COMMUNICABLE DISEASES

Topic: MALARIA
Lecturer: Dr. Edwin Fortuno
MED BLOCK 1ST Sem – OLFU-COM Batch 2020

MALARIA

 Malaria is a mosquito-borne infectious disease caused by a

eukaryotic protist of the genus Plasmodium.

 MAL (BAD) + ARIA (AIR) = MALARIA (BAD AIR)

 This “bad air” was believed to be the cause of the fever that
often developed in those who spent time around the swamps.
 In fact, the illness, now known as malaria, was due to certain
protozoon present in the mosquitoes that bred around these
swamps, and which caused recurring feverish symptoms in
those they bit.
OVERVIEW OF MALARIA
• Most important parasitic disease in humans globally.
• Causes a heavy burden among tropical countries.
• Poses a threat to non – endemic countries.
• Poses a danger to international and local travelers

MALARIA
- disease caused by protozoan parasite called Plasmodium.
- It is usually transmitted through the bite of an infected female
Anopheles mosquito.
- Malaria may also be transmitted through the following:
• Transfusing blood that is positive for malaria
DISEASE OF THE TROPICS parasites
• Sharing of IV needles (especially among IV drug
users)
• Trans -placental (transfer of malaria parasites from
an infected mother to her unborn child)

A. Plasmodium falciparum (60-70%)

B. Plasmodium vivax (30-40%)
C. Plasmodium malariae
D. Plasmodium ovale
E. Plasmodium knowlesi affects H. sapiens and Macaca
fascicularis

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Characteristic P. falciparum P. vivax P ovale P. malariae

Duration of 5.5 8 9 15
intra – hepatic
phase
Number of 30,000 10,000 15,000 15,000
merozoites
released per
infected
erythrocyte
Duration of 48 48 50 72
erythroctic
cycle in hours
RBC Young but Reticulocytes Reticulocytes Older cells
preference can invade all and cells up
cell ages to 2 weeks
old
Morphology Ring forms, Irregular Infected Bands or
banana shaped large eryhrocytes, rectangular
shaped rings and enlarged and forms of
gametocytes trophozoites, oval with trophozoites
enlarged tufted ends,
Plasmodium knowlesi RBC, schuffer’s
schuffer’s dots
 Molecular, entomological, and epidemiological data indicate dots
that human infections with P. knowlesi are not newly Pigment color Black Yellow brown Dark brown Brown black
Ability to NO YES YES NO
emergent cause relapse
 Primarily a zoonotic form.
 Potentially fatal, but if detected early enough, infections in A. Plasmodium falciparum 12 Days
humans are readily treatable. B. Plasmodium vivax 14 Days
C. Plasmodium malariae 30 Days
Plasmodium knowlesi D. Plasmodium ovale 14 Days
• Reports of its emergence from monkeys
• Isolated from Philippine macaques (Macaca fascicularis) in
1961
• Incriminated vector in Anopheles balabacensis
• Published reports of human infection
- 1965, 2004 Malaysia
- 2008 (Palawan) Phils : (2 cases)
- 2004 Thailand
- 2006 China
Presentation:
• Morphologically similar to P. malariae may be mistaken to be Parts of a mosquito:
P. falciparum because of abundant ring stages
• In Rhesus monkey studies
• High parasite densities is possible
• No significant sequestration in microcirculation
• In humans
 Reported in children and relatively older adults
 May present as mild form of malaria easily responding to
chloroquine but may also be severe and fatal
 Fever, headaches, intermittent chills, abdominal pain,
sweating and malaise
 Polymerase chain reaction is of value for diagnosis because
P. knowlesi infection is easily misdiagnosed as less
dangerous Plasmodium malariae infection with conventional
microscopy.
Do all mosquitoes carry the malaria parasite?
• No, not all mosquitoes carry the malaria parasite.
What are the common species of malaria parasites in the
• In the country, it is the adult female Anopheles mosquito that
Philippines?
can become infective and therefore carries the malaria
• Plasmodium falciparum and Plasmodium vivax are the
parasite after she bites a person infected with malaria.
common species of malaria parasites in the Philippines
• This anopheles mosquito bites from dusk to dawn and it
where 70% of malaria cases are P. falciparum while 29% are
breeds in clear, slow flowing streams that are found in
P. vivax.
mountainous/forested areas or in brackish water where salt
• There are also P. malariae cases but contributes to about <
and fresh water meet. This is usually found in coastal areas
1% of the total malaria cases.
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Can a person get malaria by drinking water in the streams with STATISTICS
mosquito eggs? THINK….. • P. falciparum and P. vivax – responsible for most new
infections.
VECTORS IN THE PHILIPPINES • No. The malaria parasite has to undergo development inside
• Anopheles sp. the adult female mosquito; therefore one cannot get malaria
o An. flavirostris from drinking water that has mosquito eggs in it.
o An. litoralis
o An. maculatus P. falciparum
o An. mangyanus • Causes severe malaria.
o An babacensis • Creates a high level of parasitemia and sequestration
causing end organ damage.
Who are at risk OF getting malaria? • Sequestration is a specific property.
• Children • Usually seen in the smears are younger forms before
• Pregnant women sequestration takes place.
• Indigenous peoples
• Forest workers, miners, soldiers RBC CHANGES
• Persons who are not from a malaria endemic area but travel • Once inside the cell, it consumes and degrades intracellular
to this area. proteins (hemoglobin).
• Alteration in RBC properties more irregular in shape and less
deformable.
• P. falciparum – causes appearances of knobs on the cell
surface.
– Mediates attachment to the capillary and venular
endothelium (cytoadherence).
• Rosette formation – infected RBCs may adhere to uninfected
RBC.
• Agglutination – infected RBCs adhere to other parasitized
RBCs.
SEQUESTRATION
• Contribute to mental changes and coma.
• End organs affected are:
– CNS, lungs and kidneys.

EPIDEMIOLOGY A combination of all these results in . . .

• Endemicity is defined as palpable spleen rates in children 2 – • Interference with microcirculatory circulation and metabolism
9 years old: especially in the brain
– < 10% - hypoendemic Other things noted in P. falciparum infection:
– 11-50% - mesoendemic • Hypoglycemia
– 51 – 75% - hyperendemic • Lactic acidosis
– > 75% - holoendemic • Severe anemia
• Africa and New Guinea • Multi - organ dysfunction secondary to hypoxia.
• Principal determinants are: • Usually occurs in travelers without immunity or young
– Biting habits children living in endemic areas.
– Density of the mosquito population
– Longevity of the anopheline mosquito INNATE IMMUNITY
• The lifecycle that takes place inside the • Depends on the host’s immunity.
mosquito is between 8 – 30 days. • P. falciparum usually results in death.
• Low temperatures are not conducive for PROTECTIVE GENETIC FACTORS
sporogony to take place. • Sickle cell disease
STABLE TRANSMISSION • Hemoglobinopathies
• Constant year round transmission. • Polymorphisms in the host’s Tumor Necrosis Factor (TNF).
• By adulthood would have achieved full immunity
CLINICAL MANIFESTATIONS
UNSTABLE TRANSMISSION
• Erratic transmission HISTORY
• Usually in hypoendemic areas • Most patients will present with fever and headache.
• Full protective immunity is not acquired • There is no neck stiffness or photophobia resembling
meningitis.
• Get a history of recent travel in those patients with high
grade fever.
• Malaria free areas:
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o Aklan, Albay, Batangas, Benguet, Biliran, Bohol, P. vivax and P. ovale

Camiguin, Capiz, Catandauanes, Cavite, Cebu,
Eastern Samar, Guimaras, Ilo-Ilo, Leyte,
Marinduque, Masbate, Northern Samar, Siquijor,
Sorsogon, Southern Leyte, Surigao del Norete,
Western Samar
o Malaria areas in and near NCR: Fairview, Antipolo
• Patient may relapse after long periods because of the
hypnozoite stage in the liver.
• Can remain dormant for months to years before entering the
blood stream to produce symptoms.
• Causes the benign form of tertian fever.
– (P. malariae causes the quartan fever.)

 Malaria is a febrile illness characterized by fever and related PHYSICAL EXAMINATION

symptoms. • Most patients will have splenomegaly.
 However, it is very important to remember that malaria is not a • Anemia
simple disease of fever, chills and rigors. • Thrombocytopenia
 In fact, in a malaria prone area, it can present with such varied • MARF
and dramatic manifestations that malaria may have to be • Acute tubular necrosis secondary to hypovolemia,
considered as a differential diagnosis for almost all the ischemia, intravascular coagulation
clinical problems. • Parameters:
 Malaria is a great imitator and trickster, particularly in areas • <1 ml/kg/hr.
where it is endemic. • Elevated creatinine

DIAGNOSTIC PROCEDURE

Since Charles Laveran first visualized the malaria parasite in blood in

1880, the main-stay of malaria diagnosis has been the microscopic
- rapidly rising fever with headache examination of blood.
- paroxysm with shaking chills
- profuse sweating Malarial Smear
- hepatosplenomegaly In this procedure, a film of blood is placed on a slide, stained, and
- myalgia (muscle pain) examined microscopically.
- orthostatic hypotension Peripheral smear examination for malarial parasite is the gold-
standard in confirming the diagnosis of malaria
• Severe anemia – usually associated with P. falciparum infections.
• May be secondary to RBC infection and a loss of infected RBC.
• Uninfected RBCs are inappropriately cleared and bone marrow
suppression may also be involved.

RENAL FAILURE
• Infected RBCs adhere to the microvasculature in the renal
cortex.
• Oliguric renal failure.
• Usually reversible.
• P. malariae can cause the nephrotic syndrome

RESPIRATORY SYMPTOMS
• Metabolic alkalosis and respiratory acidosis leading to
respiratory distress.
• Can develop pulmonary edema.

TYPICAL MANIFESTATIONS IN DIAGNOSING MALARIA

• Cerebral malaria – almost always due to P. falciparum
infections.
– Coma lasts more than 30 minutes.

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DEMONSTRATION OF THE PARASITE TREATMENT

• Must identify the asexual forms in the peripheral blood • 3 medical conditions associated with Plasmodium infection:
smear. – Uncomplicated
• Negative smears do not rule out malaria if there is a high – Treatment failure
degree of suspicion. Repeat. – Severe malaria
• Use the Giemsa stains at pH – 7.2
• Thick blood smear provides better sensitivity. UNCOMPLICATED MALARIA (falciparum, vivax)
• Thin blood smear provides better specificity and allows • Febrile
better identification of the species involved. • Parasites in blood
• Not so diagnostic in P. falciparum infections since • Absence of severe malaria and multi drug resistant P.
sequestration removes the RBCs out of the peripheral falciparum
circulation especially in the late stages. • Severe headache, chills
• Thick and thin smears done 12 – 24 hours apart at any time • Thrombocytopenia
of the infection.
•Day 0 – 2  Co Artem
THICK SMEARS • Given after high fat meals
• More sensitive than thin smears. • Contraindicated in pregnancy and lactation
• Can’t identify the species • Day 3  Primaquine
• Parasitemia can be calculated based on the number of » falciparum – gametocidal
infected RBC. » vivax – hypnozoiticidal
• Quantitative test. » Discharged if asexual forms are not seen in Day7
• Can concentrate the parasites increasing diagnostic then monitor once a week for a month.
sensitivity. Other Plasmodium parasites and mixed infections:
• P. malariae  chloroquine; Primaquine
THIN SMEARS
• Less sensitive. Multi drug resistant P. falciparum and treatment failure
• Facilitate speciation • Ability of the parasite to survive and or multiply despite the
• Qualitative test administration and absorption of a drug given in the
recommended or higher dose but within the limits of
ALTERNATIVE TESTS tolerance of the patient.
• Quantitative buffy coat – as sensitive as a thick smear but • Basis:
must still do a thin smear. • Recrudescence of asexual parasitemia from 48
• (PfHRP2)Histidine rich protein - 2 ( the only approved rapid hours after treatment
test in the US. • No parasite clearance or reduction
Objectives:
Rapid Diagnostic Test (RDT) 1. cure the infection
This is a blood test for malaria. It can be conducted outside the 2. prevent the development of severe malaria
laboratory and inside the field. 3. prevent spread of drug resistant forms of the
It gives a result within 10 to 15 minutes. parasite
This is done to detect malarial parasite antigen in the blood.
SEVERE MALARIA
• Dysfunction of organ systems secondary to:
 Effects of malaria toxins
 Sequestration of infected RBC
 Anemia
• Abnormal organ function tests
• Jaundice
• Hyperparasitemia (>2% parasitized RBC)
MALARIA SUSPECT • Severe anemia
• Patients with malaria like illness • Metabolic abnormalities
• With thrombocytopenia • Hemoglobinuria
• Relative lymphocytopenia
• Atypical lymphocytes Conditions:
• Elevated LDH • Seizures
• Impaired consciousness
OBJECTIVES FOR TREATMENT • Prostration/ weakness
• Treat the malaria • Poor urine output
• Prevent development and spread of anti malarial drug • Signs of pulmonary edema
resistance • Signs of DIC
• Abnormal spontaneous bleeding

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• US FDA and WHO: Artesunate IV BASIS FOR CHEMOPROPHYLAXIS

• DOH: may give Coartem • Each species has a specific incubation period.
– Quinine IV or artesunate IV plus treatment: • P. falciparum infection typically develops within a month of
• Quinine or artesunate + tetracycline + exposure. Rare cases have been reported up to a year
clindamycin later.
• Falciparum + either vivax or malariae • Hypnozoite form – P. vivax and P. ovale.
– CoArtem (falciparum) and Primaquine (vivax) – Parasite stays in the liver for months before
inducing initial infection.
P. vivax
• Day 0 – 2  chloroquine CHEMOPROPHYLAXIS
– No treatment failure reported yet • Doxycycline 100 mg daily for 2 – 3 days before going to an
• Days 3 – 17  primaquine endemic area, continue while in the endemic area and
continue for 4 more weeks after leaving the endemic area.
TREATMENT FAILURE
• Falciparum malaria - quinine and any of the three drugs: PERSONAL PROTECTION
doxycycline, tetracycline, clindamycin (QUININE • Reduce the frequency of mosquito bites.
PLUS) – Avoid the mosquito’s peak feeding hours.
• Vivax – CoArtem – DEET and picaridin
– If hypnozoites are suspected and fever recurs – Insecticide impregnated mosquito nets.
after 2 weeks primaquine
PREVENTION AND CONTROL
Treatment under special conditions:  Malaria case should be reported.
• Pregnant women:  A thorough screening of all infected person’s from
– Falciparum – oral quinine; Insulin secreting drug mosquitoes is important.
 monitor blood sugar levels  Mosquito breeding places must be destroyed.
– Vivax – chloroquine  Homes should be sprayed with effective insecticides
which have residual actions on the wall.
QUININE  Mosquito nets should be used especially when in infected
• No role in prophylaxis areas.
• Used with second agent in drug – resistant falciparum  Insecticide Treated Bed Nets (ITN’s) have emerged as a
infections. very important tool in malaria control in endemic areas.
 Insect repellents must be applied to the exposed portion of
FANSIDAR the body.
• Pyrimethamine –sulfadoxine o Permethrin
• Can also be used for treatment o DEET (N,N-diethyl-m-toluamide)
• Not anymore considered as a first line drug for prophylaxis o IR3535 (3-[N-acetyl-N-butyl]-aminopropionic acid
because of adverse drug reactions. ethyl ester)
o Bayrepel (1-piperidinecarboxylic acid, 2-(2-
MEFLOQUINE hydroxyethyl)-, 1-methylpropylester)
• Use of mefloquine for pregnant women in the second and  Blood donors should be properly screened.
third trimester is sanctioned by the WHO and the CDC
allow the use of mefloquine even in the first trimester of MALARIA SITUATION IN THE PHILIPPINES
pregnancy. • Malaria is a rural disease
• one of the important mosquito-borne diseases affecting far-
SUPPORTIVE MANAGEMENT flung barangays of the country
• Cerebral malaria • Out of the 79 provinces nationwide, 57 are malaria endemic
– Unarousable coma not attributed to any other
cause and persists for > 30 minutes after a MALARIA ENDEMIC AREAS
seizure
• Treatment: fluid balance, hyperpyexia,
control seizures
– No mannitol, osmotic
diuretics, steroids
• Pulmonary edema
– Increased pulmonary capillary permeability
• Hypoglycemia
• Circulatory collapse/ shock

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MALARIA CONTROL PROGRAM

Vision: malaria-free Philippines by 2020.

STRATEGIES
1) Early diagnosis and prompt treatment;
2) Vector control – insecticide-treated mosquito net as main
vector control strategy, complemented by indoor residual
spraying;
3) early management and disease surveillance;
4) monitoring and evaluation

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