2. Learning objective
Definition of malaria and types of malaria parasites
Epidemiology of malaria
Risk factor of malaria
Life cycle of malaria
Incubation period of the parasite
Pathophysiology of malaria
Signs and symptoms of malaria
Laboratory diagnosis of malaria
Treatment and prevention of malaria
Complication of malaria
3. What is malaria ?
• Malaria is a serious or life threatening disease that
spreads when you’re bitten by a Anopheles mosquito
infected by tiny parasites. When it bites, the
mosquito injects malaria parasites into your
bloodstream. Malaria is caused by the parasites, not
by a virus or by a type of bacterium.
• If it isn’t treated, malaria can cause severe health
problems such as seizures, brain damage, trouble
breathing, organ failure and death.
4. Cont…
• Is an infection of liver and RBCs caused by
protozoan parasites of the genus plasmodium.
Malaria is caused by 5 species of plasmodium:
• P. falciparum (the most common and dangerous).
• P. vivax (the most common)
• P. ovale
• P. malariae
• P. knowlesi
5. Epidemiology
• It is reported that Plasmodium vivax is more
prevalent in India, Pakistan, Bangladesh, Sri Lanka,
and Central America,
• whereas Plasmodium falciparum is predominant in
Africa, Haiti, Dominican Republic, the Amazon region
of South America, and New Guinea.
• Most of the infections with Plasmodium ovale occur
in Africa, and the distribution of Plasmodium
malariae is considered worldwide.
6. Cont…
• The commonest causes of malaria in Ethiopia are
Plasmodium falciparum and Plasmodium vivax. P.
falciparum causes virtually all the severe forms
of malaria.
• More than 50% of the total population in
Ethiopia is exposed to the risk of malaria
infection. Every year, four to five million people
are affected by malaria while a major epidemic
occurs every five to eight years.
7. Risk factor for malaria
• Living or traveling in a region where malaria is
present.
• Traveling to area where malaria is common: -
Without taking medicine to prevent malaria.
- Being outdoors, especially in rural areas
- Not taking steps to protect yourself from
mosquito bites.
• Pregnant women.
• Children under 5 years of age.
• Patients with HIV/AIDS.
8. Lifecycle of Plasmodium
• 2 stages
1) Sexual phase in the mosquito – sporogony
2) Asexual phase in humans
A, Exoerthrocytic phase ( liver stage )
B, Erythrocytic phase ( blood stage )
• The infectious stage of malaria - Sporozoite (found in
the salivary glands of female mosquitoes).
9. Exoerthrocytic Phase
• Sporozoites enters the hepatocytes and become
merozoites . Merozoites replicates asexually forming
a schizont which eventually bursts.
• In p. ovale and p. vivax, some sporozoites do not
undergo asexual replication and enter a dormant
phase known as hypnozoites which reactivate later
resulting in a relapse.
10. Erythrocytic Phase
• Merozoites release from hepatocytes invade
erythrocytes, undergoes a trophic period then
replicates in it asexually.
• It later bursts releasing merozoites which infect more
cells.
• The release of merozoites is what causes malarial
paroxyms.
11. Sporogony
• Trophozites in RBC’s undergo a sexual cycle which
differentiates into gametocytes and are then
ingested by a mosquito.
• In the mosquito: Gametocytes become gametes
which fuse to become a zygote in the mosquitos gut
which then develops into an ookinete then into an
oocyte.
• The oocyte divides asexually, ruptures and releases
sporozoites which infects the salivary gland and is
what is injected into the host.
12.
13. Incubation period
• Following the infective bite by the Anopheles
mosquito, a period of time (the “incubation period”)
goes by before the first symptoms appear. The
incubation period in most cases varies from 7 to 30
days.
14. Incubation period of the parasite
SPECIES INCUBATION PERIOD ( LIVER CYCLE )
P. falciparum 7-14 days
p. vivax 12-17 days( with relapse up to 3years )
p. ovale 9-18 days ( with relapse up to 20 years
p. malaria 13-40 days
15. Cont..
• The time between the fever episodes can be characteristics of
the infecting plasmodium species
SPECIES Duration of fever (erythrocytic cycle
)
P. falciparum 36-48hr, Malignant tertian fever
p. vivax 48hr, Benign tertian fever
p. ovale 48hr, Ovale tertian fever
p. malaria 72hr, Quartan fever
16. Pathophysiology of malaria
• New merozoites are released from the RBCs at
intervals of approximately 48h for P.vivax, P.ovale and
P.falciparum and 72h for P.malaria. The episodic
shaking, chills, and fever coincide with this release.
• The parasites destroy large numbers of infected RBC,
thereby causing a hemolytic anemia.
17. Cont..
• A characteristic brown malaria pigment derived from
hemoglobin, called hemozoin is released from
ruptured RBCs and produces discoloration of the
spleen, liver, lymph nodes and bone marrow.
• Activation of defense mechanisms in the host leads
to a marked hyperplasia of mononuclear phagocytes,
producing massive splenomegaly and occasional
hepatomegaly.
18. Common symptoms
• High temperature 38c or above
• Feeling hot or shivery
• Headaches
• Vomiting
• Diarrhea
• Muscle pain
• Generally feeling unwell
19. CLINICAL FEATURE OF
UNCOMPLICATED MALARIA
• Fever, chills, rigors, sweating
• Headache, generalized body and joint pain
(myalgia and arthralgia)
• Nausea and/or vomiting, loss of appetite,
abdominal pain (especially in children)
• Irritability and refusal to feed (in infants), flu-like
symptoms,
• Fever, usually above 38°C
• hepatosplenomegaly
20. INVESTIGATIONS AND DIAGNOSIS
Investigations
• Microscopy-thick and thin blood films for malaria
parasites
• Rapid diagnostic tests (RDT)-if microscopy is unavailable
• CBC
Diagnosis
• The diagnosis of malaria can be confirmed when malaria
parasites are demonstrated in the blood films (thick or
thin) or with Rapid Diagnostic Test (RDT).
21. Cont..
• Blood film is also helpful to estimate the degree of
parasitemia, which is very useful not only to predict
severity but gauge response to treatment.
• If neither microscopy nor rapid tests are available,
diagnosis should be made on the basis of clinical
presentation.
• Clinical diagnosis of malaria is made in a patient who has
fever or history of fever in the past 48 hours and lives in
malaria-endemic areas or has a history of travel within
the last 30 days to malaria-endemic areas
22. Treatment
Objectives
• Prevent uncomplicated malaria from progressing
to severe form
• Improve societal productivity
• Prevent death from malaria complication
• Prevent the development and transmission of
drug resistance
• Decrease malaria transmission to others
23. SUPPORTIVE TREATMENT FOR
UNCOMPLICATED MALARIA
• Fever management (axillary temp record of ≥37.50C)
Antipyretics
− Paracetamol (acetaminophen) 15 mg/kg (for adults
1000mg) every 4-6 hours, given orally or as a suppository.
Fanning and tepid sponging
• Check for signs of severity
• Assess the ability to tolerate oral medication.
• If there is any sign of severity or the patient is unable to
tolerate oral medications admit patients for parenteral
treatment.
24. PHARMACOLOGIC
• P. falciparum:
First line:Artemether +Lumefantrine(AL), fixed dose
combination
(20mg + 120mg) for 3 days + a single dose
primaquine phosphate (15mg base P.O).
• First line for pregnant women in the first trimester:
quinine
25. Cont..
• P. vivax
o Chloroquine phosphate 25 mg/kg given in divided doses
over three days
− 1 g (4 tablets) initially, then 500mg (2tablets) in 6 hours, it is
then followed by 500mg (2ablets), PO, daily for 2 days.
OR
− 1g (4 tablets) at 0 and 24 hours. It is followed by 500mg (2
tablets) at 48 hrs.
o Primaquine phosphate 15mg base, PO, daily for 14 days for
all patients after completing the three days of chloroquine.
26. Mixed infections (P. falciparum and P. vivax)
• Artemisinin based combination therapies (like AL for
3 days) should be used for mixed (falciparum and
vivax) infections, followed by 14-day primaquine
phosphate.
• Avoid primaquine in pregnant, breast-feeding
mothers less than 6 months infants, infants under six
months of age.
27. TREATMENT FAILURE
• Consider treatment failure in a patient with malaria who
was treated for malaria in the past 28 days.
• The cause might be drug resistance, poor adherence or
inadequate drug exposure (i.e. from under-dosing,
vomiting, drug interaction, misdiagnosis
or substandard medicines.
• If the cause for treatment failure identified early (e.g.
anti-malarial drug is vomited), address the cause and
reinstituted treatment with the first line anti-malarial
drug;
28. Cont…
• If a P. falciparum or P. vivax-infected patient returns
with fever or history of fever between days 4 to 28 of
treatment, microscopic blood examination should be
made (do not use RDTs).
• If parasites are detected, administer second-line
drug, e.g., quinine tablets;
• If blood smear is negative and no other obvious
causes found, reevaluate,or refer
• For treatment failure after 28 days, first line
antimalarial drugs should be used.
29. COMPLICATED (P. FALCIPARUM ) MALARIA
• Delayed presentation, delay in diagnosis or
inappropriate treatment of uncomplicated malaria
can lead to the rapid development of severe or
“complicated malaria”.
• It is commonly occurring in children under 5 years of
age, pregnant women and non-immune individuals.
Severe malaria may lead to death unless it is
diagnosed early and appropriately managed.
30. CLINICAL FEATURES
• Inability to take in fluids (or breast milk in children)
• Repetitive vomiting
• Dark or ‘cola-colored’ urine/ hemoglobinuria
• Difficulty in breathing ,
• Generalized convulsions,
• Altered consciousness, confusion, delirium, convulsions, coma
• Circulatory collapse or shock (cold limbs, weak rapid pulse)
• Tachypnea, respiratory distress and/or cyanosis
• Hyperpyrexia (axillary temperature >38.5°C)
• Hypoglycemia
• Severe anemia (Hb < 6 g/dl) or extreme pallor (severe anemia)
31. INVESTIGATIONS AND DIAGNOSIS
Investigation
• Microscopy-thick and thin blood films for malaria
parasites
• Rapid diagnostic test (RDT)-if microscopy is
unavailable
• Hemoglobin, hematocrit, CBC
• Blood glucose (RBS)
• Blood grouping and cross-matching
• BUN and creatinine
32. Cont..
Diagnosis
• The diagnosis of severe malaria is based on
clinical features and confirmed with
laboratory testing. While confirmation of the
diagnosis is necessary treatment must be
started promptly and not withheld while
confirming the diagnosis.
33. TREATMENT OF SEVERE AND COMPLICATED P. FALCIPARUM
MALARIA
Objectives
• Administer medicines parenterally to ensure
adequate blood-serum concentrations of the
medicine and rapid clearance of parasitemia
• Provide urgent treatment for life threatening
problems e.g., convulsions, hypoglycemia,
dehydration, renal impairment
• Prevent death from malaria
34. Cont..
Non pharmacologic
• Clear and maintain the airway.
• Open IV line for 8 hours of intravenous fluids including
diluents for antimalarial medicine, glucose therapy and
blood transfusion.
• Make rapid clinical assessment.
• Weigh the patient and calculate dosage.
• Exclude or treat hypoglycemia (more so in pregnant
women and children).
• Assess state of hydration.
• Measure and monitor urine output.
35. Pharmacologic
General principles of treatment
o It is a medical emergency.
o Parenteral administration required
(Artesunate >quinine)
o Also involves multiple supportive treatment
measures
36. First line
• Artesunate, 2.4mg/Kg IV or IM given on admission (time = 0),
then repeat at 12 hours, and 24 hours, then once a day for up to
5 days.
OR
• If artesunate is unavailable: Artemether, IM 3.2mg/kg loading
dose on the first day followed by 1.6mg/kg daily for five days
OR
• If artesunate and artemether are unavailable: Quinine
hydrochloride
Quinine hydrochloride loading dose: 20mg/kg in 500ml of 5% dextrose
or normal saline over 4 hours (4ml/minute). The pediatric loading dose is
the same but the fluid replacement must be based on body weight.
37. DOSING GUIDELINES FOR ANTIMALARIAL DRUGS
• Artesunate is dispensed as a powder of Artesunic acid.
• The 60mg vial of artesunate must be reconstituted in two
steps:
First: sodium bicarbonate solution (Provided separately along
with the vial)
Second: with 5ml of 5% glucose (D5W) solution.
• Full reconstitution results in either 6ml (for intravenous use,
with a concentration of 10mg/ml) or 3ml (for intramuscular
injection, with a concentration of 20mg/ml).
38. HEMATOLOGIC COMPLICATIONS (INCLUDING SEVERE
ANEMIA AND COAGULOPATHY)
Anemia
• Indication for transfusion
− If hematocrit is below 15% (Hg <5g/dl) in a normally hydrated
child or adult.
− Anemia with shock or evidence heart failure, metabolic acidosis
(deep labored breathing or high parasitemia (>20% of RBCs
parasitized)
• Volume of transfusion: 10 ml/Kg of packed RBC or 20 ml whole
blood/ kg of body weight. For adults it is equivalent to 2-3 units of
packed RBC or 2-3 units of whole blood.
• The volume of all blood products should be included in the overall
fluid balance. The patient should be closely monitored during the
blood transfusion.
39. Cont..
Bleeding tendency:
• Check for evidence of DIC (if laboratory tests are
available): platelet
count, PT/INR, and PTT
Management: Transfusion of platelet and fresh frozen
plasma or fresh whole blood (if platelet and fresh
frozen plasma are not available).
40. ACUTE RENAL FAILURE (ACUTE KIDNEY INJURY)
• Persistent oliguria, despite adequate correction of
dehydration or hypotension:
o <17 ml/hour in adults (<200ml in 12 hours or <400ml
in 24 hours); <0.3 ml/kg/hour in children.
OR
• Elevated serum creatinine: increase in serum creatinine
more than twice
(two fold) from baseline.
Management: correct dehydration, if there is any evidence of
hypovolemia. Avoid over hydration (fluid overload). If oliguria
persists, refer to a facility with dialysis service.
41. HYPOGLYCEMIA:
• Suspect in any patient who deteriorates suddenly,
decreased level of consciousness or convulsions.
• Threshold for intervention among children <5 years is <3
mmol/L (<54mg/dl); children ≥5 years and adults are <2.2
mmol/L (<40 mg/dl).
Management
• IV dextrose: initial bolus
− 40% dextrose for children: 1ml/kg/dose, diluted with
equal volume of NS, give slowly to avoid irritation of vein and
extravasation.
− 40% dextrose for adults: 80ml (4 vials of 20ml
preparation) diluted with equal volume of NS, administer
slowly.
42. NEUROLOGIC COMPLICATIONS (INCLUDE ALTERED
SENSORIUM, SEIZURE, AND COMA):
• Management of convulsions:
o Ensure the patient is in a safe environment to avoid injuries
o Position the patient laterally (sideways) to protect the
airways
o Diazepam
− Children: 0.15 mg/kg body weight IV or 0.5 mg/kg body
rectally
− Adults: 0.15 mg/kg body weight IV (maximum 10 mg)
• Management of coma
o Position the patient on the sides, change positions every 2
hours, correct hypoglycemia and regularly check blood sugar
levels.
43. Prevention
• Avoid mosquito bites: using mosquito repellants, insectides,
using mosquito nets, wearing long sleeves and trousers and
window screens.
• chemoprophylaxis for travellers and pregnant women. For all
species of Plasmodium is chloroquine phosphate 300 mg
(base) once weekly beginning 1 week prior to departure and
continued for 4 weeks after leaving an endemic area. The
pediatric dose is (5 mg) (base) per kilogram of body weight
(maximum: 300 mg).
If the traveller is going to places where there is a chloroquine
resistance : Mefloquine, 5mg base per kg weekly (1tablet for
adults >50kg, begin > 2weeks before travel to endemic area),
take weekly on the same day while in the area and for 4 weeks
after leaving the area.
44. Reference
• Dipiro pharmacotherapy : a pathophysiology
approach 7th edition
• Ministry of health - Ethiopian standard
treatment guidelines for general hospital 4th
edition 2021
• Centers for disease control and prevention
(CDC)– about malaria
