OUTLINE MALARIA

● Malaria is endemic throughout most of the tropics.

I. Malaria ● Malaria is transmitted via the bite of a female Anopheles
II. Clinical Manifestations spp mosquito, which occurs mainly between dusk and
III. Life Cycle dawn
IV. Clinical Manifestations ● Malaria occurs throughout most of the tropical regions of
A. Uncomplicated Malaria the world, with Plasmodium falciparum causing the
B. Severe Malaria largest burden of disease, followed by Plasmodium vivax.
C. Diagnosis ● As of 2019, The Department of Health (DOH) said that
D. Antimalarial Drugs only four provinces in the country remain endemic for
V. Malaria Treatment And Management malaria -- the four provinces are Palawan, Sulu,
A. Classes Of Anti-Malarial Agents Occidental Mindoro, and Sultan Kudarat.
B. Anti-Malarial Agents
1. Artemisinin And Derivatives
2. Atovaquone
3. Diaminopyrimidines: Pyrimethamine
4. Proguanil
5. Quinolines And Related Compounds
a) Chloroquine & Hydroxychloroquine
b)Quinine and Quinidine
c) Mefloquine
d)Primaquine
e)Other Drugs
C. Malarial Chemoprophylaxis
1. Prophylaxis For Infections With
Chloroquine-Sensitive P. Falciparum,A P.
Vivax, P. Malariae, And P. Ovale:
a) Chloroquine Phosphate (Aralen)
2. Prophylaxis For Infections With
Drug-Resistant Strains Of P. Falciparum B
Or P. Vivax: The Choice Of Regimen
Depends On The Local Geographic Profile
Of Drug Resistance And Other Factors
a) Atovaquone-Proguanil (Malarone)
b)Mefloquine Hydrochloride (Lariam)
c) Doxycycline Hyclate (Vibramycin Or
Doxin)
d)Primaquine Phosphate
D. Txt And Mgt: Uncomplicated Malaria *SEE APPENDIX FOR LARGER IMAGE
E. Txt And Mgt: Uncomplicated Falciparum LIFE CYCLE
Malaria ● Pathogenesis of Plasmodium falciparum is the area of
F. Malaria In Pregnancy greatest study, since this species causes the most severe
G. Txt Of Severe Falciparum Malaria clinical disease.
H. Txt Of Malaria Caused By Vivax And Ovale ● Following the bite of an infected female Anopheles
I. Problem Of Drug Resistance mosquito, the inoculated sporozoites go to the liver
J. Management where they invade the hepatocytes within one to two
K. Prevention And Control hours. These cells divide many 1000-fold until mature
Italicized gray text are speaker’s notes from lecturer’s ppt. tissue schizonts are formed, each containing thousands of

CLIN PATH 1.0 | Transcribers

 daughter merozoites. This exoerythrocytic stage is
asymptomatic.
● Individuals are generally asymptomatic for 12 to 35 days
but can commence symptoms as early as 7 days
(depending on parasite species), until the erythrocytic
stage of the parasite life cycle.
● The liver schizonts rupture after 6 to 30 days; 98 percent
of patients experience liver schizogony by 90 days (there
is typically a longer liver phase in species other than P.
falciparum). This event releases thousands of merozoites
into the bloodstream. Release of merozoites from infected
red cells when they rupture causes fever and the other
manifestations of malaria.
● Some parasites differentiate into sexual erythrocytic
stages (gametocytes)
● The gametocytes, male (microgametocytes) and female
(macrogametocytes), are ingested by an Anopheles
mosquito during a blood meal .
● The parasites’ multiplication in the mosquito is known as
the sporogonic cycle . While in the mosquito’s stomach,
the microgametes penetrate the macrogametes
generating zygotes .
● The zygotes in turn become motile and elongated
(ookinetes) which invade the midgut wall of the
mosquito where they develop into oocysts . The oocysts
grow, rupture, and release sporozoites , which make their
way to the mosquito’s salivary glands.
● Inoculation of the sporozoites into a new human host
perpetuates the malaria life cycle .
*SEE APPENDIX FOR LARGER IMAGE
CLINICAL MANIFESTATIONS
Uncomplicated Malaria
● Malaria is a common cause of fever in tropical countries
● Lack of a sense of well-being
● Headache
● Fatigue
● Abdominal discomfort
● Myalgia
CLIN PHARM | Transcribers
● The symptoms of uncomplicated malaria can be rather
nonspecific and the diagnosis can be missed if health
providers are not alert to the possibility of this disease.
● Above symptoms are all similar to the symptoms of a
minor viral illness.
● Since untreated malaria can progress to severe forms
that may be rapidly (<24 hours) fatal, malaria should
always be considered in patients who have a history of
exposure (mostly: past travel or residence in
disease-endemic areas).
Severe Malaria
● Appropriately and promptly treated, uncomplicated
falciparum malaria carries a mortality rate of <0.1%.
● However, once vital-organ dysfunction occurs or the total
proportion of erythrocytes infected increases to >2%,
mortality risk rises steeply, depending on the immunity of
the host. The major manifestations of severe falciparum
malaria are shown, and features indicating a poor
prognosis are listed here:
● Coma is a characteristic and ominous feature of
falciparum malaria and, even with treatment, has been
associated with death rates of ~20% among adults.
● Any obtundation, delirium, or abnormal behavior in
falciparum malaria should be taken very seriously. The
onset of coma may be gradual or sudden following a
convulsion.
 DIAGNOSIS against hypnozoites (which can remain dormant in the
● Prompt and accurate diagnosis of malaria is critical for liver for months and, occasionally, years after the initial
implementation of appropriate treatment to reduce infection).
associated morbidity and mortality.
● The diagnosis of malaria is definitively established in the
setting of symptoms consistent with malaria and a
positive malaria diagnostic test

*SEE APPENDIX FOR LARGER IMAGE

● To date, microscopic examination of thick and thin blood
smears is the easiest and most reliable test for malaria..
thick and thin blood smears should be prepared and
MALARIA TREATMENT AND MANAGEMENT
examined immediately to confirm the diagnosis and
● PROTECTIVE
identify the species of infecting parasite
○ Prophylaxis
○ THICK SMEAR – detecting the parasites
● CURATIVE
○ THIN SMEAR – identify the species
○ Involves use of schizonticidal drugs for the
● If initial diagnostic evaluation is negative and clinical
treatment of acute attack and in relapse, and in
suspicion for malaria persists, follow-up testing should be
radical eradication of hypnozoites
performed each day for two more days
● PREVENTIVE
● P. falciparum–specific, histidine-rich protein 2 (PfHRP2)
○ Use of gametocytocidal drugs
● Plasmodium lactate dehydrogenase (pLDH) is the
○ Interruption of the sporogonic phase when
terminal enzyme in the malaria parasite glycolytic
mosquito feeds on the blood of an infected
pathway and is produced by asexual and sexual forms of
person given the appropriate sporonticidal
all Plasmodium species
compound
● Staining of parasites with the fluorescent dye acridine
CLASSES OF ANTI-MALARIAL AGENTS
orange allows more rapid diagnosis of malaria (but not
Class I agents:
speciation of the infection) in patients with low-level
● not reliable against primary or latent liver stages or
parasitemia.
against P. falciparum gametocytes
● Molecular diagnosis by polymerase chain reaction (PCR)
● Their action is directed against the asexual erythrocytic
amplification of parasite nucleic acid is more sensitive
forms.
than microscopy or rapid diagnostic tests for detecting
● These drugs will treat, or prevent, clinically symptomatic
malaria parasites and defining malarial specie
malaria.
ANTIMALARIAL DRUGS
● When used prophylactically, the class I drugs must be
● Antimalarial drugs are used for the treatment and
taken for several weeks after exposure until parasites
prevention of malaria infection. Most antimalarial drugs
complete the liver phase and become susceptible to
target the erythrocytic stage of malaria infection, which is
therapy.
the phase of infection that causes symptomatic illness.
● The extent of pre-erythrocytic (hepatic stage) activity for Class II agents:
most antimalarial drugs is not well characterized. ● target not only the asexual erythrocytic forms but also
● Treatment of the acute blood stage infection is necessary the primary liver stages of P. falciparum.
for malaria caused by all malaria species. In addition, for ● This additional activity shortens to several days the
infection due to Plasmodium ovale or Plasmodium vivax, required period for postexposure prophylaxis.
terminal prophylaxis is required with a drug active
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Class III (Primaquine):
● unique in its spectrum of activity, which includes reliable
efficacy against primary and latent liver stages as well as
gametocytes.
● has no place in the treatment of symptomatic malaria but
rather is used most commonly to eradicate the
hypnozoites of P. vivax and P. ovale, which are responsible
for relapsing infections.
● Since none of the drugs kills sporozoites, it is not truly
possible to prevent infection but only to prevent the
development of symptomatic malaria caused by the
asexual erythrocytic forms.
● None of the antimalarials is effective against all liver and
red cell stages of the life cycle that may coexist in the
same patient. Complete cure therefore may require more
than one drug.
ANTI-MALARIAL AGENTS
1. ARTEMISININ AND DERIVATIVES
● As a class, the artemisinins are potent and fast-acting
antimalarials with no clinical evidence of resistance.
● They are particularly well suited for the treatment of
severe P. falciparum malaria and now play a key role in
the combination therapy of drug-resistant infections.
● Antiparasitic Activity:
○ Act rapidly against the asexual erythrocytic
stages of P. vivax and P. falciparum.
○ They are not cross-resistant with other drugs
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○ They have gametocytocidal activity but do not
affect either primary or latent liver stages.
2. ATOVAQUONE
● Atovaquone is a highly lipophilic analog of ubiquinone.
● it has potent activity against blood stages of plasmodia
● It is active against liver stages of P. falciparum but not
against P. vivax hypnozoites
● This compound interferes with mitochondrial functions,
such as ATP and pyrimidine biosynthesis, in susceptible
malaria parasites.
● Resistance develop readily.
● Mechanism of Action: Selectively inhibits parasite
mitochondrial electron transport.
3. DIAMINOPYRIMIDINES: PYRIMETHAMINE
Antimalarial Actions:
● A slow-acting blood schizontocide
● Effective against hepatic forms of P. falciparum is less
than that of proguanil, but at therapeutic doses,
pyrimethamine fails to eradicate the latent tissue forms
of P. vivax or gametocytes of any plasmodial species.
4. PROGUANIL
Antimalarial Actions:
● In sensitive P. falciparum malaria, proguanil exerts
activity against both the primary liver stages and the
asexual red cell stages, thus adequately controlling the
acute attack and usually eradicating the infection.
5. QUINOLINES AND RELATED COMPOUNDS
5.1 Chloroquine and Hydroxychloroquine
Antimalarial Actions:
● Chloroquine is highly effective against erythrocytic forms
of P. vivax, P. ovale, P. malariae, and
chloroquine-sensitive strains of P. falciparum.
● It is the prophylaxis and treatment of choice when travel
to chloroquine-sensitive malaria endemic areas are
contemplated.
● It exerts activity against gametocytes of the first three
plasmodial species but not against those of P. falciparum.
● The drug has no activity against latent tissue forms of P.
vivax or P. ovale.
● Chloroquine concentrates in the food vacuoles of
susceptible plasmodia, where it binds to heme as it is
released during hemoglobin degradation and disrupts
heme sequestration.
● Failure to inactivate heme or even enhanced toxicity of
drug-heme complexes is thought to kill the parasites via
oxidative damage to membranes, digestive proteases,
and possibly other critical biomolecules.
● Taken in proper doses, chloroquine is an extraordinarily
safe drug; however, its safety margin is narrow, and a
single dose of 30 mg/kg may be fatal
● Toxic manifestations relate primarily to the cardiovascular
system and the CNS.
● Chloroquine doses of more than 5 g given parenterally
usually are fatal. Prompt treatment with mechanical
ventilation, epinephrine, and diazepam may be lifesaving.
5.2 Quinine and Quinidine
Antimalarial Actions:
● Quinine acts primarily against asexual erythrocytic forms;
it has little effect on hepatic forms of malarial parasites.
● Gametocidal for P. vivax and P. malariae but not for P.
falciparum.
● Quinine is used for the treatment of
Chloroquine-resistant malaria.
● Because of its toxicity and short half-life, quinine is not
used for prophylaxis.
● Quinidine gluconate:
○ IV to both adults and children starting with a
loading dose of 10 mg of the salt per kg dissolved in
300 ml of normal saline and infused over 1 to 2
hours (maximum dose 600 mg of the salt).
○ followed by continuous infusion at the rate of 0.02
mg of the salt/kg/minute for at least 24 hours and
until oral therapy with quinine sulfate is feasible.
○ During administration of quinidine gluconate, blood
pressure (for hypotension) and ECG (for widening of
the QRS complex and lengthening of the QT interval)
should be monitored continuously and total blood
glucose (for hypoglycemia) periodically. (These
complications, if severe, may warrant temporary
discontinuation of the drug.)
● Quinine sulfate:
○ can be substituted for quinidine gluconate once
patients can take oral medication.
○ The dose for adults is 650 mg of the salt given every
8 hours. The pediatric dose is 10 mg of the salt per
kg given every 8 hours.
○ Therapy with quinidine/quinine usually is given for 3
to 7 days on the species of Plasmodium and
geographical profile of drug resistance (7 days for P.
falciparum in Southeast Asia).
Side Effects:
● The fatal oral dose of quinine for adults is about 2 to 8 g.
● Quinine is associated with a triad of dose-related
toxicities when it is given at full therapeutic or excessive
doses: cinchonism, hypoglycemia, and hypotension.
● Hypoglycemia also is common, mostly in the treatment of
severe malaria
5.3 Mefloquine
● used for the prophylaxis and chemotherapy of
drug-resistant P. falciparum and P. vivax malaria.
● It is a highly effective blood schizontocide.
● no activity against early hepatic stages and mature
gametocytes of P. falciparum or latent tissue forms of i
5.4 Primaquine
Antimalarial Actions.
● Primaquine destroys primary and latent hepatic stages of
P. vivax and P. ovale and has clinical value for preventing
relapses of P. vivax or P. ovale malaria.
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● Exerts a marked gametocidal effect against all four
species of plasmodia that infect humans, especially P.
falciparum.
● Antimalarial effect is by generating reactive oxygen
species or by interfering with electron transport in
the parasite.
5.5 Other Drugs
● Tetracyclines
● Sulfonamides and Sulfones
● Halofantrine
● Amodiaquine
● Lumefantrine
MALARIAL CHEMOPROPHYLAXIS
A. Prophylaxis for infections with chloroquine-sensitive P.
falciparum,a P. vivax, P. malariae, and P. ovale:
A.1 CHLOROQUINE PHOSPHATE (ARALEN)
● Adults take 500 mg chloroquine phosphate (300 mg base)
weekly starting 1-2 weeks before entering an endemic
area and continuing for 4 weeks after leaving.
● The pediatric dosage is 8.3 mg/kg chloroquine phosphate
(5 mg base per kg, up to the maximum adult dose) taken
orally by the same schedule.
B. Prophylaxis for infections with drug-resistant strains of P.
falciparum b or P. vivax: The choice of regimen depends on
the local geographic profile of drug resistance and other
factors
Preferred regimens:
B.1 ATOVAQUONE-PROGUANIL (MALARONE)
● Adults and children over 40 kg should take one adult
tablet per day beginning 1-2 days prior to exposure and
continuing for 7 days after exposure
Note: For P. vivax malaria, atovaquone-proguanil may not be
as effective as mefloquine. Atovaquone-proguanil is not
recommended for children under 11 kg, pregnant women, or
those breast-feeding infants. Contraindicated in persons with
severe renal impairment.
B.2 MEFLOQUINE HYDROCHLORIDE (LARIAM)
● tablet 250 mg mefloquine hydrochloride, equivalent to
228 mg mefloquine base.
● Adults and children over 45 kg body weight take 250 mg
weekly starting 1-2 weeks before entering an endemic
area and ending 4 weeks after leaving.
● Pediatric doses, taken by the same schedule, are 5 mg/kg
for children up to 15 kg; 62.5 mg (1/4 tablet) for 15-19 kg;
125 mg (1/2 tablet) for 20-30 kg; 187.5 mg (3/4 tablet)
for 31-45 kg.
Note: Mefloquine is not recommended for children weighing
less than 5 kg or individuals with a history of seizures, severe
neuropsychiatric disturbances, sensitivity to quinoline
antimalarials, or cardiac conduction abnormalities.
B.3 DOXYCYCLINE HYCLATE (VIBRAMYCIN OR DOXIN)
● The adult dose of doxycycline is 100 mg daily
● For children over 8 years of age, the dosage is 2 mg/kg
given once daily, up to the adult dose.
● Prophylaxis with doxycycline should begin 1 day before
travel to an endemic area and end 4 weeks after leaving.
● This regimen is used in geographical areas where highly
multidrug-resistant strains of P. falciparum are prevalent.
Note: Doxycycline should not be given to children younger
than 8 years of age or to pregnant women. Prophylaxis with
doxycycline can be combined with the chloroquine phosphate
regimen shown above for chloroquine-sensitive malaria. This
strategy often is used in geographic areas where infection
with more than one Plasmodium species is likely.
B.4 PRIMAQUINE PHOSPHATE
● 15 mg primaquine base per tablet
● The adult dose is 30 mg base (two tablets) daily starting
several days before exposure and continued for 7 days
after exposure.
● Same regimen at a dose of 0.6 mg/kg base for children.
● Primaquine is contraindicated in G6PD deficiency or
pregnancy
● No chemoprophylactic regimen is always effective in
preventing malaria. Recommended drug regimens always
should be used in conjunction with other protective
measures to avoid mosquito bites
TXT AND MGT: UNCOMPLICATED MALARIA
Based on WHO Treatment guidelines 2006: Malaria
● Uncomplicated malaria - symptomatic malaria w/o signs
of severity or evidence of vital organ dysfxn. In acute
falciparum malaria there is a continuum from mild to
severe malaria. Young children and non-immune adults
with malaria may deteriorate rapidly.
● To counter the threat of resistance of P. falciparum to
monotherapies, and to improve txt outcome,
combinations of antimalarials are now recommended by
WHO for the txt of falciparum malaria.
Combination therapy:
● Antimalarial combination therapy is the simultaneous use
of 2 or more blood schizonticidal drugs with independent
modes of action and thus unrelated biochemical targets
in the parasite. The concept is based on the potential of
two or more simultaneously administered schizonticidal
drugs with independent modes of action to improve
therapeutic efficacy and also to delay the development of
resistance to the individual components of the
combination.
● Artemisinin and its derivatives:
○ artesunate, artemether, artemotil,
dihydro-artemisinin
○ Produce rapid clearance of parasitemia and rapid
resolution of symptoms
○ Reduce number of parasites by a factor of 10,000 in
each asexual cycle
○ Eliminated rapidly, but when combined with
anti-malarials that are slowly eliminated, they may
require shorter courses of treatment
○ Active against the 4 species
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○ Generally well-tolerated (hypersensitivity reaction:
urticaria)
TXT AND MGT: UNCOMPLICATED falciparum MALARIA
Combination therapy:
● The ff ACTS are currently recommended:
○ Artemether- lumefantrine
○ Artesunate + amodiaquine
○ Artesunate + mefloquine
○ Artesunate + sulfadoxine-pyrimethamine
The txt of choice for uncomplicated falciparum malaria is a
combination of two or more antimalarials with different
mechanisms of action.
ACTs are the recommended txts for uncomplicated
falciparum malaria
The ff ACTs are currently recommended:
- artemether-lumefantrine, artesunate +
amodiaquine, artesunate + mefloquine,
artesunate + sulfadoxine-pyrimethamine
The choice of ACTs in a country or region will be based on
the level of resistance of the pattern medicine in the
combination:
- in areas of MDR (South-East Asia), Artesunate +
mefloquine or artemether-lumefantrine
- in Africa, Artemether- lumefantrine, Artesunate +
amodiaquine, artesunate +
sulfadoxine-pyrimethamine
The artemisinin derivative components of the combination
must be given for at least 3 days for an optimum effect
Combination therapy (alternative agents):
Alternative ACT known to be effective in the region.
Artesunate (2 mg/kgbw OD) + Tetracycline (4mg/kg bw
four times a day) doxycycline (3.5mg/kg OD) or clindamycin
(10mg/kg bw twice a day). Any of these combinations to be
given for 7 days.
Quinine (10 mg salt/kg bw three times a day)) +
tetracycline or doxycycline or clindamycin. Any of these
combinations to be given for 7 days.
MALARIA IN PREGNANCY
● The antimalarials considered safe in the first trimester of
pregnancy are quinine, chloroquine, proguanil,
pyrimethamine, and sulfadoxine-pyrimethamine. Of
these, quinine remains the most effective and can be
used in all trimesters of pregnancy.
● Inadvertent exposure to antimalarials is not an indication
for termination of pregnancy.
First trimester: quinine + clindamycina to be given 7 days.
ACT should be used if it is the only effective treatment
available.
 Second and third trimester: ACT known to be effective in
the country/region or artesunate + clindamycin to be given
for 7 days or quinine + clindamycin to be given 7 days
a: If clindamycin is unavailable or unaffordable, then
monotherapy should be given.
● The amounts of antimalarials that enter breast milk are
therefore likely to be consumed by the breast-feeding
infant are relatively small. The only exception to this is
dapsone, relatively large amounts of which are excreted
in breast milk (14%% of the adult dose), and pending
further data this should not be prescribed. Tetracyclines
are also contraindicated because of their effect on an
infant's bone and teeth.
● Lactating women should receive standard antimalarial
treatment (including ACTs) except for tetracyclines and
dapsone, which should be withheld during lactation.
TXT OF SEVERE FALCIPARUM MALARIA
Severe Malaria is a medical emergency
After rapid clinical assessment and confirmation of the
diagnosis, full doses of parenteral antimalarial txt should
be started without delay with whichever effective
antimalarial is first available
Artesunate 2.4 mg/kg IV or IM given on admission (time
=0), then ar 12h and 24h, then OD is the recommended
choice in low transmission areas or outside malaria
endemic areas
For children in high transmission areas, the ff antimalarial
medicines are recommended as there is insufficient
evidence to recommend any of these antimalarial
medicines over another for severe malaria:
- Artesunate 2.4 mg/kg bw IV/IM given on admission
(time =0), then ar 12h and 24h, then OD
- Artemether 3.2 mg/kg bw IM given on admission
then 1.6 mg/kg bw per day
- quinine 20 mg salt/ days kg bw on admission ( IV
infusion or divided IM injection), then 10 mg/kg bw
every 8h; infusion rate should not exceed 5mg salt/kg
bw per hour.
TXT OF MALARIA CAUSED BY VIVAX AND OVALE
Chloroquine 25 mg/kg bw divided over 3 days, combined
with primaquine 0.25 mg base/kg bw, taken with food OD
for 14 days is the txt of choice for chloroquine-sensitive
infxns. In Oceania and South-East Asia the dose of
primaquine should be 0.5 mg/kg bw.
Amodiaquine (30 mg base/kg bw divided over 3 days as 10
mg/kg bw single doses) combined with primaquine should
be given for chloroquine-resistant vivax malaria.
In moderate G6PD deficiency, primaquine 0.75 mg base/kg
bw should be given once a week for 8 weeks. In severe
G6PD Deficiency, primaquine should not be given.
CLIN PHARM | Transcribers
Where ACT has been adopted as the first-line treatment for
P. falciparum malaria, it may also be used for P. vivax
malaria in combination with primaquine for radical cure.
Artesunate + sulfadoxine-pyrimethamine is the exception as
it will not be effective against P. vivax in many places
PROBLEM OF DRUG RESISTANCE
● Resistance of the parasite to drugs is graded according to
the patterns of asexual parasitemia after initiation of
treatment.
● RI: mildest form characterized by initial clearance of
parasites but recrudescence occurs within a month after
start of treatment.
○ Early: clearance in first 48 hrs,
recrudescence in 14 days from start of
treatment
○ Late: clearance in first 48 hrs,
recrudescence in 14 -28 days from start of
treatment
● RII: initial reduction of parasitemia but with failure of
clearance, followed by increased parasitemia soon after
● RIII: no reduction or even increased level of parasitemia
is observed
MANAGEMENT
● The approach to antimalarial selection is determined by
whether infection was acquired in an area with
chloroquine sensitivity or resistance and further
determined based on local antimalarial drug resistance
and government treatment guidelines as well as drug
availability and tolerability.
● In general, treatment of uncomplicated malaria consists
of oral therapy with a combination of two agents (in the
case of chloroquine resistance) or chloroquine
monotherapy (in the case of chloroquine sensitivity).
● The risk of death due to severe malaria is greatest in the
first 24 hours after clinical presentation.
● Intravenous therapy should be initiated promptly, with
close monitoring of parasite density. There are two major
classes of drugs available for parenteral treatment of
 severe malaria: the artemisinin derivatives (artesunate
and artemether) and the cinchona alkaloids (quinine and
quinidine)
PREVENTION AND CONTROL
● Personal protection: well-screened areas; use of
permethrin-treated mosquito nets; appropriate clothing;
use of insect repellants
● Chemoprophylaxis for travelers
● Vector control
END OF TRANSCRIPTION
APPENDICES

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