitemia and disease but not from infection Infection without illness ,asymptomatic parasitemia is common among adults and older children living in regions with stable and intense transmission (holo- or hyperendemic areas). Immunity is mainly specific for both the species and the strain of infecting malarial parasite. Both humoral immunity and cellular immunity are necessary for protection
Slide 30 - Passively transferred IgG from immune adults has been shown to reduce levels of parasitemia in children; although parasitemia in very young infants can occur, passive transfer of maternal antibody contributes to the relative (but not complete) protection of infants from severe malaria in the first months of life
Slide 31 - Immunity to disease declines when a person lives outside an endemic area for several months or longer. Parasites may persist in the blood for months (or, in the case of P. malariae, for many years)
Slide 32 - Temperatures of 40°C damage mature parasites Tertian, every 2 days; Quartan, every 3 days) are seldom seen today
Slide 33 - Geographic Distributions Sickle Cell disease Hemoglobins C and E Hereditary Ovalocytosis Thalassemias G6PD (glucose-6-phosphate dehydrogenas edeficiency ) closely resemble that of falciparum malaria before the introduction of control measures. This similarity suggests that these genetic disorders confer protection against death from falciparum
Slide 34 - Clinical Features First symptoms of malaria are nonspecific Lack of a sense of well-being Headache Fatigue Abdominal discomfort Muscle aches followed by Fever similar to the symptoms of a minor viral illness
Slide 35 - Headache Chest pain Abdominal pain Arthralgia Myalgia Diarrhea
Slide 36 - Common Nausea Vomiting Orthostatic hypotension
Slide 37 - Classic malarial paroxysms Fever spikes Chills and rigors occur at regular intervals, are relatively unusual and suggest infection with P. Vivax or P. Ovale
Slide 38 - Fever Irregular at first (that of falciparum malaria may never become regular); the temperature of nonimmune individuals and children often rises above 40°C in conjunction with Tachycardia and sometimes Delirium.
Slide 39 - Childhood Febrile Convulsions may occur with any of the malarias, generalized seizures are specifically associated with falciparum malaria
Slide 40 - Physical Findings Fever Malaise Mild Anemia Palpable Spleen (in some cases)
Slide 41 - Anemia Common among young children living in areas with stable transmission
Slide 42 - Slight enlargement of the liver Common, particularly among Young Children
Slide 43 - Mild jaundice Common among adults; it may develop in patients with otherwise uncomplicated malaria and usually resolves over 1–3 weeks
Slide 44 - Malaria is not associated with a rash Petechial hemorrhages in the skin or mucous develop only rarely in severe falciparum malaria
Slide 45 - Severe Falciparum Malaria Appropriately and promptly treated, uncomplicated falciparum malaria (i.e., the patient can swallow medicines and food) Mortality rate of 0.1%
Slide 46 - Severe Falciparum Malaria Cerebral malaria/convulsion Acidemia/acidosis Severe normochromic, normocytic anemia Renal failure Pulmonary edema/adult respiratory distress syndrome Hypoglycemia Hypotension/shock Bleeding/disseminated intravascular coagulation Hemoglobinuria
Slide 47 - Hypoglycemia Important and common complication of severe malaria, is associated with a poor prognosis and is particularly problematic in Children and Pregnant women. Hepatic Gluconeogenesis Increase in the consumption of glucose by both host and, to a much lesser extent, the malaria parasites Quinine ,Quinidine
Slide 48 - Jaundice Mild hemolytic jaundice is common in malaria Severe jaundice is associated with P. falciparum; is more common among adults and results from: Hemolysis Hepatocyte injury Cholestasis
Slide 49 - Other HIV/AIDS predisposes to more severe malaria in nonimmune individuals Worsened by intestinal helminths, Hookworm in particular Septicemia may complicate severe malaria, particularly in children(specifically Salmonella bacteremia ) Aspiration Pneumonia
Slide 50 - در بچه ها شایعتر Anemia Convulsions Hypoglycemia
Slide 51 - در بالغین شایعتر Jaundice Renal failure Pulmonary edema
Slide 52 - Pregnancy Stable transmission area: Mothers Asymptomatic Falciparum malaria in primi- and secundigravid women is associated with Low Birth Weight Increased infant and childhood mortality Maternal HIV infection predisposes newborns to congenital malarial
Slide 53 - Pregnancy Unstable Transmission Mother: High-level parasitemia Anemia Hypoglycemia Acute pulmonary edema Fetal distress, premature labor, and stillbirth or low birth weight are common
Slide 54 - Pregnancy Congenital malaria occurs in <5% of newborns P. Vivax malaria in pregnancy is also associated with a reduction in birth weight but, in contrast to the situation in falciparum malaria, this effect is more pronounced in Multigravid
Slide 55 - Transfusion Blood Transfusion Needle-Stick Injury IVDU Organ Transplantation Incubation period in these settings is often short because there is no preerythrocytic stage Clinical features and management are the same as for naturally acquired infections. Primaquine is unnecessary for transfusion-transmitted P. vivax and P. ovale infections.
Slide 56 - Tropical Splenomegaly (Hyperreactive Malarial Splenomegaly) Chronic or repeated in some cases malarial parasites cannot be found in peripheral-blood smears Massive Splenomegaly, Hepatomegaly Hypergammaglobulinemia; normochromic, normocytic anemia Antimalarial chemoprophylaxis; results usually good
Slide 57 - Quartan Malarial Nephropathy Chronic or repeated infections with P. Malariae (and possibly with other malarial species soluble immune-complex Nephrotic Syndrome
Slide 58 - Burkitt's Lymphoma Strongly associated with Epstein-Barr virus The prevalence of this childhood tumor is high in malarious areas of Africa.
Slide 59 - Diagnosis Asexual Giemsa (preferred) Field's Wright's Leishman's stain Both thin and thick
Slide 60 - RDTs Rapid, simple, sensitive, and specific antibody-based diagnostic stick or card tests that detect P. falciparum–specific, in finger-prick blood samples are now being used widely in control programs RDTs are replacing microscopy in many areas because of their simplicity and speed, but they are relatively expensive and do not quantify parasitemia.
Slide 61 - PCR Antibody and PCR tests have NO role in the diagnosis of malaria except that PCR is increasingly used for genotyping and speciation in mixed infections
Slide 62 - Gametocytemia may persist for days or weeks after clearance of asexual parasites
Slide 63 - Phagocytosed malarial Pigment is sometimes seen inside peripheral-blood Monocytes or Polymorphonuclear leukocytes and may provide a clue to recent infection if malaria parasites are not detectable
Slide 64 - Laboratory Findings Normochromic, Normocytic Anemia is usual WBC count is generally normal, although it may be raised in very severe infections Monocytosis, Lymphopenia, and Eosinopenia, with reactive Lymphocytosis and Eosinophilia in the weeks after the acute infection ESR,CRP High Severe infections may be accompanied by prolonged PT and partial thromboplastin times and by more severe Thrombocytopenia
Slide 65 - Treatment Repeat blood smears at least every 12–24 h for 2 days Alternatively, a rapid antigen detection card or stick test
Slide 66 - Any doubt about the resistance, it should be considered resistant Antimalarial drug susceptibility testing can be performed but is rarely available, has poor predictive value in an individual case, and yields results too slowly to influence the choice of treatment
Slide 67 - Chloroquine Choice for the non-falciparum malarias Vivax Ovale Malariae Knowlesi except in Indonesia and Papua New Guinea, where high levels of resistance in P. vivax are prevalent.
Slide 68 - Chloroquine-Sensitive Vivax Malariae Ovale, Knowlesi Falciparuma
Slide 69 - Chloroquine (10 mg of base/kg stat followed by 5 mg/kg at 12, 24, and 36 h or by 10 mg/kg at 24 h and 5 mg/kg at 48 h) or Amodiaquine (10–12 mg of base/kg qd for 3 days)
Slide 70 - Radical Treatment Vivax or Ovale Primaquine (0.5 mg of base/kg qd) should be given for 14 days to prevent relapse. In mild G6PD deficiency, 0.75 mg of base/kg should be given once weekly for 6–8 weeks. Not be given in severe G6PD deficiency
Slide 71 - Falciparum Artesunatec (3 days) + Sulfadoxine/Pyrimethamine as a single dose or Artesunatec (3 days) + Amodiaquine (3 days)
Slide 72 - Multidrug-resistant Falciparum Artemether-Lumefantrinec (bid for 3 days with food) or Artesunatec (3 days) + Mefloquine (3 days )
Slide 73 - Second-line treatment/treatment of imported Artesunatec (7 days) or Quinine (tid for 7 days) plus 1 of the following 3: 1. Tetracycline (qid for 7 days) 2. Doxycycline (qd for 7 days) 3. Clindamycin (bid for 7 days) or Atovaquone-Proguanil (qd for 3 days with food)
Slide 74 - Severe Falciparum Artesunatec (IV followed by at 12 and 24 h and then daily if necessary) or, if unavailable, one of the following: Artemetherc (IM followed by qd) or Quinine dihydrochloride (infused over 4 h, followed infused over 2–8 h q8h) or Quinidine (infused over 1–2 h, followed by houriwith electrocardiographic monitoring)
Slide 75 - Very few areas now have chloroquine-sensitive P. falciparum Tetracycline and Doxycycline should not be given to pregnant women or to children <8 years of age Oral treatment should be substituted as soon as the patient recovers sufficiently to take fluids by mouth
Slide 76 - WHO now recommends Artemisinin-based combinations as first-line treatment for uncomplicated Falciparum
Slide 77 - Quinine, Quinidine Common: Hypoglycemia
Slide 78 - Chloroquine Acute: Hypotensive shock (parenteral), cardiac arrhythmias, neuropsychiatric reactions Chronic: Retinopathy (cumulative dose, >100 g), skeletal and cardiac myopathy
Slide 79 - Primaquine Massive hemolysis in subjects with severe G6PD deficiency
Slide 80 - Severe Malaria
Slide 81 - Uncomplicated Malaria
Slide 82 - ….. If there is any doubt as to the identity of the infecting malarial species, treatment for falciparum malaria should be given Nonimmune patients receiving treatment ,daily parasite counts performed until the thick films are negative. If the level of parasitemia does not fall below 25% of the admission value in 48 h or if parasitemia has not cleared by 7 days (and adherence is assured), drug resistance is likely and the regimen should be changed
Slide 83 - Radical Treatment Primaquine (0.5 mg of base/kg, adult dose) should be given daily for 14 days to patients with P. vivax or P. ovale infections after laboratory tests for G6PD deficiency have proved negative. If the patient has a mild variant of G6PD deficiency, primaquine can be given in a dose of 0.75 mg of base/kg (45 mg maximum) once weekly for 6 weeks.
Slide 84 - Radical Treatment Pregnant women with vivax or ovale malaria should not be given Primaquine but should receive suppressive prophylaxis with Chloroquine (5 mg of base/kg per week) until delivery, after which radical treatment can be given.
Slide 85 - Complications Acute Renal Failure Acute Pulmonary Edema (Acute Respiratory Distress Syndrome) Hypoglycemia Spontaneous Bleeding Convulsions Aspiration pneumonia Bacterial Sepsis
Slide 86 - Prevention no safe, effective, long-lasting vaccine is likely to be available for general use in the near future
Slide 87 - Personal Protection Against Avoidance of exposure to mosquitoes at their peak feeding times (usually dusk to dawn) Insect repellents containing 10–35% DEET (or, if DEET is unacceptable, 7% Picaridin), Suitable Clothing Insecticide-impregnated bed nets or other materials. Widespread use of bed nets treated with residual Pyrethroids reduces the incidence of malaria in areas where vectors bite indoors at night
Slide 88 - Chemoprophylaxis Chemoprophylaxis is never entirely reliable Chloroquine phosphate Atovaquone-Proguanil (Malarone) Doxycycline Mefloquine
Slide 89 - بيماري مالاريا يك بيماري انگلي بسيار قديمي است كه در هزارو هفتصد سال قبل از ميلاد مسيح در نوشته هاي چيني ها از آن ياد شده است. سقراط نيز در آثار خود اين بيماري را توضيح داده است. در آن زمان علت بيماري را شرايط بد آب و هوائي مي دانستند به همين دليل به نام مالاريا ( هواي بد باتلاق) ناميده شد . مصريان باستان اولين قومي بودند كه با خشك كردن آبهاي راكد بيماري را كنترل كردند. در ايران قديم به علت تب و لرز متناوب به تب نوبه هم نيز معروف بوده است .
Slide 90 - پلاسمودیوم فالسیپاروم عامل مالاریای سه یک بدخیم پلاسمودیوم ویواکس عامل مالاریای سه یک خوش خیم پلاسمودیوم مالاریه عامل مالاریای چهار یک پلاسمودیوم اوال عامل مالاریای اوال
Slide 91 - مرحله اول (لرز): لرز بحدي شديد است كه حتي تختخواب بيمار هم تكان ميخورد . خشكي پوست وكبودي انتهاي دست و پاها از اختصاصات اين مرحله است. نبض سريع ولي چندان پر نيست. ممكن است بيمار دچار سردرد حالت تهوع و استفراغ شود. اين مرحله معمولاً 15 دقيقه تا يكساعت به طول انجامد . حمله كلاسيك مالاریا (Paroxysm) 91
Slide 92 - حمله كلاسيك مالاریا (Paroxysm) مرحله دوم (تب): پس از قطع لرز، بيمار دچار تب شده و احساس حرارت مينمايد .تب ممكن است تا 41 درجه سانتيگراد يا بالاتر افزايش يابد و همراه با آن سرخي صورت و چشم، خشكي پوست ، نبض تند، سردرد، عطش ،تهوع و گاه استفراغ ديده ميشود. اين مرحله حدود 2 تا 6 ساعت به طول مي انجامد. 92
Slide 93 - مرحله سوم (تعریق): بيمار به سرعت دچار تعريق شديد ميگردد. تعريق ابتدا از صورت و دستها شروع ميشود و سپس از كليه منافذ بدن انجام ميگيرد، به طوري كه لباسها و ملحفه خيس و مرطوب ميشود. اين مرحله بطور معمول 2تا 4 ساعت بطول مي انجامد . حمله كلاسيك مالاریا (Paroxysm) 93
Slide 94 - علائم بين حملات مالاریا در اين مرحله بيمار كم و بيش به حالت عادي برگشته و ميل به كار و انجام زندگي عادي مينمايد. بيمار تاحدي رنگ پريده ضعيف و ناراحت بنظر ميرسد .اشتهاي او كم شده است . 94
Slide 95 - علائم مالارياي بدخيم ناتواني در نشستن و ايستادن و ناتواني در خوردن و آشاميدن استفراغ مكرر ادرار تيره رنگ مشكل در تنفس تب بالا (ركتا ل بالاي 40 درجه و يا زير بغل بالاي 5/39) كلاپس عروقي و شوك 95
Slide 96 - روش های پیشگیری مالاریا مبارزه با لارو آنوفل: خشکاندن باتلاق ها جاری کردن آب های راکد استفاده از لارو کش ها مثل نفت روش های بیولوژیک: استفاده از باکتری ها و ماهی های خاص 96
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