GENETIC MODIFICATION IN MALARIA

Several red cell inherited factors influence the morality of Plasmodium falciparum malaria. P. falciparum does not grow well in red cells that contain Haemoglobin F, C or especially S. haemoglobin S. heterozygotes (As) are protected against the lethal complications of malaria. B. thalasemia  heterozygotes enjoy a selective advantage  in malaria environment P. vivax  cannot enter red cells that lack a Duff blood  group.

 CLINICAL FEATURES
        Plasmodium falciparum is most dangerous, the onset is insidious with malaise, headache, vomiting and is often mistaken for influenza, cough and mild diahoarrdea, muscle aches, shaking chills, tiredness, are also common fever which has no particular pattern. Jaundice is haemolysis is very high or if there is hepatic dysfunction and anaemia. Without  treatment P. falciparum infection ordinarily will terminate spontaneously in  less than one year unless it ends fatally.

        P. vivax and P. ovale malaria infection starts with a period of several days of continued fever before the development of classical bouts of fever on alternate days. Fever starts with rigor. The patient feels cold and the temperature rises up to 400C. After half an hour, the hot flush phase begins, then perspiration and gradual temperature decline. The cycle is repeated every 48 hours. Relapses are common in the first two years of leaving the malarious area.  P. malariae infection is similar to the above but fever repeats third day. P. malariae causes glomerulonephitis and nephritic syndrome   in children. 
RELATED INFORMATION
Share on Google Plus

Declaimer - Unknown

The publications and/or documents on this website are provided for general information purposes only. Your use of any of these sample documents is subjected to your own decision NB: Join our Social Media Network on Google Plus | Facebook | Twitter | Linkedin

READ RECENT UPDATES HERE