Mixed Malaria

1
INTRODUCTION
Human malaria is caused primarily by 4 different species of Plasmodium namely;
P.falciparum (Pf), P.vivax (Pv), P. malaria (Pm), and P. ovale (Po). Clinical pictures,
outcome, prognostic factors, and changing clinical pattern of malaria due to individual
species infection have been studied extensively. In a geographical area when more than one
species coexist, sympatric combination of these infections in an individual cannot be ruled
out. But profile of malaria due to multiple species infection is considerably underestimated
due to lack of studies.
1

Infection with multiple Plasmodium species is common in malaria endemic regions. It
has been suggested that interactions between different species, in conjunction with
differences in seasonality and intensity of malaria transmission may underlie variation in the
epidemiology and clinical presentation of malaria. Of the four human malaria species, Pf
causes the greatest morbidity and mortality but most malaria endemic regions are coendemic
for some or all of the other three human species: Pm, Pv and Po. Individually, these species
cause less severe morbidity and fewer deaths than Pf, but they are commonly found as co-
infections with Pf. The effect of multiple species co-infections on the clinical outcomes of
malaria is unclear. Most clinical surveys of malaria focus on Pf without reference to the
potential effects of co-infecting species.
1

In South-east Asia region, India alone contributes 80% of malaria cases. Both Pf and
Pv malaria are common in this part of India. However, research on malaria due to co-existent
infection of both Pf and Pv is uncommon. Only a few studies have documented the effects of
coinfection on uncomplicated clinical malaria. Out of few available clinical studies on
coincident infection, some studies showed that Pv has a protective effect against severe
disease of Pf. On the contrary some studies showed that dual Pf and Pv infection in children
increases the disease severity. Experimental dual infection of Pf and Pv as a part of malaria
therapy in patients with neurosyphilis and mathematical model of parasitic dynamics of Pf
and Pv co-infection showed that Pv infection suppresses the severity of Pf. Prior Pv infection
reduced morbidity from subsequent Pf infections in Vanuatu and in Papua New Guinea, prior
infection with Pv or Pm protected against Pf fevers.
2

In patients with malaria mixed species infections are common and under reported. In
PCR studies conducted in Asia mixed infection rates often exceed 20%. In South-East Asia,
approximately one third of patients treated for falciparum malaria experience a subsequent
Plasmodium vivax infection with a time interval suggesting relapse. It is uncertain whether
the two infections are acquired simultaneously or separately. To determine whether mixed

2

species infections in humans are derived from mainly from simultaneous or separate
mosquito inoculations the literature on malaria species infection in wild captured anopheline
mosquitoes was reviewed.
3

The following report is a case of a child with uncomplicated mixed malaria infection
(Pf and Pv), who has been hospitalized in Prof. Dr. R. D. Kandou hospital Manado.

CASE REPORT
A 11 year 4 month old girl, KO, Christian, Minahasa tribe, was admitted to Prof. Dr. R.D.
Kandou General Hospital Manado on Febuary 23, 2014 at 00.40 pm, with a chief complaint
is fever.

History of illness (alloanamnesis, given by the mother)
Patient was brought to Prof Kandou General Hospital with major complain : fever since 2
weeks before admittance. Fever was low grade but then increase high when touched. Before
experiencing fever, patients felt cold and was shivering. Fever then decrease when given
antipyretic, when the fever disappear the patient experienced sweating. Every 2-3 days then
the fever recurs. Parents denied any convulsion, epitaksis and bleeding when the patient had
fever. Patient also complain headache since 2 weeks ago.
Her appetite was decreased than before sick. The patients experienced nausea and
vomiting for 3 times since 1 day before admittance. Defecation and urination were in normal
limit. Parents already brought her to general physician 3 days after the first episode of fever.
After took medication for 5 days, patient still had the fever. the parents told that her child
given sporetik, paracetamol and vosedon.

History of prenatal care and birth
During the pregnancy, his mother had regular antenatal care and had tetanus toxoid
immunization twice. This patient was born with sectio cesaria, immediately cried, aterm,
birth weight was approximately 3000 grams, forgot the birth length.

History of experienced illness
Patient had history of diarrhea, fever-cought dan typhoid fever.

3

Developmental milestones
Social smile : 3 months
Turning in prone position : 4 months
Sitting : 6 months
Crawling : 9 months
Standing : 10 months
Calling mama/papa : 6 months
Walking : 12 months

History of feeding
Breast feeding : birth 12 months
Milk Formula : birth 24 months
Milk porridge : 4 8 months
Soft rice porridge : 6 12 months
Rice : 1 year now

Immunization
He received basic immunization completely as recommended

Family History
No history of other family member suffers the same illness

Family Tree

4

Social, Economic and Environmental conditions
She is the second child in the family. His fathers age is 34 years old, a Highschool
graduation, while his mothers age is 32 years old, Highschool graduation, a housewife.
They live in a permanent house with 4 bedrooms, occupied by 6 adults and 8 children.
The roof made from metal platform, the wall made from rock, the floor is ceramic, restroom
is located inside the house, there is electric source, drinking water source is from the dwell,
and garbage is burned regularly.

Physical examination ( February 23
nd
, 2014)
Antropometric status
Body weight : 30 kg
Body height : 136 cm
Based on the CDC 2000 curve
normal nutritional status

General conditions : Look ill, compos mentis
Vital signs : Blood pressure : 90/60 mmHg
Pulse rate : 120 times/minutes, regularly
Respiratory rate : 28 times/minutes
Temperature : 39.2C

Head : Mesocephaly, thin black hair, not easily pulled out
Eyes : Conjunctiva not anemic and sclera was not icteric, pupil was round,
isochors, 3-3 mm, light reflex was normal
Ears : Clear meatus acusticus externus, normal ear drums, no secretes
Nose : There was no secretes and no flare
Mouth : There was no cyanosis, tonsils T1/T1 without inflammatory sign,
pharynx without inflammatory sign
Neck : There was no lymph node enlargement
Chest : Symmetrical respiratory movements, no retraction
Heart : Normal rate, regular rhythm, no thrill, no murmurs
Lungs : Symmetrical movement, symmetrical vocal fremitus,
bronchovesicular breath sound, without rales and wheezing

5

Abdomen : slim belly, not tense, with normal bowel sound,
Liver was palpable 3-3 cm below costal arch
Spleen was palpable at Schuffner I
Extremities : warm, not cyanotic, capillary refill time less than 2 seconds, normal
muscle tone, physiological reflexes normal, no pathological reflexes.
Genitalia : Female, no abnormality

Laboratory ( February 23
nd
, 2014 )
Malaria : P.Falciparum tropozoid stadium (+)
P. Vivax ring (+) Parasite count : 548 parasites /L blood
Complete Blood Count
Haemoglobin : 11.6 g/dl (11.5 15 g/dl)
Haematocrit : 34.5 % (35-45%)
Erytrocyte : 4.12 x 10
6
/mm
3
(4.0-5.2/mm
3
)
Leukocyte : 7.000 /mm
3
(5,000-10,000/mm
3
)
Thrombocyte : 306.000 /mm
3
(150,000-450,000/mm
3
)
ALT : 18 mg/dl
AST : 13 mg/dl

Working diagnosis :
Mixed Malaria (Plasmodium Falciparum, Plasmodium Vivax)

Treatment :
Artesunate 1 x 120 mg (I)
Amodiaquin 1 x 300 mg (I)
Primaquin 1 x 7.5 mg (I) for 14 days
Paracetamol 3 x 375 mg
Nutrition base on Recommended Daily Allowence (RDA)
Calory needed : 1410.0 kal/ day ( 47 kal/KgBW )
Protein needed : 30 gr/ day ( 1.0 gr/KgBW )
Fluid Needed : 1.700 cc/day ( Holliday Segar )
Given in solid form food 3 times daily

6

Planning :
Serial Thick Blood Droplets
Urinalysis, Stool analysis

Februari 24
rd
, 2014 (2nd day care)
Complaint : fever (-), nausea (-), intake (+)
Temperature : 37.0C

7

nd
, 2014 )
Malaria : P.Falciparum (+)
Urinalysis : pH 8
Epithel 2-4
Leukocyte 0-1
Erytrocyte 0-1
Stool analysis : consistancy soft
yellowish colour
blood (-)
leukocyte (-)
erytrocyte (-)

Working diagnosis :
Mixed Malaria (Pf, Pv)

Treatment :
Artesunate 1 x 120 mg (II)
Amodiaquin 1 x 300 mg (II)
Primaquin 1 x 7.5 mg (II) for 14 days

Planning :

8

Februari 25
rd
, 2014 (3
rd
day care)
Temperature : 36.5C

nd
, 2014 )
Malaria : (-)
Haemoglobin : 11.5 g/dl (11.5 15 g/dl)
Haematocrit : 34 % (35-45%)
Erytrocyte : 4.12 x 10
6
/mm
3
(4.0-5.2/mm
3
)
Leukocyte : 5.100 /mm
3
(5,000-10,000/mm
3
)
Thrombocyte : 231.000 /mm
3
(150,000-450,000/mm
3
)
MCV : 83 um
3

9

MCH : 30 pg
MCHC : 38 g/dL

Working diagnosis :

Treatment :
Artesunate 1 x 120 mg (III)
Amodiaquin 1 x 150 mg (III)
Primaquin 1 x 7.5 mg (III) for 14 days

Planning :

Februari 26
th
, 2014 (4
rd
day care)
General conditions : Look well, compos mentis
Temperature : 36.7C

10


th
, 2014 )
Malaria : (-)

Working diagnosis :

Treatment :
Primaquin 1 x 7.5 mg (IV) for 14 days
Paracetamol 3 x 375 mg if needed

Planning :

11

Februari 27
th
, 2014 (5
th
day care)
General conditions : Look well, compos mentis
Temperature : 36.7C
Spleen not palpable

th
, 2014 )
Malaria : (-)

Working diagnosis :

Treatment :
Primaquin 1 x 7.5 mg (V) for 14 days

12

Paracetamol 3 x 375 mg if needed

Planning :
Dircharge from hospital
Education, Primakuin until 14 days

13

DISCUSSION
Diagnosis of Mixed Malaria is based on anamnesis, physical examination and laboratorium
examination.
From anamnesis, patient had a fever since 2 weeks before admittance. Fever was
low grade but then increase high when touched. The presentation of uncomplicated mixed
malaria is highly variable and mimics that of many other diseases. Although fever is
common, it is often intermittent and may even be absent in some cases. The fever is typically
irregular initially and commonly associated with chills. From the literature it was found that
in single malaria infection, there are some attacks of fever with a certain interval
(paroksisme), which is punctuated by a period of free fever (intermittent). Paroksisme period
typically consists of three sumlessive stages consists of the cold stage, hot stage and sweating
stage. Paroksisme is usually clearly seen in adults and in children above five years old, in
children under five years of age cold stage is often manifest as seizures. This periodic fever
outbreak associated with a time and a number of mature schizonts release of merozoites into
the bloodstream (sporulation).
4,5

Study published by Ellis F et al with the title Fever in Patient with Mixed-Species
Malaria 2006, said that fever in mixed malaria higher than in single species malaria. It is not
clear whether higher fevers, indicate greater clinical severity or more-effective immune
responses.
6
From the study, fever does not directly correspond to parasite density, but is high
when Pf parasitemia is greater than Pv parasitemia and low when Pv parasitemia is greater
than Pf parasitemia. Effective immune responses against Pv are thought to develop after
fewer infections than those against Pf.
6-9
Parasitemia thresholds for fever are thought to be
lower with Pv than with Pf,
10-11
although with Pf, parasitemia thresholds may decrease with
age.
9
Thus, mixed-species infections may appear more often in younger age groups, perhaps
with higher densities of Pv and different patterns or intensities of fever.
A mixed-species infection in a human can result from a single bite by a mosquito
infected with multiple species or from multiple bites by mosquitoes infected with single
species. The relative frequency of these events depends on the age distribution in the vector
population, which changes during a season and year
12
; the order in which the Plasmodium
species infect may be critical to their dynamics in the human.
12
Thus, the reported frequencies
of mixed-species infections are likely to vary by season and by the particular time during a
season.

14

The patient commonly complains of fever, headache, aches and pains elsewhere in the
body and occasionally abdominal pain, nausea and vomiting. This is consistent with the
literature that describe the prodromal complaints that occurred prior to the occurrence of
fever. In a young child, there may be irritability, refusal to eat and vomiting.
13
In this case,
since 2 weeks ago, the patients appetite was decreased, the patient experienced abdominal
pain, nausea and vomitting.
Liver enlargement is due to malaria infections in which the liver Kupffer cells will be
involved in active phagocytosis. In an acute attack , the liver will be enlarged , especially on
first week.
13
The liver will enlarge as the disease progression but rarely impaired hepatic
function in children and is seen in the patient's liver function test results did not exceed 3
times the normal limit. Hepatomegaly is more common than splenomegaly and size of the
two organs showed no relationship . Hepatomegaly on malaria sometimes there is pain and
will disappear within 72 hours after the start of treatment and the size of the liver will also
decreasing.
13
Same findings in this patients , where the size of the liver begins to diminish
after starting antimalarial treatment. Hepatomegaly will have the resolution to its normal size
within 7 to 14 day.
14
In this patients when he was discharged there was still an enlargement of
the liver.
Splenomegaly was also found in this patients where the spleen in patient with malaria
infection will damed up.
13
Splenomegaly usually do not shows any symptoms. By starting
antimalarial treatment, the size of the spleen will be back to normal within 7 to 14 day.
14
This
is seen in patient where the patient spleen size decreases gradually and not palpable at the
time of discharge.
Laboratory tests that confirm the diagnosis of tropical malaria in this case
is the examination of thick blood droplets and thin blood smear. There are several kinds of
laboratory tests to diagnose malaria, among other :
13-15
1. Microscopic examination , consisting of :
Thick blood droplet
Thin blood smear
2. Examination of the RDT ( Rapid Diagnostic Test ), a test which is available at
market today contain :
a. HRP - 2 ( histidine rich protein 2 ) produced by trophozoites , schizonts and
gametocytes young Pf
b. The enzyme parasite lactate dehydrogenase ( p - LDH) and aldolase produced by
parasites asexual or sexual forms of Plasmodium falciparum, Pv, P. ovale, Pm.

15

In this case the laboratory examination of Thick Blood Droplets we found parasitemia
with Pf tropizoid form (+) and Pv ring (+) with parasite count : 548 parasites /L blood (< 5%
). The results from Complete Blood Count : Haemoglobin 11.6 g/dl, Haematocrit 33.2 %,
Erytrocyte 4.12 x 10
6
/mm
3
, Thrombocyte 306.000/mm
3
, ALT 18, AST 13.
From the anamnesa, physical examination and laboratorium result, we can diagnose
this patient with Mixed Malaria (Plasmodium Falciparum with Plasmodium Vivax).
Although the infection is mixed, this patient didnt show any sign of complication. There are
several study report that mixed malaria infection had a good prognosis than in Pf.
Infection with multiple Plasmodium species is common in malaria endemic regions. It
has been suggested that interactions between different species, in conjunction with
differences in seasonality and intensity of malaria transmission may underlie variation in the
epidemiology and clinical presentation of malaria.
16
Of the four human malaria species,
Plasmodium falciparum causes the greatest morbidity and mortality but most malaria
endemic regions are coendemic for some or all of the other three human species: Pm, Pv and
Po. Individually, these species cause less severe morbidity and fewer deaths than Pf but they
are commonly found as co-infections with Pf.
17,18
The effect of multiple species co-infections
on the clinical outcomes of malaria is unclear. Most clinical surveys of malaria focus on Pf
without reference to the potential effects of co-infecting species.
Only a few studies have documented the effects of co-infection on uncomplicated
clinical malaria.
19-24
Prior or co-infection with Pm has been implicated in protecting against
fevers caused by Pf in children in Cote dIvoire
19
and in reducing the density of asexual
stages and preventing fevers in Tanzanian children
20
. These epidemiological studies of Pm
are supported by experimental data from malaria-therapy infections in humans carried out in
the 1990s, in which prior infection with Pm reduced fever caused by Pf.
21
Prior Pv infection
reduced morbidity from subsequent Pf infections in Vanuatu
22
and in Papua New Guinea,
prior infection with Pv or Pm protected against Pf fevers
23
. In contrast to these reports of the
protective clinical effects of co-infection, an adverse effect has been described in at least one
report; carriage of multiple species was associated with greater levels of anaemia than single-
species infections in Nigerian children
24
. As well as affecting clinical outcome, interactions
between co-infecting species can modify the within-host dynamics of co-infecting malaria
parasites
25,26
and alter the transmission potential of human hosts
27
thereby impacting on the
epidemiology of malaria.
A number of studies have reported that Plasmodium species apparently suppressed
each other, in population, or in a mixedly-infected individual. It is noteworthy that the

16

emergence of Plasmodium vivax in patients' peripheral blood has led to a "total
disappearance" of Plasmodium falciparum, while passive transfer of Pf-immune IgG
exhibited weaker suppressive effects on Pf in these patients. The severity of Pf infection has
been reported to be dramatically ameliorated in patients simultaneously infected with Pv.
28,29

Mutual suppression between Plasmodium parasites has been thoroughly reviewed. These
observations have led to speculation that the much lower disease-specific mortality and case
fatality rate from malaria in Asia-Pacific region than in Africa may be due to the presence of
so-called "benign" Pv malaria, because Pf is by far the most dominant in sub-Saharan Africa.
Therefore, understanding the interaction of these Plasmodium species is important, especially
because several Pv vaccines are currently being developed. The authors hypothesized that the
host immunological reactions to infecting Pv might be playing a role in this suppression of
co-infecting Pf. Although such a notion has been long held, actual data has been rarely
available for human malaria. However, any study design that leaves a living human
volunteers (other than the researcher) untreated is unacceptable from a bioethical point of
view. By contrast, "almost all of the associated legal, ethical, and metaphysical problems
vanish" with self-recruitment of the researcher, according to the founder of modern
bioethics.
30

Mixed malaria infection is common and has been reported in many parts of the world
where malaria is endemic. In regions with low malaria endemicity regions, especially in
Thailand, mixed infection with Pf and Pv is common. When Pv was co-infected with Pf in the
malaria infection, patients had a higher fever than those with single Pf or single Pv
infections.
6
High temperature is shown to kill Pf parasites in in vitro studies. In addition,
serum from a Pv-infected donor during paroxysm inhibits maturation of Pf schizonts.
31

Together, these data support the notion that a mechanism by which Pv controls the expansion
of Pf in mixed malaria infection could be via the induction and persistency of high fever in
patients, particularly the high systemic temperature in the organs where Pf sequestered.
Antibodies to malaria, although short-lived, are the primary mechanisms of defence
against parasitic infection. Induction and maintenance of anti-malarial antibodies requires
repetitive infections. Evidence such as the existence of the asymptomatic parasitaemic
individual confirms development of immunity against malaria.
32,33

Anti-Pf and anti-Pv antibody levels in the mixed malaria infection were higher than
those of the single Pv or Pf infections. Development of a crossimmune reactivity between Pv
and Pf during acute mixed infection could be due to the activation of a pool of memory T
cells having specificities to both Pv and Pf antigens. These cells co-existed in the residents of

17

the endemic areas where there is regular exposure to malaria parasites. The antigenic cross-
stimulation by Pv antigens sharing common epitopes with Pf results in the cell-mediated and
antibody responses at high levels against Pf during the acute phase of infection. Further
investigations in the different geographical endemic areas are needed to verify the two
categories. Supporting evidence from a study in Thailand shows the antibody cross-reactivity
froma single Pv-infected patient against both the schizont extract of Pf parasite and the
PfMSP119 parasite protein. In addition, the cross-reactivity between anti-PvMSP5 and anti-
PfMSP5 antibodies was observed in single Pv or single Pf infections. Overall immunity,
effector T cells and anti-malaria antibodies to malaria among the residents of endemic areas
would be strengthened by the existence of Pv.
34

Pv suppressing Pf parasites, because Pv induces CD3+d2+T cells which are effector T
killer cells. Pv infection also elevates anti-Pf antibodies during the acute phase, and induces a
very high fever. Interaction between the host and Pv parasites could offer protection as
demonstrated in the mixed PV-PF malaria infection. Furthermore, in single Pv or Pf
infection, similar levels of T helper type 1 (Th1)/Th2 cytokine responses are shown. IL-12,
which showed the highest correlation with Pv parasitaemia, is hence likely to be (one of) the
most direct mediator(s) bridging from rupturing schizonts to fevers. It was reported that IL-12
and IFN- synergistically enhance the parasiticidal activities of peripheral blood mononuclear
cells.
30
Therefore, the sharp peaks of INF- under the presence of IL-12 observed in the
volunteer could mount an early in vivo defense against blood-stage parasites, and may
contribute to the suppressive effect of Pv on Pf. Possibility suggest that Pv infections may
suppress Pf in multiple ways including cross-reactive IgM and cytotoxicity-inducing
cytokines. To thoroughly prove that Plasmodium-specific IgM is playing a major role in

18

cross-Plasmodium suppression, such specific IgM should have been purified.
35

Figure 1 : Life cycle of Plasmodium spp. infections, with the main immune responses that
control the parasite at each stage.
Ref : Riley EM, Stewart VA. Immune mechanisms in malaria: new insights in vaccine
development. Nature medicine. 2013;19:168-178.
Figure 1 below explain us about life cycle of Plasmodium spp. infections, with the
main immune responses that control the parasite at each stage. Sporozoites, injected into the
skin by the biting mosquito, drain to the lymph nodes, where they prime T and B cells, or the
liver, where they invade hepatocytes. Antibodies (Ab) trap sporozoites in the skin or prevent
their invasion of liver cells. IFN-gproducing CD4+ and CD8+ T cells inhibit parasite
development into merozoites inside the hepatocyte. However, this immune response is
frequently insufficient, and merozoites emerging from the liver invade red blood cells,
replicate, burst out of the infected erythrocyte and invade new erythrocytes. Merozoite-
specific antibodies agglutinate and opsonize the parasite and can inhibit the invasion of red
blood cells through receptor blockade. Antibodies to variant surface proteins also opsonize
and agglutinate infected red blood cells (RBCs) and prevent their sequestration
(cytoadherence) in small blood vessels. IFN-gproducing lymphocytes activate macrophages
and enhance the phagocytosis of opsonized merozoites and iRBCs. Complement-fixing
antibodies to gametocyte and gamete antigens lyse parasites inside the mosquito gut or
prevent the fertilization and development of the zygote. Sporozoite, liver-stage and
gametocyte and gamete antigens are somewhat polymorphic, whereas merozoite antigens and
variant surface antigens are highly polymorphic. APC, antigen-presenting cell.
36

19

Figure 2 : Induction of humoral and T cellmediated immune responses against malaria
Ref : Riley EM, Stewart VA. Immune mechanisms in malaria: new insights in vaccine

Figure 2 below explain us about induction of humoral and T cellmediated immune
responses against malaria. Parasites and parasite-infected red blood cells activate dendritic
cells through PRRs, are phagocytosed and their antigens are presented to T cells. PRR
signaling leads to the secretion of cytokines that initiate the inflammation that underlies
malaria pathogenesis and direct TH1 cell differentiation. TH1 cells provide help for B cell
differentiation and antibody secretion and also secrete IFN-g, which activates macrophages.
IFN-g-activated macrophages phagocytose opsonized parasites and infected red blood cells
and subsequently kill them by NO- and O2-dependent pathways. Inflammation induces
expression of endothelial adhesion molecules to which infected red blood cells bind.
Inflammation is curtailed by the secretion of anti-inflammatory cytokines from macrophages
and regulatory populations of T cells. Treg, regulatory T cells; TCR, T cell receptor.
36

Antimalarial drug of choice for mixed malaria (Pf and Pv) are Artesunate, Amodiaquin
and Primaquin. In this patients the treatment was given in the form of oral artesunate,
amodiaquin and primaquin. Artesunate and amodiaquin was given for 3 days oral, primaquin
was given for 14 days oraly. The treatment we give to this patient based on Gebrak Malaria
book 2012. Which the protocol of treatment patient with mixed malaria infection are
Artesunate 4mg/bw/day single dose for 3 days, Amodiaquin 10mg/bw/day single dose for 2
days continued with 5 mg/bw/day single dose on day 3 and Primaquin 0,25 mg/bw/day single
dose given for 14 days. After treatment, clinical symptoms were improved, with the loss of an
attack of fever, anorexia, nausea, vommiting and adominal pain. From the physical
examination, the hepatomegaly and splennomegaly gradualy decreased.
37

Patients were discharged after being given education about the modes of transmission,
and the risk of prevention of malaria. According to the literature malaria prevention methods
generally include three things namely education, chemoprophylaxis and efforts to avoid
mosquito bites. Education is the most important factor in malaria prevention should be given
to each officer who will work in endemic areas. The main material of education is to teach
about the modes of transmission of malaria, the risk, knowing the symptoms of malaria, and
prevention of mosquito bites, and knowledge of the effort to eliminate places mosquito
breeding such as making effective drainage, and eliminate breeding sites especially marsh
mosquitoes and stagnant water.

20

The patient was discharged with a visible clinical improvement and disappearance of
parasites in blood and normal value of completed blood count. According to literature the
prognosis of malaria related to parasite responses to treatment. There for, the prognosis of
this patients is ad bonam.
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