mixed malaria

5/26/2018 Mixed Malaria

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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


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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.


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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 : birth12 months

Milk Formula : birth24 months

Milk porridge : 48 months

Soft rice porridge : 612 months

Rice : 1 yearnow

Immunization

He received basic immunization completely as recommended

Family History

No history of other family member suffers the same illness

Family Tree


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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 23nd

, 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


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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 23nd

, 2014 )

Malaria :P.Falciparum tropozoid stadium (+)

P. Vivaxring (+) Parasite count : 548parasites /L blood

Complete Blood Count

Haemoglobin : 11.6 g/dl (11.515 g/dl)

Haematocrit : 34.5 % (35-45%)

Erytrocyte : 4.12 x 106 /mm3(4.0-5.2/mm3)

Leukocyte : 7.000 /mm3(5,000-10,000/mm3)

Thrombocyte : 306.000 /mm3 (150,000-450,000/mm3)

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

Nutritionbase 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


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Planning :

Serial Thick Blood Droplets

Urinalysis, Stool analysis

Februari 24rd

, 2014 (2nd day care)

Complaint : fever (-), nausea (-), intake (+)





Temperature : 37.0C



















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, 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 :



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Februari 25rd

, 2014 (3rd

day care)






Temperature : 36.5C



















, 2014 )

Malaria : (-)

Haemoglobin : 11.5 g/dl (11.515 g/dl)

Haematocrit : 34 % (35-45%)

Erytrocyte : 4.12 x 106 /mm3(4.0-5.2/mm3)

Leukocyte : 5.100 /mm3(5,000-10,000/mm3)

Thrombocyte : 231.000 /mm3 (150,000-450,000/mm3)

MCV : 83 um3


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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 26th

, 2014 (4rd

day care)


General conditions : Look well, compos mentis




Temperature : 36.7C









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Laboratory ( February 26th

, 2014 )

Malaria : (-)

Working diagnosis :


Treatment :

Primaquin 1 x 7.5 mg (IV) for 14 days

Paracetamol 3 x 375 mg if needed






Planning :



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Februari 27th

, 2014 (5th

day care)


General conditions : Look well, compos mentis




Temperature : 36.7C















Spleen not palpable



Laboratory ( February 27th

, 2014 )

Malaria : (-)

Working diagnosis :


Treatment :

Primaquin 1 x 7.5 mg (V) for 14 days


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Paracetamol 3 x 375 mg if needed






Planning :

Dircharge from hospital

Education, Primakuin until 14 days


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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 feverin 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.6-9Parasitemia thresholds for fever are thought to be

lower with Pv than with Pf,10-11although with Pf, parasitemia thresholds may decrease with

age.9Thus, 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 year12; the order in which the Plasmodium

species infect may be critical to their dynamics in the human.12Thus, the reported frequencies

of mixed-species infections are likely to vary by season and by the particular time during a

season.


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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. 13In 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.13Same 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.14In 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.13Splenomegaly 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. 14This

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.


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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 106 /mm3, Thrombocyte 306.000/mm3, 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.17,18The 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.19-24Prior 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.21Prior Pv infection

reduced morbidity from subsequent Pf infections in Vanuatu 22and 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 25,26and alter the transmission potential of human hosts 27thereby 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


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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


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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


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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


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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

development. Nature medicine. 2013;19:168-178.

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.


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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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