PLASMODIUM

Group 1

Plasmodium

The Plasmodiidae family has a single genus, Plasmodium, which includes those parasites that undergo exoerythrocytic and pigmentproducing erythrocytic schizogony in vertabrates and a sexual stage followed by sporogony in mosquitoes. (Faust, 1974)

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 other tissues. The definitive hosts are various species of mosquitoes of the genus Anopheles.

Plasmodium

The plasmodia normally infecting men are:

Plasmodium

vivax Plasmodium ovale Plasmodium malariae Plasmodium falciparum

GENERAL LIFE CYCLE AND METHODS OF REPRODUCTION OF MALARIAL PARASITES OF MAN

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.

The general life cycle of Plasmodia have two phases:

(1)

Extrinsic Phase in Anopheles: also called as Definitve phase in which sexual reproduction occurs (2) Intrinsic Phase in man: also called Intermediate phase in which asexual reproduction occurs.

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 preerythrocitic cycle, the erythrocytic cycle, and the sporogonic cycle. (CDC)

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COMPARATIVE CHARACTERS OF PLASMODIA OF MAN AND DISTINGUISHING FEATURES

P. vivax
Early Relatively large; trophozoite usually one or ring prominent chromatin dot, sometimes two, often two rings or more in one cell

P. malariae
Compact; one chromatin dot; double infection is rare

P. falciparum

P. ovale
Compact; one chromatin dot; double infection uncommon

Small, delicate; sometimes two chromatin dots; multiple red cell infection common; appliqu forms frequent Large Large; markedly Smaller than Medium size; trophozoite ameboid; vivax; compact; usually abundant often band compact, rarely chromatin; shaped; not ameboid; prominent vacuole; ameboid; vacuole pigment in fine vacuole inconspicuous; rodlets inconspicuous; rare in pigment is peripheral coarse blood after half grown; pigment granular Mature Large Small Small schizont or segmenter

Small; compact; not ameboid; vacuole inconspicuous; pigment coarse

Medium

P. vivax

P. malariae

P. falciparum

P. ovale

Number of merozites Microgametocy tes and Macrogametoc ytes Alterations in infected red cell

12-24
Spherical

6-12

8-26

6-12
Spherical but smaller than vivax Enlarged; decolorized; prominent Schuffners dots, appear early; infected cells may be oval-shaped with fimbriated ends

Spherical but Crescent smaller and less shaped numerous Cell may seem smaller; fine stippling (Ziemanns dots) occasionally seen Normal size but may have brassy appearance; Maurers dots common; Garnhams bodies occasionally seen.

Enlarged and decolorized

P. vivax Length of 48 hours asexual phase Parasitized Enlarged. red cells Fine stippling (Schuffners dots). Primarily invades reticulocytes, young red cells Level of usual 8 000- 20 maximum 000/cu mm of parasitemia blood Distribution All forms in peripheral blood.

P. malariae 72 hours Not enlarged. No stippling (except with special stains) Primarily invades older red cells

P. falciparum 36-48 hours Not enlarged. Coarse stippling (Maurers clefts). Invades all red cells regardless of age. 1. 500 000/cu mm Only rings and crescents (gametocytes) in peripheral blood

P. ovale 49-50 hours Enlarged. Fine stippling. Cells often oval or fimbriated.

< 10 000/cu mm

< 10 000/cu mm

All forms in peripheral blood.

All forms in peripheral blood.

PATHOGENESIS

Table of Pathogenesis

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Mode of transmission

Human infection results from the bite of an infected Anopheles Mosquito

CLINICAL MANIFESTATIONS

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.

The malaria paroxysms comprise three stages:

cold

stage the hot stage sweating stage.

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 young children.Lasts for 15 to 60 min.

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 patient may become confused and delirious. The skin is flushed and hot. Lasts from 2 to 6 hours.

Sweating Stage

Defervescence or diaphoresis ensue with the patient manifesting with profuse sweating. The temperature lowers and symptoms diminish.

Take Note!

P.vivax, P. malariae, and P. ovale parasitimias is low grade , primarily because the parasites favor either young or old RBC but not both. P. falciparum invades RBC of all ages and parasitemia is very high. P. falciparum also causes the parasitized red cells to agglutinate and adhere to capillary walls , with resulting obstruction, thrombosis, and local ischemia P. falciparum also causes severe or fatal complications such as cerebral malaria, malarial hyperpyrexia, gastrointestinal disorders and algid malaria

Take Note!

P. malariae has been implicated in a nephritic syndrome in children quartan nephrosiswith 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.

DIAGNOSIS

CLINICAL DIAGNOSIS

Specimen: Blood Methods:

thick-

thin blood smear stained Romanowsky

stain Quantitative buffy coat( QBC) ParaSight F test Indirect hemagglutination(IHA) Indirect luorescent antibody test( IFAT) ELISA

THIN-FILM PREPARATIONS

Plasmodium vivax

Plasmodium ovale

Plasmodium falciparum

Plasmodium malariae

THICK-FILM PREPARATIONS

Plasmodium vivax

Plasmodium falciparum

Plasmodium malariae

LABORATORY FINDINGS

LABORATORY FINDINGS

Normocytic anemia of variable severity, with poikilocytosis and anisocytosis During paroxysms there may be transient leukocytosis. Leukopenia develops with a relative increase in large mononuclear cells. Presence of casts and protein in the urine of children with P. malariae is suggestive of quartan nephrosis. Severe P. falciparum infection , renal damage may cause oliguria and appearance of casts, protein, and RBSs.

TREATMENT

Treatment

Chloroquine is the drug of choice Pyrimethamine/ sulfadoxine or quinine is used in areas where there is higher levels of resistance to chloroquinine

PREVENTION AND CONTROL

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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