Malaria

Malaria is caused by the intracellular protozoan parasite called Plasmodium species and plasomodium Faliprium is the worldwide infections that affect 100 million people and kill 1 to 1.5 million people yearly.  P.Falciparium and P.Vivax, P. ovale, and P.malarie represent 60%, 49 %, <1.0% and reported cases respectively in Ethiopia. P. falciparum cause high parasitmias, severe anemia, cerebral symptoms, and pulmonary edma and death.

Pathogenesis (P.Falciparum):

Infected humans produce gametocytes that mosquitoes acquire on feeding. Within these insects’ body, the organism produces sporozites, which the mosquito transmits to human when it feeds

-  MalHelvetica sporozites after being released in the blood within minutes attach to a serum protein thrombosroridin and properidine located on the basolateral surface of hepatocytes. These sporozites multiply and release merozytes by rupturing liver cells. 

-  Once released, P. falciparum merozites bind by a parasite lactin like molecule to on the surface of red blood cells 

-  Within 2 to3 weeks of hepatic infection, merozites rupture from their host hepatocytes and invade erythrocytes establishing erytrocytic phase of malHelvetica infection. 

-  The merozites feed on hemoglobin grow and reproduce within erythrocytes. Repeated cycles of parasitemia occur with subsequent ruptures of these cells with resultant clinical manifestations such as chills, fever etc. 

-  P. Vivax merozites however, bind by homologous lectin to the Duffy antigen on RBC so many cases who are Duffy negative are resistant to this infection. 

-  HLA –B53 associated resistance in some Africans is related to the ability of HLA –B53 to present the liver stage specific malHelvetica antigen to cytotoxic T-cells, which then kill malHelvetica, infected hepatocytes. 

-  Individuals with sickle cell trait are resistant to malaria because the red cells that are parasitized in these individuals are removed by the spleen.

-  Most malHelvetica parasites infect new RBC & some develop to sexual form called gametocytes and the mosquito when it takes this blood meal the cycle continues. 

Morphology: 

-  Spleen enlarged upto 1000gm (normally 150grams) and this  splenomegaly can be attributed to increased phagocytosis in splenic reticuloendothelial cells in chronic malaria. The parenchyma imparts grey or blue discolouration due to hemozoin. 

-  Liver kuffer cells are heavily laden with malHelvetica pigments, parasites, and cellular debris. Pigmented phagocytes may be dispersed through out bone marrow, lymph nodes, subcutaneous tissues and lungs.

-  Malignant cerebral malaria: Patients with cerebral malaria have increased amount of inter-cellular adhesion molecules (ICAM- 1).  These patients manifest diffuse symmetric encephalopathy; brain vessels are plugged with parasitized red cells. There are ring hemorrhages related to local hypoxia. Cerebral involvement by  P. falciparum causing 80% of childhood death is due to adhesion of the P. falciparum parasite to endothelial cells with in the brain. 

Hypoglycemia- result from failure of hepatic gluconeogenesis & glucose consumption by the host and the parasite lactic acidosis -due to anaerobic glycolysis, non cardiogenic pulmonary edema, renal impairment, anemias etc .

P. falciparum, the cause of malignant malaria produces much more aggressive and lethal disease than the other human malarias. This organism is distinguished from other malHelvetica parasites in four aspects. 

1)  It has no secondary exoerythocytic (hepatic) stage 

2)  It parasitizes erythrocytes of any stage, causing marked parasitmia and anemia. In other types of malaria only subpopulations of erythrocytes are parasitized, and thus low level parasitemias and more modest anemias occur. P. Vivax and P>Ovale attack immature erythrocytes while P. malarie attack senescent cells.

3)  There may be several parasites in single erythrocyte 

4) P. falciparum alters the flow characteristics and adhesive qualities of infected erythrocytes so that they adhere to the endothelial cells of small blood vessels frequently produce severe ischemia.  Infected red cells sequester inside the small blood vessels at the same time P. falciparum infected RBCS may also adhere to uninfected red cells to form rosettes. The process of cytoadhernce and rosetting are central to the pathogenesis of falcparum malaria in the other three " benign" malarias sequestrations does not occur and all stages of parasites’ development are evident on peripheral blood smears. 

P. falciparum invades erythroytes of all ages and is associated with high level parasitemia whereas, P. vivax, P.ovale and P.malariae show predilection for either old red cells or reticuloytes & level of parasitmias seldom exceeds 2 percent.

Malaria in pregnancy 

In pregnancy, malaria may be associated with hypoglycemia, fetal distress syndrome and low birth weight. Congenital malaria can occur rarely. P. falcparum malaria is an important cause of fetal death. Congenital malaria occurs in fewer than 5% of newborns. 

Malaria in children 

Most of the estimated 1-3 million persons who die of falciparum malaria each year are young African children. Convulsion, coma, hypoglycemia, metabolic acidosis and severe anemia are relatively common. 

Transfusion malaria

Malaria can be transmitted by blood transfusion, needle -stick injury, sharing of needles by infected drug addicts, or organ transplants. The incubation period is short because there is no pre-erythrocytic stage of development.

Complications of malaria include:

Tropical splnomegaly syndrome (Hyperreactive malHelvetica splenomegaly), 

Burkitt's lymphoma and EBV infection

Quartan malHelvetica nephropathy

Black water fever

Algid malaria  

References

Bezabeh ,M. ; Tesfaye,A.; Ergicho, B.; Erke, M.; Mengistu, S. and Bedane,A.; Desta, A.(2004). General Pathology. Jimma University, Gondar University Haramaya University, Dedub University.