UNCOMPLICATED MALARIAFirst symptoms are non specific:• Headache, Lassitude, Fatigue• Abdominal discomfort, muscle and joint aches, diarrhea• Followed by fever(irregular at first), chills, rigors, perspiration, anorexia . In some cases palpable spleen and slight enlargement of liver are also present• Nausea,vomiting, & orthostatic hypotension are common Signs:• Anemia, splenomegaly, hepatomegaly
SEVERE FALCIPARUM MALARIA• Unarousable Coma / cerebral malaria, convulsions• Renal Impairment• Noncardiogenic pulmonary edema• Liver Dysfunction• Hypoglycemia• Metabolic acidosis/acidemia• Hematological abnormality like hemoglobinuria, normocytic anemia, bleeding,DIC• Other complications like jaundice, extreme weakness,hyperparasitemia, impaired consciousness• Hypotension/shock
CEREBRAL MALARIA• Coma is characteristic and ominous feature of falciparum malaria• Manifests as diffuse encephalopathy• No signs of meningeal irritation• Eyes : divergent, Corneal reflexes :preserved• Muscle tone : May be Increased/ Decreased• Tendon reflexes : Variable, Plantars : Equivocal. Abdominal & cremasteric reflexes are absent• Fundus : Retinal hemorrhages, discreet spots of retinal opacification, papilledema, cotton wool spots
• Convulsions :In children, usually generalised, often repeated• Covert seizure : manifest as Tonic clonic eye movement, hyper salivation• Residual neurological deficit (Hemiplegia, CP, cortical blindness, deafness, impaired cognition and learning) seen in children who survive cerbral malaria
Major Manifestations of MalariaAnemia Lennart Nielson (Karolinska Instituteg), Hedvig Perlmann (Stockholm University) Martin WeberCerebralmalaria George Grau Roll Back Malaria Info SheetLowbirthweight Rick Steketee National Human Genome Research Institute
• HYPOGLYCAEMIA .Increases the risk of mortality in children with cerebral malaria; may present with convulsions or a deterioration in level of consciousness. CAUSES• 1. Increased peripheral requirement of glucose consequent upon anaerobic glycolysis. 2. Increased metabolic demands of febrile illness. 3. Obligatory demand of parasites.
• ACIDOSIS This may result form renal failure, but more commonly there is a primary lactic acidosis . Lactic acidosis results from : 1. Anaerobic glycolysis due to microvascular obstruction. 2. Failure of hepatic and renal lactate clearance. 3. Production of lactate by the parasite..
• NONCARDIOGENIC PULMONARY OEDEMA This is a grave and usually fatal manifestation of severe falciparum malaria and occurs mainly in adults. Hyperparasitaemia, renal failure and pregnancy are recognised predisposing factors
• RENAL IMPAIRMENT- Tubular abnormalities consistent with acute tubular necrosis (ATN) are seen. Sequestration in glomerular capillaries, mesangial endothelial cell proliferation, and immunoglobulin deposits may be seen.• MALARIA IN PREGNANCY .Common adverse effects of malaria in pregnancy : Maternal anaemia Stillbirths Premature delivery and Intra- Uterine Growth Retardation (IUGR) result in the delivery of Low Birth weight (LBW) infants
Other complications• Septicemia may complicate severe malaria.• Liver dysfunction- mild hemolytic jaundice is common. Severe jaundice is associated with P.falciparum infections
TROPICAL SPLENOMEGALY(HYPERREACTIVE MALARIAL SPENOMEGALY)• Chronic or repeated malarial infections produce in certain situations splenomegaly• This is associated with the production of cytotoxic IgM antibodies. There is uninhibited B cell production of IgM and the formation of cryoglobulins.• This process stimulates reticuloendothelial hyperplasia and clearance activity and eventually produces splenomegaly.
• Patients with HMS present with an abdominal mass or a dragging sensation in the abdomen and occasional sharp abdominal pains suggesting perisplenitis.• Anemia and some degree of pancytopenia are usually evident, and in some cases malarial parasites cannot be found in peripheral smears• Vulnerability to respiratory and skin infections is increased.
QUARTAN MALARIAL NEPHROPATHY• Chronic or repeated infection with P.malariae may cause soluble immune-complex injury to the renal glomeruli, resulting in the nephrotic syndrome.• The histologic appearance is that of focal or segmental glomerulonephritis with splitting of the capillary basement membrane. subendothelial dense deposits are seen on electron microscopy, and imunofluorescence reveals deposits of complement and immunoglobulins
BURKITTS LYMPHOMA & EPSTEIN- BARR VIRUS INFECTION• Malaria related immunosuppression may provokes infection with lymphoma virus.• Burkitts lymphoma is strongly associated with Epstein-barr virus.