Main » Infectious diseases » Arthropod-borne Infection » Malaria
Distribution map of malaria. In spite of intensive control measures over the last 20 years, malaria is still widely distributed in the tropics and subtropics. Anopheles gambiae is the most dangerous malaria vector in tropical Africa. It breeds in small temporary collections of fresh surface water exposed to sunlight and in such sites as residual pools in drying river beds. Most important vectors in other parts of the world are also surface water breeders. Successful malaria control operations in recent years have been based largely on the destruction of house haunting anopheline vectors by spraying DDT and other insecticides on the interior walls where mosquitoes usually rest before and/or after feeding.
Photo 1. Bromeliad leaf axils, sites for specialised larvae. Some South American vectors of the subgenus Anopheles (Kerteszia) are found in bromeliads. Control of these larvae by insecticides is extremely difficult.
Photo 2. Anopheline pupa hatching.
Photo 3. Female anopheline biting. Malaria is transmitted by female Anopheles mosquitoes. Most species bite indoors at night but some are outdoor feeding. The adults are recognised by the antennae and palps(x4).
Photo 4. Life cycle of the malaria parasite.
Male gametes develop by exflagellation from microgamétocytes in the midgut of the female Anopheline. ( x 900)
Photo 5. Ookinetes in midgut. Male and female gametes fuse to produce motile ookinetes which enter midgut epithelial cells. (x 900)
Photo 6. Scanning electronmicrograph of oocysts outside anopheline midgut. Infective stages (sporozoites) develop in oocysts which lie on the outside of the mosquito midgut. (X 125)
Photo 7. Living infective sporozoites.
Sporozoites emerge from the oocysts and enter the insect's salivary glands. They are passed into the skin with saliva when the mosquito next takes a blood meal. (x 350)
Photo 8. Exoerythrocytic schizont in liver. Within 30 minutes the sporozoites enter the parenchymal cells of the host's liver where they form large 'tissue' schizonts. These mature in six to 14 days according to the species, liberating daughter cells called merozoites. (Giemsa - colophonium technique x 350).
Photo 9. Electronmicrographs of trophozoites and mature schizont of rodent malaria parasite in red cell.
The merozoites form asexual parasites which grow inside erythrocytes to form the trophozoites). These feed on red cell contents producing insoluble pigment (haemozoin) as a waste product.
Photo 10. Electronmicrographs of trophozoites and mature schizont of rodent malaria parasite in red cell. When growth is complete the parasites undergo cell division (schizogony) and the daughter cells, after rupture of the host, invade new red cells, (x 11000)
Photo 11. Malarial anaemia.The growth of intraerythrocytic parasites leads to disruption of the host cells. This (and possibly also auto-immunity) results in severe haemolytic anaemia. Jaundice can also occur.
Tetrian and quartan fever patterns. The asexual blood stages of P. falciparum. P. vivax and P. ovale require 48 hours to complete their schizogony. Fever is produced when the schizonts mature, ie at 48 hour intervals. This gives the classical tertian periodicity which is however uncommon in a primary attack of P. falciparum malaria. P. malariae requires 72 hours and is associated with quartan fever, ie 72 hours between paroxysms.
Photo 12. New Guinea child with grossly enlarged liver and spleen. Haemolysed red cells and parasite debris are phagocytosed by macrophages particularly of the spleen and liver which become enlarged. This child was seen on a field survey.
IgG increase in malaria. The characteristic immunological response is an increase in the IgG level. Cellular immunity also plays an important role.
Photo 13. Preparation of blood films. Diagnosis of malaria is based primarily on the recognition of parasites in well prepared thick and thin blood films stained with a Romanowsky stain (Giemsa, Leishman, Field, etc) at pH7.2-7.4. A small drop of blood from finger or ear is placed on a clean slide.
Photo 14. Preparation of blood films.The thin film is made by pulling a second slide away from the drop.
Photo 15. Preparation of blood films. Spreading the drop for a thick film.
Photo 16. Preparation of blood films. Comparative thicknesses of thin and thick films.
Photo 17. Life cycle of the blood stages.
Fine rings (17) predominate, mature trophozoites and schizonts (18) appearing uncommonly in the peripheral circulation because parasites mature in capillaries of the internal organs. Host cells are not enlarged. Spots of irregular shape and size (Maurer's dots) may be seen in older rings (19). Crescent-shaped gametocytes ( ♂ 20 ♀21b) are diagnostic. (Giemsa x 1800)
Photo 18. Life cycle of the blood stages (2).
Photo 19. Life cycle of the blood stages (3).
Photo 20. Life cycle of the blood stages (4).
Photo 21. Life cycle of the blood stages (5).
Photo 22. Thick blood film. Usually only young rings are seen in acute infections sometimes in very large numbers.
Photo 23. Heavy parasitaemia leads to severe haemolytic anaemia. Gametocytes appear about a week after the onset of the illness. (Field X 1800)
Photo 24. Black urine and serum taken during course of ilness. An acute haemolytic crisis resulting in haemoglobinuria occasionally occurs in severe attacks (Blackwater fever). Haemoglobinuria can also be drug induced in patients deficient in the enzyme glucose 6-phosphate dehydrogenase (G-6-PD). A = normal urine; B = patient's urine; C = patient's urine, diluted; D = normal serum; E = patient's serum.
Photo 25. Complications of malignant tertian (falciraum) malaria. A Acute renal failure. Peritoneal or haemodialysis are life saving measures. B Coma in cerebral malaria. This is one of the commonest and most lethal complications. Confusion is an early warning sign.
Photo 26a. In first infections the fever is usually irregular rather than tertian. No relapses occur after adequate treatment with blood schizontocides since no secondary liver schizogony takes place in this species (cf P. vivax).
Photo 26b. Temperature chart.
Photo 27. Gross section of brain in cerebral malaria.
Cerebral malaria results when cerebral capillaries are blocked by developing falciparum schizonts. Consequent capillary endothelial damage results in 'ring' haemorrhages. Cerebral malaria is a medical emergency which demands immediate treatment by intravenous administration of suitable antimalarials, eg quinine. Rehydration is often also needed, but overhydration may result in pulmonary oedema.
Photo 28. Microscopic section of brain ( x 100) .
Photo 29. Liver and spleen in chronic malaria. In chronic infection accumulation of malaria pigment (haemozoin) produces a dark brown coloration of liver and spleen.
Photo 30. Liver and spleen in chronic malaria(2).
Photo 31. Placental smear with falciparum schizonts and macrophage. The accumulation of falciparum schizonts in the maternal side of the placental circulation may result in the delivery of underweight infants especially in primigravidae. True congenital malaria is very rare. (Giemsa x 600).
Haemoglobin S distribution map. It is now generally recognised that haemoglobin S (AS) diminishes the severity of falciparum malaria, thus favouring the survival of the gene in tropical Africa ('balanced polymorphism').
Distribution map of chloroquine resistance. In the areas shown falciparum malaria may not respond to prevention or treatment with chloroquine and alternative drugs may have to be used.
Photo 32. Life cycle of the blood stages. All stages of asexual parasites from young trophozoites to schizonts appear in the peripheral circulation together with gametocytes.
Photo 33. The parasites are large and amoeboid, and produce schizonts with about 16 daughter cells (merozoites). In the areas shown falciparum malaria may not respond to prevention or treatment with chloroquine and alternative drugs may have to be used.
Photo 34. Thick blood film. Pigment is well developed.
Photo 35. Host red cells are enlarged and uniformly covered with fine eosinophilic stippling (Schiiffner's dots). Gametocytes are round, the male or microgamétocytes being about seven µm and the (36) ten µm or more in diameter. (Giemsa x 1800)
Photo 36. Female or macrogamétocytes.
Photo 37. Thick blood film. All stages may be present. Parasitaemia is often less heavy than in falciparum malaria. The parasites seen here are all in a single thick film. In the thicker part are seen an amoeboid trophozoite (99a), and a schizont (99b).
Photo 38. Thick blood film — schizont.
Photo 39. Often the Schiiffner's dots can be seen in 'ghost cells' in the thinner parts of the film where the host cell has been haemolysed.
Photo 40. There are seen three trophozoites and a macrogamétocyte. (Field x 1800)
Diagram of relapse patterns in vivax malaria. Relapses in vivax malaria are due to emergence of new blood forms from maturing secondary liver schizonts. In tropical areas relapses may arise within three to four months of a primary attack, but in subtropical areas usually only after nine months or more. A - Clinical symptoms; B - Overt parasitaemia; C - Subpatent parasitaemia; D - Primary and secondary tissue stages in the liver; E - Sporozoite infection; F-Exoerythrocytic schizogony; G - Radical or spontaneous cure; H - Microscopic threshold J - Clinical (pyrogenic) threshold rising with the increased immunity ; 1 - Incuba tion period; la - Pre-patent period; 2 - Primary attack composed of paroxysms 3 - Latent period (clinical latency); 4 - Recrudescence (short-term relapse) 5 - Latent period; 5a - Parasitic latency; 6 - Clinical recurrence (long-term relapse) followed by parasitic recurrence; 6a - Parasitic relapse.
Photo 41. Life cycle of the blood stages.
The parasites differ from P. vivax in being more compact, and producing about eight merozoites at schizogony (43). Host red cells contain Schiiffner's dots and tend to be ovoid and fimbriated. Diagnosis is difficult in thick films in which the parasites are easily confused with P. malariae (cf 114 & 111). As in P. vivax 'ghost cells' may be seen in thinner parts of the thick film but the contained P. ovale are more compact (cf 114 with 100). Relapses occur as in P. vivax but the disease tends to be more chronic. (Leishman x 1800)
Photo 42. Life cycle of the blood stages (2).
Photo 43. Producing about eight merozoites at schizogony.
Photo 44. Life cycle of the blood stages. All stages appear in the peripheral circulation from young trophozoites to compact schizonts with eight merozoites.
Photo 45. Band forms' are common. With special staining a very fine stippling (Ziemann's dots) is sometimes seen. Host red cells are not enlarged.
Photo 46. The compact schizonts in thick blood films.
Photo 47. The males of gametocytes.
Photo 48. Gametocytes are round and compact with distinct blackish pigment, the females usually staining a bluer colour, and the males (47) somewhat mauvish. (Leishman x 1800).
Photo 49. Younger parasites are easily recognised by their heavy pigment which may obscure the inner structure of older trophozoites and gametocytes (51). Schizonts containing about eight merozoites with a central mass of pigment (50) are characteristic. All stages are very similar to those of P. ovale, which can sometimes be identified if these parasites (114) can be found at the periphery of the thick film in 'ghost cells'. (Field x 1800)
Photo 50. Schizonts containing about eight merozoites with a central mass of pigment.
Photo 51. Older trophozoites and gametocytes.
Photo 51b. Identification of Schizonts at the periphery of the thick film in 'ghost cells'.
Photo 52. Ultrastructure of P. malarie trophozoite. Very small but regular bosses OCCur on the surface of the host erythrocyte (possibly corresponding to the Ziemann's dots). (X 11000)
Photo 53. Nephrotic child with P. malarie infectijn. A close association has been established between quartan malaria and the nephrotic syndrome in children. Note the gross oedema and ascites.
Photo 54. Immunofluorescence of immune complexe in kidney. Immunofluorescent antibody techniques have demonstrated the deposition of immune complexes on the basement membrane of the glomeruli in 'quartan malarial nephrosis', (x 350)
Photo 55. Tropical splenomegaly syndrome (TSS). Gross enlargement of the spleen is a characteristic feature of the tropical splenomegaly syndrome (TSS). The syndrome is thought to be due to an abnormal immunological response to malaria infection. High IgM levels are invariably found. Note scars due to application of indigenous medicines.
Photo 56. Massive spleen in TSS. Massive spleen in TSS Regression of the enlarged spleen occurs when longterm antimalarial therapy is given.
Photo 57. Section of liver in TSS. Section of liver in TSS Liver biopsy shows hepatic sinusoidal dilatation with marked infiltration of lymphocytes and hypertrophy of the Kupffer cells. (x500)
Photo 58. Generalised life cycle.
The figure is based on the life cycle of P. vivax and P. ovale. Sporozoites (2) injected by the mosquito enter liver parenchyma cells where they grow into the first generation of pre-erythrocytic schizonts (3). These give rise to cryptozoites which invade red blood cells, to develop into the asexual erythrocytic cycle (4). Some sporozoites in the hepatocytes stay dormant (H = hypnozoite) to mature after an interval of weeks or months into secondary exo-erythrocytic schizonts (3a, 3b). The successive waves of cryptozoites emerging from these give rise to relapse infections in the blood after months or years. Some blood stages mature to form sexual forms, the macro- and microgamétocytes (5). These enter the mosquito where the males exflagellate to fertilise the females (6). The ookinete thus produced forms oocysts on the outside of the midgut (7). Sporozoites (8 & 9) develop in the oocysts. The sporozoites enter the mosquito salivary glands (2) where they are ready to infect a new host. (In P. falciparum and P. malariae stages 3a, 3b do not exist and true relapses do not occur.)
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