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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
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
• 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.
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 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.
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.
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