Plasmodium Report

7/29/2019 Plasmodium Report

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PLASMODIUM

Group 1


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Plasmodium

The Plasmodiidae family has a single genus,

Plasmodium, which includes those parasites

that undergo exoerythrocytic and pigment-

producing erythrocytic schizogony invertabrates and a sexual stage followed by

sporogony in mosquitoes. (Faust, 1974)


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Plasmodium

The sporozoan protozoa of the genus

Plasmodium are pigment- producing ameboid

intracellular parasites of vertebrates with one

habitat in red cells and another in cells of othertissues. The definitive hosts are various

species of mosquitoes of the genus

Anopheles.


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Plasmodium

The plasmodia normally infecting men are:

Plasmodium vivax

Plasmodium ovale

Plasmodium malariae

Plasmodium falciparum


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GENERAL LIFE CYCLE

AND METHODS OFREPRODUCTION OF

MALARIAL PARASITES OF

MAN


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The malaria parasite exhibits a complex life

cycle involving an insect vector (mosquito) and

a vertebrate host (human). Four Plasmodium

species infect humans: P. falciparum, P. vivax,P. ovaleand P. malariae. All four species

exhibit a similar life cycle with only minor

variations.


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The general life cycle of Plasmodia have two

phases:

(1) Extrinsic Phase inAnopheles: also called as

Definitve phase in which sexual reproduction

occurs

(2) Intrinsic Phase in man: also called

Intermediate phase in which asexual

reproduction occurs.


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According to the CDC

The malaria parasite is a multi-stage

protozoan with a complex life cycle requiring

an insect vector and a human host. There are

three stages in its life cycle: the pre-erythrocitic cycle, the erythrocytic cycle,

and the sporogonic cycle. (CDC)


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(video presentation)


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COMPARATIVECHARACTERS OF

PLASMODIA OF MAN AND

DISTINGUISHINGFEATURES


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P. vivax P. malariae P. falciparum P. ovaleEarly

trophozoite

or ring

Relatively large;

usually one

prominent

chromatin dot,sometimes two,

often two rings or

more in one cell

Compact; one

chromatin dot;

double

infection is rare

Small, delicate;

sometimes two

chromatin dots;

multiple redcell infection

common;

appliqu forms

frequent

Compact; one

chromatin dot;

double

infectionuncommon

Large

trophozoite

Large; markedly

ameboid;abundant

chromatin;

prominent vacuole;

pigment in fine

rodlets

Smaller than

vivax; compact;often band

shaped; not

ameboid;

vacuole

inconspicuous;

pigment iscoarse

Medium size;

usuallycompact, rarely

ameboid;

vacuole

inconspicuous;

rare in

peripheralblood after half

grown; pigment

granular

Small; compact;

not ameboid;vacuole

inconspicuous;

pigment coarse

Mature

schizont or

segmenter

Large Small Small Medium


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P. vivax P. malariae P. falciparum P. ovaleNumber of

merozites

12-24 6-12 8-26 6-12

Microgametocy

tes and

Macrogametoc

ytes

Spherical Spherical but

smaller and less

numerous

Crescent

shaped

Spherical but

smaller than

vivax

Alterations in

infected red cell

Enlarged and

decolorized

Cell may seem

smaller; finestippling

(Ziemanns

dots)

occasionally

seen

Normal size but

may havebrassy

appearance;

Maurers dots

common;

Garnhams

bodiesoccasionally

seen.

Enlarged;

decolorized;prominent

Schuffners

dots, appear

early; infected

cells may be

oval-shapedwith fimbriated

ends


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P. vivax P. malariae P. falciparum P. ovaleLength of

asexual phase

48 hours 72 hours 36-48 hours 49-50 hours

Parasitized

red cells

Enlarged.

Fine stippling

(Schuffners

dots).

Primarily

invades

reticulocytes,young red

cells

Not enlarged.

No stippling

(except with

special stains)

Primarily

invades older

red cells

Not enlarged.

Coarse

stippling

(Maurers

clefts).

Invades all red

cellsregardless of

age.

Enlarged. Fine

stippling. Cells

often oval or

fimbriated.

Level of usual

maximum

parasitemia

8 000- 20

000/cu mm of

blood

< 10 000/cu

mm

1. 500

000/cu

mm

< 10 000/cu

mm

Distribution All forms in

peripheral

blood.

All forms in

peripheral

blood.

Only rings and

crescents

(gametocytes)

in peripheral

blood

All forms in

peripheral

blood.


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PATHOGENESIS


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Table of Pathogenesis

(type diagram here)


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Mode of transmission

Human infection results from the bite of an

infected Anopheles Mosquito


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CLINICALMANIFESTATIONS


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There are no absolute diagnostic clinical

features of malaria except fro the regular

paroxysms of fever with asymptomatic

intervals. Prodromal symptoms include: feeling of

weakness and exhaustion, desire to stretch

and yawn, aching bones, limbs and back,

nausea, vomiting, and sense of chillness.


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The malaria paroxysms comprise three stages:

cold stage

the hot stage

sweating stage.


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Cold Stage

feeling of cold, apprehension, mild shivering

quickly turns into violent teeth chattering and

shaking of the whole body. The patient may

vomit and febrile convulsions for youngchildren.Lasts for 15 to 60 min.


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Hot stage

patients becomes hot and manifests with

headache, palpitations, tachypnea, epigastric

discomfort, thirst, nausea and vomiting. The

temp ,ay reach up to 40 to 41 C. The patientmay become confused and delirious. The skin

is flushed and hot. Lasts from 2 to 6 hours.


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Sweating Stage

Defervescence or diaphoresis ensue with the

patient manifesting with profuse sweating. The

temperature lowers and symptoms diminish.


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Take Note!

P.vivax, P. malariae, and P. ovale parasitimias islow grade , primarily because the parasites favoreither young or old RBC but not both.

P. falciparum invades RBC of all ages andparasitemia is very high.

P. falciparum also causes the parasitized red cellsto agglutinate and adhere to capillary walls , withresulting obstruction, thrombosis, and localischemia

P. falciparum also causes severe or fatalcomplications such as cerebral malaria, malarialhyperpyrexia, gastrointestinal disorders and algid

malaria


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Take Note!

P. malariae has been implicated in a nephritic

syndrome in childrenquartan nephrosis-

with peak incidence at about age of 5. It is

characterized by generalized edema, oliguria,massive proteinuria and hypoproteinemia.

There are also presence glomerular lesions

which include basement membrane thickening

and sometimes fibrosis.


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DIAGNOSIS


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CLINICAL DIAGNOSIS

Specimen: Blood

Methods:

thick- thin blood smear stained Romanowsky

stainQuantitative buffy coat( QBC)

ParaSightF test

Indirect hemagglutination(IHA) Indirect luorescent antibody test( IFAT)

ELISA


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THIN-FILMPREPARATIONS


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Plasmodium vivax


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Plasmodium ovale


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Plasmodium malariae


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THICK-FILMPREPARATIONS


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Plasmodium vivax


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Plasmodium malariae


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LABORATORYFINDINGS


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LABORATORY FINDINGS

Normocytic anemia of variable severity, with

poikilocytosis and anisocytosis

During paroxysms there may be transient

leukocytosis. Leukopenia develops with a relativeincrease in large mononuclear cells.

Presence of casts and protein in the urine of

children with P. malariae is suggestiveof quartan

nephrosis. Severe P. falciparum infection , renal damage may

cause oliguria and appearance of casts, protein,

and RBSs.


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TREATMENT


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Treatment

Chloroquine is the drug of choice

Pyrimethamine/ sulfadoxine or quinine is used

in areas where there is higher levels of

resistance to chloroquinine


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PREVENTION ANDCONTROL


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Prevention and Control

Elimination of mosquito breeding places or

vector control

Protection against mosquitoes such as

screens, and mosquito repellants Suppressive drug therapy for exposed persons

Use of flying insect spray containing pyrethrum


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THANK YOU

Plasmodium Report

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