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Penyakit Parasitik

dr. Wiwien S Utami, M.Sc
yang mempunyai gejala
Anemia
Topik Bahasan
• Hookworm Infection
• Trichuriasis
• Diphyllobothriasis
• Schistosomiasis
• Malaria

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Ancylostoma duodenale
Necator americanus
(hookworm)
•Intestinal parasites
•World wide distribution
•However, because they feed on
blood a heavy infection can produce
severe anemia.
• habitat of adult: small intestine of man
• Infective stage: filariform larvae
• Mode of transmission: penetration of
filariform larvae in skin through bare feet.
In some cases from mother to her baby.
• Diagnosis: eggs in stool
• Disease: Hook worm infection


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MORPHOLOGY
Adults: They look like
an odd piece thread and
are about 1cm. They are
white or light pinkish
when living. ♀ is slightly
larger than ♂.The
male’s posterior end is
expanded to form a
copulatory bursa.
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1. HEAD

Buccal capsule
A. duodenale: 2 pairs of ventral teeth
N. americanus: 1 pair of ventral cutting plates
9.9
Figure 15.06
Section through hookworm
attached to dog intestine
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• Morphology

♀: the posterior end is cone-shaped
♂: elliptic and fan-shaped (copulatory bursa)

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• Characteristics of copulatory spicules

Adults of A. duodenale Adults of N. americanus
Differences between two hookworms
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Morphology

2) Egg: 64-75μm
1-8 cells or an embryo
Shells are thin and hyaline.
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2
1
3
Larva
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Filariform Rhabditiform
Larva st. 3
• L1, the feeding non-infective
rhabditiform stage
• L2, which is also in the rhabditiform
stage, will feed for approximately 7 days.
• L3 is the filariform stage of the parasite,
that is, the non-feeding infective form of
the larvae
Hookworm life cycle

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Clinical Manifestations
Larval migration
(1) Dermatitis, known as "ground itch" or
"stool poison".The larvae penetrating the skin
cause allergic reaction, petechiae 0r papule
with itching and burning sensation. Scratching
leads to secondary infection.
(2) pneumonitis (allergic reaction), Loeffier's
syndrome: cough, asthma, low fever, biood-
tinged sputum or hemoptysis, chest-pain,
inflammation shadows in lungs under X-ray.
These manifestations go on about 2 weeks.
2. Adults in small intestine
(1) Epigastric pain as that of a duodenal ulcer.
(2) A large worm burden results in microcytic
hypochromatic anemia (character manifestation).
The symptoms are lassitude, edema, palpitation
of the heart. In severe case, death may result
from cardiac failure or physical exhaustion.
(3) Allotriophagy (orpica) is due to the lack of
trace element iron .
(4) Amenorrhea, sterility, abortion may take
place in women.
(5) Gastrointestinal bleeding
• Clinical Manifestations
Pathogenesis
1. Pathogenesis of the larvae
(1) Dermatitis (“ground itch”)
due to working in farmland, contacting
with the soil
Susceptible locations: between fingers and
toes
(2) Symptoms caused by larva migration
from pulmonary capillaries to alveoli
a dry cough, sore throat,, etc

Maculopapule & erythema
Cause ground itch
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• Humans occasionally get
infected by L3 larvae of dog
and cat hookworms (e.g.
Ancylostoma caninum or
brazilienzis again by skin
penetration)
• The larvae can not establish a
productive infection in
humans, but wander about in
the subcoutaneous tissue,
causing significant
inflammation and painful
swelling
• Responds well to treatment
Cutaneus Larva Migrans
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2. Pathogenesis of the adults

• Worms burrow through the mucosa with
buccal capsule, teeth, cutting plates,
feed on blood, secret anticoagulants and
proteinases
• Worms continuously suck blood, but
digest a little, the large amount of blood
is passed.
• Worms change places and leave the
wound bleeding.
PATHOGENESIS
Adults in intestinal mucosa
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(1) Anemia
The amount of blood loss
N. americanus: 0.02~0.10 ml per worm a
day
A. duodenale: 0.14~0.26 ml per worm a day
In children a hookworm infection can stunt growth
and cause a general lack of energy.
(2) Gastrointestinal symptoms
Epigastric discomfort, pain
Nausea, vomiting, diarrhea, etc
Aberrations of appetite
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Diagnosis
1. Direct fecal smear (egg and
Rhabditiform larvae (noninfective) in old
stool samples.
2. Culture of hookworm larvae Harada-
Mori culture: collection of larvae from eggs
hatched on strips of filter paper with one
end immersed in water
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Prevention & Control
• Sanitation!
• Clean water
• Proper waste disposal

• Proper footwear

• Identification of high-risk people

• School-based deworming
• School-based children are most high risk!
• Evidence-based efficacy

Diagnosis
Criterion:
1. hemoglobin is lower than 12g/dL in man, 11g/dL in
woman.
2. find hookworm egg
1.Direct visualization – gold standard
- Uses stool samples
- N. americanus and A. duodenale eggs are
indistinguishable from each other!
2.Morphologic differentiation of larval culture
3.PCR










Treatment
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• Mebendazole 500 mg tab single dose

• Albendazole 400 mg tab single dose

• Pyrantel pamoate 11 mg/kg/d x 3 days,
max of 1g/day


* Same dosage for children >2 years old
• Mebendazole 500 mg tab single dose

- Prevents microtubule formation
- Irreversible blockage of glucose uptake

• Albendazole 400 mg tab single dose
• Pyrantel pamoate 11 mg/kg/d x 3 days, max of
1g/day

• * Same dosage for children >2 years old
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• Mebendazole 500 mg tab single dose

• Albendazole 400 mg tab single dose
- Inhibits cytoplasmic tubulin polymerization
- Decreases ATP production
- Results in immobilization/energy depletion

• Pyrantel pamoate 11 mg/kg/d x 3 days, max of
1g/day

* Same dosage for children >2 years old
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• Mebendazole 500 mg tab single dose
• Albendazole 400 mg tab single dose
• Pyrantel pamoate 11 mg/kg/d x 3
days, max of 1g/day

- Depolarizing neuromuscular blocker
- Causes paralysis
* Same dosage for children >2 years old
Lanjut
Whipworm:
Trichuris trichiuria
• Adult habitat: caecum, colorectum
• No extra-intestinal phase
• Lifespan: 1 - 3 years
• 90% infections are asymptomatic
• Symptoms with heavy infections
–Intensity of infection peaks by age 10
Pre-patency:
2 months
Whipworm:
Trichuris trichiuria
• Clinical Features:
–Asymptomatic
–Physical Weakness, Anemia
–Stunted Growth, Cognitive Deficits
–Stool frequency (12+/day), nocturnal
stooling
–Trichuris dysentery syndrome
–Trichuris colitis
–Rectal prolapse
• Treatment: Albendazole
Whipworm: Trichuriasis Colitis
Rectal Prolapse from Trichiuriasis
Whipworm Egg: 2 polar plugs
Lanjut
CESTODA
Diphyllobothrium latum
• Hospes Definitif : Manusia
• Hospes Reservoar : Anjing, kucing dan 22 jenis
mamalia lainnya, seperti: walrus, singa laut,
babi dan serigala.
• Hospes Perantara I : Cyclops, Dioptomus
• Hospes Perantara II : Ikan
• Nama Penyakit : Diphyllobothriasis

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Diphyllobothrium latum
Morfologi
• Panjangnya mencapai ± 900 cm, lebar 2,5 cm.
• Terdiri atas 4000 proglotid.
• Mempunyai sepasang celah penghisap
(bothria) dibagian ventral dan dorsal pada
skoleks.
• Hermafrodit
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Daur Hidup
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Telur
• Mempunyai
operkulum
• Berukuran 70×45
mikro

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Patologi dan Gejala Klinis
Bila cacing sudah hidup di permukaan usus, gejala yang
ditimbulkan:
- Anemia megaloblastik
( Defisiensi B12 )
- Sumbatan usus secara mekanis bila cacing banyak
- Obstruksi usus → cacing membentuk benang kusut

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Gejala Diphyllobothriasis:
• Gangguan saraf
• Gangguan pencernaan
• Sakit perut
• Berat badan turun
• Lemah
• Kurang gizi
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Diagnosis
Gravid proglottids burst to release eggs, or
drop off
and burst later in the feces.
Diagnosis is based on the identification
of eggs, which are oval and operculated,or
proglottids in the feces.

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Treatment
• Praziquantel is highly effective  10mg/kgBB
• Obat Atabrin dalam keadaan perut kosong,
disertai Na-Bikarbonas, dosis 0,5 gr
• Niclosamid (Yomesan), 4 tablet (2gr) dikunyah
setelah makan hidangan ringan
• Vitamin B12 supplements are required for
patients with anemia

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Pencegahan
• Memasak ikan air tawar sampai betul-betul
matang atau membekukannya sampai -10°C
selama 24 jam.
• Mengeringkan dan mengasinkan ikan secara
baik.
• Dilarang membuang tinja di kolam air tawar.
• Memberikan penyuluhan pada masyarakat.
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TREMATODA DARAH


TREMATODA DARAH SCHISTOSOMA

• Schistosoma japonicum
• Schistosoma mansoni
• Schistosoma haematobium
• Schistosoma intercalatum
• Schistosoma mekongi
• Schistosoma binatang

Schistosoma
• Penyakit : skistosomiasis= bilharziasis
• Morfologi dan Daur Hidup
–Hidup in copula di dalam pembuluh darah
vena-vena usus, vesikalis dan prostatika.
–Di bagian ventral cacing jantan terdapat
canalis gynaecophorus, tempat cacing
betina.
–Telur tidak mempunyai operkulum dan
berisi mirasidium, mempunyai duri dan
letaknya tergantung spesies.
• Telur dapat menembus keluar dari
pembuluh darah, bermigrasi di
jaringan dan akhirnya masuk ke lumen
usus atau kandung kencing
• Telur menetas di dalam air
mengeluarkan mirasidium.
Cacing dewasa schistosoma
HP Schistosoma
Serkaria Schistosoma
Daur hidup Schistosoma sp.
Schistosoma waktu kopulasi
Patologi dan Gejala Klinis
• Perubahan yang terjadi disebabkan oleh 3
stadium cacing yaitu serkaria, cacing dewasa
dan telur.
• Perubahan-perubahan pada skistosomiasis
dibagi dalam 3 stadium:
1. Masa tunas biologik
– Gejala kulit dan alergi : eritema, papula
disertai rasa gatal dan panas hilang dalam
2-3 hari.
–Gejala paru : batuk, kadang-kadang
pengeluaran dahak yang produktif
–Gejala toksemia : timbul minggu ke-2 sampai
ke-8 setelah infeksi. Berat gejala tergantung
jumlah serkaria yang masuk
• Gejala berupa : lemah, malaise, tidak nafsu
makan, mual dan muntah. Diare disebabkan
hipersensitif terhadap cacing
• Hati dan limpa membesar dan nyeri raba.
2. Stadium Akut
– Mulai sejak cacing bertelur
– Efek patologis tergantung jumlah telur yang
dikeluarkan dan jumlah cacing .
– Keluhan : demam, malaise, berat badan
menurun
– Pada infeksi berat Sindroma disentri
– Hepatomegali timbul lebih dini disusul
splenomegali; terjadi 6-8 bulan setelah
infeksi.
3. Stadium menahun :
– Penyembuhan dengan pembentukan
jaringan ikat dan fibrosis
– Hepar kembali mengecil karena fibrosis. Hal
ini disebut sirosis
– sirosis  sirosis periportal
– Gejala : splenomegali, edema tunbgai
bawah dan alat kelamin, asites dan ikterus.
– Stadium lanjut sekali dapat terjadi
hematemesis.
• Diagnosis :
–Menemukan telur dalam tinja, urin
atau jaringan biopsi
–Reaksi serologi
Pengobatan
• Umumnya tidak ada yang aman atau agak
toksik
• Semuanya mempunyai risiko
• Pengaruh obat anti schistosoma dapat
menyebabkan terlepasnya cacing dari p. darah
dan mengakibatkan tersapunya cacing ke
dalam hati oleh sirkulasi portal disebut
hepatic shift.
• Obat-obat anti schistosoma :

–Emetin (tartras emetikus)
–Fuadin stibofen, Reprodal, neo-antimosan
–Astiban TW 56
–Lucanthone-HCl, Miracil D. Nilodin
–Niridazol
–Prazikuantel (Embay® 8440;
Droncit®,Biltricide®)
Epidemiologi
• Penyakit skistosomiasis merupakan masalah
kesehatan masyarakat di berbagai negara. Di
Indonesia hanya skistomiasis japonikum
ditemukan endemik di Sulawesi Tengah.
• Berhubungan erat dengan air dari irigasi dengan
adanya fokus keong sebagai hospes perantara
• Infeksi berlangsung pada orang yang bekerja di
sawah.
• Kelompok usia yang terkena 5 – 50 tahun.
Schistosoma japonicum
• Hospes : Manusia, kucing, anjing,rusa, tikus
sawah (rattus), sapi, babi rusa dll.
• Penyakit : Oriental schistosomiasis,
skistosomiasis japonika, penyakit Katayama
atau penyakit demam keong.
• Penyebaran geografis :
–Di Indonesia hanya di Sulteng daerah D.
Lindu dan lembah Napu.
Schistosoma japonicum
TELUR
BENTUK : BULAT AGAK LONJONG DNG
TONJOLAN DI BAGIAN
LATERAL DEKAT KUTUB
UKURAN : 100 x 65 µm
TELUR BERISI EMBRIO
TANPA OPERKULUM
SERKARIA
Schistosoma sp
EKOR BERCABANG
Morfologi S. japonicum
Telur S.japonicum
Telur S.japonicum
Telur S. japonicum
S. japonicum jantan dan betina
DAUR HIDUP Schistosoma sp
Daur S. japonicum
INANG ANTARA Schistosoma japonicum
Oncomelania sp
Patologi dan Gejala Klinis
• Satdioum I :
– Gatal-gatal (urtikaria)
– Gejala intoksikasi : demam hepatomegali dan
eosinofilia tinggi
• Stadium II :
– Sindroma disentri
• Stadium III :
– Sirosis hepatis dan splenomegali serta
hematemesis
Diagnosis
• Menemukan telur dalam tinja atau jaringan
biopsi
• Reaksi serologi :
–COPT (circumoral precipitin test)
–IHT (Indirect haemagglutinination test)
–CFT (complement fixation test)
–FAT (Fluorescense antibody test)
–ELISA(Enzyme linked immunosorbent assay)

Schistosoma mansoni
• Hospes : Manusia dan kera babon di Afrika sbg
hospes reservoir.
• Penyakit : skistomiasis usus
• Patologi dan gejala Klinis :
–Seperti pada S. japonicum, tetapi lebih
ringan.
–Splenomegali dapat jadi berat sekali.

Morfologi S. mansoni
Telur S. mansoni
Telur S. mansoni
Daur S. mansoni
INANG ANTARA Schistosoma
mansoni
Biomphalaria sp
Telur S. mansoni dlm usus
Telur S. mansoni pada jaringan usus (pd lapisan mukosa
dan submukosa)
Schistosoma haematobium
• Hospes : Manusia. Babon dan kera lain sbg
hospes reservoir.
• Penyakit : skistosmiasis vesika urinaria
• Tidak ditemukan di Indonesia.
• Patologi dan Gejala Klinis:
–Hematuria dan disuria bila terjadi sistitis
–Sindroma disentri bila terjadi kelainan di
rektum.
Diagnosis : Menemukan telur di dalam urin.
Morfologi S. haematobium
Telur S. haematobium
Telur S. haematobium
Daur S. haematobium
INANG ANTARA Schistosoma haematobium
Bulinus sp
Telur S. haematobium pada jaringan kandung kencing,
terlihat telur terkalsifikasi
Telur S. haematobium pada jaringan
kandung
Lokasi S. haematobium dlm Plexus V. vesicalis
S. haematobium S. mansoni S. japonicum
Cacing jantan

Ukuran 10-15 x 1 mm 10 x 1 mm 12-20 x 0.5 mm
Kutikula Tuberkula halus Tuberkula kasar Tidak bertuberkel
Testis 4-5, berkelompok 8-9, deret zig-zag 6-7, berderet
Cacing betina

Ukuran 20 X 0.25 mm 14 x 0.25 mm 26 x 0.3 mm.
Ovarium Posterior pertengahan badan Anterior pertengahan badan Pertengahan badan
Telur dalam uterus 20-30 butir 1-3 butir 50 butir atau lebih
Sekum yang menyatu Panjang (menyatu di pertengahan
badan)
Terpanjang(menyatu di anterior
perte-ngahan badan)
Pendek(menyatu di posterior
perte-ngahan badan)
Hospes perantara Bulinus (Physopsis dan
Planorbarius)
Biomphalaria dan Australorbis Oncomelania hupensis
Hospes Definitif Manusia
Babon
Manusia
Babon
Manusia & hewan domestik
Penyebaran Geografis Afrika, Timur Tengahd & Timur
Dekat
Afrika dan Amerika Selatan Timur Jauh (Oriental)
Habitat Pleksus vena vesikalis dan
prostatika
Plexus mesenterikus daerah
sigmoidorektal
(v. mesenterika inferior dan
cabang-cabangnya
Plexus mesenterikus daerah
ileocaecalis (v. mesenterika
superior dan cabang-cabangnya)
Telur Duri terminal Duri lateral Bejolan lateral
Malaria
Key Morphological in Blood Smear:
• P. falciparum :
- numerous rings
- smaller rings
- no trophozoites or
schizonts
- cresent-shaped
gametocytes

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Plasmodium vivax
• enlarged erythrocyte
• Schüffner's dots
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Plasmodium malariae
• P. malariae :
- compact parasite
- merozoites in
rosette

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Plasmodium ovale
- similar to P. vivax
- compact trophozoite
- fewer merozoites in
schizont
- elongated erythrocyte
- 'ameboid' trophozoite


Plasmodium ovale
• P. ovale :
• Infected RBCs are
often slightly
enlarged and may
exhibit fimbriation
and Schüffner's dots.
• Pigment is less-
coarse and diffuse.
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Morphological Differences Between Human Plasmodium
Species in Blood Smear


Plasmodium falciparum
RING STAGE
Ring-form trophozoites (rings) of Plasmodium falciparumare often thin and
delicate, measuring on average 1/5 the diameter of the red blood cell. They may
be found on the periphery of the RBC (accolé, appliqué) and multiply-infected
RBCs are not uncommon. There is usually no enlargement of infected RBCs.
Plasmodium falciparum
TROFOZOIT
Developing trophozoites of P. falciparum tend to remain in ring form,
but may become thicker and more compact. The amount of pigment
and chromatin may also increase. Compact or amoeboid forms may be
seen
Plasmodium falciparum
SKIZON MASAK
Schizonts are rarely seen in peripheral blood of Plasmodium
falciparum infections, except in severe cases. When seen, schizonts
contain anywhere from 8-24 merozoites. A mature schizont usually
fills about 2/3 of the infected RBC.
MIKROGAMETOSIT
Plasmodium falciparum
• BTK GINJAL/PISANG GEMUK
• PLASMA MERAH MUDA
• INTI BESAR TERSEBAR,
PUCAT
• PIGMEN MAL TERSEBAR DI
ANTARA INTI
MAKROGAMETOSIT
Plasmodium falciparum
• BENTUK LANGSING
SPT PISANG AMBON
• PLASMA WARNA BIRU
• INTI PADAT KOMPAK,
LETAK DI TENGAH
• PIGMEN MAL TERSEBAR
DI SEKITAR INTI
GAMETOSIT
Plasmodium falciparum
MAKROGAMETOSIT
MIKROGAMETOSIT
Plasmodium vivax
Plasmodium malariae
Plasmodium malariae
SCHIZONT Plasmodium malariae
TROFOZOIT Plasmodium ovale
SIKLUS HIDUP




• waktu antara sporozoit masuk dalam
badan hospes sampai timbulnya gejala
demam, biasanya berlangsung antara 8-
37 hari, tergantung pada spesies parasit,
pada beratnya infeksi dan pada
pengobatan sebelumnya atau pada
derajat resistensi hospes.
MASA
TUNAS
INSTRINSIK
• berlangsung sejak saat infeksi sampai
ditemukan parasit malaria dalam darah
untuk pertama kali
MASA PRE-
PATEN
• parasit malaria yang ditularkan melalui
nyamuk kepada manusia adalah 12 hari
untuk plasmodium falciparum, 13-17 hari
untuk plasmodium ovale dan vivax, dan
28-30 hari untuk plasmodium malariae
(malaria kuartana).
MASA
TUNAS
EKSTRINSIK
gejala khas terutama
pada malaria yang
menahun.
Perubahan limpa biasanya
disebabkan oleh kongesti, tetapi kemudian limpa
berubah warna menjadi hitam, karena pigmen yang
ditimbun dalam eritsosit yang mengandung kapiler
dan sinusoid
Pada malaria menahun
jaringan ikat bertambah
tebal, sehingga limpa
menjadi keras.
SPLENOMEGALI
Derajat anemia
tergantung pada spesies
parasit yang
menyebabkannya
Jenis anemia pada malaria adalah hemolitik,
normokrom dan normositik.

Pada serangan akut kadar hemoglobin turun secara
mendadak.
Anemia terutama tampak
jelas pada malaria
falsiparum dengan
penghancuran eritrosit yang
cepat dan hebat dan pada
malaria menahun.
ANEMIA
Gejala klasik, biasanya ditemukan pada
penderita yang berasal dari daerah
non endemis malaria atau yang belum
mempunyai kekebalan (immunitas); atau yang
pertama kali menderita malaria
GEJALA
Manifestasi klinik
• Bervariasi, ringan – berat
• Gejala utama (cardinal signs)  trias malaria:
• Febris paroksismal
• Anemia (hemolitik)
• Splenomegali
• Gejala-2 prodromal: tidak selalu ada  masa
inkubasi intrinsik
• Masa inkubasi tergantung beberapa faktor (agent +
host)
 Berbeda utk msg-2 spesies:
• P. vivax + ovale : 13-17 hari
• P. falciparum : ± 12 hari
• P. malariae : 28-30 hari

Hepato-splenomegaly
10-15% die - survivors partially immune
often with splenomegaly
Malarial (Pf)
anemia in
Kenyan child
Malarial (Pf)
Jaundice in
Vietnamese man
Peters & Pasvol, Tropical Medicine
and Parasitology, 5
th
Ed., 2002

Immunopathology
• Fever
– correlates with schizont rupture
– IL1 & TNF
• Anaemia
– common complication exceeds parasitemia & may
worsen after treatment
– T cell control of spllenomegally/bone marrow
Pathogenesis of Malaria

Pathophysiological Mechanisms of Complication
• There is tissue hypoxia caused by :
- sequestration
- cytoadherence
- rosetting
- reduced erythrocyte deformability
SEQUESTRATION
Sequestration :
The removal of infected RBCs from the
peripheral circulation by binding to the
vascular endothelium (postcapillary
venules of deep tissue) often
accompanied by uninfected RBCs
CYTOADHERENCE
• Cytoadherence :
The binding of mature infected RBCs to the
vascular endothelium
• The advantages for the parasites :
- microaerophilic environment is better
suited for their maturation
- to escape the clearence by the spleen
Possible
Pathophysiology
cytoadherence

cerebral ischemia

hypoxia,
metabolic effects,
cytokines (eg, TNF-)

coma

death
ROSETTING
• The spontaneeous binding of normal RBCs to
malaria-infected RBCs
• Five rosetting receptor have been identified
on RBCs :
- blood group antigens A and B
- CD 36
- complement receptor 1 (CR1)
- HS-like GAGs

MECHANISM OF ROSETTING
Reduced Erythrocyte Deformability
• Erythrocyte become more rigid
• Several factors contribute to erythrocyte
deformability :
- reduced sphingomyelin and
phosphatidylcholine in the infected erythrocyte
membrane
- increased membrane stiffness
- increased cytoplasmic viscosity
Malaria - Prevention