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KONSEP DASAR INFEKSI

PARASIT

A. PENDAHULUAN
Tujuan Belajar
Mahasiswa mampu menjelaskan:
Klasifikasi Parasit
Respon Imun pada infeksi parasit
Beberapa penyakit infeksi parasit utama

Immunopathogenesis
Gejala klinis
Pemeriksaan laboratorium dan interpretasi
Penatalaksanaan

B. KLASIFIKASI PARASIT
Helminth =
cacing
Protozoa

Phylum

Class

Nemathelminthes =
Cacing gilig/spt benang

Nematoda

Platyhelminthes =
Cacing pipih

Cestoda

Sarcomastigophora

Flagellata

Apicomplexa
Ciliophora

Trematoda

Rhizopoda
Sporozoea
Ciliata

Arthropoda = serangga

B. KLASIFIKASI PARASIT
Nematoda

Bentuk bulat memanjang


Kulit luar tidak bersegmen
Memiliki rongga badan
Jenis kelamin terpisah

Metamorfosis telur larva dewasa


Manusia berperan sbg hospes definitif
Habitat cacing dewasa bisa di usus
atau jaringan
Ditularkan secara langsung atau
melalui vektor serangga
Bentuk infektif bisa berupa stadium
telur atau larva

B. KLASIFIKASI PARASIT
Trematoda

Bentuk spt daun =pipih dorsoventral


Badannya dilapisi integumen
Memiliki 2 batil isap untuk melekat
pada tempat hidupnya (BIM dan BIP
Tidak memiliki rongga badan
Jenis kelamin sebagian besar
hermaphrodit kecuali Schistosoma
Metamorfosis telur larva dewasa
Manusia berperan sbg hospes definitif
Habitat cacing dewasa bisa di usus atau
jaringan
Ditularkan melalui vektor invertebrata
Bentuk infektif bisa berupa stadium larva
cercaria/metacercaria

B. KLASIFIKASI PARASIT
Cestoda

Bentuk spt pita = pipih dorsoventral


Tubuhnyanya terdiri dari bagian kepala
(=scolex), leher dan badan (= strobila)
Scolex memiliki alat mulut berupa batil isap
atau lekuk isap
Strobila bersegmen-segmen disebut proglotid
terdiri dari 3 kelompok (proglotid immatur,
matur, dan gravid)
Tidak memiliki rongga badan
Jenis kelamin hermaphrodit pada setiap proglotid

Metamorfosis telur larva dewasa


Manusia berperan sbg hospes definitif
Habitat cacing dewasa bisa di usus
Bentuk infektif berupa stadium larva melalui
atau tanpa hospes perantara

B. KLASIFIKASI PARASIT
Flagellata

Parasit sel tunggal


Terdapat stadium trofozoit dan kista
Trofozoit memiliki flagel sebagai alat gerak
Kista mrp stadium reproduktif kecuali
Trichomonas
Reproduksi aseksual dengan pembelahan
biner longitudinal

Habitat di usus(Giardia lamblia) atau


jaringan (Trichomonas vaginalis,
Trypanosoma, Leishmania)

B. KLASIFIKASI PARASIT
Rhizopoda

Stadium trofozoit, protoplasma tidak


dibungkus membran yang disebut
pseudopodia
Sebagian besar hidup di alam bebas
(Fam. Amoebidae), beberapa saja yang
bersifat parasit (Fam. Endamoebiadae).
Amoeba hidup bebas ada yang dapat
menimbulkan kelainan pada otak
manusia
Genus dibedakan dari bentuk inti spt
Entamoeba, Endolimax, Iodamoeba

B. KLASIFIKASI PARASIT
Sporozoea

tidak memiliki alat gerak


pada salah satu tahapan dalam siklus
hidupnya memiliki bentuk seperti spora
Seluruh jenis Sporozoa hidup sebagai
parasit
reproduksi secara aseksual dan seksual
Reproduksi aseksual dilakukan dengan
pembelahan biner.
Reproduksi seksual dilakukan dengan
pembentukan gamet
Contoh: Toxoplasma gondii, Plasmodium

B. KLASIFIKASI PARASIT
Ciliata

Terdapat rambut getar ( silia )


Bentuk tubuhnya oval
Memiliki dua inti, yaitu makronukleus
dan mikronukleus
Pembelahan biner
Ada yang hidup bebas ada juga yang
hidup parasit

Habitat di usus (Balantidium


coli)

D. PENYAKIT AKIBAT INFEKSI


PARASIT

D.1. MALARIA
40% of the worlds population lives in endemic
areas
3-500 million clinical cases per year
1.5-2.7 million deaths (90% Africa)
increasing problem (re-emerging disease)
resurgence in some areas
drug resistance ( mortality)

MALARIA
Adalah penyakit infeksi disebabkan
oleh parasit genus Plasmodium,
ditularkan oleh nyamuk Anopheles,
dengan gambaran klinis berupa
demam intermitten, anemia,
pembesaran limpa, atau dapat
disertai berbagai kumpulan gejala
oleh karena adanya komplikasi ke
beberapa organ seperti otak, hati,
dan ginjal.

MALARIA
causative agent =
Plasmodium species
protozoan parasite
member of
Apicomplexa
4 species infecting
humans
transmitted by
anopholine mosquitoes

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

Life Cycle

sporozoites injected
during mosquito
feeding
invade liver cells
exoerythrocytic
schizogony
(merozoites)
merozoites invade RBCs
repeated erythrocytic
schizogony cycles
gametocytes infective
for mosquito
fusion of gametes in
gut
sporogony on gut wall
in hemocoel

Transmission
sporozoites injected
with saliva
enter circulation
trapped by liver
(receptor-ligand)

Anopheles

Exoerythrocytic
Schizogony
hepatocyte invasion

asexual replication
6-15 days
1000-10,000 merozoites
no overt pathology

Hyponozoite
some EE forms
exhibit delayed
Forms

replication (ie, dormant)


merozoites produced months after
initial infection
only P. vivax and P. ovale
relapse = hypnozoite
recrudescence = subpatentt

Erythrocytic
Stage
intracellular parasite
undergoes trophic phase
young trophozoite called
ring form
ingests host hemoglobin
cytostome
food vacuole
hemozoin (malarial
pigment)

Erythrocytic
Schizogony

nuclear division =
begin schizont stage
6-40 nuclei
budding merozoites =
segmenter
erythrocyte rupture
releases merozoites
blood stage results in
disease symptoms

Clinical Features
characterized by acute febrile attacks
(malaria paroxysms)
periodic episodes of fever alternating with
symptom-free periods

manifestations and severity depend on


species and host status
immunity, general health, nutritional state,
genetics

recrudescences and relapses can occur


over months or years
can develop severe complications
(especially P. falciparum)

Malaria
Paroxysm
paroxysms associated with
synchrony of merozoite
release
between paroxysms temperature is normal and patient
feels well
falciparum may not exhibit
classic paroxysms
(continuous fever)
tertian malaria
quartan malaria

erythrocytic schizogony
48 hr in Pf, Pv, Po
72 hr in Pm
gametocytes

Gametocytogenesis
alternative to asexual replication
induction factors not known
drug treatment #'s
immune response #'s

ring gametocyte

Pf : ~10 days
others: ~same as schizogony

sexual dimorphism
microgametocytes
macrogametocytes

no pathology
infective stage for mosquito

Gametogenesis
occurs in mosquito gut
exflagellation most
obvious
3X nuclear replication
8 microgametes formed

exposure to air induces


temperature (2-3oC)
pH (8-8.3)
result of pCO2

gametoctye activating
factor in mosquito
xanthurenic acid

Sporogony
occurs in mosquito (9-21 d)
fusion of micro- and
macrogametes
zygote ookinete (~24 hr)
ookinete transverses gut
epithelium ('trans-invasion')

Sporogony
ookinete oocyst

between epithelium and


basal lamina

asexual replication
sporozoites
sporozoites released

Sporogony
sporozoites migrate
through hemocoel
sporozoites 'invade'
salivary glands

Invasive Stages
Merozoite
erythrocytes
Sporozoite
salivary glands
hepatocytes
Ookinete
epithelium

D.2. FILARIASIS
Lymphatic Filariasis / Elephantiasis

Onchocerciasis (river blindness)

Loiasis

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What is it ?
Wuchereria bancrofti and Brugia
malayi are filarial nematodes
Spread by several species of night feeding mosquitoes
Causes lymphatic filariasis, also
known as Elephantiasis
Commonly and incorrectly
referred to as Elephantitis
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Definitive Host

Humans are the definitive host for


the worms that cause lymphatic
filariasis
There are no known reservoirs for
W.bancrofti.
B.malayi has been found in
macaques, leaf monkeys, cats and
civet cats
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Intermediate Host

Anopheles

Aedes

W.bancrofti is transmitted by
Culex, Aedes, and Anopheles
species
B.malayi is transmitted by
Anopheles and Mansonia
species.
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Culex

Mansonia

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Lymphatic Filariasis by the numbers


Endemic in 83 countries
1.2 billion at risk
More than 120 million people
infected
More than 25 million men suffer
from genital symptoms
More than 15 million people suffer
from lymphoedema or elephantiasis
of the leg
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Morphology I
Adult: White and thread-like. Two
rings of small papillae on the head.
Female:5~10cm in length
Male: 2.5~4cm and a curved tail
with two copulatory spicules.

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Morphology II
Microfilaria: 177~296 m in length, a
sheath with free endings. Bluntly
rounded anteriorly and tapers to a
point posteriorly. A nerve ring with no
nuclei at anterior 1/5 of the body.

Wuchereria bancrofti

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Brugia malayi

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Morphology - B.malayi
B.malayi microfilariae are slightly smaller
than those of W.bancrofti.
Microfilariae are sheathed, and about 200
to 275 m.
Not much is known about the adult
worms, as they are not often recovered
One distinctive feature of B.malayi is that
the microfilarial nuclei extends to the tip
of the tail
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The morphological differences between two microfilaria

W.bancrofti

Size

Cephalic space

Nuclei

Terminal nucleus

244~296 m
Shorter

B. malayi
177~230 m
Longer

Equal sized

Unequal sized

clearly

coalescing

countable

uncountable

No

Two

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Characteristic of life cycle


Host: Mosqutoes (intermediate host)
Human (final host)
Location: Lymphatics and lymph
nodes
Infective stage: Infective larvae
Transmission stage: Microfilariae
Diagnostic stage: Microfilariae
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Life cycle
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Wuchereria Life Cycle

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Nocturnal periodicity

Phenomen which the number of


microfilariae in peripherial blood is very
low density during daytime, but
increase from evening to midnight and
reach the greatest density at 10p.m to
2 a.m.May be related to cerebral
activity and vasoactivity of pulmonary
vessels.
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Larva deposited by mosquito bite


Travel through dermis to lymphatic vessels
Growth (approx 9 months) to mature
worms(20-100mm long)
Worms live 5-7 years (occasionally up to15
years)
Mate->Microfilariae (1st stage larva)
Females->release up to 10,000
microfilariae/day into bloodstream
Microfilarie taken up by mosquito bite
Develop into 2nd and 3rd stage larva over 1014 days inside mosquito vector
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Lymphatic System

Network of vessels
that collect fluid that
leaks out of the blood
into tissues (lymph)
Redirects lymph back
into the blood stream
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Clinical Course
Initially asymptomatic
Symptoms develop with increasing numbers
of worms
Less than 1/3 of infected individuals have
acute symptoms
Clinical Course is 3 phases:
Asymptomatic Microfilaremia
Acute Adenolymphangitis (ADL)
Chronic/Irreversible lymphedema
Superimposed upon repeated episodes of
ADL
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Acute ADL
Presents with sudden onset of fever
and painful lymphadenopathy
Retrograde Lymphangitis
Inflammation spreads distally away
from lymph node group
Immune mediated response to dying
worms
Most common areas: Inguinal nodes
and Lower extremities
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o Inflammation spontaneously resolve


after 4-7 days but can recur
frequently
o Recurrences usually 1-4 times/year
with increasing severity of
lymphedema
o Secondary bacterial infections in
edematous(elephantatic) areas
o Filarial fever (fever w/o lymphangitis)
o Tropical Pulmonary Eosinophilia
o Hyperresponsiveness to microfilariae
trapped in lungs
o Nocturnal Wheezing
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Chronic Manifestations
o Lymphedema

o Mostly LE and inguinal, but can


affect UE and breast
o Initially pitting edema, with gradual
hardening of tissues
hyperpigmentation & hyperkeratosis
o GenitaliaHydroceles

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Chronic Manifestations
o Renal involvement

o Chylurialymph discharge into


urine
o Loss of fat and protein
hypoproteinemia & anemia
o Hematuria, proteinuria from ?
immune complex nephritis
o Secondary bacterial/fungal infections
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Elephantiasis: accumulation of lymph in


extremeties, fibrosis, and thickening of
skin.

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Onchocerciasis (river blindness)


Debilitates millions of humans by
scarring eyes & causing
permanent blindness
Affects people along rivers in West
& Central Africa (native) & South
America (introduced via slavery)

Caused by Onchocerca volvulus


Adult females are up to 500mm
long & males up to 40mm long
Adults live up to 14 years
Restricted to humans (no known
animal reservoirs)

Transmitted by black flies


(Simuliidae)
Larvae live in fast-flowing water
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Onchocerciasis (river blindness)

Black flies ingest microfilariae from


blood
Move from gut to flight muscles &
mature into infective larvae (L3)
L3 larvae migrate to head & enter
humans via bite wound; mature
into adults (2-4 months)
Adults accumulate in subcutaneous
nodules (1cm diameter) which
dont cause much damage
Mating in nodules produces
microfilariae

Nodules

Live under skin causing rashes &


wrinkles
Cause blindness when invade
eyes tissues & die there
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Damaged
eye tissues

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Onchocerciasis (river blindness)

Early stages of eye damage can


be reversed by drug treatment
Parasiticide ivermectin is most
popular

Transfer of worms affected by


feeding behaviour of flies
Waggle mouth parts during biting
to increase wound size & create
pool of blood (pool feeders)

Main vector = Simulium


damnosum
Complex of >40 sibling species in
West & East Africa
Not all sibling species transmit
worms
Insecticide applications used to
control larvae in rivers
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Loiasis
Microfilariae in human blood

Caused by infection with Loa loa

Adult worms move under human skin


Observed beneath skin or passing
through conjunctiva of eyes (eye
worms)
Worms = 2 races (attack humans or
arboreal primates)

Transmitted by horse flies (Tabanidae)


in genus Chrysops
Day-feeding & forest-dwelling
Rare case of Tabanidae = biological
vectors

Disease endemic to rain forest regions


of West & Central Africa

Adult in human eye

Generally mild & painless (chronic)


with 10-15 year incubation period
May cause swellings of skin (Calabar
swelling)

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Diagnosis

The standard method for diagnosing


active infection is the identification of
microfilariae by microscopic
examination
However, microfilariae circulate
nocturnally, making blood collection
an issue

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Diagnosis
A card test for parasite antigens
requring only a small amount of
blood has been developed
Does not require laboratory
equipment
Blood drawn by finger stick
Urinalysis, CBC and Comprehensive
Chemistries
Foot Biopsy: Normal Skin with areas
of chronic inflammation
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Microfilariae are seen in blood


smears and are DIAGNOSTIC

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Blood Smear Microfilaria


Note wavy
microfilarial
worm in the
thick part of
blood film.
Dark blue
structures are
nuclei
Tail end tapering
(no nuclei)
Sheath covering
worm.
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Blood Smear Microfilaria


Note wavy
microfilarial
worm in the
thick part of
blood film.
Head end of the
worm rounded
(no nuclei)
(Sheath is not
clearly seen)
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Blood Smear Microfilaria


Note wavy
microfilarial worm
in the thick part of
blood film.
Dark blue
structures are
nuclei
Tail end - tapering
sheath (no nuclei)
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Hydrocele fluid cell


block.
Note wavy
microfilarial
worms.
Inflammatory
cells
lymphocytes.
Hemorrhagic
fluid sediment

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Hydrocele fluid cell


block.
Note wavy
microfilarial
worms.
Inflammatory
cells
lymphocytes.
RBC

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Hydrocele fluid cell


block.
Note wavy
microfilarial
worms.
Inflammatory
cells
lymphocytes.
RBC

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Hydrocele fluid cell


block.

Inflammatory
cells
Microfilaria.
lymphocytes.
RBC

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Control
As with malaria, the most effective
method of controlling the spread of
W.bancrofti and B.malayi is to avoid
mosquito bites
The CDC recommends that anyone in
at-risk areas:
Sleep under a bed net
Wear long sleeves and trousers
Wear insect repellent on exposed
skin, especially at night
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Vector control
Covering water-storage containers
and improving waste-water and solidwaste treatment systems can help by
reducing the amount of standing
water in which mosquitoes can lay
eggs.
Killing eggs (oviciding) and killing or
disrupting larva (larviciding) in
bodies of stagnant water can further
reduce mosquito populations.
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Treatment
Treatment of filariasis involves two
components:
Getting rid of the microfilariae in
people's blood
Maintaining careful hygiene in
infected persons to reduce the
incidence and severity of secondary
(e.g., bacterial) infections.
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Drugs, Drugs, Drugs!


Anti-filariasis medicines commonly used
include:
Diethylcarbamazine (DEC)
reduces microfilariae concentrations
kills adult worms
Albendazole
kills adult worms
Ivermectin
kills the microfilariae produced by adult
worms
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And more drugs!


The disease is usually treated with
single-dose regimens of a combination
of two drugs, one targeting
microfilariae and one targeting adult
worms (i.e.,either diethylcarbamazine
and albenadazole, or ivermectin and
albendazole
In some areas, DEC laced table salt is
used as a prophylactic
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