MALARIA

Dr. Ian Katanga

ECOHS
Objectives
 To be able to recognize malaria presentation
 To understand investigations for malaria
 To be able to manage malaria as well as its complications
Outline
 Introduction
 Etiology and life cycle of malaria parasites
 Clinical features
 Diagnostics
 Classification and management of malaria
 Complications
 Cerebral malaria
 Prevention of malaria
Malaria
 Malaria is a potentially life‑threatening tropical infectious
disease caused by Plasmodium parasites.
 transmitted through the bite of an infected female Anopheles
mosquito.
 Most cases of malaria occur in tropical Africa (West and
Central Africa).

 Transmission also occurs in other tropical and subtropical

regions eg South and Southeast Asia, and Central and South
America
 The vector

Malaria has probably killed

many people than any other
disease!
Global distribution of endemic malaria
Etiology of malaria
 Pathogen: protozoa called plasmodia
 Different types with different geographic distribution
 Vector: female anopheles mosquito
 Host: humans

 Therefore, getting exposed to mosquito bites increases

the risk of getting malaria parasites.
 Public health centre of malaria control
 Types of plasmodium and their characteristics
Plasmodia type Disease name Characteristics
Fever spikes
P. Falciparum Falciparum malaria most virulent and causes the most severe disease
dominant in Africa
Irregular fever spikes

P. Vivax Tertian malaria less virulent and causes milder disease

every 48 hours dominant in endemic areas outside Sub-saharan Africa (e.g., Southeast
Asia)

P. Ovale Tertian malaria

every 48 hours Less common and cause milder disease.
Both can be found in sub-Saharan Africa, but ovale also in Asia and
P. Malerie Quartan malaria central America
every 72 hours
P. Knowlesi Quotidian malaria Causes severe disease
possibly zoonotic
every 24 hours found in Southeast Asia
Protection against malaria
 Carriers of sickle‑cell mutation
 Individuals with either certain Duffy antigens or no Duffy antigens are
resistant to P. vivax and P. knowlesi
 Other hemoglobinopathies (e.g., thalassemia, HbC)
 Infection with malaria
 leads to production of plasmodium antibodies
 may result in partial immunity (less than a year)
Life cycle of malaria parasites
Asexual development in humans
 Mosquito bite → sporozoites travel to the liver of the host
 Liver: sporozoites enter hepatocytes
 sporozoites multiply asexually to make schizonts containing
thousands of merozoites → release of merozoites into the
bloodstream.
 In circulation. TWO pathways involved.
 1. Merozoites enter RBC: schizonts with merozoites → release
merozoites into the bloodstream → penetration of erythrocytes
recurs
 2. Merozoites enter RBC → differentiation into gametocytes (male
or female)
Life cycle of malaria parasites conti…
Sexual development in female Anopheles mosquito
 A mosquito bites an infected human
 ingests gametocytes
 gametocytes mature in intestines
 sporozoites are formed and migrate to the salivary glands
 transmission of sporozoites to humans via mosquito bite
Clinical features of malaria
 Flu‑like symptoms SPECIFICS FEATURES
 Headache  Blood
 Thrombocytopenia- bleeding risk
 Diaphoresis/ sweating
 Hemolytic anemia: weakness,
 Fever and chills
paleness, dizziness, dyspnea
 Joint and muscle pains
 general body aches  Liver: hepatosplenomegaly,
 Sweating jaundice.
 Nausea and vomiting
 CNS (cerebral malaria):
 Diarrhea, abdominal pain hallucinations, confusion, impaired
consciousness, seizures, coma
Diagnosis (Parasitological testing for malaria)
 Rapid diagnostic tests (RDTs)
 Detects specific malaria antigens (e.g., HRP2, pLDH, aldolase)
 Allows for quick diagnosis if high‑quality microscopy is
unavailable or delayed.
Blood smear
 Gold standard test: visualization of parasites in RBCs via microscopy
 Thick blood smear: high sensitivity; best initial test
 Enables calculation of malaria parasitemia
 the percentage of RBCs containing a Plasmodium organism; used to classify
severity and monitor response to therapy

 Thin blood smear: lower sensitivity, high specificity; confirmatory test

 Allows identification of Plasmodium species

 Patients may be symptomatic before parasites can be detected on

smear.
 If an initial test result is negative, repeat every 12–24 hours for a total of 3
tests. Malaria is negative if all are negative
Blood smear

Immature throphozoite gametocytes

Other investigations in malaria
 FBC:
 Hemolytic anemia: ↓ Hb, ↑ reticulocytes
 Thrombocytopenia
 WBC changes uncommon except in severe disease.

 RBS: Hypoglycemia and AKI can occur in severe malaria.

 Urinalysis: Hemoglobinuria may occur with intravascular hemolysis.

 Other (as clinically indicated): ABG, LFTs, blood and urine cultures, CSF
analysis
UNCOMPLICATED MALARIA
 Uncomplicated malaria refers to a symptomatic, diagnostically
proven malaria without features of severe malaria (without
complications).
 Can be caused by all species of plasmodium

 The first step of malaria infection

 Management of uncomplicated Malaria
 Usually managed as outpatients or short stay observation
 Treat symptoms with analgesia and antipyretics eg paracetamol

 Lumefantrine artemether (LA) - first-line drug

 Comes in two forms:
 Dispersible (LA-D)- for children < 25kg
 Non-dispersible (LA-ND)- for children >25kg and adults
 LA-ND further comes in regular LA or double strength LA

 Artesunate-Amodiaquine (ASAQ) - second-line

 Given in treatment failure or contraindications with LA
 Suitable for patients weighing > 5kg
Dispersible LA prep. and dosing
Double strength LA dosing
ASAQ dosing

Patients with failure on LA and are <5kg or <8 yrs: give quinine and clindamycin.

Patients with treatment failure with ASAQ: quinine and doxycycline for 7 days.
 SEVERE MALARIA
 Malaria infection with potentially fatal manifestation or with complications
 Most commonly from falciparum malaria.

Risk factors for developing severe malaria

 Children under 5 years
 Returning after a long stay or visitors from non-malaria countries
 Pregnant women;
 Splenectomy individuals
 Patients with HIV/AIDS
Pathophysiology of S. malaria
 Infected RBCs occlude capillaries, which can lead to severe organ
dysfunction.

1) Infected RBCs deform and are sticky.

2) May stick to post capillary endothelium.
3) Sticky RBCs can build up, causing blockage, hypoxia and micro
infarcts in the affected organs (sequestration)
4) This leads to dysfunctional organs, particularly vital ones.
 Brain, kidney, liver, etc
 Severe malaria conti…
Criteria for s. malaria: Proven malaria + 1 or more of the following:
System Features Laboratory test findings
General Prostration (severe weakness)
• Severe anemia < 5 g/dL or PCV <15%
CNS hallucinations, confusion, impaired
• Hypoglycemia: < 40 mg/dL
consciousness, seizures, coma
Cardiac shock (e.g., hypotension, capillary refill • Acidosis (with or without lactemia):
time ≥ 3 seconds), heart failure • Hyperlactatemia: lactate > 4 mmol/L
Pulmonary respiratory distress (acidotic breathing), • AKI: creatinine > 3 mg/dL or urea > 20 mmol/L
pulmonary edema, ARDS
• Hyperbilirubinemia: bilirubin > 3 mg/dL
Renal flank pain, oliguria, hemoglobinuria, (dark
colored urine) AKI • Hemoglobinuria
GIT jaundice • Electrolyte imbalance
Hematopoietic Extreme pallor (anemia), significant • High malaria parasitemia??
bleeding
Complications of Malaria
Complication Possible pathogenesis
Hypoglycemia Diminished hepatic gluconeogenesis
Depletion of liver glycogen stores
Increase consumption by host or parasite)
Quinine-induced hyperinsulinemia
Acidosis Ηурοvоlеmiа
Parasite lаϲtate production
Insufficient hepatic and renal laϲtаtе clearance
Pulmonary edema Sequestration o RBC in lung vessels
Anemia Ηеmοlysiѕ of parasitized RBCs
splenic sequestration and clearance
Cytokine suppression of hеmаtοроiеѕiѕ
Shortened erythrocyte survival
Liver dysfunction ϳаսոdiϲe due to hеmоlysiѕ, hepatocyte injury, and cholestasis
Bacterial infections Salmonella bacteremia a common association
Coagulopathy Thrombocytopenia with/without DIC
Differences between severe malaria in adults
and children
Management of Severe malaria:
Pre referral at Health centre
 Severe malaria is a medical emergency and treatment should begin
immediately.
 The commencement of lifesaving therapy must not be delayed.

 At a health centre level, initial treatment may be:

 Rectal artesunate
 IM artesunate (same dose as IV)
 IM quinine (10mg/kg or 0.2ml/kg)
Suppository and IM administration
Management of severe malaria: Inpatient
 ABCD approach and manage accordingly
 Secure IV line and give fluids accordingly (including shock)
 Make a thick blood smear for immediate malaria parasite count
 MRDT if smear not available
 Control fever if temperature is ≥38 ºC:
 Tepid sponge, fanning and paracetamol
 Manage convulsions: diazepam or paraldehyde
 Check for hypoglycemia and treat with glucose
 Start malarial treatment with
 Artesunate IV or IM (first-line)
 Quinine IV or IM (second-line)
Artesunate IV/IM dosing
 Patients < 20 kgs: artesunate 3 mg/kg
 Patients > 20kgs or adults: artesunate 2.4 mg/kg

 Artesunate is given at 0, 12 and 24 hour interval,

 then once daily for not more than six days (if unable to eat).
 Or switch to LA if patient is taking orals
 Start LA at least 8 hours after last dose of artesunate
Quinine dosing
 Quinine is administered with fluids as infusion
 5% dextrose or half strength Darrow's
 Loading dose 20 mg/kg diluted into 10 ml/kg and infuse over 3-4 hours.
 If patient received loading dose somewhere;
 give 10 mg/kg (same dilution) given over 3-4 hours-no loading dose.

 Subsequently: 10 mg/kg run for 3-4 hrs every 12 hours.

 Continue IV fluid (10 ml/kg given over 3 – 4 hours) between doses of

quinine.

 Switch to LA when patient able to take orals

Monitoring of admitted malaria patient
 Level of consciousness (using BCS or any coma score)
 Vital signs every 4 hours (T, PR, RR, BP)
 Fluid balance (input and output, signs of fluid overload)
 Increasing anemia (pallor, heart failure)
 Occurrence of convulsions
 Blood glucose every 4 hours while unconscious and also if convulsions
occur
 Hb/ Packed Cell Volume – at least daily, or more often if anemia is
suspected
 Ability to suck, drink, eat, sit and walk – measures of overall strength
Cerebral malaria (CM)
 It is a severe neurological syndrome of malaria caused by the
plasmodium falciparum (Pf) affecting mainly children.

 Criteria for cerebral malaria

 Coma (BCS<2, or GCS<11)
 No other cause of coma present
 Not in postictal phase or hypoglycemia excluded
 Normal CSF (or any cause of encephalopathy)

 Asexual forms of malaria parasites on BF

Clinical features of CM
 Impaired consciousness,
 convulsions, (focal seizures unusual),
 opisthotonos position
 conjugate gaze deviations
 respiratory rhythm abnormalities
 Cerebral edema and elevated intracranial pressure
 Retinopathy (on fundoscope)
 Cotton wool spots, retinal opacifications, vessel damage
Retinal changes in CM
Cerebral malaria long term sequelae
 Neurologic sequelae are more common among children than
adults (about 50 vs 3 percent, respectively)
 These deficits may include
 hemiplegia,
 cerebral palsy,
 cortical blindness,
 deafness,
 epilepsy,
 language deficit, and
 impaired cognition
Prevention of malaria
 Avoid exposure
 Exercise particular caution during peak biting periods
 Mosquito nets
 Protective clothing (covering most of the skin, light colors)
 Mosquito repellent, such as DEET (N,N-diethyl-meta-toluamide)

 Mosquito control
 Reduce breeding sites (e.g., eliminate pools of water, optimize plant watering)
 Insecticide spraying

 Prophylaxis
 SP in pregnancy and SCD
 Visitors? Doxycycline, chloroquine
TITHELE POMPA
KWA LERO
References
1. Guidelines for the treatment of malaria in malawi 5th Edition,
August 2020.
2. Protocols for the management of common childhood
illnesses in Malawi. QECH White book- 2017 edition
3. WHO Pocket book of Hospital care for children 2 nd edition
4. AMBOSS
5. UpToDate