Clinical features (fever)• Cold stage: rigor (cold and shivers)

headache (half-1hour)

• Fever (hot) stage:

temperature rises to maximum ,sever headache pain in back and joints vomiting and diarrhea (1-4h)

• Sweating stage patient perspires temperature fall and patient relieved until the next rigor (1-4h).

• Cold- hot- sweating - normal

• Incubation period

• Primary attack

Malarial paroxysm cold -hot –sweating normal

• Repeated attack Relapse (P.vivax & P.ovale) recrudescence

• Recrudescence of falciparum it is caused by parasites persisting in circulation at sub clinical level following previous attack.

• Malarial relapse due to delayed development of hypnozoites in liver

• There is no hypnozoites in falciparum

Plasmodium falciparum

IN life cycle of P.falciparum• There is No hypnozoite stage no relapse.• Erythrocytic cycle takes 36-48 hours • Schizont contain 8-32 merozoites .• Large number of RBCs infected and many cell contain more than one trophozoite.• only ring stage and gametocyte in peripheral blood.

Anemia can be sever and rapid

• Mainly due to mechanical distraction of parasitised RBCs.

• RBCs Phagocytosed in spleen and destroyed Due to lose of deformability .

• Aplastic anemia due to effect of malarial toxins on B.M.

• Hemolytic destruction (immune sensitization).

• Erythrocytic schizogony take place in capillaries of deep organs.

(Ring and gametocyte only that appeared in blood film).

• Adhererance phenomena lead to congestion ,hypoxia ,blockage and rupture of small blood vessels, (DIC) disseminated intravascular coagulation.

• High level of parasitaemia up to 30-40 % of RBCs infected (5% considers sever).

• Cerebral malaria :parasitized RBCS and fibrin block capillaries and small bl. Vessels (may causing un-arousable coma)

• Black-water fever :rapid and massive intravascular hemolysis of both parasitized and non-parasitized RBCs

Urin appears dark red to brown-black Renal failure hemoglbinurea

• Diarrhea and vomiting • Pulmonary edema • Hypoglycemia• Hyperpyrexia• Pregnant women

• Child with severe malaria, anemia, acidosis and respiratory distress

• P. ovale and P. vivax infect immature red blood cells • P. malariae infects mature red cells. • P. falciparum infects both.

Laboratory Diagnosis• microscopic identification of

parasites in blood is most certain method of confirming infection with plasmodium.

• Examination of thick (large amount) and thin blood film relation of parasite to RBCs and rate of infection

• Serologloy used in epidemiology.

Thick smear should be examined in all suspected cases of malaria because of its ability to detect parasites even when the parasitemia is low.

A thin film is used for species and stage identification and to provide information regarding erythrocytes, leukocytes, and platelets.

High parasitemia, growing stages of parasites (trophozoites and schizonts) and pigment-laden neutrophils indicate poor prognosis.

In case of uncertainty in identification of the species in severe malarial patients, it should always be considered as

P. falciparum.

P.f. ring

Plasmodium falciparum schizonte

Plasmodium falciparum gametocyte

P. falciparum

Plasmodiun vivax• infected RBC usually not exceed 2% - infection less sever than P.f.• P.v synchronized :regular 48h pattern

of fever • All form of parasites

trophozoites ,schizontes and gametocyte can be found in blood films.

• enlargement of RBCS, schuffner`s dotes

• Spleen enlargement and anemia• Relapse are feature of P.vivax• Patient must receive treatment both

for attack and against relapsing form. (primaquine)

Plasmodium vivax ring stage of trophozoite

Plasmodium vivax schizontes

Plasmodium vivax gametocyte

Plasmodiun vivax

Plasmodium malariae• Cycle synchronized every 72 h.

(quarten)• Spleen enlarge early.

• Nephrotic syndrome which progress to renal failure caused by damage to kidney following deposion of antigen-antibody complex on glomerular membrane of kidney (proteinuria ,low serum albumin oedema)

• Recrudescence can occur.

Plasmodium malariae trophozoit

Plasmodium malariae schizont

Plasmodium malariae gametocyte

Plasmodium malariae

Plasmodium oval ring, ameboid, schizont

Plasmodium oval gametocyte

Disease Severity and Durationvivax ovale malariae falciparu

m

Initial Paraoxysm Severity

moderate to severe

mildmoderate to severe

severe

Average Parasitemia (mm3)

20,000 9,000 6,00050,000-500,000

Maximum Parasitemia (mm3)

50,000 30,000 20,000 2,500,000

Symptom Duration (untreated)

3-8+ weeks

2-3 weeks3-24 weeks

2-3 weeks

Maximum Infection Duration (untreated)

5-8 years12-20 months

20-50+ years

6-17 months

Anemia ++ + ++ ++++

Complications renal cerebralModified from Markell and Voge's Medical Parasitology

Exoerthrocytic shizogony ( Liver) Primary hepatic form and hypnozoites

Clinical symptoms

Patent parasitemia

Subpatent parasitemia

Diagnosis• history of being in endemic

area • symptoms: fever, chills,

headache, malaise • splenomegaly, anemia • microscopic demonstration of

parasite (blood smear)• antigen detection PCR

amplification of parasite DNA

Treatment Blood stages:

erythrocytic stages (Asexual schizogony)

• Chloroquine• Quinine• pyrimethamine +sulfadoxine (fansidar)• Mefloquine, halofantrine• Gametocytes: primaquine• Liver stages (in vivax, ovale

species) primaquine

In malignant malaria all is right except:

1.black water fever.2.Relapse .3.disseminated

intravascular coagulation (DIC).

4.Adhesion phenomena.5.Cerebral malaria.6.Acute renal failure

In benign tertian malaria all can occur except :

1.attack every 48 hours.2.Relapse 3.Splenomegaly 4.Un arousable coma

In Erythrocytic cycle of P.vivax:

1.Enlargement of RBCs.2.schuffner`s dots.3.DIC.4.Splenomegaly+ anaemia5.Black water fever

In P.falciparum1.High parasitemia2.Multiple infection.3.Enlargement of RBCs4.Erythrocytic tertian or sub

tertian schizogony.5.Maurer`s dots6.Adhesion phenomena

(DIC)

In P. malariae:1.Splenomegaly2.Band shape trophozoites.3.Recrudescence4.Antigen antibodes complex

depostion in glomeruli with nephrotic syndrome

5.relapse

High parasitemia, growing stages of parasites (trophozoites and schizonts) and pigment-laden neutrophils indicate poor prognosis.

In case of uncertainty in identification of the species in severe malaria,it should always be considered as P. falciparum.

Inoculation of the sporozoites into a new human host lead to inchoation of:

1 Exo-erythrocytic cycle (Tissue cycle) Pre-erythrocytic cycle

2 -Erythrocytic cycle.3 -Sporogonic cycle.4 -Sexual cycle.

Malarial releapse is due to1. Merozoite.2. Sporozoite.3. Hypnozoite.4. trophozoite5. schizonte

The clinical manifestations of the disease is due to:

1. Erythrocytic cycle. 2. Exo-erthrocytic cycle.3. Sporogonic cycle.4. Rupture of infected RBC and

release malarial pigments and toxin.

Infective stage in saliva of female Anopheles is:

1. Merozoite.2. Schizonte.3. Trophozoite.4. Sporozoite.

Geographical Distributions• p.vivax widespread in tropical and

subtropical areas • range extends into temperate areas • relatively uncommon in Africa • P falciparum. widespread, but

primarily in tropics and subtropics • P malariae broad, but spotty

geographical distribution • P. ovale• primarily tropical Africa, especially

western coast