PROTOZOAL INFECTIONS

MALARIA
Clent Banaay, RMT, MD, MPM-HSD, CFP
Department of Microbiology and Parasitology
Southwestern University PHINMA School of Medicine
Objectives:

1. To discuss the Epidemiology and Life Cycle of

Plasmodium spp.
2. To discuss the Pathogenesis of Malarial infection
3. To describe the clinically important species of
Malaria in terms of Clinical manifestations,
Diagnosis and treatment
4. To establish competence in differentiating the
different species
5. To be able to recognize malarial infections
The disease was formerly called ague
or marsh fever due to its association
with swamps
Charles Louis Alphonse Laveran ,a French army surgeon
described the disease (1880)

Ronald Ross, a British officer in the Indian Medical Service,

was the first to demonstrate that malaria parasites could be
transmitted from infected patients to mosquitoes (1897)

Laveran
MALARIA
Plasmodium spp., the causative agent of
malaria, belongs to a larger phylum of
obligate intracellular parasites,
the Apicomplexa.
There are six species that cause malaria in
humans:
• Plasmodium falciparum,
• P. vivax,
• P. ovale curtisii, P. ovale wallikeri,
• and P. malariae
• P. knowlesi -is predominantly a zoonotic parasite
of Southeast Asian macaques, with as yet no
definitive evidence of primary human-to-human
transmission
 Epidemiology of Malaria

• Malaria remains the world's most devastating human parasitic infection.

• Malaria affects over 40% of the world's population.
• WHO, estimates that there are 350 - 500 million cases of malaria worldwide.
• In India 2 million cases and 1000 deaths annually.
• Malaria affects birds, lizards, rodents, non-human primates and humans

• Technically, in human malaria, the mosquito vector is the “definitive host”

because the parasite reproduces in them –Malaria (Plasmodium) needs
ananopheline mosquito and a vertebrate host to complete its cycle –The life cycle
complexity and tight species associations suggest co-evolution
• P. falciparum (also known as cerebral malaria) is the most
lethal
–estimated to cause 200 million clinical cases, and 1-3 million deaths
(including many children) every year world-wide

• Each year 350–500 million cases of malaria occur worldwide, and over
one million people die, most of them young children in sub-Saharan
Africa.
• In areas of Africa with high malaria transmission, an estimated 990,000
people died of malaria in 1995 –over 2700 deaths per day, or a death
every 30 seconds.
• One bite from an infected mosquito can mean weeks of fever and
exhaustion, preventing children from going to school and adults from
working to provide for their families.
• Estimated 5-fold reduction in GDP in countries –Estimated $12 billion
loss to Africa annually due to malaria
• •Close to 90% of malaria cases occur in Africa.
The malaria life cycle is a complex system with both sexual and asexual aspects .
cycle of all species that infect humans is basically the same.
There is an exogenous sexual phase in the mosquito called sporogony during which the parasite multiplies.
There is also an endogenous asexual phase that takes place in the vertebrate or human host that is called
schizogeny
Transmission

 Man – Intermediate host.

 Mosquito – Definitive host

– Sporozoites are infective

forms
 Present in the salivary gland
of female anopheles
mosquito
 After bite of infected
mosquito sporozoites are
introduced into blood
circulation.
Another mosquito arriving to
feed on the blood may suck up
these gametocytes into its gut,
where flagellation of
microgametocytes occurs, and
the macrogametocytes are
fertilized.
The resulting ookinete
penetrates the wall of a cell in
the midgut, where it develops
into an oocyst.

Sporogeny within the oocyst

produce many sporozoites and,
when the oocyst ruptures, the
sporozoites migrate to the
salivary gland, for injection
into another host.
Human Cycle

1 Pre erythrocytic
schizogony
2 Erythrocytic Schizogony
3 Gametogony
4 Exoerythrocytic
schizogony
Pre erythrocytic cycle
 Sprozoites undergo
developmental phase in the
liver cell
 Multiple nuclear divisions
develop to Schozonts
 A Schizont contains 20,000 –
50,000 merozoites.
Period of Pre erythrocytic cycle

 1 P.vivax 8 days
 2 P.falciparum – 6 days

 3 P. malariae - 13 – 16 days,

 4 P.ovale -9 days

On maturation Liver cells rupture Liberate

Merozoites into blood stream
Erythrocytic cycle
 Merozoites released invade red cells
 P.vivax infects young erythrocytes
 P.malariae Infects old erythrocytes
 P.falciparum infects RBC of all ages
 The Merozoites are pear shaped 1-5 microns in length
 The receptors for Merozoites are on red cells in the
glycoprotein
Erythrocytic Schizogony
 Liberated Merozoites
penetrate RBC
 Three stages occur

1 Trophozoites
2 Schizont
3 Merozoite
Exo-erythrocytic (tissue) phase
 P. malariae or P. falciparum sporozoites do not
form hypnotizes, develop directly into pre-
erythrocytic schizonts in the liver
 Schizonts rupture, releasing merozoites which
invade red blood cells (RBC) and hepatocytes in
liver
Gametogony
 Merozoites differentiate into Male and female
gametocytes
 They develop in the red cells
 Found in the peripheral blood smears
 Microgametocyte of all species are similar in size
 Macro gametocytes are larger in size.
Mosquito cycle: Sexual cycle
 Sexual cycle will be initiated in the Humans by the
formation of Gametocytes
 Develop further in the female Anopheles Mosquito
 Fertilization occurs when a Microgametocyte
penetrate into Macrogametocyte
 ZYGOTE is formed matures into OOKINETE
 OOKINETE to OOCYST
 OOCYST matures with large number of Sporozoites
( A few hundred to thousands)
Mosquito cycle
A definitive Host – Mosquito
Life cycle
Pathogenesis of Malarial infection
 The merozoites of P. falciparum develop in the parasitophorous vacuolar membrane (PVM) within the mature
red cells and modify the structural and antigenic properties of these cells.
 Malaria in the blood cell takes up the hemoglobin, causing Anemia, Dizziness, light-headedness, weakness,
arthralgia (general joint aches)
 The parasites feed on the hemoglobin resulting in the production of pigment known as hematin
 Body responds with a Spiking fever –different species cause different temperatures, cycles and durations.
 Also alters the cell surface, making it “sticky”, so it sticks to blood vessel walls, causing further anemia and
blockage of capillaries in the brain – Cerebral malaria
 P.vivax and P. ovale can hang out in the liver for a long time and periodically re-emerge –Longest recorded
incubation of vivax is 30 years –They can also go straight from there, and rip up the liver cells–causes
hepatitis issues
 Malaria can clog up lots of organs –the spleen, the liver, the brain, the kidneys –Renal failure can manifest as
“Blackwater Fever” wherein the hemoglobin from ruptured cells appears in the urine
 Cerebral issues cause developmental problems in children, especially from repeated infections
 Interaction with Host erythrocyte

EBA= Erythrocyte Glycophorins

the merozoite's apical end contains organelles and structures, 
 RBPs- Reticulocyte Binding Proteins
including micronemes (Attachment) and rhoptries (Invasion), which
 AMA1- RON= Apical Membrane Antigen
1 (AMA1) and the Rhoptry Neck
facilitate invasion upon erythrocyte contact Proteins (RONs).
Resistance from Malarial infection
 he three major types of inherited genetic resistance
(sickle-cell disease, Thalassemia, and glucose-6-
phosphate dehydrogenase deficiency)

 Glycophorin C deficiency and Absence of Duffy

antigen on the erythrocytes, because such blood
disorders confer a selective advantage against
malaria infection.
 9 days to 3 years incubation
period
 Onset of symptom: 8 days
30 days
 EARLY SIGNS AND
SYMPTOSM
➢ The common first symptoms –
fever, headache, chills and
vomiting – usually appear 10 to
15 days after a person is
infected.
➢ If not treated promptly with
effective medicines, malaria can
cause severe illness and is often
fatal.
➢ Malarial Paroxysm
Malaria stages of the Malarial
Paroxysms
Malarial Paroxysmal stages

Stage 1(cold stage)

 Chills for 15 minutes to 1 hour

 Caused due to rupture from the host red cells escape into
Blood
 Preset with nausea, vomiting, headache

Stage 2 (hotstage)
❑ Fever may reach upto 400c may last for several hours starts
invading newer red cells.
Clinical Malaria
Stage 3 (sweating stage)
❑ Patent starts sweating, concludes the episode

Cycles are frequently Asynchronous Paroxysms occur

every 48 – 72 hours.

In P. Malariae pyrexia may last for 8 hours or more

and temperature my exceed 410c
Malarial Paroxysm:
Periodicity can be clue in Diagnosis and species relation

 Malaria tertiana: 48h

between fevers (P.
vivax and ovale)

 Malaria quartana:
72h between fevers
(P. malariae)

 Malaria tropica:
irregular high fever (P.
falciparum)
Malaria the disease
Why Falciparum Infections are Dangerous

 Can produce fatal complications,

1.Cerebral malaria
2.Malarial hyperpyrexia
3.Gastrointestinal disorders.
4.Algid malaria(SHOCK)
5 Black water fever can lead to death
SEVERE COMPLICATED MALARIA
Confusion, or drowsiness with extreme weakness (prostration).
In addition, the following may develop:

➢ Alteration in the level of consciousness (ranging from drowsiness to deep

coma)
➢ Cerebral malaria (unrousable coma not attributable to any other cause in a
patient with falciparum malaria)
➢ Respiratory distress (metabolic acidosis bicarb less than 15 meq/l)
➢ Multiple generalized convulsions (2 or more episodes within a 24 hour
period)
➢ Shock (circulatory collapse, septicaemia)
➢ Pulmonary oedema
➢ Abnormal bleeding (Disseminated Intravascular coagulopathy)
➢ Jaundice
➢ Haemoglobinuria (black water fever)
➢ Acute renal failure - presenting as oliguria or anuria
➢ Severe anaemia (Haemoglobin < 5g/dl or Haematocrit < 15%)
➢ High fever
➢ Hypoglycaemia (blood glucose level < 2.2.mmol/l)
Pernicious Malaria
 Is a life threatening complication in acute falciparum
malaria
 It is due to heavy parasitization

 Clinical Manifestatiom:

1 Cerebral malaria – it presents with hyperpyrexia,

coma and paralysis.
2 Algid malaria – presents with clammy skin leading to
peripheral circulatory failure.
Cerebral Malaria

Malignant malaria can

affect the brain and the
rest of the central
nervous system. It is
characterized by
changes in the level of
consciousness, convulsions
and paralysis.
Cerebral Malaria

 Present with
Hyperpyrexia
 Can lead to Coma
 Paralysis and other
complications.
 Brain appears
congested
Pathogenesis of Cerebral malaria

High cytokine levels could be toxic on their own

High levels of cytokine also enhance the second process
thought to be responsible for cerebral malaria: sequestration
of infected RBCs
Sequestration & cytoadherence

 Rosetting (adhesion of
infected RBCs to other RBCs)
and clumping (adhesion
between infected cells) was
first observed in in vitro
culture
Black Water Fever
 In malignant malaria a large number of the
red blood corpuscles are destroyed.
Haemoglobin from the blood corpuscles is
excreted in the urine, which therefore is dark
and almost the colour of cola
Malaria Relapses

 In P. vivax and P. ovale infections, patients having

recovered from the first episode of illness may suffer
several additional attacks ("relapses") after months or
even years without symptoms.

 Relapses occur because P. vivax and P. ovale have

dormant liver stage parasites ("hypnozoites") that
may reactivate.
Relapse versus Recrudescence

 Without treatment P.falciparum will terminate in less

than 1 year.
 But in P.vivax and P.ovale persist as hypnozoites
after the parasites have disppeared from blood.
 Produce Periodic relapses upto 5 years
 In P. malariae may last for 40 years called as
Recrudescence
LABORATORY DIAGNOSIS
OF MALARIA
Diagnostic Tools
for Human Infections with Malaria

 Blood film examination(Microscopy)

 QBC (Quantitative Buffy Coat) system

 Rapid Diagnostic Tests" (RDTs)

 Antibody Detection Test

 PCR
 Microscopy
 Malaria parasites can be identified by
examining under the microscope a drop
of the patient's blood, spread out as a
"blood smear" on a microscope slide.
 Conventional approach by preparing a
thin and thick smears.
 Prior to examination, the specimen is
stained (most often with the Giemsa stain)
to give to the parasites a distinctive
appearance.
 This technique remains the gold standard
for laboratory confirmation of malaria.
 Comparison of Malarial species
Parameters P. falciparum P. vivax P. Ovale P. Malariae

Infected RBCs All RBCs Young RBCs Young RBCs Mature RBCs

Stages seen in the Ring forms and All stages All stages All stages
peripheral blood gametocytes
Length of asexual 48 hrs 48 hrs 48 hrs 72 hrs
cycle
Incubation period 8-15 days 12-20 days 11-16 days 18-40 days

Fever (attack) 48 hrs 48-72 hrs 48-72 hrs 72 hrs

pattern (alternating days) (alternating days) (on day 4)

Factors that influences the incubation period are; parasite strain, dose of sporozoites
inoculated, immune status of the host, chemoprophylaxis history.
 QBC system has evolved as rapid and
precise method in Diagnosis

 The QBC Malaria method is the

fastest, simple and sensitive method
for diagnosing the following diseases.
 Microcentrifugation, fluorescence and
density gradient of RBCs.
 91 % sensitivity, 94 % specificity
 Malaria
 Babesiosis
 Trypanosomiasis (Chagas disease,
Sleeping Sickness)
 Filariasis (Elephantiasis, Loa-Loa)
 Relapsing Fever (Borreliosis)
 Antigen Detection Methods

Antigen Detection
 Various test kits are available to detect antigens derived from
malaria parasites and provide results in 2-15 minutes. These
"Rapid Diagnostic Tests" (RDTs).
 Rapid diagnostic tests (RDTs) are immunochromatographic tests
based on detection of specific parasite antigens.
 Tests which detect histidine-rich protein 2 (HRP2) are specific
for P.falciparum while those that detect parasite lactate
dehydrogenase (pLDH)
 or aldolase have the ability to differentiate between
P.falciparum and non-P.falciparum malaria
 Newer Diagnostic methods

Molecular Diagnosis
 Parasite nucleic acids are detected using polymerase
chain reaction (PCR).
 This technique is more accurate than microscopy.
 However, it is expensive, and requires a specialized
laboratory (even though technical advances will likely
result in field-operated PCR machines).
 Treatment of Malaria
 The objectives of antimalarial treatment are to prevent severe
malaria and, for patients residing in endemic areas, to interrupt
transmission via anopheline vectors, among others.
 The National Malaria Program aims to eliminate the disease by
2030; thus, compliance to guidelines and treatment with highly
effective drugs are critical.
 Response to malaria treatment must be monitored with daily blood
film microscopy until the end of administration of the first line drugs,
then weekly until the 28th day after the start of treatment.
 The second line drug is administered when asexual forms of the
parasite are detected in blood films during this specified period.
 Recurrence of asexual parasitemia with the first line drugs must also
be immediately reported to the Department of Health
 THE PHARMACOLOGY OF ANTIMALARIALS
Class Definition Class Definition Examples Class Definition Examples
Examples
Blood Act on (erythrocytic) stage of the Quinine, artemisinins,
schizonticidal parasite thereby terminating amodiaquine, chloroquine,
drugs clinical illness lumefantrine, tetracyclinea ,
atovaquone, sulphadoxine,
clindamycina , proguanila
Tissue Act on primary tissue forms of Primaquine, pyrimethamine,
schizonticidal plasmodia which initiate the proguanil, tetracycline
drugs erythrocytic stage. They block
further
development of the
infection
Gametocytocidal Destroy sexual forms of the Primaquine, artemisinins,
drugs parasite thereby preventing quinineb
transmission of infection to
mosquitoes
a Slow acting, cannot be used alone to avert clinical symptoms
b Weakly gametocytocidal
 THE PHARMACOLOGY OF ANTIMALARIALS (cont.)

Class Definition Class Definition Examples Class Definition Examples

Examples

Hypnozoitocidal drugs These act on persistent Primaquine, tafenoquine

liver stages of P.ovale
and P.vivax which cause
recurrent illness

Sporozontocidal drugs These act by affecting Primaquine, proguanil,

further development of chlorguanil
gametocytes into oocytes
within the mosquito thus
abating transmission
 1. Treatment of severe falciparum malaria
Preferred regime Alternative regime

➢IV Artesunate (60mg): 2.4mg/kg on ➢IV Quinine loading 7mg salt /kg over 1hr
admission, followed by 2.4mg/kg at 12h & followed by infusion quinine 10mg salt/kg over
24h, then once daily for 7 days. 4 hrs, then 10mg salt/kg Q8H or IV Quinine
20mg/kg over 4 hrs, then 10mg/kg Q8H.
➢Once the patient can tolerate oral therapy, Plus
treatment should be switched to a complete ➢Adult & child >8yrs old: Doxycycline
dosage of Riamet (artemether/lumefantrine) (3.5mg/kg once daily)
for 3 day. or
➢Pregnant women & child < 8yrs old:
Clindamycin (10mg/kg twice daily). Both drug
can be given for 7 days.
➢Reconstitute with 5% Sodium Bicarbonate & ➢Dilute injection quinine in 250ml od D5%
shake 2-3min until clear solution obtained. and infused over 4hrs.
Then add 5ml of D5% or 0.9%NaCl to create
total volume of 6ml. ➢Infusion rate should not exceed 5 mg salt/kg
➢Slow IV injection with rate of 3-4ml/min or per hour.
IM injection to the anterior thigh.
➢The solution should be prepared freshly for
each administration & should not be stored.
 2. Treatment of uncomplicated p.falciparum
Preferred regime Alternative regime
Artemether plus lumefantrine(Riamet) Quinine sulphate (300mg/tab)
(1 tab: 20mg artemether/120mg lumefantrine)
Weight Day 1 Day 2 Day3 Day 1-7: Quinine 10mg salt/kg PO
Group Q8H
5-14kg 1 tab stat then 1 tab 1 tab
8hr later Q12H Q12H Plus
*Doxycycline (3.5mg/kg once a day)
15-24kg 2 tab stat then 2 tab 2 tab
8hr later Q12H Q12H OR
25-34kg 3 tab stat then 3 tab 3 tab
8hr later Q12H Q12H *Clindamycin (10mg/kg twice a day)
>34kg 4 tab stat then 4 tab 4 tab
8hr later Q12H Q12H *Any of these combinations should be
given for 7 days.
Take immediately after a meal or drink containing at Doxycycline: Children>8yr
least 1.2g fat to enhance lumefantrine absorption. Clindamycin: Children<8yr
Add primaquine 0.75mg base salt/kg single dose if gametocyte is present at any time during
treatment.
 Children under 5 kg or below 4 months should not be given Riamet instead treat
with the following regimen (see table).

Dosage and administration Plasmodium falciparum for young infant

Weight
Age Group Artesunate or *Quinine
group

Oral Quinine
** IM first dose 10
Artesunate 1.2 ***Oral Artesunate mg/kgTDS
0 - 4 months <5 kg mg/kg or IM 2mg/kg/day day 2 for 4 days
Arthemeter 1.6 to day 7 then 15-20
mg/kg) mg/kg TDS
for 4 days

Source: Malaria in Children, Department of tropical Pediatrics, Faculty of Tropical Medicine, Mahidol University.

** Preferably Artesunate/Artemether IM on day 1 if available

*** When Artesunate/Artemether IM is unavailable, give oral Artesunate from day 1 to day 7
* Treat the young infant with Quinine when oral Artesunate is not available
3. Treatment of malaria caused by p.knowlesi &
mixed infection (p. falciparum + p. vivax)

 Treat as P. falciparum
 4. Treatment of of malaria caused by p.vivax, p. ovale or p. malariae.

CHLOROQUINE
PRIMAQUINE
(150 mg base/tab) 25 mg
(7.5 mg base/tab)
base/kg divided over 3 days

Day 1 Day 2 Day 3

➢Start concurrently with CHLOROQUINE 0.5
mg base/kg Q24H for 2 weeks
➢Take with food
10mg ➢Check G6PD status before start primaquine
base/kg 5mg 5mg ➢In mild-to-moderate G6PD deficiency,
stat, then base/kg base/kg primaquine 0.75 mg base/kg body weight
5mg Q24H Q24H given once a week for 8 weeks.
base/kg ➢In severe G6PD deficiency, primaquine is
contraindicated and should not be used.

1 tab of chloroquine phosphate 250mg equivalent to 150mg base. Calculation of dose for
chloroquine is based on BASE, not SALT form. 1 tab of primaquine phosphate contains 7.5mg
base.
 Treatment in specific population & situations

Specific Preferred regime Alternative regime

populations
Pregnancy Quinine plus clindamycin to be given for 7 day Artesunate plus Clindamycin for 7
days is indicated if first line
treatment fails
Lactating Should receive standard antimalarial treatment (including ACTs) except for dapsone,
women primaquine and tetracyclines, which should be withheld during lactation

Hepatic Chloroquine: 30-50% is modified by liver, appropriate dosage adjustment is needed,

impairment monitor closely.
Quinine : Mild to moderate hepatic impairment-no dosage adjustment, monitor
closely.
Artemisinins : No dosage adjustment
Renal Chloroquine : ClCr<10ml/min-50% of normal dose.
Impairment Hemodialysis, peritoneal dialysis: 50% of normal dose.
Continuous Renal Replacement Therapy(CRRT) :100% of normal dose.
Quinine : .ClCr 10-50ml/min : Administer Q8-12H, CLCr<10ml/min : administer
Q24H,Severe chronic renal failure not on dialysis : initial dose: 600mg followed by
300mg Q12H, Hemo- or peritoneal dialysis: administer Q24H ,Continuous
arteriovenous or hemodialysis: Administer Q8-12H.
Artemisinin : no dosage adjustment.
 Treatment of complications of malaria

 Severe & complicated falciparum or knowlesi

malaria is a medical emergency that requires
intervention and intensive care as rapidly as
possible.
 Fluid, electolyte glucose & acid-base balance

must be monitored.Intake & output should be

carefully recorded.
 Immediate clinical management of severe manifestations and
complications of P. falciparum malaria

Definitive clinical features Immediate management/treatment

Come (Cerebral malaria) Monitor & record level of consciousness using Glaslow coma
scale, temperature, respiratory, and depth, BP and vital signs.
Hyperpyrexia (rectal body Treated by sponging, fanning &with an antipyretic drug.
temperature >40°C) Rectal paracetamol is preferred over more nephrotoxic drugs
(e.g. NSAIDs)
Convulsions A slow IV injection of diazepam(0.15mg/kg, maximum 20mg
for adults).
Hypoglycaemia (glucose Correct with 50% dextrose (as infusion fluids). Check blood
conc. <2.8mmol/L) glucose Q4-6H in the first 48hrs.
Severe anaemia (hb < Transfuse with packed cells. Monitor carefully to avoid fluid
7g/dl) overload. Give small IV dose of frusemide, 20mg, as necessary
during blood transfusion to avoid circulatory overload.
Acute pulmonary Edema Prop patient upright (45°), give oxygen, give IV diuretic (but
most patient response poorly to diuretics), stop intravenous
fluids. Early mechanical ventilation should be considered.
 Immediate clinical management of severe manifestations and
complications of P. falciparum malaria (cont.)

Definitive clinical features Immediate management/treatment

Acute renal failure (urine ➢Exclude pre-renal causes by assessing hydration status.
output <400ml in 24hrs in ➢Rule out urinary tract obstruction by abdominal examination or
adults or 0.5ml/kg/hr, ultrasound.
failing to improve after ➢Give intravenous normal saline
rehydration & a serum ➢If in established renal failure add haemofiltration or
creatinine of >265μmol/L) haemodialysis, or if unavailable, peritoneal dialysis.
Disseminated intravascular ➢Transfuse with packed cell, clotting factors or platelet.
Coagulopathy (DIVC) ➢Usual regime: Cryoprecipitate 10units,platelets 4-8units, fresh
frozen plasma(10-15ml/kg).
➢For prolonged PT, give vitamin K, 10mg by slow IV injection.

metabolic acidosis ➢Infuse sodium bicarbonate 8.4% 1mg/kg over 30min and
repeat if needed.
➢if severe, add haemodialysis.
Shock (hypotension with ➢Suspect septicaemia, take blood for cultures; give parenteral
systolic blood pressure broad-spectrum antimicrobials, correct haemodynamic
<70mmHg) disturbances.
 Monitoring & follow-up

 Blood smear should be repeated daily (twice daily in severe

infection). Within 48-72 hr after start of treatment, patients usually
become afebrile and improve clinically except in complicated cases.
 All patients should be investigated with repeated blood film of
malarial parasite one month upon recovery of malarial infection, to
ensure no recrudescence.
 Malaria surveillance is the continuous and systematic collection,
analysis and interpretation of malaria-related data, and the use of
that data in the planning, implementation and evaluation of public
health practice. Improved surveillance of malaria cases and deaths
helps ministries of health determine which areas or population
groups are most affected and enables countries to monitor changing
disease patterns
WHO strategy for elimination
The WHO Global technical strategy for malaria 2016–2030 provides a
technical framework for all malaria-endemic countries. It is intended to
guide and support regional and country programs as they work towards
malaria control and elimination.

The strategy sets ambitious but achievable global targets, including:

 reducing malaria case incidence by at least 90% by 2030

 reducing malaria mortality rates by at least 90% by 2030

 eliminating malaria in at least 35 countries by 2030

 preventing a resurgence of malaria in all countries that are malaria-

free
 Prevention and Control
Avoid mosquito bites:
➢Wearing long sleeves, trousers.

➢Insecticide Treated Bed nets

➢Repellent creams or sprays.

❑ Vaccination
➢ WHO also recommends broad use of the
RTS,S/AS01 malaria vaccine among
children living in regions with moderate to
high P. falciparum malaria transmission. The
vaccine has been shown to significantly
reduce malaria, and deadly severe
malaria, among young children.
Vector Control

 Anopheles gambiae from northeast Brazil and thus from the New World was
achieved in 1940 by the systematic application of the arsenic-containing compound
Paris green to breeding places, and of pyrethrum spray-killing to adult resting
places.
 Dichloro-Diphenyl Trichloroethane (DDT) – insecticides for houses and
buildings.
 Pyrethrum- (from the flowering plant Chrysanthemum [or Tanacetum] cineraria
folium) is an economically important source of natural insecticide Pyrethrins attack
the nervous systems of all insects.
 Chemoprophylaxis

 Indicated for travellers travel to endemic

areas.
 Mefloquinine 250mg weekly (up to 1 year)

or doxycycline 100mg daily (up to 3

month), to start 1 week before and
continue till 4 weeks after leaving the area.
Dosing schedule for Mefloquine
Weight Age No of tablets per
week
< 5 kg < 3 months Not
recommended
5 - 12 kg 3 - 23 months 1/4
13 - 24 kg 2 - 7 yrs 1/2
25 - 35 kg 8 - 10 yrs 3/4
36 and above 11 yrs and above 1
Dosing schedule for doxycycline

Weight in kg Age in years No of tablets

< 25 <8 Contraindicated
25 - 35 8 - 10 ½
36 - 50 11 - 13 ¾
50+ 14+ 1