malaria klinis.pptx

7/23/2019 malaria klinis.pptx

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Malaria Pathogenesis andClinical Presentation


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Plasmodiumspecies whichinfect humans

Plasmodium vivax(tertian)

Plasmodium ovale(tertian)

Plasmodium falciparum(tertian)

Plasmodium malariae(quartian)

Plasmodium knowlesi (?/)


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Exo-erythrocytic(hepatic) cycle

Sporozoites

Mosquito SalivaryGland

Malaria Life Cycle

Gametocytes

ocyst

ErythrocyticCycle

!y"ote

Schizogony

Sporogony

#ypnozoites(for P. vivaxand P. ovale)


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Malaria Transmission Cycle

Parasite undergoes

sexual reproduction in

the mosquito

Some merozoites

differentiate into male or

female gametocyctes

Erythrocytic Cycle:

Merozoites infect red

blood cells to form

schizonts

Dormant liver stages

hypnozoites! of P.

vivax and P. ovale

Exo"erythrocytic hepatic! Cycle:

Sporozoites infect liver cells and

develop into schizonts# $hich release

merozoites into the blood

MOSQUITO HUMAN

Sporozoires in%ected

into human host during

blood meal

Parasites

mature in

mosquito

midgut and

migrate to

salivary

glands


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Components of the Malaria LifeCycle

Mosquito Vecto

Human Host

Sporogonic cycle

nfecti!e "erio#

Mosquito $itesgametocytemicperson

Mosquito $ites

uninfecte#person

"repatent "erio#

ncu$ation "erio#

Clinical llness

"arasites !isi$le

%eco!ery

Symptom onset


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&'oerythrocytic (tissue)phase loo# is infecte# with sporo*oites a$out

+, minutes after the mosquito $ite

The sporo*oites are eaten $y

macrophages or enter the li!er cellswhere they multiply -

preerythrocytic schi*ogeny

P. vivaxan# P. ovalesporo*oites formparasites in the li!er calle# hypno*oites


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&'oerythrocytic (tissue)phase

P. malariaeor P. falciparumsporo*oites #o not formhypno*oites. #e!elop #irectly into

preerythrocytic schi*onts in theli!er

"reerythrocytic schi*ogeny taes

010 #ays post infection Schi*onts rupture. releasing

mero*oites which in!a#e re# $loo#

cells (%C) in li!er


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%elapsing malaria&'oerythrocytic (tissue) phase

P. vivax and P. ovale hypno*oitesremain #ormant for months

They #e!elop an# un#ergoe pre

erythrocytic sporogeny The schi*onts rupture. releasing

mero*oites an# pro#uce clinical

relapse


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&rythrocytic phase

"repatent perio# - inter!al $etween#ate of infection an# #etection ofparasites in peripheral $loo#

ncu$ation perio# - time $etweeninfection an# 2rst appearance of clinicalsymptoms

Mero*oites from li!er in!a#e peripheral(%C) an# #e!elop causing changes inthe %C

There is !aria$ility in all + of thesefeatures #epen#ing on species ofmalaria


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&rythrocytic phasestages of parasite in %C

Tropho*oites are early stages with ringform the youngest

Tropoho*oite nucleus an# cytoplasm

#i!i#e forming a schi*ont Segmentation of schi*ont3s nucleus an#

cytoplasm forms mero*oites

Schi*ogeny complete when schi*ont

ruptures. releasing mero*oites into $loo#stream. causing fe!er

These are ase'ual forms


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&rythrocytic phasestages of parasite in %C

Mero*oites in!a#e other %Cs an#schi*ongeny is repeate#

"arasite #ensity increases untilhost3s immune response slows it#own

Mero*oites may #e!elop intogametocytes. the se'ual forms ofthe parasite


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Schi*ogenic perio#icity an# fe!er patterns

Schi*ogenic perio#icity is length ofase'ual erythrocytic phase 45 hours in P.f.. P.v.. an# P.o.(tertian)

67 hours in P.m8 (quartian) nitially may not see characteristic fe!er

pattern if schi*ogeny not synchronous

9ith synchrony. perio#s of fe!er or

fe$rile paro'syms assume a more#e2nite + (tertian) or 4 (quartian) #aypattern


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Clinical presentation

&arly symptoms Hea#ache

Malaise

:atigue ;ausea

Muscular pains

Slight #iarrhea

Slight fe!er. usually not intermittent Coul# $e mistaen as in


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Clinical presentation

=cute fe$rile illness. may ha!e perio#icfe$rile paro'ysms e!ery 45 - 67 hours with

=fe$rile asymptomatic inter!als

Ten#ency to recru#esce or relapse o!ermonths to years

=nemia. throm$ocytopenia. >aun#ice.hepatosplenomegaly. respiratory #istress

syn#rome. renal #ysfunction.hypoglycemia. mental status changes.tropical splenomegaly syn#rome


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Types of nfections

%ecru#escence e'acer$ation of persistent un#etecta$le parasitemia.

#ue to sur!i!al of erythrocytic forms. no e'oerythrocytic cycle (P.f., P.m.)

%elapse reacti!ation of hypno*oites forms of parasite in li!er.

separate from pre!ious infection with same species (P.v.and P.o.)

%ecurrence or reinfection e'oerythrocytic forms infect erythrocytes. separate

from pre!ious infection (all species)

Can not always #ierentiate recru#escence fromreinfection


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Clinical presentation Varies in se!erity an# course

"arasite factors

Species an# strain of parasite @eographic origin of parasite

Si*e of inoculum of parasite

Host factors =ge

mmune status

@eneral health con#ition an# nutritional status

Chemoprophyla'is or chemotherapy use

Mo#e of transmission Mosquito

loo#$orne. no hepatic phase (transplacental. nee#lestic.

transfusion. organ #onation/transplant)


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"resentation of "8!8

Hea#ache.#i**iness. muscle pain.malaise. anore'ia. nausea. !aguea$#ominal pain. !omiting

:e!er constant or remittent "ostural hypotension. >aun#ice. ten#er

hepatosplenomegaly


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Common features of P.vivax

infections

ncu$ation perio# in nonimmunes 1716#ays $ut can $e 5A months or longer

Some strains from temperate *ones show

longer incu$ation perio#s. 7B,0+6 #ays :irst presentation of importe# cases - 1

month - o!er 1 year post return fromen#emic area

Typical pro#romal an# acute symptoms Can $e se!ere

Howe!er. acute mortality is !ery low


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Common features of

P.vivaxinfections

Most people of 9est =frican #escentare resistant to P.v. Lac uy $loo# group antigens nee#e#

for %C in!asion Mil# - se!ere anemia.

throm$ocytopenia. mil# >aun#ice.ten#er hepatosplenomegaly

Splenic rupture carries high mortality More common with P.v.than with P.f.


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Common features of

P.vivaxinfections

%elapses 0,D untreate# or ina#equately treate#

will relapse

Time from primary infection to relapse!aries $y strain

Treat $loo# stages as well as gi!e

terminal prophyla'is for hypno*oites

u


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. u cases Hea#ache.#i**iness. muscle pain. malaise.

anore'ia. nausea. !ague a$#ominal pain. !omiting

:e!er constant or remittent "ostural hypotension. >aun#ice. ten#er

hepatosplenomegaly

Can progress to se!ere malaria rapi#ly in nonimmune patients

Cere$ral malaria can occur with P.f.

"arasites can sequester in tissues. not #etecte# onperipheral smear


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Some characteristics of infection withfour species of human Plasmodia

P.v. P.o. P.m. P.f.

Pre-erythroctic

stage (days)

6-8 9 14-16 5.5-7

Pre-patentperiod (days)

11-13 10-14 15-16 9-10

Incuation

period (days)

15 (1!-17)

or up to 6-1! "onths

17 (16-18)

or #onger

!8 (18-40)

or #onger

1! (9-14)

$rythrocyticcyc#e (hours)

48 (aout) 50 7! 48


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Some characteristics of infection withfour species of human Plasmodia

P.v. P.o. P.m. P.f.

In%asionre&uire"ents

'uy %e#ood

group

* * *

+e#apses ,, ,, - -

+ecrude-

scences

, , - -


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C&%&%=L


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&9 M8=%L=; 1/70/7,,A 71

Cerebral Malaria

General

&tiologyE Plasmodium falciparum8

Mortality rate is high for malaria cases #ue to

cere$ral

malaria (1BD a#ult F 7,D chil#ren)8

Early stage: schizont in liver will rupture in

4 days afterinfection8

Microscopic e'aminationE only ring an# gametocyte

stages8

Tropho*oite an# schi*ont will #isappear in peripheral

$loo# (74 hours) an# stay in internal organ capillary8

ncu$ation perio#e E A14 #ays8

&9 M8=%L=; 1/70/7,,A 71


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Cerebral Malaria

&9 M8=%L=; 1/70/7,,A 77


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Cerebral Malaria

&9 M8=%L=; 1/70/7,,A 7+

PathogenesisComple'. at times confusing F

con


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Cerebral Malaria

&9 M8=%L=; 1/70/7,,A 74

Cerebral Malaria

Pathogenesis

Slu#ging hypothesisParasitised cells in cerebral capillaries

Large late tropho%oites Et schi%ont (rosetting)

Obstruction to microcirculation&' tissue anoxia

"ermea$ility hypothesisCerebral edema is common at autopsy

Cytokines: increase permeability of capillaries

PF4 inolement!

74


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Cerebral Malaria

&9 M8=%L=; 1/70/7,,A 7B

PathogenesisGMechanicalE cytoa#herence

o"opular hypothesis with lots of molecular

$iology inputs

oIntimate apposition of endothelialcells and

infecte# %C

o%eceptorligan#s interaction

o

Mo#ulate# $y cytoines


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Cerebral Malaria

&9 M8=%L=; 1/70/7,,A 70

Expressed adhesins eg PfMP!"


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#osetti

ng

$e%uestra

tion

$ludgi

ng

$ludginghypothesis


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Cerebral Malaria

Pathogenesis

"mmunological hypothesis"mportant in certain seere manifestations

#cute glomerulonephritisBlack water fever: auto-immune

disorder

Lack of se$uestration in some cases: asculitisdue to hyper&allergic reaction

'oeer no eidence of inflammatory cells

infiltration

&9 M8=%L=; 1/70/7,,A 75


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&9 M8=%L=; 1/70/7,,A 7A

C it l l i


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Congenital malaria Transplacental infection

Can $e all 4 species

Commonly P.v.an# P.f.in en#emic areas P.m.infections in nonen#emic areas #ue to long

persistence of species

;eonate can $e #iagnose# with parasitemia within 6#ays of $irth or longer if no other ris factors for

malaria (mosquito e'posure. $loo# transfusion) :e!er. irrita$ility. fee#ing pro$lems. anemia.

hepatosplenomegaly. an# >aun#ice

e min#ful of this pro$lem e!en if mother has not$een in malarious area for years $efore #eli!ery


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&Malaria Rapid Diagnostic Tests (RDTs)

DIAGNOSA MALARIA'()

Konfirmasi diagnosa dilakukan secaramikroskopik sebelum diberikan pengobatan;kecuali pasien yang diduga dengan malariaberat dimana pemeriksaan dengan hapusan

darah tidak dapat dilakukan segera. Malaria Rapid Diagnostic Tests (RDTs)


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Plasmodium falciparum

Plasmodium vivax

Malaria mortality


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PE*G+,-.-*: '/)

"e#oman pertama E 7,,B =CT

ire!isi E 17 to$er 7,,6=CTs E =rtesunate/=mo#iaquine

=ltemether =n# Lumenfantrine (=/L)

-0.E#*-.I1

Jom$inasi =rtesunate/Sulfametho'y "yra*ine "yrimethamine(=s/SM")

=s/SM" #ilaporan le$ih $ai #ari =/L

Menun>uan E Ti#a ter#apat reru#ensi #an le$ih ren#ahnyareinfesi

=s/SM" E 74 >am #an + hari sangat efetif AA #an 1,,D

PE*G+,-.-* M-0-#I- 1-0CIP-#2M


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PE*G+,-.-* M-0-#I- 1-0CIP-#2M.-*P- 3+MP0I3-$I'4)

Terapi Jom$inasi =rtemisin (=CT) a#alahpengo$atan yang #ipilih #alam semua asusmalaria falciparum tanpa ompliasi termasuE

ayi

"en#erita HV/=S

Kntu penanganan malaria #i rumah

9anita hamil trimester e#ua #an etiga

JecualiE

Jehamilan trimester pertama Menggunaan =CT hanya >ia ti#a a#a

antimalaria alternatif yang efetif

PE*G+,-.-* M-0-#I-


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PE*G+,-.-* M-0-#I-1-0CIP-#2M .-*P- 3+MP0I3-$I '5)

"enggunaan =CT yang #ireomen#asian oleh9HE

=rtemetherlumefantrine6 =rtesunate amo#iaquine

=rtesunate metloquine =rtesunate sulfa#o'inepyrimethamine

ABD sem$uh #alam e$anyaan asus

"engo$atan lini pertama pa#a penelitian e2asiteraupeti pa#a suatu negara

%espon pengo$atan tergantung #ari pengun>ungyang $erasal #ari #aerah infesi


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.E#-PI -*.I!#E0-P$P-7- M-0-#I- 8I8-9 '4)

"engo$atan ra#ial E relaps harus #icegah #enganpem$erian primaquine

"a#a #aerah transmisi ren#ah. manfaatpeme$rian primaquine le$ih $esar #ari resionya

osis "rimaquine ,.7B mg/g/hari (#osis#ewasa 1B mg) #apat #i$erian selama 14 hari -ti#a a#a $uti $ahwa pem$erian >anga pen#ea#alah efetif

nfesi plasmo#ium !i!a' #i n#onesia #anceania #i$utuhan #osis primaquine yang le$ihtinggi yaitu ,.B, mg/g per hari selama 14 hari


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EVENTION


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'4)

Mulai ,erhenti#egimen

3emoprola;sis

7ian


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Than

Nou

malaria klinis.pptx

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