Life cycle of malarial parasite

Signs:

Physical examination usually demonstrates an increased temperature, tachycardia, and warm flushed Skin. The spleen is often palpable in initial infection, but this is more likely in subsequent attacks. It is usually soft and may be tender. The liver is often enlarged and may be tender; jaundice is not unusual. Orthostatic hypotension often occurs during initial infections. Mental confusion and cyanosis are sometimes encountered.

Lab Diagnosis of Malaria:

The definitive diagnosis of malaria is made by the identification of malaria parasites in a peripheral blood film. However, Malaria shares signs and symptoms with other tropical illness including typhoid fever, rheumatic fever, and bacterial meningitis. Therefore, diagnosis of malaria requires an increased level of suspicion and diligent screening. Screening all febrile patients possibly exposed to malaria transmission.

The screening tool of choice for malaria diagnosis is microscopic examination of thick and thin blood smears. Thick smear examination detects the presence of any organism; thin

smear examination identifies the specific infecting Plasmodium species.

Timing of Screening:

Symptoms often precede detectable parasitemia by 1-2 days. Therefore, screen blood obtained through fingersticks or other techniques several times a day (frequency is more important than timing) until a diagnosis of malaria is made or ruled out. Thin smear diagnosis for causal species is crucial, as P. falciparum infections are life threatening and require specific treatment. After diagnosis, blood smears should continue to be monitored for response to therapy. Decreasing parasite count (concentration) signifies favorable response to therapy; frequency of testing depends on therapeutic response and severity of illness. For example, seriously ill patients should be tested 2-3 times daily until they significantly improve, then daily until parasite level is zero.

Early diagnosis and treatment is life saving; falciparum malaria kills 25% of non-immune adults within 2 weeks if treatment is not started early in the infection. If the diagnosis of malaria is suspected, treat, then arrange for definitive diagnosis.

Other Laboratory Findings:

Abnormal laboratory findings reflect the severity of hemolysis. A normocytic, normochromic anemia with leukopenia and thrombocytopenia is sometimes present on initial screening, but it is almost always present following medication therapy with resultant clearing of parasitemia. Massive P. falciparum infections cause acute decreases in hemoglobin, hematocrit, and an increase in reticulocyte count. Trace to moderate protein, urobilinogen, and conjugated bilirubin may be found on urinalysis. In severe P. falciparum infections, massive hemolysis combined with circulating immune complexes produces acute renal insufficiency or failure ("blackwater fever") with laboratory findings of hemoglobinuria, proteinuria, and an elevated serum creatinine. Fever and dehydration may cause an increase in BUN and creatinine, but if serum creatinine rises disproportionately higher than BUN (BUN to creatinine ratio is normally 10 or 12 to 1), renal failure must be considered.

Liver:

Liver impairment may occur, though hyperbilirubinemia normally results from hemolysis. Abnormalities in liver function tests, increased ALT, AST, and prolonged prothrombin time, sometimes occur causing diagnostic confusion with viral hepatitis. Serum albumin is usually decreased. Hypoglycemia, commonly seen in P. falciparum infections and pregnancy, is due to the 75-fold increase in glucose consumption by parasitized red blood cells. In addition, quinine may stimulate insulin secretion, causing clinically significant hypoglycemia when used for treatment, especially when given intravenously. If a patient deteriorates during convalescence, especially with a deterioration in neurologic function, hypoglycemia should be considered as a possible cause.

Hyperparasitemia:

Patients with P. falciparum infections that are hyperparasitemic have a higher risk of death. Hyperparasitemia is defined as a parasite count of greater than 250,000 per microliter (>250,000/_l), or as having greater than 5% of red blood cells parasitized. Risk of death is due to extensive microvascular disease, and severe metabolic effects from the parasite load.