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Recent changes in behavior of plasmodium
Recent Changes in Behavior of Plasmodium This document discusses recent changes observed in the behavior of the Plasmodium parasite, which causes malaria. It notes that Plasmodium vivax, previously considered a benign infection, has shown a new potential for severe and life-threatening disease. The document also reviews the epidemiology and pathophysiology of malaria, including clinical manifestations like anemia, renal failure, pulmonary edema, and complications in pregnancy. It discusses investigations, treatment approaches for uncomplicated and severe malaria, drug prophylaxis, emerging drug resistance, and strategies for controlling the mosquito vector.
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Recent changes in behavior of plasmodium
- 1. Recent Changes inBehavior of Plasmodium Dr. Suresh Kumar. S
- 2. Introduction • Malaria iscaused by protozoa of genus PLASMODIUM. • Transmitted to human by the bite of infected female ANOPHELES mosquito. • Mainly 4 species P. vivax, P.falciparum, P.ovale and P. malaria • P. knowlesi a zoonotic malarial parasite, important cause of malaria in south east Asia but not reported in India
- 3. Cont… • Malaria causesmorbidity and mortality significantly in developing countries of tropics • In India 20 million confirmed cases each year • 15 – 20,000 deaths occur yearly in India due to malaria • In India 60-65% is due to P. vivax and 35% due to P. falciparum. • Only few cases of P. Malariae have been reported in Odissha and Karnataka.
- 4. Cont… • Initially itwas thought that only P. falciparum causes severe and complicated malaria but with recent advances, it has been found that P. vivax could also result in severe life threatening disease • There is a recent change in benign behavior of P. vivax to malignant behavior
- 5. Epidemiology • P. vivaxhas wide geographical distribution due to better survival of the parasite in anopheles mosquito at lower temperature and higher altitude. • P. knowlesi a zoonotic parasite seen in soth east asian region can cause a spectrum of disease and potentially fatal but if detected early can be treatable.
- 7. Pathophysiology of Clinicalfeatures • Anaemia • Renal failure • Fluid space and electrolyte changes. • Pulmonary oedema • Coagulopathy and thrombocytopenia. • Blackwater fever • Liver dysfunction • Acidosis • Hypoglycaemia • Gastroinstestinal dysfunstion.
- 8. Anemia • Anaemia • Thepathogenesis is multifactorial. It results from the obligatory destruction of red cells containing parasites at merogony. • The shortened survival of red cells from which parasites have been extracted by the spleen, and accelerated destruction of non-parasitized red cells all compunded by bone marrow dyserythropoeisis. • In severe malaria anaemia develops rapidly because of the rapid haemolysis of the red cells and decline in the haematocrit.
- 9. Renal Failure • Thereis renal vasoconstriction and hypoperfusion in severe falciparum malaria. The renal injury in severe malaria results from acute tubular necrosis. • ATN results from renal microvascular obstruction and cellular injury consequent upon sequestration in the kidney and the filtration of nephrotoxins
- 10. Fluid and ElectrolyteChanges • In view of the general vasodilatation and a falling haemtocrit there will be increase in the plasme renin activity, anti diuretic harmone concentrations reflecting an appropriate homeostatic mechanisms to maintain adequate circulating blood volume. • Mild hyponaterima and hypochloremia are common in sever malaria. • Sreum potassium concentrations are usually normal.
- 11. Pulmonary edema • Pulmonaryoedema in malaria results from a sudden increase in pulmonary capillary permeability. • The cause of this increase in the pulmonary permeability is not exactly known, although the presence of sequestered RBC and host leucocytes in pulmonary capillaries may have a role in causing pulmonar y capillary endothelial dysfunction. • Acute renal failure, severe metabolic acidosis, and coma are confined mainly to the falciparum malaria. • Acute pulmonary oedema may also occur in vivax malaria
- 12. Coagulopathy and Thrombocytopenia •In acute malaria coagulation cascade activity is increased with accelerated fibrinogen turnover, consumption of antithrombin III, reduced factor XIII and increased concentrations of fribrin degardation products. • In severe malaria infections the antithrombin III, protein S and protein C are further reduced and prothrombin and partial thromboplastin times may be prolonged. • Thrombocytpenia is common to all the four malaria species.
- 13. Liver Dysfunction • Jaundiceis common in adults with severe malaria, and there is other evidence of hepatic dysfunction with reduced metabolic clearance of the antimalarial drugs and failure of gluconeogenesis which contributes to lactic acidosis and hypoglycaemia. • Jaundice in malaria appears to have haemolytic, hepatic and cholestatic components. • Cholestatic jaundice may persist well into the recovery period. There is no residual liver damage following malaria.
- 14. Acidosis • Acidosis isthe major cause of death in severe falciparum malaria, both in adults and children. • In severe malaria the arterial, capillary, venous and CSF concentrations of lactate rise in direct proportion to disease severity. • Lactate-pyruvate ratios often exceed 30, reflecting tissue hypoxia and anaerobic glycolysis.
- 15. Hypoglycemia • Hypoglycaemia isan important manifestation of severe malaria. • An increased peripheral requirement for glucose consquent upon anaerobic glycolysis, the increased maetabolic demands of febrile illness. • The obligatory use of glucose by parasite and failure of hepatic gluconeogenesis and glycogenolysis.
- 16. Malaria in Pregnancy •Malaria is more common in pregnancy compared to the general population. Immuno suppression and loss of acquired immunity to malaria could be the causes. • Malaria in pregnancy being more severe, also turns out to be more fatal, the mortality being double (13 %) in pregnant compared to the non-pregnant population (6.5%). • Some anti malarials are contra indicated in pregnancy and some may cause severe adverse effects. Therefore the treatment may become difficult, particularly in cases of severe P. falciparum malaria.
- 17. • In pregnantwomen the morbidity due to malaria includes anemia, fever illness, hypoglycemia, cerebral malaria, pulmonary edema, puerperal sepsis and mortality can occur from severe malaria and haemorrhage. • The problems in the new born include low birth weight, prematurity, IUGR, malaria illness and mortality.
- 18. Transfusion Malaria • Malariacan be transmitted by blood transfusion, needle-stick injury, sharing of needles by infected injection drug users. • The incubation in this setting is often short because there is no pre erythrocytic cycle . • The clinical features are same as of naturally acquired malarias. • Radical therapy with primaquine is unnecessary in transfusion related malaria.
- 19. Cerebral Malaria • Definitionof cerebral malaria requires the presence of P.falciparum parasitemia and the patient to be unrousable . And other causes (e.g.hypoglycemia, bacterial meningitis and viral encephalitis) ruled out. • To distinguish cerebral malaria from transient postictal coma, unconsciousness should persist for at least 30 min after a convulsion. The deeper the coma, the worse is the prognosis.
- 20. • If necessary,a lumbar puncture should be performed to rule out bacterial meningitis. • However, all patients with P. falciparum malaria with neurological manifestations of any degree should be treated as cases of cerebral malaria.
- 21. Neurological signs ofCerebral Malaria • As per the definition, patient should have unarousable coma, not responding to noxious stimuli with a Glasgow coma scale of <7/15. • Mild neck stiffness may be seen. • Retinal haemorrhages occur in about 15% of cases. • Pupils are normal. • Corneal reflexes are preserved. • Papilloedema is unusual and is a sign of poor prognosis
- 22. • Fixed jawclosure and tooth grinding(bruxism) • The corneal reflexes are preserved except in case of deep coma. • Motor abnormalities like decerebrate rigidity, decorticate rigidity and opisthotonus can occur. • Deep jerks and plantar reflexes are variable. • The patients may also have anemia, jaundice and hepatosplenomegaly.
- 23. • Lumbar punctureand CSF analysis may have to be done in all doubtful cases and to rule out associated meningitis. • EEG may show non-specific abnormalities. CT scan of the brain is usually normal.
- 24. Severe Malaria • Definitionsof severe malaria are useful for clinical and epidemilogical purposes. • Definitions were proposed by WHO in 1990 and 2000. • In severe malaria there is often evidence of multiple organ dysfunction. • More than one of the criteria are fulfilled. Pateints can be treated for severe malaria even if they don’t fall clearly into any of the criteria.
- 25. Manifestation of severemalaria
- 28. Investigations • Microscopy :thin and thick smears • Rapid diagnostic tests • Polymerase Chain Reaction • Immunofloroscence
- 29. Approach to malariadiagnosis
- 30. Treatment of uncomplicatedmalaria
- 32. Treatment of complicatedand severe malaria
- 34. Drug prophylaxis ofmalaria Drug Dosage Comments Atovaquone/proguanil Only in areas with chloroquine or mefloquine resistant P.f 250mg of atovaquone and 100 mg of proguanil OD Begin 1-2 days before and for 7 days after leaving such areas. Chloroquine phosphate (Sensitive p.f strains) 300mg base once a week on the same day each week Begin 1-2 days before and for 4 weeks after leaving such areas. Doxycycline(chloroquine or mefloquine resistant P.f) 100mg PO OD Begin 1-2 days before and for 4 weeks after leaving such areas Mefloquine (Chloroquine resistant areas) 228mg base=250mg tablet 1 tablet once a week on the same day each week. Begin 1-2 days before and for 4 weeks after leaving such areas
- 35. Drug Resistance Plasmodium DrugResistance Region P. vivax Antifolates WIdespread P. falciparum Chloroquine Africa P. falciparum Sulfadoxine- Pyrimethamine East Asia, Southern and Central Africa and Central America P. falciparum Quinine Brazil P. falciparum Mefloquine Artemesnin Western Cambodia and eastern Myanmar
- 36. Anti Adult Measures •Residual spraying : the spraying of houses with residual insecticides(eg: DDT, malathion, fenitrothion) is still most effective measure to kill the adult mosquito. • Space application : it involves the application of pesticides in the form of fog or mist using special equipment. • Individual protection : man vector control can be reduced by other preventive measures such as use of repellents, protective clothing, bed nets.
- 37. Anti Larval Measures •Larvicides : anti larval measures such as oiling the collection of standing water. • Source reduction : techniques to reduce mosquito breeding sites which include drainage, flushing, management of water level, intermittent irrigation.
- 38. References • Harrisons principlesof internal medicine.19th edition • API Medicine Update – 2016-1 • National Drug Policy on Malaria – 2013. Directorate of National Vector Borne Disease Control Programme. Govt. of India. New Delhi. 2013
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