Introduction To Malaria • Malaria is an acute and chronic illness characterized by paroxysms of fever, chills, sweats, fatigue, anemia, and splenomegaly • It is protozoa d/se w/ch is mostly transmitted by a vector Anopheles mosquitoes. • The most important of the parasitic disease of humans =>107 countries, 3 billion people, 1-3 million deaths/yr
ETIOLOGY & PATHGENESIS • Malaria is caused by intracellular Plasmodium protozoa transmitted to humans by female Anopheles mosquitoes. • Four species of the genus plasmodium cause nearly all malarial infections in humans. • Almost all deaths are by P.falciparum. • The pathogensis in human is as a result of direct effects of RBC destruction.
Major Malaria Parasites • P. falciparum ( 60%) • P. vivax ( 40%) • P. malariae (rare) < 1% • P. ovale (rare) • Major Malaria Vectors • An. arabiensis (family of An. gambiaecomlex) • => primary vector • An. funestus • An. phareonsis • An. nili
Life cycle of malaria • Plasmodium species exist in a variety of forms and have a complex life cycle that enables them to survive in different cellular environments in the human host (asexual phase) and the mosquito vector (sexual phase). • The exoerythrocytic phase begins with inoculation of sporozoites into the bloodstream by a female Anopheles mosquito. • Within minutes, the sporozoites enter the hepatocytes where they develop and multiply asexually as a schizont. • After 1–2 wk, the hepatocytes rupture and release thousands of merozoites into the circulation. The tissue schizonts of P. falciparum and P. malaria rupture once and do not persist in the liver.
There are 2 types of tissue schizonts for P. ovale and P. vivax. The primary type ruptures in 6–9 days, while a secondary type remains dormant in the liver cell in the hypnozoite form for weeks, months, or as long as 5 yr before releasing merozoites, and thereby causing relapses of infection. • The erythrocytic phase of Plasmodium asexual development begins when the merozoites from the liver penetrate erythrocytes. Once inside the erythrocyte, the parasite transforms into the ring form, which then enlarges to become a trophozoite. • The trophozoite multiplies asexually to produce a number of small erythrocyticmerozoites that are released into the bloodstream when the erythrocyte membrane ruptures, which is associated with fever.
Over time, some of the merozoites develop into male and female gametocytes that complete the Plasmodium life cycle when they are ingested during a blood meal by the female Anopheline mosquito. • The male and female gametocytes fuse to form a zygote in the stomach cavity of the mosquito
Life cycle • Female Anopheles mosquito (sexual cycle) • Gametocytes • Sporozoites injected • In man (Asexual cycle) • Exo-erythocytic (hepatic) stage • Liver (schizogony) = Merozoites or Hypnozoites • Erythrocytic stage • Merozoites and Gametocytes
Types of Clincal Features • Benign tertian malaria • Paroxysim(AFI) of 48 hrs =>P. vivax and ovale • Malignant tertian malaria • Paroxysim of 48 hrs => P. falcipurum • Quartan malaria • Paroxysim of 72 hrs => P. malarie
Malignacy of P. falcipurum • High parasitemia(up to 60%), fatal >25% • Multiple parasites in RBC • Endothelial adherence (sticky nobes) • Children and new immigrants
EPIDEMOLOGY • Malaria occurs throughout most of the tropical regions of the world. • Global distribution • prevalence of 500 million people/yrly • Two million death/yrly • 40% of the world population living in tropical/subtropical climates are exposed to malaria.
MALARIA IN ETHIOPIA • Malaria is one of the leading public health problems in Ethiopia • 75% of the country is malarious (<2000m), with about 68% of the population (50 million) at risk • Major impediment to socio-economic development, coincides with major planting and harvesting season
Malaria Epidemiology • Bimodal type of transmission: • Major: Sep - Dec, following the main rainy season from Jun to Aug • Minor: Apr–May, following a short rainy season from Feb to Mar • Major epidemics occur every 5-8years, focal outbreaks are common • Distribution varies from place to place depending on climate and altitude
Malaria in Ethiopia is Unstable Unstable malaria • Seasonal • Lack of immunity • Epidemic common • All age groups affected Malaria in Ethiopia Stable malaria • Intense, perennial • High immunity • Epidemic uncommon • Children & pregnant women more affected
Trend of an epidemic malaria in Adami Tulu District. Microscopically confirmed malaria cases at Zeway MCL, 1999-2004. Malaria in Ethiopia is Seasonal
Malaria Burden in Ethiopia • More than 600,000confirmed and >9 million clinical cases each year • Cause about 70,000deaths each year • Health and health related indicator (2005/06) of the FMOH: • 18% of OPD cases (1st) • 14% of admission (2nd) • 9% of hospital deaths (2nd) • Poor health information system
ENDEMICITY • Endemicity is defined in terms of parasitemia rates or palpable-spleen rates in children 2-9 yrs of age as-hypo/meso/hyper/holo-endemic. • Infant parasite rate- most sensitive index of transmission of malaria to a locality • Epidemic can occur under some conditions
Clinical features • Malaria is a very common cause of fever in tropical countries. • Non-specific symptoms
Predisposing factors for complications • (1.) Extremes of age. • (2.) Pregnancy, especially in primigravidae and in 2nd half of pregnancy. • (3.) Immunosuppressed - patients on steroids, anti- cancer drugs, immunosuppressant drugs. • (4.) Immunocompromised - patients with advanced tuberculosis, HIV and cancers. • (5.) Splenectomy. • (6.) Lack of previous exposure to malaria (non-immune) or lapsed immunity • (7.) Pre-existing organ failure.
Complications of P. falciparum malaria • Cerebral malaria ( coma ) • Severe anemia • Metabolic (Lactic) Acidosis • renal failure • Pulmonary odema & ARDS • hypoglycemia • Hypotention & shock • Bleeding & clotting disorder(DIC) • Algid Malaria(CR-Collapse) • Convulsions • haemoglobinuria • hyperparasitemia • Hyperpyrexia • Jaundice • Prostration • Complications of P. vivax / P. malariae • Rupture of spleen • Hepatic dysfunction • Thrombocytopenia • Severe anemia • malarial nephropathy
…cerebral malaria • Cerebral malaria manifests as diffuse symmetrical encephalopathy • No meningial sign • Primitive reflexes are absent • Corneal reflexes are reserved • muscle tone either increase or decrease • Flexor or extensor posturing may be seen. • Approximately 15% of pts have retinal haemorrhage
… • coma is a characteristic and ominous feature (MR 15-20% despite treatment). • Any obtundation, delirium, or abnormal behaviour should be taken seriously.
… • Generalized convulsion(50%) vs covert seizure • Neurological deficit in 3-15% • 1o% of children has language deficit • The incidence of epilepsy increase • Life expectancy decrease among these children.
HYPOGLACEMIA • Plasma glucose level of <2.2mmol/l(<40mg/dl) • Indicate poor prognosis • Causes: • Failure in hepatic gluconeogensis • Increase consumption • drugs
Direct Diagnosis • Blood smears • for asexual P.falciparom parasite is the gold standard. • Thick and thin blood films are made on clear grease-free glass slides. • Thick film is for parasite identification. • Thin film is for species identification.
Treatment of uncomplicated falciparum malaria: • • Artemether-Lumefantrine: (Coartem 20/120): is most widely used in Ethiopia. • Tablet containing 20 mg Artemether plus 120 mg Lumefantrine in a fixed dose combination. • Adult Dosage: < 35 kg: 3 tabs PO BID for 3 days • > 35 Kg: 4 tabs PO BID for 3 days
b) Quinine: • Adult dose : 600 mg PO TID for 5 – 7 days alone or in combination with + Tetracycline 500 • mg PO QID or Doxycycline 100mg PO /day for the same period • Side effects: • Cinchonism: Tinnitus, hearing loss, dizziness, tremor, nausea, resteleness, blurring • Hypogycemia: is the commonest adverse effect
The treatment of Malaria is supportive and specific • Supportive treatment may include the following: • Reducing the temp. if hyperpyrexia is present specially common with P.falciparum infection. • Rehydration specially when vomiting and diarrhea have been prominent and in acidosis. • Monitoring renal output and taking corrective measures if necessary (such as hypovolemia and oliguria maintain careful flood balance.) • Monitoring the need for blood transfusion which may be life-saving.
5. Terminating convulsion with appropriate drugs-rectal diazepam or lorazepam, rectal or intramuscular paraldehyde, and intramuscular phenobarbital are some options. 6. Monitoring of blood glucose and correction of hypoglycaemia where necessary (10-40mL) of 50% dextrose diluted three times with saline and infused over 5-10min.) 7. Reducing acidaemia. Rehydration blood transfusion and anti malaria therapy are usually sufficient for this purpose
Treatment of Severe and complicated falciparum malaria: • A) Drug Treatment: • i) Quinine: is drug of choice for severe and complicated malaria. • Dosage and Adminstration: • Where IV administration of quinine is possible • Loading dose: Quinine 20 mg salt/kg of body weight by infusion over 4 hours, in 5 % • dextrose in saline (5-10 ml/kg of body weight depending on the patient's overall fluid • balance). • Maintenance does: Twelve hours after the start of the loading dose, give quinine 10 mg • salt/kg of body weight in dextrose saline over 4 hours. Repeat the same dose of quinine • (i.e. 10 mg salt/kg) every 8 hours until the patient can take oral medication.
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