MALARIA

by
Collins Atta Poku
Department of Nursing

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 Malaria
• Nearly half of the world’s population was at risk of malaria
• In 2020, there were an estimated 241 million cases of
malaria worldwide
• The estimated number of malaria deaths stood at 627,000
in 2020 (reported)
• The WHO African Region carries high share of the global
malaria burden – 95% of morbidity and 96% of mortality.
• Children under 5 accounted for 80% of all malaria death

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 Malaria
• In 2015, all countries in the WHO European Region
reported, for the first time, zero indigenous cases of
malaria, down from 90,000 cases in 1995.
• Outside the region, 8 countries reported zero cases of
the disease in 2014; Argentina, Costa Rica, Iraq,
Morocco, Oman, Paraguay, Sri Lanka and United Arab
Emirates

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 Malaria - Classification
• Sporozoa belong to the phylum Apicomplex
• The parasites of class Haematozoa occur in the blood
of their vertebrate hosts
• The class contain two orders:
1. Haemosporida, containing the genus plasmodium
which causes malaria
2. Piroplasmida, containing the genus babesia
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 Plasmodium parasite
Five (5) parasites but three species cause malaria in Ghana
1. P. falciparum mono infection
2. P. malariae mono infection
3. P. ovale mono infection
4. P. vivax has not yet been seen in blood films in Ghana
5. P. knowlesi has recently been identified in Malaysia but
not yet identified in Ghana

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 Malaria - Prevalence
• Malaria generally occurs in areas where
environmental conditions allow parasite
multiplication in the vector.
• Malaria is usually restricted to tropical and sub-
tropical areas but this distribution might be affected
by climatic changes, especially global warming and
population movements.
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 Malaria - Prevalence
• Prevalence of malaria parasites globally according to
species is as
• p. falciparum account for 50% of malaria cases,
• p. vivax 40%
• p. malariae about 7% and
• p. ovale less than 3%

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Life cycle of anopheles mosquitoes
Average Life span 3-4 Wks.
Mosquitoes have Most lay up to 3 batches (100-
4 different stages 150/ batch)
in their life cycle: Rarely up to 7 batches. Have
Egg different breeding habitat
Larva preferences
Pupa
adult

Pupal stage
takes 2-4 days
First instars but temperature
hatch within 2- dependent
3 days Larval development
takes 8-10 days but
temperature dependent

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Life Cycle of Plasmodium (Malaria)
Parasite

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Mode of transmission
There are four main modes of malaria transmission:
1. Through the bite of an infective female anopheles
mosquito (the main method of transmission)
2. An accidental transmission via blood transfusion
(transfusion malaria)
3. Through the use of contaminated syringe and needle
particularly in drug addicts

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Mode of transmission
4. Transmission of infection to fetus in utero from
mother through placental defect during pregnancy
or parturition (congenital malaria)
• The above conditions are also known as trophozoite
induced malaria, in which there is no primary and
secondary exo-erythrocytic schizogony, short
incubation period and there is no relapse

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Predisposing (Host) factors
All individuals are predisposed, however

Genetic

1. Hemoglobin S (HbS)/ Sickle cell - persons who have

the sickle cell trait are relatively protected against P.
falciparum.

• Heterozygotes for the sickle gene (AS) are relatively

protected against the danger of dying of malaria
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Predisposing (Host) factors cont’d
Reasons:
1. Biochemical –
a. Reduced intra-erythrocytic growth of P. falciparum in
HbAS red blood cells
b. Reduced cytoadherence
2. Immunological –
a. Enhanced phagocytosis of parasitized HbAS red blood
cells
b. Higher IgG levels in HbAS individual (Increased humoral
immune response)

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Predisposing (Host) factors cont’d
2. Glucose-6-phosphate dehydrogenase deficiency (G6PDD)
protects against malaria

• G6PD deficiency leads to increased oxidative stress in red blood

cells, this may in turn have a negative influence on the parasite.

• As such, individuals who possess this mutation have some

protection against malaria.

• There is no effect on the number of clinical cases/episodes of

malaria caused by the parasite, but there is an effect on
parasite density and hence severe malaria (risk reduced)
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Predisposing (Host) factors cont’d
3. Acquired immunity - after repeated attacks of malaria,
a person may develop a partially protected immunity.

• Persons can be infected but not likely to present

with symptoms of severe disease.

• However, in contrast to many viral infections, multiple

infections with malaria do not confer long lasting,
sterile protective immunity
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 At risk of SEVERE DISEASE
• Age: Children < 5 years in highly malaria endemic countries
• Sex and pregnancy status: Sex is not a major factor but
pregnant women have higher degree of susceptibility

• Non-immune individuals
• Travelers from non-endemic malaria
• Residents of endemic areas who have stayed for 6 months
continuously or more in non-endemic areas
• Immunosuppressed
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General clinical features

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Clinical features (cardinal)
• After an incubation period
• P. falciparum - 12 days,
• P. vivax and ovale – 13-17 days,
• P. malariae – 28-30 days,
• Patients will develop typical picture of malaria that
consists of febrile paroxysm, anaemia, and
splenomegaly.

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Clinical features – Febrile paroxysm
• Febrile paroxysms follow the completion of
erythrocytic schizogony when the mature schizont
ruptures releasing merozoites, malarial pigment and
other parasitic debris
• Macrophages engulf these and releases endogenous
pyrogens leading to pyrexia.

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Clinical features – Febrile paroxysm
It generally begins in the early afternoon and comprises
of 3 successive stages
• Cold stage (15 to 60 mins of intense cold and
shivering)
• Hot stage (2 to 6 hours of feeling intense hot.
Fever of 40°C to 40.6°C, severe headache, nausea
and vomiting)
• Sweating stage (crisis of profuse sweating)
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Clinical features - Anaemia
• Anaemia after few paroxysms develops as a result of:
1. Mechanical destruction of parasitized RBCs
2. Reduced erythropoiesis in the bone marrow
3. Lysis and phagocytosis of uninfected RBCs

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Clinical features - anaemia
• In a small number of patients with malignant tertian
malaria, there is autoimmune destruction of RBCs
• Consumption of more than 70% of haemoglobin in
RBCs by the parasite
• Failure of the liver to cover liberated iron

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Clinical features – splenomegaly
• After few paroxysms, spleen gets enlarged and
becomes palpable
• Splenomegaly is due to massive proliferation of
macrophages which phagocytize both parasitized and
non-parasitized RBCs
• Jaundice can also occur due to rupture of RBCs

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Diagnostic investigation
1. Clinical picture is highly suggestive, especially the
characteristic paroxysm
2. Microscopic identification of parasite (stages) in
blood film is the method most frequently used to
demonstrate an active infection
3. Malaria antibody detection test can detect past (not
active) infections

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Diagnostic investigation cont’d

4. Rapid diagnostic tests (RDTs) are based on detection

of antigen derived from lysed blood cells using
immunochromatographic methods
5. Molecular diagnostic techniques can complement
other tests especially in species identification

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Complications cont’d
Pernicious anaemia: It is a complex of life-threatening
complications that sometimes supervene in acute
falciparum malaria
It is due to heavy parasitisation and causes
1. Cerebral malaria
2. Algid malaria
3. Septicaemic malaria
4. Blackwater fever
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Complication cont’d
• Septicemic malaria is characterised by high degree of
prostration; there is high continuous fever with involvement
of various organs.
• Blackwater fever
• is a manifestation of repeated infections with p. falciparum
which were inadequately treated with quinine.
• Sometimes resumption of quinine for new attack is followed
by massive destruction of RBCs, fever, haemoglobinuria and
renal failure.
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Treatment
• Chloroquine was the standard treatment for many years
but resistance has made a problem so quinine is an
alternative
• Primaquine is used to eliminate the exo-erythrocytic
phase. However, this drug may precipitate hemolysis in
individuals who are deficient in the enzyme glucose-6-
phosphate dehydrogenase (G6PD)
• Artemeter combined therapy (ACT)
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Prevention
1. Spraying insecticides
2. Spraying larvicides in breeding sites
3. Wearing long sleeve clothing and trousers to avoid
bites
4. Using bed nets
5. Early diagnosis and prompt treatment of patients

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 Prophylaxis
1. Taking prophylactic treatment (Chemoprophylaxis)
e.g. Sulphadoxine pyrimethamine
2. Malaria vaccine: A completely effective vaccine is NOT
yet available for malaria, although several vaccines are
under development
• SPf66 was tested extensively in endemic areas in
the 1990s, but clinical trials showed it to be
insufficiently effective
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Prophylaxis cont’d
• Several potential vaccines targeting the pre-
erythrocytic stage are being developed, with RTS,
S/AS01 showing the most promising results
• The RTS, S/AS01 (commercial name, mosquirix) was
engineered using genes from the outer protein of P
falciparum and a portion of hepatitis B virus, plus a
chemical adjuvant to boost immune response

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Nursing management

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