Notes on Malaria in Children- MD5 - 2021.ppt

Malaria in pediatrics

1. 6/17/2024 Levina J. Msuya 1
MALARIA IN CHILDREN
Prof(Dr) L. J. Msuya
MD, MMED, Ped Endocrinologist.

2. Case -1
15 days old baby girl presented with inability
to breast feed, fever, vomiting. On physical
examination inactive baby, febrile T-39
0
C, and
pale mucous membrane, weight 3kg.
1.What might be the differential diagnosis?
2.How will you manage the baby?
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3. Case 2
A 10 years old child is brought unconscious. On
assessment GCS 5/15, febrile T-38.5
0
C, wt –25kg,
neck rigidity. mRDT result from referring hospital
was positive.
1.What is the provisional diagnosis?
2.Which investigations will you perform?
3.How will you manage the child?
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4. Outline
•Introduction
•Etiology
•Transmission
•Pathogenesis
•Clinical features
•Diagnosis
•Treatment
•Prevention
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5. Objectives
Be able to:
•Define malaria and how it is transmitted.
•Describe the pathogenesis of malaria.
•Outline the clinical presentation of malaria in
different age groups.
•Diagnose and treat uncomplicated and severe
malaria.
•Treat anemia in children.
•Describe the prevention and control of malaria.
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Introduction -1
•Name is derived from Italian Mal’ aria or bad air.
•A vector borne disease cased by protozoan
parasites.
•Malaria has been eradicated from Europe, most
of North America, USA, South America, Korea
and Japan.
•It is widespread in tropical and subtropical
regions, including parts of the America, Asia, and
Africa.

7. Introduction -2
•A parasitic acuteand chronicprotozoan
infection infecting red blood cells.
•Malaria continues to be most important cause
of fever and morbidity in the Tropical world.
•Most deaths occur in infants and young
children(6 months –5 years)
•P. Falciparum malaria may be life threatening.
•Exclude in every feverish traveler from the
tropics.
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Etiology
Intracellular Plasmodium protozoa transmitted to
humans by female anopheles mosquitoes
5 Species in human
•Plasmodium falciparum
•P. vivax
•P. ovale
•P. malariae
•P. Knowlesi -malaria in macaques but can infect
human.

9. Zoonotic malaria(other types)
•P. cynomolgi
•P. inui
•P. coatneyi.
•Inability to invade RBCs.
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11. •Relapse
oP.vivax and P.ovale
oAfter months –years
oDue to the presence of hypnozoitesin the liver
•Recrudescense
oP. falciparum and P. malariae
oIf blood stages are not completely destroyed by the
antimalarials, the persistent blood stage can cause re-
infection.
oInterval –months.
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Relapse& RecrudescenseMalaria

12. Transmission -1
The female anopheles mosquito is the vector for human malaria.
1. Vector transmission: Thefemale anopheles mosquito bites
man between 5 PM and 7 AM, with maximum intensity at
midnight.
2. Direct transmission: Blood transfusion (Transfusion malaria)-
can survive 14 days in blood bottles in –4
0
C.
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13. Transmission -2
3. Congenital transmission:Mother to the
growing fetus/newborn(via placenta)
4. Use of contaminated needle (stick injury)
oDrug addicts who share syringes and needles
Do not occur <16
0
C and >33
0
C
Do not occurs > 2000 meters altitude.
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14. Pathogenesis -1
•Man –Intermediate host.
•Mosquito –Definitive host.
•Sporozoites are infective forms.
•Present in the salivary gland of female
anopheles mosquito.
•After bite of infected mosquito sporozoites are
introduced into blood circulation.
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Pathogenesis -1
Several hypotheses
1.The sludging–RBCs with parasites stuck together
obstructing microcirculatory flow with release of
toxic materials.
2.The permeability –increase in cerebral capillary
permeability with outward leakage of plasma
leading to edema.

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Pathogenesis-2
3. The mechanical –microcirculatory obstruction –local hypoxia,
ischaemia.
4. Knobscontains at least 2 histidinerich proteins (parasites derived)
5. PfEMP-1 (P. falciparum erythrocyte membrane protein 1) is the most
on the surface of infected cells
6. ICAM 1 –rolling receptor for adherence of IRBCs espin the brain
7. CD36 –stable and stationary adherence of IRBCs

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Pathogenesis -4
Anemia
•Destruction of RBCs
•Sequestration of RBCs in the spleen and other organs
•Suppression of RBCs production of bone marrow
•Accelerated destruction of non parasitized RBCs
•Cytokines –TNF depress erythropoiesis
•RBCs survival is shortened
•Immune mediated hemolysis
•Lowered threshold for splenic clearance of abnormal
erythrocytes.

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Pathogenesis -5
Hypoglycaemia
•Increased peripheral requirement for glucose
•Increased metabolic requirement in febrile illness
•Parasite use glucose as their major fuel
•Failure of hepatic gluconeogenesisand glycogenolysis
(reduced supply)
•Hepatic glucogenexaustedrapidly in 2 days in adults, 12
hours in children
•Quinine stimulate βcells to secrete insulin and there is
decrease tissue sensitivity to insulin

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Pathogenesis -6
Cerebral malaria
•Sequestration of RBCs containing mature forms of the
parasites in deep vascular beds.
•Microcirculatory obstruction –decreased cerebral
blood flow, local hypoxia, ischaemia.
•Arterial lactate and cerebral lactate are increased
•Anaerobic cerebral glycolsisdue to cerebral hypoxia
and parasite glycolyticmetabolism.

20. Pathogenesis -7
Bleeding and Coagulation Abnormalities
•Due to thrombocytopenia and/or disseminated
intravascular coagulation.
•Mature parasitized red cells and cytokines activate
the coagulation cascade.
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21. Pathogenesis -8
TSS-hyperreactivemalarial splenomegaly)
•Repeated malarial infection
•Production of IgM-antisuppresorIg
•Inhibition of Suppressor T cells
•Uninhibited B-cell stimulation
•Overproduction of IgM and cryoglobulins
•Reticuloendothelial system overstimulation
•Progressive enlargement of spleen n liver
•Spleen -Massively enlarged
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Pathogenesis
Jaundice
•Hepatic dysfunction
•Sequestration in the hepatic microcirculation
•Liver blood flow is reduced
•Hemolytic, hepatic and cholestatic

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Pathogenesis
Black water fever(hemoglobinuria)
•Massive intravascular hemolysis
•G6PD def use of oxidant drugs –unable
to synthesize adequate quantity of
NaDPHthrough pentose shunt.

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Immunity
•Incomplete immunity occurs
•Subsequent severe disease is averted.
•Complete eradication or prevention of future
infection is not achieved.
•Malaria parasites circulates for a long time but
are prevented from multiplying and causing
severe illness.

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Malaria Case Definition

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Clinical features -1
Incubation period
•P. falciparum 9-14 days.
•P. vivax 12-14 days ( 6-12mo).
•P. ovale16-18 days.
•P. malariae18-40 days.
•Clinical manifestations vary according to
species, strain, and host immunity.

27. Affinity of parasite to Erythrocytes
•P. vivax –Young blood cells
•P. ovale–Young blood cells
•P. malariae-Old red blood cells
•P. falciparum –infect all age groups, adhere to
endothelial lining of blood cells causing
obstruction, thrombosis and local ischemia,
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Clinical features -2
•Infants–recurrent bouts of fever, irritability,
poor feeding, vomiting, jaundice and
splenomegaly.
•Older children –headache, backache, chills
myalgia and fatigue pallor, fever, malaise,
vomiting, body weakness, vomiting,
hepatosplenomegaly.

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Features in neonate
•The signs and symptoms resemble those seen in
the newborn septicaemia.
•Fever, lethargy, unable to be breastfeed.
•Vomiting, irritability, respiratory distress.
•Seizures, jaundice, pallor, hepatomegaly.
Laboratory
•Presence of MPS, hyperbilirubinemia. Anemia.
Hb< 13.5g/dl, hypoglycemia and acidosis.

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•Children may be asymptomatic.
•Fever occur every third day (tertian fever) in
vivax and ovalemalaria, or every fourth day
(quartanfever) in malariaemalaria.
•In falciparum malaria the fever is less regular.
•Non specific symptoms -abdominal pains.
diarrhoea, vomiting, malaise, joint pains.
Clinical features -4

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33. Severe malaria
•Cerebral malaria
•Anemia
•Hypoglycemia
•Prostrations
•Respiratory
distress
•Repeated
convulsions
•Circulatory
collapse/shock
•Pulmonary oedema
•Bleeding
tendency/DIC
•Jaundice
•Acute renal failure
•Hemoglobinuria
•Behavioral changes
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34. Differential diagnosis -1
•URTI (Flu, tonsillitis)
•LRTI (Pneumonia)
•UTIs
•Gastrointestinal infections(Enteric fever, gastro
entritis)
•Skin conditions (Scabies)
•Abscesses
•Trauma-infected bite/wounds/cut
•Parasitic infections(trypanosomes)
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Differential diagnosis -2
•Viral infections such as influenza and hepatitis
•Sepsis
•Meningitis
•Encephalitis
•Endocarditis
•Pyelonephritis
•Brucellosis
•Tuberculosis

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Congenital malaria -1
•Risk of transmission to fetus higher in semi-immune or non
immune mothers (7-10%) than in immune mothers (1-4%)
•May be difficult to distinguish from post natallyacquired
infection
•Symptom onset usually 2-8 weeks of age
oPoor feeding
oVomiting
oFever
oDiarrhea
oIrritability

37. Congenital malaria -2
oAnemia
oThrombocytopenia
oJaundice
oHepatosplenomegaly
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Diagnosis
Clinical diagnosis
1)Uncomplicated malaria-symptomatic malaria without
signs of severity or evidence of vital organs
dysfunction(clinical or laboratory)
2)Severe malaria
Laboratory investigations
1)Malaria blood smear (Thick and Thin)
2)Antigen detection(Rapid diagnostic tests)
3)Polymerase Chain Reaction-(parasite genetic materials)
4)Fluorescent microscopy (acridineorange)
5)Serology –antibody detection(past infection)
6)QBC

39. Blood smear
•Thick
oMore sensitive
oDifficult to read
•Thin
oParasite species identification
oParasite density
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41. (mRDTs)
Parasite antigen detection.
•Most detect histidinerich protein-2 (HRP-2)(P. falciparum
specific), PlasimodiumLactate dehydrogenase (pLDH) and
Aldolase.
oSensitivity 88-98%, specificity 95-100% vsmicroscopy
oHRP-2 persists in blood after acute infection
oRemains positive even after therapy
•Require only a finger prick blood specimen
•Results within 10-15 minutes
•Vulnerable to high temperature and humidity
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42. Quantitative Buffy Coat (QBC)
Test
•Is a new method for identifying the malarial
parasite in the peripheral blood.
•It involves staining of the centrifuged and
compressed red cell layer with AcridineOrange
and its examination under UV light source
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43. QBC
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44. Supportive investigations
•Blood glucose in patients with altered consciousness
•Haematocritand haemoglobin level
•Lumbar puncture to exclude meningitis
•Serum creatinineor urea
•Electrolytes
•FBP
•Blood gases, pH and anion gap –to diagnose acidosis
•CXR –look for pulmonary oedema/lobar consolidation
•Plasma and CSF lactate concentrations
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Other laboratory investigations
•Blood culture
•Urine culture
•Blood group and X match
•Urine microscopy
•Stool microscopy

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47. Treatment
•Uncomplicated malaria
•Severe malaria
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Treatment of Uncomplicated Malaria
Combination Therapy (ACTs )are combinations of two components:
1. Artemisinin and its derivatives
oArtesunate,
oArtemether, and
oDihydroartemisinin
2. Antimalarial with a known good efficacy profile
oLumefantrine,
oPiperaquine,
oMefloquine,
oAmodiaquine).

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Treatment of Uncomplicated Malaria
Using Combination Therapy
•The Artemisinin compounds are active against all
four species of malaria parasitesthat infect humans
and are generally well tolerated.
•A 3-day course of the Artemisinin is required for the
ACTs to eliminate at least 90% of the parasitaemia.
•This ensures that only about 10% of the parasitaemia
is present for clearance by the partner medicine.

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Uncomplicated malaria
Using combination therapy.
1. Artemetherlumefantrine(Alu) oral fixed combination
tablet of 20mgartemetherand lumefantrine120mg.
•Lumefantrinehas a longer elimination half-life of up to 10
days
•Artemether2days
•ALu1.5/12mgbody weight twice a day for 3 days
(strength 20/120mg)

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Alu administration
•First dose as DOT in a health facility
•If vomited within 30 minutes repeat the dose
•Should be taken with meal to enhance
absorption.
•Second dose after 8 hours
•Subsequent doses twice daily in the second
and third day.

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Non response to Alu
•Vomiting the drug
•Poor quality of the drug
•Inadequate dosage
•Fever/symptoms from a cause other than
malaria
•Parasite resistance to the drug rare
•Treat with second line -artesunate
•Treat fever with paracetamol, asprin

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2. Dihydroartemisinin-Piperaquine (DPQ)
Available Formulations:
•Fixed-dose combination with tablets containing
Dihydroartemisinin(a derivative of Artemisinin) and
Piperaquine.
oTwo strengths for the above formulation are:
•40mg DHA+ 320mgDPQ
•20mg DHA + 160MGDPQ (for paediatric)
.

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DPQ
•Indications:
oAlternative medicine of choice for treatment of
uncomplicated malaria.
oTreatment of uncomplicated malaria where ALuis
contraindicated.
oTreatment of uncomplicated malaria where ALuhas
failed.
•Contraindications:
oHypersensitivity to either Dihydroartemisininor
Piperaquine.

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DPQ
Adverse Effects:
oSinus bradycardia and
oAsymptomatic prolongation of QT interval.
oIt is therefore to be given with caution in patients
with cardiac illness.
oOther -nausea, anorexia, body weakness
(asthenia), dizziness and headache.

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DPQ
Dosage Regimen:
oA target dose: 4mg/kg/day of
Dihydroartemisininand 18mg/kg/day of
Piperaquine; once a day for 3 days.

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3. Artesunate-Amodiaquine
Available Formulations:
oFixed-dose formulation: Tabs containing 25/67.5mg,
50/135mg or 100/270mgof artesunateand
Amodiaquine.
oSeparate tablets: Tablets containing 50 mg of
artesunateand 153 mg base of Amodiaquine
respectively.
Indications:Treatmentof uncomplicated malaria.
Contraindicated: First trimester of pregnancy.
Dosage Regimen: 4 mg/kg/day and 10 mg/kg/day
Amodiaquineonce a day for 3 days.

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4. Artesunate-Mefloquine
Available Formulations:
oThis is currently available as blister packs with
separate scored tablets containing 50 mg of
artesunateand 250 mg base of mefloquine.
Adverse Effects:
oIncreased incidence of nausea, vomiting, dizziness,
dysphoriaand sleep disturbance in clinical trials, but
these are seldom incapacitating.
oWhere this ACT has been deployed it has been well
tolerated.

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Artesunate-Mefloquine
Indications: Treatment of uncomplicated malaria
Not Recommended: First trimester of pregnancy
Dosage Regimen: Artesunate 4mg/kg/daygiven
once a day for 3 days and 25 mg/kg of mefloquine split
over 2 days as 15 mg/kg and 10 mg/kg.

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Principles of Management of Severe Malaria
•Use of injectable monotherapy in the first 24
hrs.
•4 management principles
oRapid clinical assessment
oManagement of emergency conditions
oSpecific antimalarial treatment
oSupportive care

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Principle 1:
Rapid Clinical Assessment of the Patient
•A rapid assessment: Airway, Breathing,
Circulation, Coma, Convulsion, and
Dehydration status.
•Weigh the patient
•Perform malaria tests and relevant
supportive investigation.
•Think of differential diagnosis

62. Coma scales
Pediatric Glasgow Coma Scale
Score
Best motor response
•None
•Extension to pain
•Flexion to pain
•Withdrawal from pain
•Localizes pain
•Obeys commands
1
2
3
4
5
6
Best verbal response
•None
•Moans to pain
•Persistent cries to pain
•Inappropriate words
•Appropriate words/ phrases
1
2
3
4
5
Eye movements
•None
•Opens to pain
•Opens to verbal command
•Opens spontaneously
1
2
3
4
Blantyre Coma Scale
Score
Best motorresponse
•Localizes painful stimulus
•Withdraws limb from painful stimulus
•No response or inappropriate response
2
1
0
Best verbal response
•Criesappropriately with painful stimulus,
or if verbal, speaks
•Moan or abnormal cry with painful
stimulus
•No vocal response to painful stimulus
2
1
0
Eye movements
•Watchesor follows
•Fails to watch or follow
1
0
© 2007 Baylor College of
Medicine

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Principle 2:
Management of Emergency Conditions
A:An open airway should be secured in
unconscious patients
B:Breathing supported
C:Circulation maintained, convulsion
stopped and coma managed.
D:Severe Dehydration corrected.

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Principle 3:
Specific Antimalarial Treatment
•The drug of choice for treatment of severe
malaria isinjectable Artesunate.
•The alternative treatments are injectable
Artemetherorinjectable Quinine.

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Principle 4:
Supportive Care
•Supportive treatments are provided to any
complication which appears.
•Supportive treatment is determined by level
of health care delivery and existing capacity.

66. Treatment of Severe Malaria with
Injectable Artesunate
1. Artesunateis a water-soluble derivative of
Artemisinin.
oThe only Artemisininanalogue that can be given
intravenously.
•It produces rapid parasite clearance in
falciparum malaria.
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67. Treatment of Severe Malaria with
Injectable Artesunate
Available Formulations:
•Each box contains:
o1 vial of Artesunate60mg
o1 ampoule of 1ml of 5% Sodium
bicarbonate solution
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68. Treatment of Severe Malaria with
Injectable Artesunate
Preparation:
•Injectable Artesunatehas 2-steps dilutions:
oStep 1:The powder for injection should be diluted
with 1ml of 5% sodium bicarbonate and shaken
vigorously for 2-3 minutes till the solution becomes
clear.
oStep 2:For I.V. add 5 ml (for I.M. add 2ml) of Normal
Saline or 5% of Dextrose and mix again.
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69. Treatment of Severe Malaria with
Injectable Artesunate
•For slow intravenous infusion (3-4 minutes),
add 5 ml of 5% dextrose or normal saline, to
obtain a Artesunateconcentration of 10
mg/ml
•For deep intra-muscular injection, add 2 ml of
5% dextrose or normal saline to obtain
Artesunateconcentration of 20 mg/ml.
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70. Treatment of Severe Malaria with
Injectable Artesunate
Dose:
•Dose of 2.4 mg/kgb/wt IV or IM given on
admission (time = 0 hour), then at 12 hours and
24 hours. (< 20kg start with 3mg/kg/dose.)
•If the patient can tolerate oral medication after
24 hours provide a full treatment course of ALu.
•Initiate the first dose of ALu8 hours after the last
injection
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71. Pre referral treatment
•Rectal artesunate 10mg /kg
•< 10kg < 12months = 100mg (1supp)
•10 –19kg 1-5yrs = 2x100mg (2)
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Treatment of Severe
Malaria with Injectable Artemether
•Artemether is a lipid soluble Methylether of
Dihydroartemisinin
Formulation:
oFormulation advised by the WHO are
ampoules of injectable solutions for
intramuscular injection containing 80 mg
artemether in 1 ml oil solution for adults or
40 mg artemether in ml for paediatric use.

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Treatment of Severe Malaria with
Injectable Artemether
•Administration and Dosage:
oDose of 3.2 mg/kgloading dose) IM start
othen 1.6mg/kgbody weight (time = 0h then
at 24 hrs and 48 hrs).
oIf the patient can tolerate oral medication
after 24 hours provide a full treatment
course of ALu.

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Treatment of Severe Malaria with
Injectable Artemether
oInitiate the first dose of ALu 8 hours
after the last injection.
oArtemether injections need additional
supplies such as tuberculin syringes.
oArtemether injectable can be deployed
effectively in malaria epidemics.

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General management
•Airway
•Semi prone position
•Breathing
•Circulation
•Blood slide for MPS
•Blood glucose
•HB estimation

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General management
•Insert IV cannula
•NGT for feeding and medication
•Catheterization if indicated
•Nursing care and monitoring –fluid input
and output, level of consciousness, T, PR,
RR, BP

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Emergency management of severe malaria.
•Convulsions–diazepam 0.15mg/kg IV bolus
or rectal route 0.5 –1.0mg/kg
•Hypoglycaemia–glucose < 2.5mmol/l give
5mls/kg of 10% dextrose, or2.5mls/kg of
25% or 50%.
•In adults 125mls of 10% or 50mls of 25%
dextrose
•Sugar water: 20gm in 200mls clean water

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Neonatal malaria
•Neonatal malaria –symptoms attributable to
malaria with evidence of ring forms of malaria
parasite in the blood of an infant within the
first 28 days (4 weeks) of life.
•The signs and symptoms resemble those seen
in the new-born with septicemia.
•Malaria in this age group is life threatening and
requires immediate action.

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Treatment of Malaria in
Neonates
•Broad spectrum antibiotics –ampicillin and
Gentamycin
•Parental Artesunate is 1st line treatmentfor neonates
and infants below 5kg with severe malaria.
•Injectable quinine remains a suitable alternative
where Artesunate is not available.
•Give 10% glucose IV 60ml/kg/24hours If a neonate is
not able to breast feed,
•Give blood transfusion if Hb is <10g/dl

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Treatment of Malaria in
Neonates
•Nursing Care and Monitoring
oMonitor vital signs (PR, RR & Temperature)
oMonitor input/output
oCheck BS for malaria parasite daily
oEnsure feeding
oAdvise on use of LLINs

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Definition of Anaemia
•The reduction of red blood cells or Hb
concentration or both below the normal range
for the age and sex of the individual.

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Normal Hbconc. levels
by Ages and Sex
Category Hb g/dl
New-born 13.5 -20
Children<6years 11 -13
Adultfemales,notpregnant 12 -16
Adultfemales,pregnant 11 -15
Adultmales 13.-17

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Relationship Between Malaria
and Anaemia
•The aetiologyof anaemiain malaria endemic areas is
often multi-factorial:
oNutritional deficiencies
oInfectious
oInherited red blood cell disorders.
•Anaemiadue to malaria is usually normocyticand
normochromicin nature.
•During the course of malaria infection, red blood
cells are destroyed.

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Clinical Presentation of
Anaemia
Symptoms Signs
•Easy fatigue/ tiring
•Inability to feed and drink
(Infants and children)
•Dizziness and
breathlessness on exertion
in pregnant women
•History of eating soil
(especially in children or
pregnant women)
•Pallor (palms, soles, nails beds,
conjunctivae and tongue)
•Signs of respiratory distress (nasal
flaring, chest in drawing and deep
breathing or grunting)
•Signs of CCF -(dyspnoea, tachycardia,
gallop rhythm, basal crepitations,
oedema, puffy eyes, raised JVP and
enlarged tender liver)

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Effects of Malaria on Morbidity in
Pregnant Women, Foetusand Newborns
Pregnant
Woman
Foetus New born
Effects of
Malaria
Severe
malaria(*)
Intrauterine
growth
retardation
Low birth
weight
Anaemia Congenital
Infection
Prematurity
Premature
labour
Congenital
/neonatal
malaria
(*) especially cerebral malaria and pulmonary oedema

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Malaria in HIV/AIDS Infected
Children
•Effect of malaria in HIV infection children
includes increased risk of illness and anaemia
•HIV infection does not undermine the
response to treatment with antimalarial
medicines in uncomplicated malaria.
•Avoid Amodiaquine-containing ACT regimens
treatment in HIV-infected patients on
zidovudineor efavirenz.

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Prevention of Malaria in People
Living With HIV/AIDS
•Individuals with advanced immunosuppression
(CD4 T-cell count ≤ 200 µl) should receive co-
trimoxazoleprophylaxis until their CD4 count is
above 200 µl.
oThis is to prevent them from respiratory tract
infections and malaria
•HIV positive pregnant women should be referred to
PMTCT services and should alwaysbe protected by
LLINs.

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Importance of Malaria in Sickle
Cell Disease
•SCD patients have low risk or malaria
infection.
•SCD patients are at higher risk of mortality
when they get malaria.
•Malaria is the most common precipitating
cause of crises in sickle cell disease in malaria-
endemic countries.

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Management of Malaria in Sickle
Cell Disease
•Depending on classification of the malaria
diagnosis, full treatment with anti-malarials
should be given according to the guidelines.

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Prevention
Mosquito bite avoidance
•LLITNs, ITNs, IRS
Antimalarial chemoprophylaxis
•Chloroquin5mg/kg, mefloquin5mg/kg weekly, proguanil
3mg/kg daily, malarone(proguanil/atovaquin) daily,
doxycyclline100mg daily > 12yrs.
Vector control
Accessto diagnostic testing of suspected malaria and
treatment of confirmed cases.
IPTp,andIPTi.
Vaccine?

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Malaria chemoprophylaxis
•Sickle cell anemia
•Non immune travelers
•Non immune pregnant women
•TSS-Tropical splenomegaly syndrome.

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SCD –Sickle Cell Disease
1.Chemoprophylaxis monthly
1.Proguanil/Atovaquine
2.Dihydroartemisinin-Piperaquine
2.LLINs
3.Access to prompt diagnosis and
treatment
4. Health Education

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Non immune travellers
•Proguanil25mg/Atovaquine62.5mg
•Mefloquine5mg/kg weekly
•Doxycyclline100mg daily > 12yrs

95. POST DISCHARGE MALARIA
CHEMOPREVENTION
•< 5 YEARS with diagnosis of severe anemia,
severe malaria
•Monthly ACT long term acting DP for 6
months.
•Use LLINs
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MASS DRUG ADMINSTRATION
•ACT –DP and PQ
•All age groups/targeted community
members
•Cure asymptomatic infections
•Prevent reinfection
•Reduces the prevalence and incidence of
malaria in a short term.

97. FOCAL AND MASS TESTING and
TREATMENT
•Test using mRDT all individuals
•Treat those who are positive
•Active case detection
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98. WHO -package of interventions for the
prevention and treatment of malaria in children
•Use of LLINs
•In areas with highly seasonal transmission of the Sahel sub-
region of Africa, seasonal malaria chemoprevention (SMC) for
children aged between 3 and 59 months;
•In areas of moderate-to-high transmission in SSA, IPT for
infants (IPTi10 weeks, 14 weeks and 9 months)-Seasonal
Malaria Chemoprophylaxia-SMC
•Prompt diagnosis and effective treatment of malaria
infections.
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Vaccination
•The development of vaccines that interrupt
transmission.
•Pre-erythrocytic(liver stage) vaccines block the
entry of sporozoitesinto hepatocytes or destroy
infected hepatocytes, thereby preventing clinical
disease.
•Radiation-attenuated sporozoites

100. Figure 4
The Lancet 2010; 375:1468-14DI:10.1016/S0140-6736(10)60447-3)
Terms and Conditions
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