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David P. Humber School of Biosciences University of East London

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1 David P. Humber School of Biosciences University of East London
Pathology of Malaria David P. Humber School of Biosciences University of East London

2 Learning Outcomes Know the parasites, vector & epidemiology
Understand of the life cycle Know the principal clinical features and pathology and the basis of diagnosis Appreciate the difficulties of control

3 The Problem At Risk Deaths Chemotherapy Vector control Vaccination
More than 40% of the world population Deaths More than 2 million per year Chemotherapy Limited Drugs & drug resistance Vector control Vaccination

4 The Parasite - Taxonomy
Phylum - Apicomplexa (Sporozoa) Class Haemosporidea (Sporozoea) Order - Haemosporidia Genus - Plasmodium

5 Species Infecting Humans
Common & Severe Rare & Mild Plasmodium falciparum Malignant tertian (Cerebral) Plasmodium vivax Tertian Plasmodium ovale Plasmodium malariae Quartan

6 Species Infecting Humans
Relapses Fevers No Yes No Rare & Mild Plasmodium falciparum Tropical Africa, Asia, Latin America Plasmodium vivax Worldwide Plasmodium ovale Tropical West Africa Plasmodium malariae Worldwide but very patchy

7 Epidemiology >400 million cases annually 3 million deaths
majority 2-5 years 103 endemic countries most in Africa most due to P.falicparum Need 15oCfor 4 weeks <300m 64oN to 32oS

8 Distribution of Malaria

9 Life Cycle Liver Schizont Sporozoite Trophozoite Oocyst RBC Merozoite
Ookinete Gametocytes

10 Infected Liver CellHepatocyte
Pre-erythrocytic schizonts

11 Erythrocytic forms (signet)
Young ring form trophozoites

12 Gametocytes P.falciparum Macro Micro

13 P. vivax produces 8 microgamentes
Exflagellation P. vivax produces 8 microgamentes in mosquito’s midgut

14 Clinical Features Pre-patent Period
Time taken from infection to symptoms P. falciparum 6-12 days P. vivax 10-17days P ovale 14 days P. malariae days

15 Clinical Features of Malaria
Cold stage hr Headache/shiver/rapid weak pulse Hot stage 6hrs Intense headache/nausea/thirst/distress Sweating stage 4hrs Profuse sweating Sleep! Prepatent period Flu-like initially Intermittent fever Recurrence Coma/death Chronic infection Relapses

16 Tertian Malaria - P. vivax & P. ovale
Rarely fatal- relapses common Prodrome myalgia, headache, chilliness, low grade irregular fever (no sync maturation cycle) 5-7 days - paroxysms on alternate days Spleen palpable days P. ovale milder with shorter initial attacks

17 Qartan Malaria - P. malariae
Paroxysms every third day Mildest and most chronic of the 4 immune complex nephropathy seasonal variation with P.f (wet season)

18 Falciparum Malaria Cause of virtually all malaria deaths
asynchronous cycle onset insidious - fever variable Rapid onset of splenomegaly Severe anaemia, jaundice, hyperventilation, cns dysfunction (delirium, stupor, coma)

19 Fever Charts

20 Untreated P. falciparum malaria
Sequestration - (schizogony completed) Bind to endothelia cells surface receptors eg ICAM1 - via membrane “knobs” with histidine rich protein Reduced in some individuals - splenectomy & genetic background Clumping also occurs (platelets involved?)

21 Site Specific Sequestration
Brain measurable reduction in blood flow Intestines diarrhoea Placenta intervillus space

22 Hepatosplenomegaly Hepatic dysfunction
Hyperplasia of splenic/liver macrophages Normally transient related to parasite load Tropical splenomegally Proportion of adult develop very large spleens Genotype/IR genes

23 Hepato-splenomegaly 10-15% die - survivors partially immune
often with splenomegaly

24 Cerebral Malaria Coma 6- 96 hours 20% fatality
shorter in children 20% fatality Hepatoslenomegaly common Retinal haemorrhages

25 Numerous small haemorrhages
Cerebral Malaria Numerous small haemorrhages of grey matter

26 Brain section - P. falciparum

27 Nephrosis Renal failure common in adults Transient Nephrosis
poor prognosis Transient Nephrosis all species Nephrotic Syndrome P. malariae - IC mediated

28 Nephrosis P. Malariae quarten nephrosis

29 Blackwater Fever Massive intra vascular haemolysis Mortality 20-30%
haemoglobinuria acute renal failure tubule necrosis parasitemia may be absent nonimmune or G6PD deficiency + treatment - autoimmuninty? Mortality 20-30%

30 Pregnancy Serious complication in pregnancy
maternal deaths, foetal death (x10) & foetal retardation Placental sequestration & clumping accumulation of intervillus macrophages & fibrin deposits

31 Section of Placenta

32 Diagnosis Clinical symptoms Stained fixed blood smear Blood
Regular fevers / possible exposure Stained fixed blood smear Thick film - presence/absence Thin film - morphology/species Blood Capillary - fluorescence Antigen capture PCR/Mabs

33 Chemotherapy Quinine Extract of tree bark used since 17th century
g/day for days Tonic water! Methylene blue pamaquine mepacrine

34 Synthetic antmalarials
Chloroquine Developed by Bayer in 1934 (toxic!) Rediscoved in the mid 1940’s selective uptake by food vacuole intefers with haem polymersiation/detox reactive oxygen species Resistance in humans early 1960’s

35 Other Antimalarials Proguanil - 1948 Primaquine - 1951
Pyrimethamine Cycloquanil Resistant strains by late 1960’s

36 Treatment v Prophylaxis
Monotherapy Treatment high dose short term Prophylaxis low dose long term

37 Immune Mechanisms Antibody blocks merozoite infection of RBC’s
passive transfer experiment in the Gambia Enhance clearance through opsonisation ADCC likely NK activity Decrease in circulating T cells Down regulation of T cell function Spleen - spleenectomy!

38 Cytokines IL1 TNF IL10

39 Stage specific Anti sporozoite antibodies in adults in endemic areas- blocks liver invasion Anti sporozoite/merozoite antibodies - block rbc invasion TNF blocks merozoite development Erythrocyte clearance - liver and spleen Block cyto-adherence

40 Immunomodulation Poly clonal T & B activation Immunodepression
auto antibodies - anaemia? Immunodepression humoral & cellular - T, B & macrophage

41 Immunopathology Fever Anaemia correlates with schizont rupture
IL1 & TNF Anaemia common complication exceeds parasitemia & may worsen after treatment T cell control of spllenomegally/bone marrow

42 Immunopathology 2 Cerebral malaria Glomerulonephritis
highly reversible Under T cell control - IL1/TNF Glomerulonephritis Not very common - acute nephritis reversed by treatment IgM, IgG & C3 - autoimmune? treatment mediated

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