Malaria PDF

# MALARIA ## Epidemiology - 40% of the world population live in areas endemic of malaria. - Affect Malaria 270 millions people each year and has mortality rate of 1%, so 1-2.7 millions die of malaria, most of them in Africa within the age of 2-30 year. - P.Falciparum reported in most African coun...

# MALARIA ## Epidemiology - 40% of the world population live in areas endemic of malaria. - Affect Malaria 270 millions people each year and has mortality rate of 1%, so 1-2.7 millions die of malaria, most of them in Africa within the age of 2-30 year. - P.Falciparum reported in most African countries, pacific ocean and central south America. - P.Vivax → north Africa. - P.ovale → west Africa. - P.Malariae → rare outside of Africa. - In the Sudan → p.falciparum is common, vivax and malariae occur but ovalae not very common. ## Etiology - 4 species: - P.falciparum → malignant tertian - P.vivax, P.ovalae → benign tertian - P.malariae → Quartan malaria ## Transmission - By bite of infected female anopheles mosquitos. - 45% of them are considered to be efficient for transmission of malaria due to: - Longevity - Efficiency of biting - Other ways ## Life Cycle - **Sexual cycle:** in mosquitos, which takes 8-35 days. - **Asexual cycle:** bite for feeding [sporozoites] → circulation → hepatocytes[merozoites] → RBCs [erythrocytic cycle], some of them reinvade the liver cells and remain dormant - relapse. - Complete cycle from the liver to the RBCs takes 5 days {p.F}, 8 days{ P.vivax}, 9days{ P.ovalae} and 15 days {P.malariae}. ## Erythrocyte Cycle - RBCs infected by merozoites → many asexual cycles → some form gametocytes & majority ring forms & trophozoites. - P.V&P.O → invades new RBCs. - P.F → invades all RBCs especially young, so produce the most severe form of malaria. - In the RBC ring stage [12hrs], trophozoite[36hrs] then schizonts. - Gametocytes in P.V&P.O[4days]&PF [10 DAYS] ## Immunology ### Natural - Sickle cell trait - Thalassemia - G6PD deficiency - West African with negative blood for Duffy antigen - HLA antigens - Spleen versus splenectomy ### Acquired - Due to macrophages stimulation by activated T lymph's but each generation of merozoites produce Ags different from previous ones →antigenic diversity ## Path Physiology and Pathogenesis - Sequestration of parasitized RBCs in the vital organs → ischemia → hypoperfusion → anaerobic glycolsis. - Liberation of substance like TNF and IL1 when merozoites rupture → inhibiton of gluconeogenesis → 'hypoglycemia. - Brain → loss of consciousness due to: - Increased CSF lactate - Interference with neurotransmission. - Kidneys → blockage of the glomeruli by parasites → ischemia → hypo perfusion in the medullary → ATN - Lungs → oedema due to ↑ permeability. - Blood → anemia due to RBCs destruction, short life span of the RBCs and dyserythropoeisis. - Metabolic changes - Lactic acidosis due to: - Anaerobic glycolysis. - Failure of the kidneysaliver to remove lactate. - High production of lactate by the parasites. - Hypoglycemia due to: - Failure of hepatic gluconeogenesis. - Increased demand by febrile patients. - Increased demand for glucose by the parasites. ## Clinical Picture - **IP:** 10-14 days in P.vivax,ovalae and falciparum and 18 days to 6 wks in P.malariae. - **Prodromal symptoms:** Flue like. - **Classical malaria:** 3 stages - Cold stage last 30 m - one hr, characterized by marked vasconstriction. - Hot stage last 2-6 hrs due to vasodilatation. - Sweating stage - patient feels exhausted. ## Other Features - Herpes labials in 1/2. - Enlarged spleen by day 10. - Large tender liver. - Leucopenia with relative lymphocytosis. ## P.Falciparum Malaria - This is the most severe type due to: - P.F affects all types of cells. - Produces more parasites. - Causes more multiplication in the tissues and RBCs - **Indication for severity:** - More than 5% of RBCs parasitized. - More than 10% of parasitized RBCs contain more than one ring. - Schizonts in the PBP. ## Complications - **Cerebral malaria:** Disturbed consciousness, convulsions, agitation and coma. - O/E papilledema, cranial nerve palsies. - MR → 15% in children - MR → 20% in adults. - **Convulsions**. - **Post malarial neurological syndrome:** Seen in 3% of adultsa 10% of children. - **Early:** hemiplegia, hemi sensory loss, cortical blindness and some cranial nerve palsies. - **Prognosis:** 50% recovery, 25% partial recovery and 25% no recovery. - **Late:** Psychosis,encephalopathy and cerebellar ataxia. - **GIT syndrome:** Due to heavy infiltration resulting in: - Bilious remittent fever. - Dysenteric malaria. - **Aligid malaria**. - **Black water fever:** In non immune treated with quinine G6PD given primiquine. Result from I/V hemolysis leading to rapid onset of fever,hemoglobinuria, jaundice. vomiting and ARF. - MR 20-50% - **Acute renal failure:** - **Early:** seen in pts with serious complication. - **Late:** tends to occur after recovery of malaria. - **Metabolic acidosis**. - **Hypoglycemia:** 30% of children and 8% of adult mainly in non immune,children and pregnant ladies. - **Pulmonary oedema:** MR 80% - **Anemia**. - **Hyperpyrexia**. ## Clinical Picture of Vivax and Ovalae - **IP:** 10-15 days. - **Tertian fever**. - 1/3 have herpes labials. - Exoerythrocytic cycle is responsible for relapsea difficult eradication. ## Clinical Feature of P. malariae - **IP:** 30-40 days. - **Fever occurs** every 72 hrs. - May be self limited. - Persistent type of up to 20 years with chronic splenomegaly, high gamma globulin a nephrotic syndrome. ## Chronic Complication - Cachexia. - Hepatomegly. - Splenomegaly. - Tropical splenomegaly syndrome. - Quatrain malaria nephropathy. ## Definition of Severity of Malaria - Cerebral malaria - Severe anemia. - Renal failure. - ARDS. - Hypoglycemia. - DIC. - Convulsion ≥ 2 - Acidemia. - Degree of parasitemia 5-10% - Jaundice ## Diagnosis - B.F for malaria is +ve in most cases but the most sensitive is bone marrow. - Trophozoites in B.F is important for diagnosis, gametocytes alone are not enough. - Tow types of the blood film - Thick blood film → for Δ. - Thin blood film → for identification of the species and severity. ## ICT - Identify P.F and P. vivax Ags HRP-2 found in the whole blood. - The Abs used is impregnated in strip paper, its Ag -Ab reaction. - Limitations of the test the HRP-2 may be detectable after drug therapy even if the parasites no longer seen in the B.F. ## Antimalarial Drugs - Management of malaria involves: - Vector control - Prophylaxis with drugs. - Treatment of established infection. - The drugs can be classified according to parasitic life cycle they affect.