Learning objectives At the end of this unit, the students will be able to know about: Epidemiological aspects of blood, and tissue sporozoan Life cycle and pathogenesis of each blood, and tissue sporozoan Necessary laboratory procedures for the detection and identification of blood, and tissue Sporozoa.

1. Blood and tissue Apicomplexa (coccidia)
Learning objectives
At the end of this unit the students will be able to:
• Describe the epidemiological aspects of blood & tissue sporozoa
• Discuss the characteristics of each blood & tissue sporozoa
• Explain the life cycle and pathogenesis of each blood & tissue
sporozoa
• Apply the necessary laboratory procedures for the detection and
identification of blood & tissue sporozoa
1

2. Outline
• Blood and tissue sporozoa
• Summary of taxonomic classification of protozoa
• blood and tissue sporozoa
• For each species:
Epidemiology , morphology, transmission life cycle ,
pathogenesis, clinical features, laboratory diagnosis
treatment, prevention& control
2

3. classes
• Found inside blood , blood forming
organs or tissues
• Blood and tissue sporozoa include
• Plasmodium species
• Babesia species
• Toxoplasma gondi
• Intestinal coccidian
3

4. Plasmodium species
• Causative agents of malaria: an acute and/or chronic infection
caused by protozoans of the genus Plasmodium
• Five plasmodium species cause human malaria
– Plasmodium falciparum (P. falciparum)
– P. vivax
– P. malariae
– P. ovale
– P. knowlesi
4

5. • Widespread species
• P. falciparum: most prevalent in the hotter and
more humid regions of the world.
• P. vivax: more common in temperate region than
in the tropics
• Less widespread species
P. malariae: confined mainly to tropical Africa (25%)
P. Ovale: Low & restricted distribution
 Occurs primarily in tropical west Africa (10%)
5

6. General feature of Plasmodium species
• Obligate intracellular parasites (liver cell & RBC)
• Life cycle
– Alternation of generation ~ alternation of hosts
– Requires two hosts:
 Man (IH)
Female Anopheles mosquitoes (DH)
• Sexual and asexual reproduction
• No animal reservoir host except for P. malariae?, P. knowlesi
6

7. History of Malaria
• Known since antiquity (oldest diseases to mankind )
– Early medical writings from India and China - periodic fever
malaria
– Hippocrates described symptoms (500 BC)
– Italians – named mal aria (bad air) in 17th century
– Laveran identified parasites (1880)
– Ronald Ross demonstrated mosquito transmission (1898). He
observed parasite forms in mosquito stomach cells.
7

8. …
– P. falciparum described by Welch in 1897 and Schaudinn in 1902
– P.vivax described by Grassiand and Felletti in 1890 and Labbe in
1989
– P. malariae described by Laveran in 1881 and Grassiand and
Felletti in 1890
– P.ovale described by Stephens in 1922
– Garnham described liver stage in1940’s
– WHO Launch worldwide malaria eradication in 1955
8

9. Burden of malaria
According to the 2017 malaria report by WHO (from 91 countries),
• There were 219 million cases of malaria worldwide
• The WHO African Region accounted for most global cases of
malaria (200 million, 92%)
• There were an estimated 435 000 malaria deaths worldwide (266,
000, 61% were under 5 children).
• Most of these deaths occurred in the African Region (93%)
Ethiopia
• Reported confirmed cases (health facility): 1,530,739
• Reported deaths: 356 9

10. 10

11. …
• Plasmodium species in Ethiopia
– P. falciparum =60%
– P. vivax = nearly 40%
– P. malariae =1% cases ,focal distribution like in Humera
– P. ovale = less than 1% cases , found in Setit Humera ,
Gambela & Arbaminch
Epidemiology of Malaria in Ethiopia
The risk of malaria varies highly from season to season and from place
to place
Transmission- Seasonal (Unstable)
– Mainly depends on rain fall and Temp
11

12. ….
Characteristics of stable malaria:
• ~ Constant incidence over several years
• Includes seasonal transmission
• Immunity and disease tolerance developed by adults
• Usually affects children
Characteristics of unstable malaria:
• Malaria incidence varies from day to day, week to week, month to
month, year to year.
• Communal immunity of the population low.
• Makes the region prone to malaria epidemics.
• High morbidity and mortality
12

13. 13

14. …
• Two major transmission periods in Ethiopia
– Major - September to December after main rainy season
– Minor- April to June following small showers of rain in autumn.
• Dega zone(> 2,500 m) mean annual temperature of 10-150C , is malaria
free
• Weyna dega zone( 1,500 - 2,500 m) mean annual temperatures range from
15-20o c
• Malaria most often occurs below 2,000 meters, with short-lived
transmission following the rains
• Kolla zone (< 1,500 m), mean annual temperatures are 20-25oc, malaria
transmission is endemic
14

15. …
Terms: endemic, epidemic, sporadic, pandemic
• Endemicity: defined in terms of parasitemia rates or palpable
spleen rates in children 2 to 9 years of age as
– hypoendemic (<10%)
– mesoendemic (11 to 50%)
– hyperendemic (51 to 75%)
– holoendemic(>75%)
 Hyperendemic and Holoendemic malaria are found in areas of
stable malaria transmission
 Hypo and Mesoendemic : are found in areas of unstable malaria
transmission
15

16. Transmission and life cycle of malaria
• Principal mode of transmission
– Bites of female anopheles mosquito
60 species of mosquito
Sucks the gametocytes during blood meal
Bites between 5 PM and 7 AM, with
maximum intensity at midnight.
• In Ethiopia : A.gambiae, A.funestus, A.nili,
A.arabiensis & A.pharonensis are main vectors
A. arabiensis is responsible for most epidemics in the
country
Anopheles
• …
16

17. 17

18. 18

19. Life Cycle:
19

20. Other modes of transmission
1. Blood transfusion (Transfusion malaria):
Donor blood should be screened
2. Blood transfusions malaria
– Infective stage-trophozoites/merozoites
– shorter incubation period,because no exo-erythrocytic shizogony
– No relapses possible (vivax/ovale)
– Clinical features & management of cases are the same as naturally
acquired infection
3. Mother to the growing fetus (congenital malaria)
– Occurs in 5 % of new borne whose mothers are infected
– Relatively rare although placenta is heavily infected
– Congenital malaria is more common in first pregnancy, among non -
immune populations
4. Needle stick injury:
– Accidental transmission can occur among drug addicts who share
syringes and needles
20

21. Clinical Features & Pathology
Characterized by acute febrile attacks (malaria paroxysms)
• Caused by the release of toxins (when erythrocytic schizonts
rupture) stimulate the secretion of cytokines from leucocytes
and other cells
Manifestations and severity depend on parasite species,
parasitemia and host status, i,e immunity, general health, nutritional
state, genetics
21

22. …
Prodromal Symptoms
Malaria paroxysm preceded by Prodromal period
– 2-3 days before 1st paroxysm
– Includes: malaise, fatigue, headache, muscle pain, nausea,
anorexia (i.e., flu-like symptoms)
– Can range from none to mild to severe
Febrile Attack (Malaria Paroxysm), 4-8 hr
• Periodic febrile episodes alternating with symptom-free periods
• Initially fever may be irregular before developing periodicity
• May be accompanied by splenomegaly, hepatomegaly (slight
jaundice), anemia
• P. falciparum can be lethal in non-immune cases
• Paroxysms comprise of three successive stages: cold stage, hot
stage and sweating stage
22

23. 23

24. cold stage
• Feeling of intense cold
• Vigorous shivering, rigor
• Lasts 15-60 min
24
hot stage
• Intense heat
• Dry burning skin
• Throbbing headache
• Lasts 2-6 hours
sweating stage
• Profuse sweating
• Declining temperature
• Exhausted, weak  sleep
• Lasts 2-4 hours

25. • Paroxysms associated with
synchrony of merozoite release
• Between paroxysms
temperature is normal and
patient feels well
• Falciparum may not exhibit
classic paroxysms
• continuous fever
• 24 hr periodicity
25
Tertian malaria

26. Complications of acute malaria
Malaria caused by P. falciparum
 Without treatment, P.vivax, P. ovale and P. malaria ultimately may result
in spontaneous cure
 P. falciparum can develop severe complications
 Almost all deaths are due to falciparum malaria
 Falciparum/subtertian/malignant malaria
Factors for Malignancy of P.falciparum
• Rapid multiplication
• Infected red blood cells become "stick“ (cytoadherence)
• Infects all age group of red blood cells
• A single red blood cell can be infected by more than one parasite
• Erythrocytic schizogonic reproduction takes place in the deep capillaries
of organs such as brain, lung, heart, spleen, bone-marrow, placenta,
intestine.
26

27. 1.Higher Parasitemia in Falciparum
Malaria
• all erythrocytes invaded
• up to 32 merozoites
• Pv/Po = reticulocytes
• Pm = senescent RBC
P.falciparum.
-Up to 30-40% of RBC
- sever if > 5% RBC are infected.
P.vivax & P.ovale rarely exceeds 2%
P.malariae. Usually < 1%
Pathogenecity of P. falciparum
27

28. 28

29. Sequestration
Hypothesis
cytoadherence

cerebral ischemia

hypoxia, metabolic effects

coma

death
29

30. Severe falciparum Malaria
Complications
Features Indicating Poor
Prognosis
Cerebral malaria
Black water fever
Anemia
Hypoglycemia
GI and liver syndromes
Pulmonary edema
Algid malaria (shock)
Hyper-reactive malaria
splenomegaly (Tropical
splenomegaly syndrome)
impaired consciousness
repeated convulsions
respiratory distress
shock
acidosis/hyperlactemia
hypoglycemia
jaundice or other liver
malfunctions
renal impairment
high parasitemia
(>500,000/mm3)
30

31. Hyper-reactive malaria splenomegaly
31

32. Predisposing factors for complications of P. falciparum malaria
1. Extremes of age.
2. Pregnancy, especially in primigravidae and in 2nd half of pregnancy.
3. Immunosuppression - patients on steroids, anti-cancer drugs,
immunosuppressant drugs
4. Splenectomy.
5. Lack of previous exposure to malaria (non-immune) or lapsed
immunity
6. Pre-existing organ failure.
32

33. Genetic factors that Provide Protection Against Malaria
1. Nature of hemoglobine
– Hgb S (Sickle cell anemia trait) –P.f
– Thalassemia Hgb-P.f
– Fetal Hgb – all spp.
– Hgb E – P.v
2. Enzyme content of erythrocyte
– Glucose-6-phosphate dehydrogenase deficiency ,-P.f
3. Presence or absence of certain factor
– Ovalocytosis -P.f & P.v
– Duffy blood group antigens negative RBCs-P.v
33

34. Laboratory diagnosis
Clinical Diagnosis
Microscopic
•Thin film
•Thick film
• BC/QBC
Immunological
Ag /enzyme… RDT
Ab…..ELISA
Molecular
PCR
Malaria Diagnosis
MALALRIA Diagnostic approaches
34

35. Microscopic examination of blood film
Materials Required
35

36. Blood Sample Collection : Capillary Blood
• The ideal sample as the density of trophozoites or schizonts is
greater in blood from capillary-rich area.
• Obtained by pricking a fingertip or big toe
• For adults:
 the lateral side of the 3rd or 4th finger is best.
• For infants :
 the big toe is preferred.
36

37. Procedure for collecting finger prick blood
37
Transferring of blood to slide
Thick and thin blood film preparation

38. Qualities of Good Thin Blood film
– Uniformly spread over the slide
– Thin enough so that It is tongue shaped
– Consists of a single layer of RBCs
– Feathery end
Qualities of Good Thick Blood film
– It should be 10 mm away from the edge of the slide
– Rectangular or round in shape with a diameter of about 10 mm
– News print read under thick film before staining
– Its thickness contains 10 layers of RBCs
– At least 10-12 WBCs should be visible / 100x field.
38

39. Common Mistakes in Making Blood Films
1. Too much blood
2. Too little blood
3. Blood films spread on a greasy slide
4. Edge of spreader slide chipped
5. Badly positioned blood films
39

40. Fixation
Fixation methods
Done for 10-20 seconds using one of these three methods:
1. Dropping absolute methanol while holding the slide with the
thin portion down
2. Dipping in a jar containing absolute methanol.
3. Dabbing it with cotton wool dampened with methanol
Note: Avoid methanol, or its fumes encountering the thick film.
40

41. Staining: Romanowsky stains
The main components of a Romanowsky stain are:
1. A cationic or basic dye such as azure B/methylene blue
– which binds to anionic sites and gives a blue-grey colour to nucleic acids
(DNA or RNA), nucleoproteins, granules of basophils , malaria cytoplasm and
weakly to granules of neutrophils
2. An anionic or acidic dye such as eosin Y
– which binds to cationic sites on proteins and gives an orange-red colour to
haemoglobin , chromatin dot of malaria parasite and eosinophil granules.
Giemsa stain, Field’s stain, Leishman’s stain , Wright’s stain…
41

42. Giemsa stain
• Giemsa stain is an alcohol-based Romanowsky stain.
• Is a mixture of eosin, which stains parasite chromatin and stippling
shades of red or pink, and methylene blue, which stains parasite
cytoplasm blue.
• White-cell nuclei stain blue to almost black, depending on the
type of white cell.
• The recommended stain for identification of malaria parasite.
• Composed of giemsa powder, Absolute methanol and Glycerol
42

43. Staining blood films
There are two methods of staining with Giemsa stain:
1. The rapid (10%) method
2. The slow (3%) method.
• The rapid method is used in laboratories where a quick
diagnosis is an essential part of patient care.
• The slow method is used for staining larger numbers of slides,
such as those collected during cross-sectional or
epidemiological surveys and field research.
43

44. …
1. The rapid (10%)methods
• Filter the stock Giemsa solution
• Prepare fresh 10% (1:10 ratio) working Giemsa stain solution
– Add 10ml of Giemsa stock solution to 90 ml of buffered
distilled water or 5ml to 45 ml of buffered distilled water
• Pour the diluted solution into a staining jar
• Immerse completely dried slides in a jar.
• Make sure that the stain cover the entire surface of films on the
slide.
44

45. …
• Leave the slides in the stain
for minimum of 10 minutes.
• Wash the stain in a jar
containing water.
• Remove the slides and
clean the back of each
slide with dry gauze.
45

46. Staining …
• Place the slides with the film side down wards in a
drying rack to drain and dry at room temperature.
• Make sure that the thick film does not touch the edge
of the rack.
46

47. Examining blood film
• Both thick and thin films should initially be examined with 10 x
and 40x to avoid missing large parasites such as microfilariae
and trypanosomes.
Required materials, reagents and equipments
47

48. Approach to examination of thick film
• Thick films are performed to
– To detect parasites
– To measure parasite density
• A slide can be pronounced negative only after examination of at
least 100 fields in thick film.
In nonimmune patients, symptomatic malaria can occur at lower
parasite densities, and screening more fields (e.g., 200, 300, or even
the whole film) is recommended.
48

49. Method
1. Place the stained slide on the mechanical stage.
2. Scan the entire film at a low magnification.
3. Examine the film using the 100× .
4. Select an area that is well-stained, free of stain precipitate, and
well-populated WBCs (10-12WBCs/field).
5. Move the blood film following the pattern shown in the diagram.
6. If you see parasites, make a tentative species determination on
the thick film and then examine the thin film to confirm the
species present.
49

50. Examining the thin film
• Thin films are examined for
– Species identification
– Quantification e.g. Percentage of infected red cell
– Useful in high parasitaemia.
– Difficulty in examination of thick film.
• Since it takes more time (~10 x) as compared to examination of a
thick film, routine examination of thin films is not recommended.
50

51. Method
1. Place a drop of immersion oil on the edge of the middle of the film.
2. Scan using low magnification. if this has not been done on the thick
films.
3. Carefully examine the film using the 100× .
– If doubtful diagnosis examine more fields
51

52. Identification of malaria parasite species and stages
using Romanowsky stains
– Chromatin: Round in shape and stains red.
– Cytoplasm : Form a ring shape to a totally irregular shape and
stained blue.
– Malaria pigment: Shades from yellow – gold through brown to
black
– Stippling: stains in shades of pink which vary among different
species
– Vacuole: Non stained area of the parasite
52

53. Species differentiation on thin films
Feature P. falciparum P. vivax P. ovale P. malariae
Enlarged
infected RBC
No Yes Yes No
Infected RBC
shape
Round Round, distorted
Oval,
fimbriated
Round
Stippling in
infected RBC
Mauerer’s clefts Schuffner spots
Schuffner spots
(James’s dots)
Zieman’s dots
Trophozoite
shape
Small ring,
Delicate
Large ring,
amoeboid
Large ring,
compact
Small ring,
compact
Chromatin dot Often double Single Single Single
Mature
schizont
Rare, 12-32
merozoites
12-24 merozoites 4-12 merozoites 6-12 merzoites
Gametocyte Crescent shape large, round large, round compact, round
53

54. Species differentiation on thick films
Feature P. falciparum P. vivax P. ovale P. malariae
Uniform trophozoites + +
Fragmented
trophozoites
++ +
Compact trophozoites + +
Pigmented
trophozoites
+
Irregular cytoplasm + +
Schizonts visible Very rarely Often Often Often
Gametocytes visible Occasionally usually usually usually
54

55. Artefacts
– Vegetable spores, yeast, pollen, algae and
bacteria in the stain or on the slide
– Platelets
– Howell-jolly, Cabot ring bodies in anaemic
patients
– Ghosts of immature red cells mimicking
Schüffner’s dots.
55

57. Plasmodium falciparum
Diagnostic points:-
• RBCs not enlarged.
• Maurer’ dot may be present
• No Schuffener’s dot
• Rings appear fine and delicate
• May be several in one cell.
• Some rings with 2 chromatin
dots.
• Presence of marginal or appliqué
forms/acolle formation/.
• Gametocytes crescent/banana
shape
• Usually trophozoites +
gametocytes seen
• Schizont rarely seen
57

58. Plasmodium vivax
Diagnostic points:-
• RBCs are usually enlarged.
• Schuffner's dots are
frequently present in the
red cells.
• The mature ring forms tend
to be large and coarse.
• Trophozoites, schizonts &
gametocytes seen
• Developing forms are
frequently present
58

59. Plasmodium ovale
Diagnostic points:-
• Red cells enlarged.
• Comet forms common
(top right)
• Rings large and coarse.
• Schuffner's dots, when
present, may be
prominent.
• Mature schizonts similar
to those of P. malariae
but larger and more
coarse .
59

60. Plasmodium malariae
Diagnostic points :-
• RBC not enlarged
• Ring forms may have a
Squarish appearance.
• Band forms are a
characteristic of this
species.
• Mature schizonts may
have a typical daisy head
appearance with up to
ten merozoites.
60

61. Estimating Parasitaemia
• Important for clinical purposes
– To monitor the progress of the disease and
– The efficacy of therapy.
• Methods
1. Number of parasites/µL of blood (thick film)
2. Number of parasites/µL of blood (thin film)
3. Proportion of parasitized erythrocytes (thin film)
4. Semi quantitative count (thick film):
61

62. 1. Number of parasites/µL of blood
(thick film):
• Requires observation of at least 100 fields
while you count 200 WBCs.
•Number of asexual parasites and WBCs
should be counted in each field until the
number of WBCs reaches 200.
• If number of WBCs is unknown, it can be
assumed to be 8000/µL

63. Example:
• Patient WBC = 8000/ µl
• Parasite count against 200 WBCs = 650
• Parasite count/µl = 650 x 8000/µl
200
= 26 000 parasites/µl
63

64. 2. Number of parasites/µL of blood (thin film)
• Requires the preliminary determination of RBCs number present in the
average microscopic field.
• The number of asexual parasites is counted in at least 25 microscopic
fields.
• The number of RBCs in the average microscopic field is about 200, so total
RBCs counted in 25 fields is about 200 x 25 = 5000.
• RBCs/µl is assumed to be 5 millions/µl for males and 4.5 millions/µl for
females.
64

65. Example:
• Parasite counted against 5000 RBCs/25 fields/= 50
• # of RBCs in 25 fields= 5000
• RBC count = 5 million/Male patient/µl
50 x 5,000,000
5000
• 50,000/µl of blood.
65

66. 3. Proportion of parasitized erythrocytes (thin
film):
• Indicate the percentage of erythrocytes that are
infected by malaria parasites.
• The number of parasitized erythrocytes (asexual
forms) present in 25 microscopic fields is counted
divided by the total number of erythrocytes present
in these fields (about 5000), and multiplied by 100.
66

67. Example
– Average # of RBCs/25 fields=5000
– # Parasitized RBCs/25 fields=100
– % of parasitized RBCS= 100 X 100
5000
– 2% of RBCs are infected with asexual for of
malaria parasite.
67

68. 4. Semi quantitative count (thick film):
• Very quick but less accurate.
• Used only when not possible to perform more
accurate methods.
• Reporting:
– + 1-10 asexual parasites / 100 thick film fields
– ++ 11-100 asexual parasites / 100 thick film fields
– +++ 1-10 asexual parasites / single thick film field
– ++++ > 10 asexual parasites / single thick film field
68

69. Reporting of BF results
If positive :
• Check the presence of
• Different stages (Throphozoits, schizonts and
gametocytes).
• Mixed infection
• Report the species, stage and density of parasites and if
present malaria pigments .
• If negative after examination of a minimum of 100 thick film
fields, Report No parasite or hemoparasite found.
69

70. 12/23/2023 70
RDT (Antigen detection tests)
WHO Recommended:
Prompt parasitological confirmation of all malaria suspected
patients
Treatment solely on the basis of clinical suspicion should only be
considered when a parasitological diagnosis is not accessible
RDT
• Detects specific antigen derived from blood stage parasites
• Good alternative in the absence of microscopy
• Sensitivity & specficity of RDT is comparable to filed microscopy
• Improves diagnosis and quality of patient care

71. Formats of RDT
1. Cassette –
• Expensive but safe and
easy to use
• Widely used
2. Card
3. Strip /Dipstick/
71

72. 12/23/2023 72
12/23/2023 7:22:50 AM 72
Rapid Diagnostic Tests: Target Antigens
1. HRP II (Histidine-Rich Protein II)
- produced by P. falciparum only
- Target for Pf only RDTs
- persists after parasite death
2. pLDH (parasite Lactate Dehydrogenase enzyme)
- produced by all Plasmodium species
- D/t isomers of pLDH for each species
- Target for combination RDTs
- Closely reflects parasite viability
3. pan-specific Aldolase ~ found in all spp.
- Monoclonal antibodies are pan-specific
- Closely reflects parasite viability
72

73. 12/23/2023 73
12/23/2023 7:22:50 AM 73
• Dye-labeled antibody is pre-deposited on nitrocellulose strip.
• Bound Ab specific for target antigen (Ag) is bound on the test line
• Ab specific for dye labeled Ab is bound at the control line.
unbound
labeled Ab
bound Ab
RDT mechanism of action…
Dye labeled Ab
Test band
(bound Ab)
Control band
(bound Ab)
73

74. 12/23/2023 74
12/23/2023 7:22:50 AM Sindew M / EHNRI 74
Parasite Ag captured
by labeled Ab
buffer
Parasitized
blood
Blood and labeled Ab flushed along strip
• Blood is lysed with buffer to release more Ag
• Parasite antigen binds to the labeled antibody.
• Buffer flushes labeled Ag-Ab complex along the test strip.
Mechanism …
74

75. 12/23/2023 75
12/23/2023 7:22:50 AM Sindew M / EHNRI 75
• Some labeled Ag-Ab complex is trapped on the test line
• Excess labeled Ab is trapped on the control line
Labeled Ag-Ab
complex captured by
bound Ab at test line
Labeled Ab
captured by
bound Ab of
control band
Captured labeled
Ag-Ab complex
Captured
labeled Ab
Mechanism …
75

76. 12/23/2023 76
RDT Interpretation
In PfHRP2/PMA and the pLDH tests
• Control line and pan specific lines positive
– Positive for non- Pf ( Pv, Pm and/or Po )
76
Color change on all 3 lines
Positive for Pf or mixed infection with non- Pf

77. 12/23/2023 77
Strengths and Challenges of RDT
Strengths
 Easy to use with minimal training
 Give rapid results & permitting immediate treatment in the site
 Do not rely electricity and special equipment
 Do not require refrigeration
 Uses whole blood
 Reinforce patient confidence in the diagnosis & health service
Challenges
• Costs per test exceed microscopy
• Short shelf-life,
• Requires effective transportation, storage and distribution systems
• Can’t estimate parasite density (qualitative test)
• Intensity of test varies with parasite density
• Undetermined quality- Can be affected at manufacturing, Testing, transport
and storage
• Inability to distinguish new infection (HRP2 targeted RDTs)
77

78. …
Supportive tests
• Measurement of haemoglobin or packed cell volume
• Measurment of blood glucose to detect hypoglycaemia
• Total white cell count and platelet count (severe falciparum
malaria)
• Testing urine for free haemoglobin if black water fever is suspected
• Blood urea or serum creatinine to monitor renal failure
• urine protein if nephritic syndrome is suspected
78

79. Treatment Strategies
chloroquine sensitive
• chloroquine
• CQ + primaquine (vivax/ovale)
chloroquine resistance (or unknown)
• mefloquine, quinine, artemisinin derivatives
severe malaria
• i.v. infusion of quinine or quinidine (or CQ, if sensitive)
• i.v. artemisinin derivatives
79

80. Prevention and Control
Reduce human-mosquito contact
•Impregnated bednets
•Repellents, protective clothing
•Screens, house spraying
Reduce vector density
•Environmental modification
•Larvicides/insecticides
•Biological control
Reduce parasite reservoir
•Case detection and treatment
•Chemoprophylaxis
Screen blood to be donated
80