MALARIA

BACKGROUND

DEFINISI
Malaria adalah penyakit yang disebabkan oleh infeksi
protozoa plasmodium yang pada awal nya menyerang sel
darah merah dan sel hati. Transmisi penyakit tersebut
melalui gigitan nyamuk anopheles (Jarang: transfusi darah).
EPIDEMIOLOGI

Berdasarkan hasil Survei Kesehatan Rumah

Tangga (SKRT) tahun 2001, terdapat 15 juta
kasus malaria dengan 38.000 kematian setiap
tahunnya. Dari 295 kabupaten/kota yang ada
di Indonesia, 167 kabupaten/kota merupakan
wilayah endemis malaria
ETIOLOGI

Plasmodium Falciparum
Plasmodium Vivax
Plasmodium Ovale
Plasmodium Malarie
Plasmodium Knowlesi
PATOGENESIS

Incubation:
P. Falciparum: < 1 month
P. Vivax and Ovale: Weeks to 3 months * rarely
1 year
P. Malarie: >3 months
P. Knowlesi: Unspecific
SIKLUS TRANSMISI
PERUBAHAN PADA ERITROSIT

Merozoites masuk ke eritrosit konsumsi dan

degradasi intracellular protein (primarily
Hemoglobin) Toxic heme All 5
Parasit mengubah membran RBC dengan Protein
Plasmodium
alterance strain-specific erythrocyte membrane
adhesive protein PfEMP1) cytoadherance
Irregular shaped RBC and increased adhesiveness
to blood vessel endothelium
P. Falciparum
Formation of Rosettes Sticks to other healthy RBC
Capillary and Venule Blockage
Agglutination Sticks to parasite infected RBC
Sequestration
PERUBAHAN PADA ERITROSIT

P. Vivax, P. Ovale, dan P. Malarie tidak

mengalami process sequestration.
Parasitemia tidak setinggi P. falciparum

terhadap RBC
P. Vivax & P. Ovale:- Predileksi menyerang RBC
muda
P. Malarie:- Predileksi menyerang RBC tua
 HOST RESPONSE
Aktivasi
Stops Severe
Plasmodium nonspesic
Parasitemia
menyerang Host defense
mechanism

Fungsi activation of macrophages and

Parasitized RBC
Immunologic release of proinflammatory
rupture in
dan clearance mononuclear cellderived
Schizont Phase
Spleen cytokines

Fever > 39 C,
Fever and Other Synchronized
damages mature
S&S Parasitic Cycle
parasitized RBC

Patternized fever
DIAGNOSIS

Riwayat Penyakit (History Taking)

Manifestasi Klinis

Gejala
Pemeriksaan Fisik
Pemeriksaan Penunjang
STATUS PASIEN
(HISTORY TAKING)
Riwayat Kunjungan ke daerah endemic
Pekerjaan (1 4 weeks)
Tempat Tinggal
Status Imun
Usia
Gejala-gejala
MANIFESTASI KLINIS

Initially flu like symptoms

Symptoms

Headache NO NECK STIFFNESS/PHOTOPHOBIA

Cough
Fatigue
Malaise
Shaking Chills
Arthralgia
Myalgia
GI Symptoms
Paroxysm of Fever (Up to 48 - to 72 HRS,
depending on infecting parasite)
SYMPTOMS
ACCORDING TO SPECIES
Plasmodium Falciparum
Malignant Tertian Fever
Rarely becomes regular
Plasmodium Vivax and Ovale
Benign Tertian Fever
Symptoms up to 6 12 months
Hypnozoites Longer Relapse
 Plasmodium Malariae
Quartan Fever
No Hypnozoites Phase
Longer Asymptomatic Phase (symptoms usually
manifest years after initial infection)
* Plasmodium Knowlesi:
Usually found in pigtail macquau monkeys
Under the microscope similar to P. Malariae
Symptoms patter similar to P. Malariae but manifest
as a severe form
Severe Falciparum
PEMERIKSAAN FISIK

Demam (37,5oC)
Kunjunctiva atau telapak tangan pucat
Pembesaran limpa
Pembesaran hati
 Temperature rectal 40oC
Nadi capat dan lemah
Tekanan darah sistolik <70 mmHg pada orang dewasa dan <50 mmHg
pada anak-anak.
Frekuensi napas >35 kali permenit pada orang dewasa atau >40 x/ pada
balita, dan >50 kali permenit pada anak dibawah 1 tahun
Penurunan kesadaran
Manifestasi perdarahan: petekie, purpura, hematom
Tanda-tanda dehidrasi.
Tanda-tanda anemia berat
Sklera mata kuning.
oligouria sampai anuria.
kaku kuduk, refleks patologis positif
KOMPLIKASI

Cerebral Malaria
Severe Anemia
Renal Failure
Respiratory Symptoms
Hypoglycemia
Acidosis
Liver Dysfunction
Tropical Splenomegaly
Quartan Malarial Nephropathy
Burkitts Lymphoma & EBV- Infection
Cerebral Malaria

Caused by P falciparum infection

Coma may occur; coma can usually be

distinguished from a postictal state secondary to

generalized seizure if the patient does not
regain consciousness after 30 minutes.
Onset: Gradual or sudden following a convulsion

Death rates of 20% among adults and 15%

among children
Symptoms:

diffuse symmetric encephalopathy

Liver Dysfunction

Mild hemolytic jaundice is common in malaria

Severe jaundice is associated with P. falciparum infections
When accompanied by other vital-organ dysfunction (often

renal impairment), liver dysfunction carries a poor

prognosis.
Hepatic dysfunction contributes to:

Hypoglycemia
Lactic acidosis
Impaired drug metabolism
Falciparum malaria may develop deep jaundice (with
hemolytic, hepatic, and cholestatic components) without
evidence of other vital-organ dysfunction.
Severe Anemia
Usually associated with P falciparum
infection.
In nonimmune patients, anemia may be

secondary to erythrocyte infection and a

loss of infected RBCs.
Uninfected RBCs are inappropriately

cleared, and bone marrow suppression may

be involved.
Acute Renal Failure
Rare complication
Infected erythrocytes adhere to the

microvasculature in the renal

cortexoliguric renal failure.
Renal failure is typically reversible,

Supportive dialysis is often needed until kidney

function recovers.
In rare cases, chronic P malariae infection results
in nephrotic syndrome.
Respiratory Distress
Development of metabolic acidosis and
associated respiratory distress
Pulmonary edema can occur
Signs of malarial hyperpneic syndrome:

Alar flaring
chest retraction (intercostals or subcostal)
use of accessory muscles for respiration, or
abnormally deep breathing.
Hypoglycemia

Hypoglycemia, an important and common complication of severe

malaria
Associated with a poor prognosis
Problematic in children and pregnant women.
Hypoglycemia in malaria results from a failure of hepatic
gluconeogenesis increase in the consumption o glucose by both
host and malarial parasites.

Quinine (and quinidine) is a powerful stimulant of pancreatic insulin secretion.

Hyperinsulinemic
hypoglycemia is especially troublesome in pregnant women receiving quinine
treatment
Symptoms and Signs (sweating, gooseflesh, tachycardia) are absent
The
neurologic impairment caused by hypoglycemia cannot be distinguis
hed from that caused by malaria
Quartan Malarial
Nephropathy

Chronic/repeated infections with P. malariae cause soluble immune-

complex injury to the renal glomeruli nephrotic syndrome
Histologic appearance:
Focal or segmental glomerulonephritis with splitting of the capillary basement
membrane.
Electron microscopy:
Subendothelial dense deposits
Immunofluorescence:
deposits of complement and immunoglobulins
P. malariae antigens are often visible.
Coarse-granular pattern of basement membrane immunofluorescent deposits
(predominantly IgG3) with selective proteinuria better prognosis
Fine-granular, predominantly IgG2 pattern with nonselective proteinuria worse
prognosis
Quartan nephropathy usually responds poorly to treatment with either
antimalarial agents or glucocorticoids and cytotoxic drugs.
 Tropical
Splenomegaly
Chronic or repeated malarial infections produce
hypergammaglobulinemia
normochromic, normocytic anemia
splenomegaly.
Residents of malaria-endemic areas in tropical Africa and
Asia exhibit an abnormal immunologic response to
repeated infections
Massive splenomegaly, hepatomegaly, marked elevations in
serum titers of IgM and malarial antibody, hepatic sinusoidal
lymphocytosis, and (in Africa) peripheral B cell lymphocytosis.
Symptoms
Abdominal mass or a dragging sensation in the abdomen
Sharp abdominal pains perisplenitis.
Anemia and some degree of pancytopenia are usually evident
Vulnerability to respiratory and skin infections is increased;
Many patients die of overwhelming sepsis.
Persons with HMS who are living in endemic areas
should receive antimalarial chemoprophylaxis; the
results are usually good
Mechanism

Production of cytotoxic IgM antibodies to CD8+ T

lymphocytes, antibodies to CD5+ T lymphocytes,
and an increase in the ratio of CD4+ T cells to
CD8+ T cells
Uninhibited B cell production of IgM and the

formation of cryoglobulins (IgM aggregates and

immune complexes)
This immunologic process reticuloendothelial

hyperplasia and clearance activity

splenomegaly
PEMERIKSAAN PENUNJANG

Routine Laboratory Examination

Malarial Triad
Elevated Lactate Dehydrogynase (LDH)
Thrombocytopenia (60 %)
Atypical Lymphocytes
Decrease in Hemoglobin (25 %)
Abnormal Liver Function (50 %)
Blood Smears
Microhematocrit Centrifugation
Polymerase Chain Reaction Assay
Lumbar Puncture
Rapid Diagnostic Test (RDT)
Peripheral Blood Smears

200-300 oil-immersion fields should be examined

One negative smear does not exclude malaria

Several more smears should be examined over a 36-

hour period.
Thick Smears (Quantitative)
Thick smears are 20 times more sensitive than thin
smears, but speciation may be more difficult.
Parasitemia can be calculated based on the number of
infected RBCs.
Thin Smears (Qualitative)
Species identification
Histologic Findings
Plasmodium Falciparum
Plasmodium Vivax
Plasmodium Ovale
Plasmodium Malariae
PENATALAKSANAAN

Prevention
Uncomplicated Malaria
Severe Malaria
Complications
Prevention
Uncomplicated Malaria
Severe Malaria
PROGNOSIS

Uncomplicated malaria exhibit marked

improvement within 48 hours after the
initiation of treatment
Fever free after 96 hours.
P falciparum infection carries a poor
prognosis with a high mortality rate if
untreated.
Diagnosing early and treated appropriately, the
prognosis is excellent
Mortality
Internationally, malaria is responsible for
approximately 1-3 million deaths per year.
Majority are in children aged 5 years or younger,
and 80-90% of the deaths each year are in rural
sub-Saharan Africa.
Malaria is the fourth leading cause of death for
children under the age of 5 years old
Malaria is preventable and treatable
THANK
YOU!!!