Malaria

Prof. O. Ojurongbe
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Malaria

 Malaria is a major public health problem

in warm climates especially in
developing countries.
 It is a leading cause of disease and
death among children under 5 years,
pregnant women and non-immune
travellers/immigrants.
 In 2017, there were an estimated 219
million cases of malaria in 87 countries
 The estimated number of malaria deaths
stood at 435 000 in 2017 Children under 5 are the major at risk group in malarious
regions. Inset: An Anopheles mosquito taking a blood meal
 What is malaria ?
Malaria is a disease caused by the protozoan parasites of the genus Plasmodium. The five
species that commonly infect man are:

Species Major features

P. falciparum  The most important species as it is responsible for 50% of all malaria cases
worldwide and nearly all morbidity and mortality from severe malaria
 Found in the tropics & sub-tropics
P. vivax  The malaria parasite with the widest geographical distribution
 Seen in tropical and sub-tropical areas but rare in Africa
 Estimated to cause 43% of all malaria cases in the world
P. ovale  This species is relatively rarely encountered
 Primarily seen in tropical Africa, especially, the west coast, but has been
reported in South America and Asia

P. malariae  Responsible for only 7% of malaria cases

 Occurs mainly in sub-tropical climates
P. knolwlesi Is now considered the fifth species of Plasmodium causing malaria in humans
It is recorded In South-East Asia,
It is a zoonotic malaria
 The burden of malaria

The “indirect” burden of malaria

• Human development: Impaired intellectual development, developmental abnormalities (especially following

cerebral malaria), lost school attendance and productivity at work
• Economics: The cost of a single bout of malaria is equivalent to over 10 working days in Africa. The cost of
treatment is between $US0.08 and $US5.30, depending on the type of drugs
 Geographical Distribution of Malaria
• Although previously widespread, today, malaria is confined
mainly to Africa, Asia and Latin America.
• It is endemic in 91 countries, with small pockets of
transmission occurring in a further 8 countries.
• The female anopheles mosquito transmits malaria.
• Factors that affect mosquito ecology, such as temperature
and rainfall, are key determinants of malaria transmission.
Mosquitoes breed in hot, humid areas and below altitudes
of 2000 meters.
• The malaria parasite develops optimally between 25 and
30oC and stops below 16oC. Indigenous malaria has been
recorded as far as 64oN and 32oS.
• The major factor for the spread of malaria is drug-resistant
parasites.
• Other important factors include poverty, HIV/AIDS,
mosquito resistance to insecticides, weak health services,
conflict, population migration, and, more recently, the
COVID-19 outbreak
 Endemicity
 Endemicity refers to the amount or severity of malaria in an area or community.
Malaria is said to be endemic when there is a constant incidence of cases over a
period of many successive years.
Endemic malaria may be present in various degrees. Recognised categories of
endemicity include
A. Hypoendemicity - little transmission and the disease has little effect on the
population.
B. Mesoendemicity - varying intensity of transmission; typically found in the small, rural
communities of the sub-tropics.
C. Hyperendemicity - intense but seasonal transmission; immunity is insufficient to
prevent the effects of malaria on all age groups.
D. Holoendemicity - intense transmission occurs throughout the year. As people are
continuously exposed to malaria parasites, they gradually develop immunity to the
disease. In these areas, severe malaria is mainly a disease of children from the first few
months of life to age 5 years. Pregnant women are also highly susceptible because the
natural immune defence mechanisms are impaired during pregnancy.
 How is malaria transmitted?
• Malaria parasites are transmitted from one
person to another by the bite of a female
anopheles mosquito.
• The female mosquito bites during dusk and
dawn and needs a blood meal to feed her
eggs.
• Male mosquitoes do not transmit malaria as
they feed on plant juices and not blood.
• There are about 380 species of anopheles
Female Anopheles mosquito taking a blood meal
mosquito but only about 60 are able to
Source:http://phil.cdc.gov/phil/quicksearch.asp
transmit malaria.
• Like all mosquitoes, anopheles breed in water
- hence accumulation of water favours the
spread of the disease.
 How does infection develop ?
• Plasmodium infects the human and insect host alternatively and several phases of the parasite
life cycle are described.
• During feeding, saliva from the mosquito is injected into the human blood stream. If the
mosquito is carrying malaria, the saliva contains primitive stages of malaria parasites called
sporozoites.
• Hepatic, tissue or pre-erythrocytic phase: Sporozoites invade and develop in liver cells. The
infected hepatocyte ruptures to release merozoites.
• Erythrocytic phase: Merozoites then invade red blood cells. The red cells lyse and this
causes bouts of fever and the other symptoms of the disease. This cycle repeats as
merozoites invade other red cells.
• Sexual phase: Sexual forms of the parasites develop and are ingested when another female
anopheles mosquito feeds. These develop into sporozoites in the gut of the insect host and
travel to its salivary glands. Then the cycle starts again…
• The life cycle of the malaria parasite is shown on the next slide
Life cycle of malaria parasite
 Severity of disease and host factors

In addition to parasite factors, several host factors determine the outcome of exposure to malaria:

• Naturally-acquired immunity. People who are constantly exposed to malaria gradually acquire immunity,
firstly against clinical disease and later against parasite infection. Clinical manifestations of malaria are
most severe in the non-immune. In holoendemic areas, these are children aged <5 years and pregnant
women (especially primagravidae). People of any age from areas that are free from malaria, or have
limited malaria transmission, are at risk when they are exposed to malaria.

• Red cell and haemoglobin variants. Well known examples of inherited factors that protect against
malaria are Haemoglobin S carrier state, the thalassaemias and Glucose-6-phosphate dehydrogenase
(G6PD) deficiency. Malaria provides the best known example whereby an environmental factor (malaria)
has selected human genes because of their survival advantage.

• Foetal haemoglobin (HbF): High levels of HbF occur in neonates, and in some people with inherited
haemoglobin variants, protect against severe forms of P. falciparum malaria.

• Duffy blood group: P. vivax requires the Duffy blood receptor to enter red blood cells. Therefore, people
who do not carry the Duffy blood group are resistant to this malaria species. This explains the rarity of P.
vivax in Africa, as most Africans are Duffy blood group negative.
 Other host factors that could affect
severity of malaria

 We hypothesize that Toll-interacting proteins (TOLLIP),  CD14 is a multifunctional receptor expressed on many cell
vitamin D receptor (VDR) and TNF -α genes are significant types and has been shown to mediate immune response
contributors to susceptibility and disease severity in Pf resulting in the activation of an inflammatory cascade
infection.  We present a detailed analysis of genetic
diversity of CD14 promoter gene (snp -159 C/T; rs2519190)
 Our aim is to explore the genomic diversity and haplotype polymorphism between a malaria-infected group and
frequency of these genes, as well as extrapolate possible uninfected controls and its association with clinical parameters
association with markers of severity, between malaria of disease.
infected and healthy controls
 Our results show a significant diversity in the genotypic
 no difference in genotypic or allelic frequencies of frequency of the rs2569190 mutant variant between the
TOLLIP and VDR polymorphisms. malaria-infected group and controls, respectively.
 The mutant allele had the lowest frequency among the
 However, a significant difference in the genotypic (p = malaria-infected group demonstrating its necessity for
2.20E-16) and allelic frequencies (p = 2.20E-16) of infection.
theTNF-α (snp rs1800629) polymorphism was found.  How this affects disease severity between sub-regional and
continental groups deserves further clarification,
 The clinical course of P. falciparum

Following a bite by an infected mosquito, many people do not develop

any signs of infection. If infection does progress, the outcome is one of
three depending on the host and parasite factors enumerated in the
previous slides:

A. Asymptomatic parasitaemia (“clinical immunity”)

B. Acute, uncomplicated malaria
C. Severe malaria
 A. Asymptomatic parasitaemia

 This is usually seen in older children and adults who have acquired
natural immunity to clinical disease as a consequence of living in areas
with high malaria endemicity.
 There are malaria parasites in the peripheral blood but no symptoms.
These individuals may be important reservoirs for disease
transmission.
 Some individuals may even develop anti-parasite immunity so that they
do not develop parasitaemia following infection.
 B. Simple, uncomplicated malaria
 This can occur at any age but it is more
likely to be seen in individuals with some
degree of immunity to malaria. The
affected person, though ill, does not
manifest life-threatening disease.

 Fever is the most constant symptom of

malaria. It may occur in paroxysms when
lysis of red cells releases merozoites
resulting in fever, chills and rigors
(uncontrollable shivering). Children with malaria waiting to be seen at a
malaria clinic in the south western part of
Nigeria. Identifying children with severe malaria,
and giving them prompt treatment, is a major
challenge when large numbers attend clinics.
 The periodicity of malaria fever
 Erythrocytic schizogony is the time
taken for trophozoites to mature into
merozoites before release when the
cell ruptures.
 It is shortest in P. falciparum (36
hours), intermediate in P. vivax and P.
ovale (48 hours) and longest in P.
malariae (76 hours).
 Typical paroxysms thus occur every Note how the frequency of spikes of fever
differ according to the Plasmodium species.
2nd day or more frequently in P. In practice, spikes of fever in P. falciparum,
falciparum (“sub-tertian” malaria) 3rd occur irregularly - probably because of the
presence of parasites at various stages of
day in P. vivax and P. ovale (“tertian” development.
malaria) 4th day in P. malariae
infections, (“quartan” malaria)
 Other features of simple,
uncomplicated malaria include:
o Vomiting
o Diarrhoea – more commonly seen in young children and, when vomiting also occurs, may be
misdiagnosed as viral gastroenteritis
o Convulsions – commonly seen in young children. Malaria is the leading cause of convulsions with fever in
African children.
o Pallor – resulting mainly from the lysis of red blood cells. Malaria also reduces the synthesis of red blood
cells in the bone marrow.
o Jaundice – mainly due to haemolysis.

Malaria is a multisystem disease. Other common clinical features are:

o Anorexia
o Cough
o Headache
o Malaise
o Muscle aches
o Splenomegaly
o Tender hepatomegaly

These clinical features occur in “mild” malaria. However, the infection requires urgent diagnosis and
management to prevent progression to severe disease.
 C. Severe and complicated malaria

Nearly all severe disease and the estimated >1 million deaths from
malaria are due to P. falciparum. Although severe malaria is both
preventable and treatable, it is frequently a fatal disease.

The following are 8 important severe manifestations of malaria:

Click on each severe manifestation for details

1. Cerebral malaria 5. Acute renal failure

2. Severe malaria anaemia 6. Pulmonary oedema
7. Circulatory collapse, shock or
3. Hypoglycaemia
“algid malaria”
4. Metabolic acidosis 8. Blackwater fever

Note: It is common for an individual patient to have more than

one severe manifestation of malaria!
 1. Cerebral malaria - clinical
• The most well-known severe manifestation of malaria
• Defined as:
– unarousable coma persisting for more than one hour
– with asexual forms of P. falciparum in the peripheral
blood
– other common causes of encephalopathy excluded*
• Occurs most commonly in young children although non-
immune adults are also at risk
• Cerebral malaria can rapidly progress to death, even
with appropriate treatment. Case fatality is between 20-
30%.
• In survivors, resolution of coma usually occurs within 1-2 A 4 year old boy who was deeply
days in children and within 2-4 days in adults but may be comatose and had persistent
complicated by neurological sequelae in ~5% adults and
>10% of children. deviation of the eyes

• The illness may start with drowsiness and confusion and then progress to coma. The loss of
consciousness is often preceded by repeated convulsions. Retinal haemorrhages may be seen on
fundoscopy.

• None of the clinical features are pathognomonic, malaria parasitaemia is common in people living in
endemic areas and coma may complicate many illnesses. Therefore, a clinical diagnosis of cerebral
malaria is made only after other common causes of coma (e.g. meningitis) have been excluded.
 Summary of differences in the clinical features
of severe malaria in adults and children
Frequency of occurrence

Clinical Manifestation Children Adults

Similar in adults and children
• Prostration +++ +++
• Circulatory collapse + +
More common in children
• Cerebral malaria +++ ++
• Severe anaemia +++ +
• Multiple convulsions +++ +
• Metabolic acidosis +++ +
• Hypoglycaemia ++ +/-
More common in adults
• Jaundice + +++
• Pulmonary oedema +/- ++
• Haemoglobinuria +/- +
• Abnormal bleeding +/- +
• Renal failure +/- +
 1. Cerebral malaria - pathophysiology
The exact pathogenesis of cerebral malaria is not
well understood. It is believed to result from
sequestration of parasitised red cells in the small
blood vessels in the brain. The consequences of
this include:
• reduced cerebral blood flow
A young girl with cerebral malaria. Note the • cerebral hypoxia
abnormal, decerebrate posturing
•release of cytokines which in turn induce the
release of nitrous oxide, a known depressor of
consciousness

Sequestration of parasitised red cells in different

tissues probably underlies most severe
manifestations of malaria

A 3 year old boy with impaired consciousness,

grimacing and marked extensor posturing of the arms
 2. Severe malaria anaemia

Defined as a haematocrit of <15% or haemoglobin

concentration <5 g/dl. Occurs commonly in young children
and pregnant women.

Anaemia in malaria results from a combination of factors:

• Destruction of parasitised red blood cells
• Destruction of unparasitised red cells by complement-
mediated lysis
• Bone marrow suppression by cytokines produced by
malaria parasites
• Haemolysis induced by medications in individuals with
glucose-6-phosphate dehydrogenase deficiency

Many patients require urgent transfusion. The condition may

be rapidly fatal when blood transfusion is delayed. Marked pallor in an African child
with severe anaemia due to P.
falciparum infection
 Partners in Global Health Education
3. Hypoglycaemia
1. How to use this
module
2. Learning outcomes
3.
4.
Plasmodium species
Malaria burden
• Blood sugar <2.5 mmol/L
5. Question 1
6. Transmission • Increases the risk of mortality and sequelae in children
7. Life cycle
8.
9.
Question 2
Disease severity
with cerebral malaria; may present with convulsions or a
10.
11.
Question 3
Clinical malaria
deterioration in level of consciousness.
12. Question 4
13. Diagnosis • Results from a combination of factors:
14. Treatment
15. Prevention and
control
– reduced glycogen stores because of reduced food
16.
17.
Pregnancy
Question 5 intake
18. Information sources
– increased metabolism due to fever and repeated
convulsions
– glucose consumption by malaria parasites
22 of 49 – cytokine or quinine-stimulated hyperinsulinaemia
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 Partners in Global Health Education

1. How to use this

2.
3.
module
Learning outcomes
Plasmodium species
4. Metabolic acidosis
4. Malaria burden
5. Question 1
6. Transmission
7.
8.
Life cycle
Question 2
• Lactic acidosis is a major contributor and probably
9. Disease severity
10. Question 3 results from tissue anoxia and anaerobic glycolysis
11. Clinical malaria
12. Question 4
13. Diagnosis
14.
15.
Treatment
Prevention and
• Presents with deep, rapid respirations (as in diabetic
control
16. Pregnancy ketoacidosis)
17. Question 5
18. Information sources

23 of 49

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 Partners in Global Health Education

1.

2.
How to use this
module
Learning outcomes
5. Acute renal failure
3. Plasmodium species
4. Malaria burden
5. Question 1
6.
7.
Transmission
Life cycle
• occurs almost exclusively in adults and older children in
8. Question 2
9. Disease severity areas of unstable malaria
10. Question 3
11. Clinical malaria
12. Question 4
13.
14.
Diagnosis
Treatment
• affected patients are usually oliguric (urinary output <400
15. Prevention and
control ml/day) or anuric (<50 ml/day)
16. Pregnancy
17. Question 5
18. Information sources
• serum creatinine levels are elevated

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 6. Acute pulmonary oedema
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1. How to use this This is a grave and usually

module
2.
3.
Learning outcomes
Plasmodium species
fatal manifestation of severe
4. Malaria burden
5. Question 1 falciparum malaria and occurs
6. Transmission
7. Life cycle
8. Question 2 mainly in adults.
9. Disease severity
10.
11.
Question 3
Clinical malaria
Hyperparasitaemia, renal
12. Question 4
13.
14.
Diagnosis
Treatment
failure and pregnancy are
15. Prevention and
control recognised predisposing
16. Pregnancy
17.
18.
Question 5
Information sources factors and the condition is
Acute pulmonary oedema, developing shortly after
commonly associated with delivery in a woman with severe P. falciparum
malaria
hypoglycaemia and metabolic
acidosis.
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 7. Circulatory collapse, shock, “algid
Partners in Global Health Education
malaria”
1. How to use this
module
2. Learning outcomes
3. Plasmodium species
4. Malaria burden
5. Question 1 Features of circulatory collapse (cold/clammy skin,
6. Transmission
7.
8.
Life cycle
Question 2
hypotension, peripheral cyanosis, weak/thready pulses)
9. Disease severity
10.
11.
Question 3
Clinical malaria
may be seen in patients with severe P. falciparum malaria.
12. Question 4
13. Diagnosis
14. Treatment
15. Prevention and
control
16.
17.
Pregnancy
Question 5
“Algid malaria” is characterised by hypotension, vomiting,
18. Information sources
diarrhoea, rapid respiration and oliguria. This condition is
associated with a poor prognosis.

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 8. Haemoglobinuria or “Blackwater Fever”
Partners in Global Health Education

1. How to use this This results from massive intravascular Typical, dark urine of haemoglobinuria on
module day 0 which has cleared by day 3
2. Learning outcomes haemolysis. The condition presents with
3. Plasmodium species
4. Malaria burden
severe pallor, jaundice and passage of
5. Question 1 dark urine due to haemoglobinuria. It
6. Transmission
7. Life cycle may be associated with acute renal
8.
9.
Question 2
Disease severity
failure.
10. Question 3
11. Clinical malaria
12. Question 4
13. Diagnosis
14. Treatment
15. Prevention and
control
16. Pregnancy
17. Question 5
18. Information sources

A 3 year old boy with severe anaemia

(Hb 3.3 g/dl) and dark urine (shown in
27 of 49 the container)

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 Relapse Vs Recrudesence
• Depending upon the cause, malaria recurrence can be classified
either as recrudescence or relapse
• Recrudescence is when symptoms return after a symptom-free
period. It is due to parasites surviving in the blood due to
inadequate or ineffective treatment.
• Relapse is when symptoms reappear after the parasites have been
eliminated from blood but persist as dormant hypnozites in liver
cells.
• Relapse is common in P.ovale and P.vivax infection
• Recrudescence is commonly seen in P. falciparum
 Diagnosis
Malaria is a multisystem disease. It presents with a wide variety of non-specific clinical features:
there are no pathognomonic symptoms or signs. Many patients have fever, general aches and
pains and malaise and are initially misdiagnosed as having “flu”.

P. falciparum malaria can be rapidly progressive and fatal. Prompt diagnosis saves lives and
relies on astute clinical assessment:

• A good history
– Residence or a recent visit (in the preceding 3 months) to a malaria endemic area
– History of fever (may be paroxysmal in nature)
– Recognise significance of non-specific clinical features such as vomiting, diarrhoea,
headache, malaise
• Physical examination
– Identify signs consistent with malaria: fever, pallor, jaundice, splenomegaly
– Exclude other possible causes of fever (e.g. signs of viral and bacterial infections)

The diagnosis of malaria should be considered in any unwell person who has been in a
malarious area recently
 Investigations
Blood Film Examination
Thick and thin blood films (or “smears”) have
remained the gold standard for the diagnosis of
malaria. The films are stained and examined by
microscopy.
Thick blood film - Used for detecting malaria: a
larger volume of blood is examined allowing
detection of even low levels of parasitaemia. Also
used for determining parasite density and
monitoring the response to treatment.
Thin blood film – Gives more information about the
parasite morphology and, therefore, is used to
identify the particular infecting species of
Plasmodium.
Thick blood film
A drop of blood is spread over a
small area. When dry, the slide is
stained with Field’s or Giemsa
stains. The red cells lyse leaving
behind the parasites.

• Used to detect parasites,

even if parasitaemia is low
• Less useful for speciation

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 A small drop of blood is
Thin blood film spread across a microscope
slide, fixed in methanol and
stained with Giemsa stain.

The microscopist finds the

area of the film where red
cells are lying next to each
other. The fine details of the
parasites can be examined to
determine the species.

• Used for speciation

• Does not detect low
parasitaemia

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 Appearance of P. falciparum in thin
blood films
Ring forms or trophozoites; many
red cells infected – some with more
than one parasite

Gametocytes (sexual stages); After a blood

meal, these forms will develop in the
mosquito gut

http://phil.cdc.gov/phil/quicksearch.asp
 Rapid Diagnostic Technique
 RDTs are lateral flow immuno-chromatographic antigen-detection tests, which rely on the capture of
dye-labeled antibodies to produce a visible band on a strip of nitro-cellulose, often encased in
plastic housing, referred to as cassettes.
 In RDTs, the dye-labeled antibody first binds to a parasite antigen, and the resultant complex is
captured on the strip by a band of bound antibody, forming a visible line (T-test line) in the results
window.
 A control line (C- control line) gives information on the integrity of the antibody-dye conjugate, but
does not confirm the ability to detect parasite antigen.
 The RDTs come in a number of formats: Card, Dipstick, Hybrid cassette-dipsticks & Plastic cassette
 The three main groups of antigens detected by commercially available RDTs are:
• Histidine-rich protein 2 (HRP-2), specific to P. falciparum. It is an abundant soluble, heat
stable antigen that is present in the cytoplasm and membrane of infected erytocytes.
• Parasite specific plasmodium lactate dehydrogenase (pLDH), currently available as P.
falciparum specific, pan-specific, and P. vivax-specific.
• Aldolase (pan-specific). These two antigens are conserved major enzymes in the glycolytic
pathway of malaria parasites, they are abundant and are soluble in the parasite.
  A total of 511 febrile
children were enrolled out
of which 309 (61%) were
positive by RDT.
 The presence of pfhrp2 and
pfhrp3 genes were
analyzed in 66 PCR positive
samples comprising of 31
RDT false negative and 35
RDT true positive randomly
selected samples.

 The pfhrp2 and pfhrp3 genes failed to amplify in 17% (11/66) and 6% (4/66) samples, respectively.
Seven of the eleven samples had only pfhrp2 deletion while four had both pfhrp2 and pfhrp3
deletions.
 The absence of the pfhrp2 gene may be responsible for the seven RDT false negative cases
observed.
 Three RDT positive cases lacked pfhrp2 whereas pfhrp3 was absent in only four RDT false
negative cases.
 The pfhrp2 and pfhrp3 amino acid repeat sequences were highly diverse.
 The P. falciparum isolates lacking pfhrp2 and pfhrp3 genes may be circulating and contributing to
RDT false negativity in Nigeria.
 PCR based techniques

• Polymerase chain reaction (PCR) assays are the most sensitive and
specific method to detect malaria parasites

• Numerous PCR assays have been developed for the laboratory

diagnosis of malaria, including conventional and real-time PCR
techniques

• PCR allow the differentiation of all five species of human Plasmodium

spp. It is also use for the detection of drug resistant genes of
Plasmodium spp

• However, the time lag between sample collection, transportation and

processing, and dissemination of results back to the physician limits the
usefulness of PCR in routine clinical practice.
 Other methods of diagnosis of malaria

These are not routinely used in clinical practice. They include :

a) Antigen capture kits. Uses a dipstick and a finger prick blood sample. Rapid
test - results are available in 10-15 minutes. Expensive and sensitivity drops with
decreasing parasitaemia.
b) Fluorescent techniques. Relatively low specificity and sensitivity. Cannot
identify the parasite species. Expensive and requires skilled personnel.
c) Serologic tests. Based on immunofluorescence detection of antibodies against
Plasmodium species. Useful for epidemiologic and not diagnostic purposes.
 Malaria in pregnancy
More than 45 million women (30 million in
Africa) become pregnant in malaria endemic areas each
year.
Common adverse effects of malaria in pregnancy include:
• Maternal anaemia
• Stillbirths
• Premature delivery and intrauterine growth retardation
result in the delivery of low birth weight infants
The WHO now recommends intermittent preventive
treatment (IPT): administering anti-malarial drugs (e.g.
sulphadoxine-pyrimethamine (sp)) during antenatal
care whether or not women show symptoms.
IPT-sp has been shown to substantially reduce the risk of
Source:
maternal anaemia in the mother and low birth weight in http://phil.cdc.gov/phil/quicksearch.asp
the newborn.
 Malaria Treatment
 In Nigeria, Artemisinin-based Combination Therapy (ACT) became the
recommended treatment for uncomplicated malaria, as resistance emerged to
conventional monotherapies, including sulphadoxine-pyrimethamine (SP),
chloroquine and amodiaquine, thereby reducing their therapeutic efficacy
 The first-line recommended treatment is artemether-lumefantrine (AL),
 Treatment with artesunate-amodiaquine (ASAQ), artesunate-mefloquine
(ASMQ) and dihydroartemisinin-piperaquine (DHAPQ) are also considered
acceptable
 Sulfadoxine-pyrimethamine is recommended for intermittent preventive
treatment in pregnancy,
 Cases of severe malaria should be treated using quinine injection, artemether
injection, or artesunate (either as an injection or suppository);
 The use of monotherapies is no longer recommended.
 Malaria Vaccine
 RTS,S/AS01 is the only approved vaccine as of 2021
 It has the potential for considerable impact when used in combination with existing
tools
 RTS,S/AS01 (commercial name Mosquirix), was engineered using genes from the
outer protein of P. falciparum malaria parasite and a portion of a hepatitis B virus
plus a chemical adjuvant to boost the immune response
 Phase 3 trial showed high impact in high transmission settings
 Thousands of malaria episodes prevented per 1000 children vaccinated over 4
 years follow-up
 Impact provided by RTS,S/AS01 was in addition to that achieved with ITNs
 It is estimated that one life is saved for every 200 children vaccinated
 Malaria Control
The five key intervention areas for malaria prevention activities in
Nigeria include
 Long-Lasting Insecticide-treated nets (LLINs): the mainstay of malaria
prevention, especially in sub-Saharan Africa
 Indoor residual spraying (IRS),
 larval source Management (LSM),
 Provision of Intermittent Preventive Treatment of malaria in
pregnancy (IPTp) to all pregnant women and infants (IPTi); and
providing seasonal chemoprevention (SMC) for children less than five
years of age
 Vector sentinel surveillance and resistance monitoring and quality
assurance of commodities