MALARIA

MEDICINE AND MEDICAL

NURSING

LECTURE BY
C.J SIMUYEMBA
E/N, R/N, BSc Student UNZA
 INTRODUCTION

 Malaria has been haunting mankind for many years.

 Has killed more people than all the wars.
 Globally, about 3.2 billion people are at risk of malaria, and 1.2
billion are at high risk.
 In 2015, malaria caused 214 million infections and 438000
deaths. Nearly 90% of these deaths occurred in Africa, and 70%
occurred in children <5 years.
HISTORY AND DISTRIBUTION
 Plasmodium vivax is the most widely distributed, being most
common in Asia, North Africa, and Central and South America.
 Plasmodium falciparum, the predominant species in Africa,
Papua New Guinea, and Haiti, is rapidly spreading in South-
east Asia and India.
HISTORY AND DISTRIBUTION

 Plasmodium malariae is present in most places but is rare,

except in Africa.
 Plasmodium ovale is virtually confined to West Africa where it
ranks second after P. falciparum.
 OBJECTIVES

GENERAL OBJECTIVE
 At the end of the lecture, students are expected to gain
knowledge and understanding about Malaria.
SPECIFIC OBJECTIVES
 At the end of the lecture, students should be able to;
 Define the Malaria
 Mention the causative agent of Malaria
OBJECTIVES
 Explain the life cycle of Malaria in a mosquito and in man
 Discuss the pathogenesis of Malaria
 State the signs and symptoms of Malaria
 Explain the stages of fever in malaria
 Discuss the management of Malaria
 Outline the complications of Malaria
 Explain the preventive measures of Malaria
 DEFINITION
 Malaria is a protozoa infection of the genus plasmodium
transmitted through the bite of an infected female anopheles
mosquito characterized by paroxysms of chills, fever, sweating,
splenomegaly and a chronic relapsing course.” (MOH, 2013).
DEFINITION

 Malaria is a parasitic infection caused by a parasites injected

into the blood stream from a female anopheles mosquito bite
characterized by fever, headache, joint pains and general body
malaise.
VECTOR

 Human malaria is transmitted by over 60 species of female

Anopheles mosquito.
 The male mosquito feeds exclusively on fruits and juices.
 The female needs at least 2 blood meals, before the first batch
of eggs can be laid.
CAUSATIVE AGENTS OF HUMAN
MALARIA (SPECIES OF MALARIA
PARASITE)
 Plasmodium vivax: Benign Tertian Malaria.
 Plasmodium falciparum: Malignant Tertian Malaria.
 Plasmodium malariae: Benign Quartan Malaria.
 Plasmodium ovale: Benign Tertian Malaria.
 LIFE CYCLE
 Malaria parasite passes its life cycle in 2 hosts which include a
Definitive host (Female Anopheles mosquito) and Intermediate
host (Man).
 It also involves two phases.
 An asexual phase occurring in humans, which act as the
intermediate host and a sexual phase occurring in mosquito,
which serves as a definitive host for the parasite.
 LIFE CYCLE
ASEXUAL PHASE (SCHIZOGONY)
 In this phase the malaria parasite multiplies by division or
splitting a process designated to as Schizogony (from schizo: to
split, and gone: generation).
 This asexual phase in man, is also called vertebrate, intrinsic, or
endogenous phase.
LIFE CYCLE
 In humans, schizogony occurs in 2 locations in the red blood
cell (erythrocytic schizogony) and in the liver cells
(exoerythrocytic schizogony or the tissue phase).
 The products of schizogony, whether erythrocytic or
exoerythrocytic, are called merozoites (meros: a part, zoon:
animal).
 LIFE CYCLE
SEXUAL PHASE (SPOROGONY)
 The sexual phase takes place in the female Anopheles mosquito.
Maturation and fertilization take place in the mosquito, giving
rise to a large number of sporozoites (from sporos: seed).
 Hence this phase of sexual multiplication is called sporogony.
 It is also called the invertebrate, extrinsic, or exogenous phase.
 LIFE CYCLE
LIFE CYCLE IN MAN
 Human infection comes through the bite of the infective female
Anopheles mosquito during which the sporozoites, which are
infective forms of the parasite are present in the salivary gland of
the mosquito.
 They are injected into blood capillaries when the mosquito feeds
on blood after piercing the skin, usually, 10–15 sporozoites are
injected at a time.
 LIFE CYCLE
Pre-erythrocytic stage:
 Within an hour of being injected into the body by the mosquito,
the sporozoites reach the liver and enter the hepatocytes to
initiate the stage of pre-erythrocytic schizogony or merogony.
 LIFE CYCLE
 The sporozoites undergo repeated nuclear division to become
schizonts. Mature liver stage schizonts contain 2000–50,000
merozoites.
 Mature schizonts rupture in 6–15 days and release thousands of
merozoites into the blood stream.
 The merozoites infect the erythrocytes.
 LIFE CYCLE
Erythrocytic Stage:
 The merozoites released by pre-erythrocytic schizonts invade the
red blood cells. These young parasites are, therefore called the
ring forms or young trophozoites.
 Late trophozoite form transform into mature schizonts.
 LIFE CYCLE
 Mature schizont contains 8–32 merozoites and hemozoin.
 The mature schizont bursts releasing the merozoites into the
circulation.
 The merozoites invade fresh erythrocytes within which they go
through the same process of development.
 LIFE CYCLE
 This cycle of erythrocytic Schizogony or merogony is repeated
sequentially leading to progressive increase in the parasitemia,
till it is arrested by the development of host immune response.
 Rupture of mature schizont releases large quantities of pyrogens.
 This is responsible for the febrile paroxysms characterizing
malaria.
 LIFE CYCLE
 In P. falciparum, erythrocytic schizogony always takes place
inside the capillaries and vascular beds of internal organs.
 The parasite feeds on the hemoglobin of the erythrocyte.
 It does not metabolize hemoglobin completely and therefore,
leaves behind a hematin-globin pigment called the malaria
pigment or haemozoin pigment, as residue.
 LIFE CYCLE
Gametogony
 After a few erythrocytic cycles, some of the merozoites that
infect RBC's do not proceed to become trophozoites or schizonts
but instead develop into sexually differentiated forms, the
gametocytes.
 Development of gametocytes takes place within the internal
organs, only the mature forms appear in circulation.
 LIFE CYCLE
 The mature gametocytes are round in shape, except in P.
falciparum, in which they are crescent-shaped. In all species,
the female gametocyte is larger (macrogametocyte).
 In the smaller male gametocyte (microgametocyte).
 Female gametocytes are generally more numerous than the
male.
 LIFE CYCLE
 Gametocytes appear in circulation 4–5 days after the first
appearance of asexual form in case of P. vivax and 10–12 days
in P. falciparum.
 A person with gametocytes in blood is a carrier or reservoir.
 The gametocytes do not cause any clinical illness in the host,
but are essential for transmission of the infection.
 LIFE CYCLE
LIFE CYCLE IN A MOSQUITO
 When a female Anopheles mosquito ingests parasitized
erythrocytes along with its blood meal the asexual forms of
malaria parasite are digested but the gametocytes are set free in
the midgut (stomach) of mosquito and undergo further
development.
LIFE CYCLE
 The nuclear material and cytoplasm of the male gametocytes
divides to produce 8 microgametes with long, actively motile,
whip-like filaments (exflagellating male gametocytes).
 LIFE CYCLE
 The female gametocyte does not divide but undergoes a process of
maturation to become the female gamete or macrogamete.
 It is fertilized by one of the microgametes to produce the zygote.
 The zygote, which is initially a motionless round body, gradually
elongates and within 18–24 hours, becomes a vermicular motile
form called the ookinete (‘travelling vermicule’).
 LIFE CYCLE
 The ookinete develops into oocyst which is yet another
multiplication phase, within which numerous sporozoites are
formed.
 The mature oocyst ruptures releasing sporozoites which find their
way to the salivary glands.
 The mosquito is now infective and when it feeds on humans the
sporozoites are injected into skin capillaries to initiate human
LIFE CYCLE
 The time taken for completion of sporogony in the mosquito is
about 1–4 weeks (exitrinsic incubation period) depending on
the environmental temperature and the species.
INCUBATION PERIOD

 The average incubation periods of different species of

Plasmodium are as follows –
P. vivax—14 (8–31) days
P. falciparum—12 (8–14) days
P. ovale—14 (8–31) days
P. malariae—28 (18–40) days
 INCUBATION AND PRE-PATENT

 The incubation period: is the interval between the entry of

sporozoites into the host and the earliest manifestation of clinical
illness is the incubation period.
 The pre-patent period: is the interval between the entry of the
parasites into the host and the time when they first become
detectable in blood.
 RECRUDESCENCE

 In P. falciparum and P. malariae infections after the primary

attack, sometimes there is a period of latency during which there
is no clinical illness.
 But some parasites persist in some erythrocytes, although the
level of parasitemia is below the fever threshold or sometimes
below the microscopic threshold.
 Fresh malarial attacks then develop after a period of latency.
 LIFE CYCLE
 Usually within 8 weeks after the primary attack and resulting
from persistence of the erythrocytic cycle of the parasites are
called recrudescences.
 Recrudescence may be due to waning immunity of the host or
possibly due to antigenic variation.
 In P. falciparum infections, recrudescences are seen for 1–2 years,
while in P. malariae infection, they may last for long periods, even
up to 50 years.
 RELAPSE
 It is seen in P. vivax and P. ovale infections.
 In both these species, 2 kinds of sporozoites are seen some of
which multiply inside hepatocytes promptly to form schizonts and
others which remain dormant.
 RELAPSE
 These latter forms are called hypnozoites (from hypnos: sleep).
Hypnozoites remain inside the hepatocytes as uninucleated
forms, 4–5 μm in diameter, for long periods.
 Such new attacks of malaria, caused by dormant exoerythrocytic
forms.
 Reactivated usually from 24 weeks to 5 years after the primary
attack are called relapses.
 PATHOGENESIS
 The infection of the red cells by malaria parasites, particularly
P. falciparum, results in progressive and dramatic structural
changes biochemical, and mechanical modifications of the red
cells.
 PATHOGENESIS
 Several pathophysiological factors occur:
the parasite biomass; ‘malaria toxin(s)’ and inflammatory
response;
cytoadherence, resetting and sequestration;
altered deformability and fragility of parasitized erythrocytes;
endothelial activation,
The above have been found to be involved in the development
PATHOGENESIS
 All these phenomena are more profound in P. falciparum
infection.
 As a result, complications such as cerebral malaria,
hypoglycemia, metabolic acidosis, renal failure, and
respiratory distress are more commonly seen in P.
falciparum infections
 PATHOGENESIS
 CYTOADHERENCE, SEQUESTRATION, AND
ROSETTING
 Structural changes in the infected red cells and the resulting
increase in their rigidity and adhesiveness are major contributors
to the virulence for P. falciparum malaria.
 PATHOGENESIS
 Owing to the increased adhesiveness, the red cells infected with
late stages of P. falciparum adhere to the capillary and
postcapillary venular endothelium in the deep microvasculature
(cytoadherence).
 The infected red cells also adhere to the uninfected red cells
resulting in the formation of red cell rosettes (rosetting).
 PATHOGENESIS
 Cytoadherence leads to sequestration of the parasites in various
organs such as the heart, lung, brain, liver, kidney, intestines,
adipose tissue, subcutaneous tissues, and placenta.
 PATHOGENESIS
 Due to the sequestration only the ring-stage trophozoites of P.
falciparum are seen circulating in the peripheral blood,
Cytoadherence-rosetting-sequestration of infected and
uninfected RBCs in the vital organs can lead to ultimately
blocking blood flow, limits the local oxygen supply, therefore
contributing to the development of severe disease.
 CLINICAL FEATURES
UNCOMPLICATED MALARIA
This is the form of Malaria in which the signs and symptoms are
mild to moderate and is not life threatening.
 Fever with rigor- due to the presence of toxins and heamolized
RBCs in circulation which stimulate the production of pyrogens
hence a fever and rigors.
 CLINICAL FEATURES
 Headache- this is due to cerebral hypoxia occurring from
occlusion of the cerebral microcirculation by the dead RBCs and
other toxic substance.
 CLINICAL FEATURES
 Nausea- due to accumulation, occlusion and irritation of the
mesenteric circulation by heamolised RBCs.
 Vomiting- as a result of irritations and stimulation of the
vomiting center by the toxins and dead RBCs.
 CLINICAL FEATURES

 Joint pains- due to blockage in the microcirculation by the

heamolysed RBCs and other dead tissues which interfere with
oxygen supply to the joints.
 Back pains- due to reduced blood flow to the spine with
subsequent hypoxia
 STAGES OF MALARIA FEVER
The febrile paroxysm comprises of 3 successive stages which
includes cold stage, hot stage, and sweating stage.
1. Cold stage
 In the cold stage, that lasts for 15–60 minutes, the patient
experiences intense cold and uncontrollable shivering.
 Patient feels intensely cold and shivers with teeth usually
chattering.
STAGES OF MALARIA FEVER
 Demanding for extra linen or wanting to bask in the sun or
sitting near a fear.
 The temperature is rapidly elevated reaching its highest about
40 degrees Celsius.
 Vomiting frequently occur.
 STAGES OF MALARIA FEVER

2. Hot stage
 Patient feels very hot and may be delirious
 The temperature mounts to 41°C or higher.
 It occurs 30 minutes after the cold stage.
 Vomiting may continue.
 The patient may complain of heat in the body and simultaneously
feeling cold on the outside.
STAGES OF MALARIA FEVER

3. Sweating stage
 Occurs about 1-6 hours after hot stage
 The patient sweats profusely
 Temperature drops and the patient becomes relatively
comfortable.
 The fever reoccurs after 48-72 hours
COMPLICATED (SEVERE) MALARIA

 Infection with Plasmodium Falciparum Malaria, in the

presence of any life-threatening condition is considered as
Severe Malaria or Complicated Malaria.
 All life-threatening conditions with the presence of a danger
sign in acute febrile illness should be suspected to be severe
malaria (MOH, 2013).
COMPLICATED (SEVERE) MALARIA
 This is the most serious and fatal type of malaria which is caused
by P. falciparum.
 When not treated promptly and adequately, dangerous
complications develop.
 These may present in various forms, the most important of
which are the cerebral, algid, and septicemic.
 C. Malaria is the most common cause of death (15% of
 CLINICAL PICTURE OF SEVERE
MALARIA
 Convulsions- due to excessive accumulation of the debilitated
RBCs and toxins in the cerebral circulation causing irritations to
the meninges
 Coma- due to severe hemolysis and hypoxia as well as
engorgement of the cerebral circulation/ irritations.
 CLINICAL PICTURE

 Jaundice- due to severe RBC hemolysis leading to an increase in

the amount of bilirubin in circulation which is then deposited on
the mucous membrane and cornea giving it a yellowish
discoloration.
 Severe anemia- due to excessive RBC destruction by the
parasites.
 CLINICAL PICTURE
 Hyperpyrexia- due to the presence of the parasites, toxins and
heamolized RBCs in circulation which stimulate the production
of pyrogens hence a fever and rigors.
 Excessive vomiting- as a result of irritations and stimulation of
the vomiting center by the parasites, toxins and dead RBCs .
MANAGEMENT
Diagnosis of malaria involves
 Clinical diagnosis which includes:
 Clinical picture: Signs and symptoms
 History of travel to endemic areas
 Laboratory Diagnosis
 Microscopic examination- thin or thick smear (BS FOR MPs)
 MANAGEMENT
 Serological examination- immuno- sorbent assay- to detect
antibodies, indirect fluorescent antibody test (IFAT), Enzyme
linked immuno-sorbent assay(ELISA)
 Microscopic examination- thin or thick smear (Blood Slide for
Malaria Parasites).
 MANAGEMENT

 Serological examination- immuno- sorbent assay- to detect

antibodies.
 Immunochromatographic method: Rapid Diagnostic Test
(RDT) for malaria.
 TREATMENT

FIRST LINE TREATMENT;

 Involves treatment of uncomplicated malaria.
 Administer anti- Malarial drugs- Coarterm (atermether +

lumefantrine) give Artemether 20mg + Lumefantrine 120mg

tablets.
 Adult dose is given 4 tablets start, then 4 tablets after 8 hours and

continue with 4 tablets 12 hourly for 2 days.

TREATMENT
AGE (YEARS) WEIGHT (KG) NUMBER OF ARTEMETHER(A
TABLETS PER ) +
DOSE LUMEFANTRINE
(L) PER DOSE

<1 <5 Not recommended

1 to 5 5 to 14 1 20mg A + 120mg L

6 to 8 15 to 24 2 40mg A + 240mg L

9 to 12 25 to 34 3 60mg A + 360mg L

Over 12 >35 4 80mg A + 480mg L

 TREATMENT

 Antipyretics/ Analgesics- paracetamol 1g 8 hourly for 3 days.

 Fluids are also given IV to maintain the hydration status of the
patient eg. 5 or 10% dextrose and ringers lactate.
TREATMENT
SECOND LINE TREATMENT;
 Given in complicated or severe Malaria:
 Complicated Malaria is a medical emergence and the patient
requires urgent attention and treatment in order to save her life.
 TREATMENT

Emergence management
 Admit the patient for close management.
 Establish and maintain clear airway for improved gaseous
exchange.
 Give oxygen of patient has breathing problems.
 Give anticonvulsants in case of convulsions.
TREATMENT
 Give 10% Dextrose to treat for hypoglycaemia.
 Evaluate for anaemia (check FBC)
 Monitor blood sugar 12 hourly
 Monitor urine output.
 Assess condition regularly.
TREATMENT
DRUGS:
 Alternatively, injection Artesunate 2.4mg/kg body weight
IM/IV 12 hourly until patient is able to take orally, then
switched to Coartem orally. If no response, switch to;
 Quinine 20mg/kg body weight loading dose IV diluted in 5%
or 10% Dextrose solution 10mls/kg body weight over 4 hours .
TREATMENT
 After 8 hours a maintenance dose of 10mg/kg body weight
given over 4 hours, repeated 8 hourly, until patient can swallow
or after coma resolution, then oral quinine 10mg/kg body
weight 8 hourly for 7 days.
 Haematinics: Folic Acid 5mg orally daily
 Analgesics: Paracetamol 1g orally daily for 3 days.
 PREVENTIVE MEASURES
 Early diagnosis and treatment – treat early to reduce parasite
load, hence spread; prevent deaths
 Treat completely to prevent spread and relapse
 Ensure compliance with complete treatment
 Intermittent preventive treatment (IPTp): 3 doses SP in 2 nd. & 3rd.
Trimesters and by chemoprophylaxis (for travelers).
 PREVENTIVE MEASURES
 Environmental degradation to get rid of mosquito breeding sites
near residential areas.
 Use the long lasting insecticide treated mosquito nets (LLITNs).
 Provide health education information on malaria on how it is
transmitted and prevented.
 Use of indoor residue spraying to kill the mosquitos and prevent
them from resting on the walls of the house.
COMPLICATIONS OF MALARIA

 Cerebral malaria
 Hypoglycemia

 Metabolic acidosis
 Renal failure
 Respiratory distress
 NURSING CARE
Nursing care is approached according to the stage of the malaria
fever.
1. DURING THE COLD STAGE
 Provide extra linen as the patient feels very cold in this stage.
 If available, switch on the heater to provide some warmth to the

patient.
 Provide hot drinks such as tea to keep the patient warm.
 Hot water bottles can provide some warmth for the patient.
NURSING CARE

2. DURING THE HOT STAGE

 Remove extra linen to help the body cool faster.
 Give ice cubes to suck or a cold drink to reduce temperature.
 Provide a fan if available to reduce fever.
NURSING CARE
 Carry out tepid sponging in order to reduce temperature and
promote comfort.
 Open near-by windows allow for free flow of air in the room
to cool the patient.
 Give antipyretics: Paracetamol 1g orally 8 hourly.
NURSING CARE CONT……
3. DURING THE SWEATING STAGE
 Provide towel for patient to wipe the sweat away.
 Open near-by windows to promote air flow into the room to
cool the patient’s temperature.
 Change wet linen for patient’s comfort.
 Offer a bath for patient’s comfort.
 SUMMARY
 We have come to the end of our discussion on Malaria in
pregnancy and it is a common problem in most developing
countries and a major cause of morbidity and mortality especially
in malaria endemic areas.
 In pregnancy, Malaria has a significant impact on the health of the
fetus as well as that of the mother.
 Most of maternal deaths in Africa have been attributed to Malaria.
EVALUATION

 What is Malaria?
 What is the causative organism for Malaria?
 How is malaria transmitted?
 What happens in the life cycle of malaria?
 What are the signs and symptoms of Malaria?
EVALUATION
 How is the diagnosis made for malaria?
 What is the management of malaria in pregnancy?
 What are the effects of Malaria in pregnancy?
 How do you prevent malaria?
ASSIGNMENT

 Write notes in your note book on the complications of malaria.

 To be reviewed in the next class.
 REFERENCES
 MOH (2013), Standard Treatment Guideline, 3rd edition, Lusaka,
Zambia, ZNFC
 Raynor M. and Marshall J. (2014), Myles Textbook for Midwives,
16th edition, Churchill Livingstone, London, England
 CBOH (2002), Intergrated Technical Guidelines for Frontline
Healthworkers, 2nd Edition, Lusaka, Zambia.
 CBOH (2003), Malaria During Pregnancy Facilitator’s Guide, 4th
Edition, Lusaka, Zambia.