INTERNAL MEDICINE 3A—INFECTIOUS DISEASES: MALARIA
• Merozoites invade RBCs to become trophozoites and
MALARIA
• Protozoan disease transmitted by the bite of an
infected female Anopheles mosquito
• Most important parasitic disease in humans
• Transmitted in 106 countries; 200 deaths per day
ETIOLOGY AND PATHOGENESIS
• 6 species of genus Plasmodium: P. falciparum (most
severe infection), P. vivax, P. ovale (2 identical species),
P. malariae, and P. knowlesi (monkey malaria parasite
in SEA)
• P. falciparum à malignant tertian; rupture of RBCs on
the 3rd day; ovale and vivax are benign tertian;
knowlesi is quotidian
• P. ovale not seen in the PH
• Almost all deaths are caused by P. falciparum; P. vivax
and P. knowlesi also can cause severe illness
• Human infection begins when a female Anopheles
mosquito inoculates sporozoites from its salivary
glands during a blood meal
• Carried rapidly to the liver via the bloodstream à
invades parenchymal cells à begins
preerythrocytic/intrahepatic schizogony or merogony
(asexual reproduction)
• Single sporoizote produces 10,000 to >30,000 daughter
merozoites
• Swollen infected liver cells eventually burst à release
of motile merozoites into the bloodstream
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multiply 6-20 fold
o P. knowlesi: every 24 hrs (quotidian)
o P. malariae: every 72 hrs
o P. vivax, ovale, falciparum: every 48 hrs
• Symptomatic stage begins when the parasite density
reaches 50/uL of blood (~100 M parasites in the blood
of an adult)
• P. vivax and P. ovale à not all intrahepatic forms
divide immediately but remain inert for a period
ranging from 3 weeks to ≥ 1year
o Dormant forms or hypnozoites à cause of
relapses
• Entry to RBCs is made by attachment mediated via
specific erythrocyte surface receptors
o P. falciparum: Reticulocye-binding protein
homologue 5 (PfRh5) and its erythrocyte
receptor Basigin
o P. vivax: receptor is related to the Duffy
blood-group antigen Fya or Fyb
§ Duffy-negative FyFy phenotypes
are resistant to P. vivax malaria
(West Africans)
• Early stage of development à small “ring” forms
appear similar
• As trophozoites enlarge, species-specific
characteristics become evident
o Pigment becomes visible
o Parasite assumes an irregular or amoeboid
shape
• By the end of the intraerythrocytic life cycle à parasite
has consumed 2/3rds of the RBC’s hemoglobin and
occupies most of the cell à schizont à undergoes
multiple nuclear divisions à RBC ruptures releases 6-
30 daughter merozoites à invade new RBCs and
repeat cycle
• Disease is caused by direct effects of the asexual
parasite (RBC invasion and destruction) and host
reaction
• Blood-stage parasites eventually develop into longer-
lived sexual forms (gametocytes) which is ingested by
the mosquito
• Male and female gametocytes unite in the mosquito’s
midgut to form a zygote à matures into an ookinete
which penetrates and encysts in the gut wall à oocyst
 INTERNAL MEDICINE 3A—INFECTIOUS DISEASES: MALARIA
• Oocyst divides asexually and bursts, releasing motile
sporozoites which then migrate in the hemolymph to
the salivary gland of the mosquito
• Infective stage to HUMAN: sporozoite
• Infective stage to MOSQUITO: gametocyte
Remember DLSU for the vector of Dengue:
Daybiting, Low-flying, Stagnant water, Urban areas
Opposite of this would be MALARIA! Night-biting,
High-flying, Running water, rural areas
EPIDEMIOLOGY
• Occurs throughout most of the tropical regions
• P. falciparum à Africa, New Guinea, and Hispaniola
(DR and Haiti)
• P. vivax à more common in Central America
• P. malariae à sub-Saharan Africa, much less common
• P. ovale à unusual outside of Africa and comprises <1%
of isolates
• P. knowlesi à Borneo and SEA
• Endemicity à based on parasetemia rates and
palpable-spleen rates in children 2-9 years
o Hypoendemic (<10%)
o Mesoendemic (11-50%)
o Hyperendemic (51-75%)
o Holoendemic (>75%)
• Holo- and hyperendemic areas à more than 1
infectious mosquito bite per day à morbidity and
mortality are high during early childhood; adults are
mostly asymptomatic (immunity)
• Stable transmission—constant, frequent, year-round
infection
• Unstable transmission—low, erratic, or
transmission
o Full protective immunity is not acquired
o Symptomatic disease in all ages
o Usually in hypoendemic areas
• Increased mosquito breeding and transmission during
rainy season à increased incidence of symptomatic
malaria
• Changes in environmental, economic, or social
conditions (heavy rains, migrations) à epidemic may
develop à considerable mortality in all age groups
• Principal determinants of epidemiology of malaria
o Number (density)
INTERNAL MEDICINE 3A—INFECTIOUS DISEASES: MALARIA STRAWBERRY
o Human-biting habits
o Longevity of anopheline mosquito vectors
• Gametocyte ingestion to inoculation lasts 8-30 days,
depending on ambient temperatue
• To transmit malaria, mosquito must survive for >7
days
• Sporogony is not completed in cooler temperatures à
transmission does not occur below these
o <16C for P. vivax
o <21C for P. falciparum
• Characteristics of the most effective mosquito vectors
(Anopheles gambiae)
o Long-lived
o High densities in tropical climates
o Breed readily
o Preference for biting humans
• Entomologic inoculation rate à most common
measure of malarial transmission
o the number of sporozoite-positive mosquito
bites per person per year
o <1 in Latin America and SEA; >300 in Africa
ERYTHROCYTIC CHANGES IN MALARIA
• Growing parasite progressively consumes and
degrades intracellular proteins, mainly hemoglobin
• Heme is potentially toxic à detoxified by lipid-
mediated crystallization to biologically inert
hemozoin (malarial pigment)
• RBC membrane alteration
o Changing transport properties
o Exposing cryptic surface Ag
o Inserting new parasite-derived proteins
focal
• RBC becomes more irregular in shape, more antigenic,
and less deformable
• Plasmodium Falciparum à membrane protuberances
appear 12-15h after cell invasion
o “knobs” extrude erythrocyte membrane
adhesive protein (PfEMP1) à mediates
attachment to receptors on venular and
capillary endothelium à cytoadherence
o Several vascular receptors
§ Intercellular adhesion molecule 1
in the brain
 INTERNAL MEDICINE 3A—INFECTIOUS DISEASES: MALARIA

§ Chondroitin sulfate B in the • Genetic disorders confer protection against death from
placenta falciparum malaria:
§ CD36 in other organs o Sickle cell disease
o Infected RBCs stick inside blood vesselsà o Hemoglobins C and E
obstructed capillaries and venules o Hereditary ovalocytosis
o Infected RBCs may also adhere to uninfected o Thalassemias
RBC (rosettes) and other parasitized RBC o G6PD deficiency
(agglutination) • HbA/S heterozygotes (sickle cell trait) à 6-fold
o Sequestration of RBCs with mature parasites reduction in the risk of dying from severe falciparum
in vital organs (brain) malaria
o Splenic processing and filtration: • Hemoglobin S-containing RBCs à impair parasite
sequestered parasites continue to develop out growth at low oxygen tensions
of reach of the host defense mechanism • Hemoglobin S and C à reduced cytoadherence d/t
o Only the younger ring forms are seen reduced surface adhesion PfEMP1
circulating in peripheral blood • α-thalassemia à more frequent malaria (vivax and
o Level of peripheral parasetimia falciparum) à infection pattern appears to protect
underestimates true number of parasites in them from severe disease
the body • Ovalocytosis à rigid RBCs à resist invasion by
o Reduced deformability of uninfected RBCs merozoites; hostile intracellular milieu
à shortened RBC survival • Exposure to sufficient strains à protection from high-
• Sequestration does not occur in other human malarias: level parasitemia and disease but not infection
all stages of development are evident on PBS • State of infection without illness à premunition
• P. vivax and ovale à predilection for young RBCs • Asymptomatic parasitemia common among adults
• P. malariae à predilection for old RBCs and older children living in regions with stable and
intense transmission
HOST RESPONSE • Immunity is mainly specific for both strain and species
• Both humoral and cellular immunity are needed for
• Initial response à activation of nonspecific defense
protection
mechanisms à stops expansion of infection
• Immune individuals have a polyclonal increase in
• Strain-specific immune response à controls infection
serum levels of IgG, IgM, and IgA
• Splenic immunologic and filtrative clearance functions
• Antibodies to parasitic antigens limit in vivo parasitic
are augmented
replication (most important of these antigens is surface
• Removal of both parasitized and uninfected RBCs is
antigen PfEMP1)
accelerated
• Passively transferred IgG from immune adults to
• Parasitized RBCs escaping splenic removal are
children à reduces level of parasitemia in the latter
destroyed when the schizont ruptures à release of
• Maternal antibodies contribute to relative protection
proinflammatory cytokines and activation of
(not complete) of infants from severe malaria in the 1st
macrophages à fever
months of life
• Temperatures of ≥40C damage mature parasites
• Immunity to disease declines when a person lives
àfurther synchronize the parasitic cycle à regular
outside an endemic area for several months or longer
fever spikes and rigors
• Parasites may persist in the blood for months or years
o Quotidian: daily
if treatment is not given
o Tertian: every 2 days
o Quartan: every 3 days

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 INTERNAL MEDICINE 3A—INFECTIOUS DISEASES: MALARIA

CLINICAL FEATURES • CEREBRAL MALARIA à COMA is a characteristic
and ominous feature; death rates of ~20% in adults and
• First symptoms are nonspecific (lack of sense of well- 15% among children
being, headache, fatigue, discomfort, muscle aches o Secondary to tissue anoxia
followed by fever) à similar to a minor viral illness o Onset may gradual or sudden following a
• Headache may be severe à NO photophobia and neck convulsion
stiffness like that seen in meningitis o Manifests as diffuse symmetric
• Myalgia may be prominent à not usually as severe as encephalopathy (focal neurologic signs are
that of dengue and muscles are not tender like in unusual)
leptospirosis or typhus o (-) signs of meningeal irritation; with SOME
• Nausea, vomiting, and orthostatic hypotension are passive resistance to head flexion
common o Corneal reflexes intact (except in deep coma)
• Classic malarial paroxysms (fever spikes, chills, and o Muscle tone may be increased or decreased
rigors at regular intervals) à relatively unusual and o Tendon reflexes variable; plantar reflexes
associated with P. vivax or P. ovale may be extensor/flexor; (-) cremasteric and
• Fever is usually irregular at first; temp. rises above abdominal reflexes
40C in children and nonimmune individuals, with o Flexor or extensor posturing may be seen
delirium and tachycardia o Fundoscopic abnormalities:
• Generalized seizures à P. falciparum; heralds § Retinal hemorrhages with pupillary
development of cerebral malaria dilation à15%
• Uncomplicated malaria à few abnormal PE findings § Discrete spots of retinal
other than fever, malaise, mild anemia, and palpable opacification à 30-60%
spleen § Papilledema à 8% in children, rare
• Anemia à common in young children living in areas in adults
with stable transmission with resistance to § Cotton wool spots à <5%
antimalarials § Decolorization of a retinal vessel or
• Spleen takes several days to be palpable in nonimmune vessel segment à occasional
individuals; splenic enlargement is found in a high o Generalized and repeated convulsions à 10%
proportion of otherwise healthy individuals in in adults, 50% in children
endemic areas à indicates repeated infections § Covert seizure activity in children :
• Liver findings: mild enlargement (young children); repetitive tonic-clonic eye
mild jaundice among adults with uncomplicated movement and hypersalivation
malaria, resolves in 1-3 weeks § Adults rarely suffer neurologic
• No associated rash! sequelae (<3%)
• Petechial hemorrhages à only VERY RARE in severe § Residual neurologic deficits in
falciparum malaria children (10% of surviving cases esp.
with hypoglycemia, severe anemia,
SEVERE FALCIPARUM MALARIA repeated seizures, and deep coma)
• Hemiplegia
• Uncomplicated malaria if appropriately and promptly
Cerebral palsy
treated à mortality rate of <0.1%
• Cortical blindness
• Vital-organ dysfunction OR total infected
• Deafness
erythrocytes increases to >2% à mortality rate rises
• Impaired cognition
steeply
(learning, planning,
executive, attention,

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 INTERNAL MEDICINE 3A—INFECTIOUS DISEASES: MALARIA

memory and nonverbal § Anaerobic glycolysis in tissues
functioning) where sequestered parasites
• Persistent language deficit interfere with microcirculatory flow
• Increased rates of epilepsy § Lactate production by parasites
• Decreased life expectancy § Failure of hepatic and renal lactate
clearance
• HYPOGLYCEMIAà important and common
complication of severe malaria • NONCARDIOGENIC PULMONARY EDEMA
o Associated with a poor prognosis and o Pathogenesis is unclear
particularly problematic in pregnant women o Mortality is >80%
and children o Can be aggravated by overly vigorous
o Results from a failure of hepatic administration of IV fluid
o Can develop in otherwise uncomplicated
gluconeogenesis and increased glucose
vivax malaria à recovery is usual
consumption by the host and parasites
o Quinine à powerful stimulant of
• RENAL IMPAIRMENT à AKI common in severe
pancreatic insulin secretion à falciparum malaria; oliguric RF rare in children
hyperinsulinemic hypoglycaemia in o Related to RBC sequestration and
pregnant women being treated with agglutination interfering with renal
quinine microcirculation and metabolism
o Usual physical signs of hypoglycaemia o Manifests as acute tubular necrosis
(sweating, gooseflesh, tachycardia) à o Renal cortical necrosis NEVER DEVELOPS!
o ARF may occur simultaneously with other
ABSENT à makes dx difficult
vital-organ dysfunctions
o Neurologic impairment
o Urine flow resumes in a median of 4 days and
indistinguishable from cerebral malaria
serum creatinine normalizes in 17 days

o Early dialysis or hemofiltration à enhances
• ACIDOSIS à important cause of death
likelihood of survival particularly in
o d/t accumulation of organic acids
hypermetabolic RF
o hyperlactatemia commonly coexists with
hypoglycemia
• HEMATOLOGIC ABNORMALITIES
o coexisting renal impairment compounds
o Anemia à accelerated removal of RBCs by
acidosis in adults; ketoacidosis in children
the spleen, obligatory RBC destruction at
o Acidotic breathing “respiratory distress” à
parasite schizogony, and ineffective
sign of poor prognosis
erythropoiesis
o Often followed by circulatory failure
o Reduced deformability of both infected and
refractory to volume expansion or inotropic
uninfected RBC à prognosis and
drug treatment à respiratory arrest
development of anemia
o Serum bicarbonate or lactate à best
o Increased splenic clearance of all RBCs
biochemical prognosticators in severe
o Anemia develops rapidly and transfusion is
malaria
required in nonimmune individuals and in
o Hypovolemia à NOT a major contributor to
areas with unstable transmission
acidosis
o Anemia is a common consequence of
o Lactic acidosis à if severe, poor prognosis!
antimalarial drug resistance à repeated or
continued infection

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 INTERNAL MEDICINE 3A—INFECTIOUS DISEASES: MALARIA
o Mild thrombocytopenia is usual (if platelet
count is normal, QUESTION THE DX OF
MALARIA!)
o <5% have significant bleeding w/ evidence of
disseminated intravascular coagulation
o Hematemesis from stress ulceration or acute
gastric erosion à also may occur rarely
• LIVER DYSFUNCTION
o Mild hemolytic jaundice is common
o Severe jaundice associated with P. falciparum;
adults > children; results from cholestasis,
hemolysis, and hepatocycte injury
o Poor prognosis if accompanied by other vital-
organ dysfunction (often renal impairment)
o Deep jaundice w/o other vital-organ
dysfunction à good prognosis
• OTHER COMPLICATIONS
o HIV/AIDS and malnutrition predispose to
more severe malaria
o Worsened by concurrent infections with
intestinal helminths (hookworm)
o Septicemia à young children
o Salmonella bacteremia à assoc. with P.
falciparum infection
o Chest infections and catheter-induced
urinary tract infections common among
patients unconscious for >3 days
o Aspiration pneumonia following
generalized convulsions
MALARIA IN PREGNANCY
• In early pregnancy à abortion needle-stick injury, sharing of needles by infected
• Low birthweight and increased infant mortality rates injection drug users, or organ transplantation
INTERNAL MEDICINE 3A—INFECTIOUS DISEASES: MALARIA STRAWBERRY
• Infected mothers in areas of stable transmission à
asymptomatic despite intense accumulation of
parasitized RBCs in placental microcirculation
• HIV infection à more frequent and higher density
malarial infection
o Predisposes newborn to congenital malarial
infection
o Exacerbates birth weight reduction
• Unstable transmission à pregnant women prone to
severe infections and vulnerable to high parasitemias
with anemia, hypoglycaemia, and acute pulmonary
edema
• Fetal distress, still births, premature labor, or LBW;
fetal death in severe malaria
• Congenital malaria à <5% in newborns of infected
mothers
o Frequency and level of parasitemia related
directly to parasite density in maternal blood
and placenta
• P. vivax à LBW associated more with multigravids
than primigravids
• Maternal death from hemorrhage at childbirth à
malaria-induced anemia
MALARIA IN CHILDREN
• Most of the 660,00 persons who die of falciparum
malaria each year are young African children
• Convulsions, coma, hypoglycemia, metabolic
acidosis, and severe anemia – relatively common
with severe malaria
• Deep Jaundice, Oliguric Acute Kidney Injury and
Acute Pulmonary Edema are unusual
• Severely anemic children may present with labored
deep breathing usually caused by metabolic acidosis,
often compounded by hypovolemia.
• In general children tolerate antimalarial drugs well
and respond rapidly to treatment
TRANSFUSION MALARIA
• Malaria can be transmitted by blood transfusion,
 INTERNAL MEDICINE 3A—INFECTIOUS DISEASES: MALARIA
• Incubation period is often short because of no
preerythrocytic stage of development.
• Clinical features and management are the same as for
naturally acquired infections.
• Radical chemotherapy with primaquine
unnecessary for transfusion-transmitted P.vivax and P.
ovale infections
DIAGNOSIS
• Diagnosis of malaria rests on the demonstration of
asexual forms of the parasite in stained peripheral-
blood smears.
• Negative blood smears à Repeat smears if with high
degree of suspicion
• Level of parasitemia is expressed as the number of
parasitized erythrocytes per 1000 RBCs.
• In severe malaria, a poor prognosis is indicated by a
predominance of more mature P.falciparum parasites
in the peripheral-blood film or by the presence of
phagocytosed malarial pigment in >5% of neutrophils.
• Molecular diagnosis by polymerase chain reaction
(PCR) amplification of parasite nucleic acid is more
sensitive than microscopy or rapid diagnostic tests.
LABORATORY FINDINGS
• Normochromic, normocytic anemia is usual
• WBC count is generally normal; may be raised in very
severe infections
• There is slight monocytosis, lymphopenia, and
eosinophilia, with reactive lymphocytosis
eosinophilia in the weeks after the acute infection
• ESR, plasma viscosity, CRP and other acute phase
proteins are high
• Severe infections à prolonged PT and PTT and
severe thrombocytopenia
• Uncomplicated malaria à electrolytes,
creatinine are normal
• Severe malaria à metabolic acidosis, low plasma
glucose, sodium, bicarbonate, calcium, phosphate,
urate, muscle and liver enzymes, and conjugated and
unconjugated bilirubin
INTERNAL MEDICINE 3A—INFECTIOUS DISEASES: MALARIA STRAWBERRY
TREATMENT
• The drug of choice depends on the likely sensitivity of
the infecting parasites
is • Despite increasing evidence of chloroquine resistance
in P. vivax, chloroquine remains a first-line
treatement for the non-falciparum malarias except in
Indonesia and Papua New Guinea, where high levels
of resistance in P.vivax are prevalent
• In all endemic areas, the WHO now recommends
artemisin-based combinations (ACTs) as first-line
treatment for uncomplicated falciparum malaria
• It is now accepted that, to prevent resistance,
falciparum malaria should be treated with drug
combinations and not with single drugs in endemic
areas
• If the level of parasitemia does not fall below 25% of
the admission value in 48 hours or if parasitemia has
not cleared by 7 days (and adherence is assured), drug
resistance is likely and the regimen should be changed
• 3-day ACT regimens are all well tolerated, although
mefloquine is associated with increased rates of
vomiting and dizziness.
• Patients should be monitored for vomiting for 1 hour
after the administration of any oral antimalarial drug.
If there is vomiting, the dose should be repeated.
• To eradicate persistent liver stages and prevent
relapse (radical treatment), primaquine (0.5 mg of
base/kg or, infections acquired in temperate areas,
0.25 mg/kg) should be given daily for 14 days to
and patients with P.vivax or P. ovale infections after
laboratory tests for G6PD deficiency have proved
negative.
• If the patient has a mild variant of G6PD deficiency,
primaquine can be given in a dose of 0.75mg of
base/kg (45 mg maximum) once weekly for 8 weeks.
BUN,
 INTERNAL MEDICINE 3A—INFECTIOUS DISEASES: MALARIA

• Hemofiltration and hemodialysis are more
effective than peritoneal dialysis and are
associated with lower mortality risk.
• Renal function usually improves within days,
but full recovery may take weeks.
• Acute Pulmonary Edema (ARDS)
• Patients should be positioned with the head of
the bed at a 45° elevation and given oxygen and
IV diuretics.
• Pulmonary artery occlusion pressure may be
normal, indicating increased pulmonary
capillary permeability
• Hypoglycemia
• An initial slow injection of 50% dextrose (0.5g/kg)
should be followed by an infusion of 10%
dextrose (0.10 g/kg per hour)
• Blood glucose level should be checked regularly
thereafter as recurrent hypoglycemia is common,
particularly among patients receiving quinine or
quinidine.
• In severely ill patients, hypoglycemia commonly
occurs together with metabolic (lactic) acidosis
and carries a poor prognosis.

COMPLICATIONS

• Acute Renal Failure

• If plasma level of BUN or creatinine rises despite
adequate rehydration, fluid administration
should be restricted to prevent volume overload.

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 INTERNAL MEDICINE 3A—INFECTIOUS DISEASES: MALARIA

CHEMOPROPHYLAXIS

• Travelers should start taking antimalarial drugs 2 days to 2

weeks before departure so that any untoward reactions can be
detected and so that therapeutic antimalarial blood
concentrations will be present when needed

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 INTERNAL MEDICINE 3A—INFECTIOUS DISEASES: MALARIA

ADD IT ION AL N OTE S FR OM D R. T AN ’S LEC TUR E • PROPHYLAXIS
• Malaria from blood transfusion: P. falciparum malaria o Mefloquine à DOC; taken
• You can get blood anytime, no need to get blood at peak of once a week
the fever § Safe for pregnant
• Gold standard for malaria: malarial smear microscopy women
o Peripheral blood smear (thin and thick) § (-) photosensitivity
o For quantification of parasitemia o Doxycycline à taken everyday
o Identification of species (based on the size) o Chloroquine à can be given if
§ Same size: Falciparum and malariae resistance pattern is known
§ Bigger: vivax or ovale • All antimalarials can kill merozoites
• Antigen detection kit: used for resource-limited settings EXCEPT Primaquine à kills
only; cannot be used for diagnosis hypnozoites and gametocytes only!
• PCR: used for species identification
• TREATMENT is in combination due to high-resistance: • Knowlesi can only be diagnosed by PCR
Artemisin Combination Therapy (ACT) à very similar to P. malariae in smear
(NO NEED TO MEMORIZE DOSES!) microscopy!
o Give 1 atremisin-based drug plus another drug
with different MOA NICE TO KNOW FOR HIV: J
o Artemether + Lumefatrine (Co-Artem) à only • Needle prick: 0.3% chance of getting
preparation available in the PH HIV
o Pregnant women: Quinine + clindamycin • Splash of blood in mucous membranes:
o Chloroquine can be used as TREATMENT and 0.09% chance of getting HIV
PROPHYLAXISà not DOC anymore due to high
resistance
o Complicated or severe malaria/cerebral malaria
à give 3rd-tier tx: Quinine per IV
§ Loading dose: 20 mg/kg
§ Maintenance dose:10 mg/kg
§ Watch out for cardiotoxicity: connect
patient to cardiac monitor/ECG à watch
out for prolonged QT interval
§ CBG monitoring à hypoglycemia
§ Cinchonism: headache, tinnitus
o Primaquine: kills hypnozoites! à main reason
why it is given to vivax and ovale is to prevent
relapse
§ Indication for falciparum malaria: to kill
gametocytes Highlighted pink text and boxed text were the
§ Gametocidal and hypnocidal key points emphasized during the lecture.
§ Longer tx course for vivax and ovale
According to Dr. Tan, he will be the one
compared to falciparum
making questions for Malaria and Typhoid. J
o Uncomplicated malaria: main objective is to
eradicate parasite Dr. Salandanan will make questions for TB and
à Give Artemether-Lumefantrine HIV.
o Complicated malaria: main objective is to
INTERNAL MEDICINE 3A—INFECTIOUS DISEASES: MALARIA
prevent death STRAWBERRY