raed z. ahmed, medical parasitology lab.,2012. comparison

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Raed Z. Ahmed, Medical Parasitology Lab.,2012

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Page 1: Raed Z. Ahmed, Medical Parasitology Lab.,2012. Comparison

Raed Z. Ahmed, Medical Parasitology Lab.,2012

Page 2: Raed Z. Ahmed, Medical Parasitology Lab.,2012. Comparison

ComparisonComparison

Raed Z. Ahmed, Medical Parasitology Lab.,2012

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• Either thick or thin films may be used depending on the circumstances.

• The thick film is more sensitive in detecting parasite and also saves time in examination.

• The thin film technique cause very little distortion of the parasite, and permits species identification when it may not be possible in thick films, but many fields must be examined to detect parasite when they are few in number.

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Blood ProtozoaBlood Protozoa

Raed Z. Ahmed, Medical Parasitology Lab.,2012

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Raed Z. Ahmed, Medical Parasitology Lab.,2012

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Life cycleLife cycleRaed Z. Ahmed, Medical Parasitology Lab.,2012

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Trypanosoma sppTrypanosoma spp..

• Trypanosoma cruzi (Americans) cause Chaga’s disease.• Trypanosoma bruzi (Africans) cause sleeping sickness disease. • Trypanosoma have many stages:

– Amastigote, Promastigote, Epimastigote and Trypomastigote.• Reservoir host: mammalian animal.• Intermediate host:

– Tsetse fly (Glossina spp.) for Trypanosoma bruzi– Reduviidae bug(kissing bug) for Trypanosoma cruzi

• Definitive host: Human.• Infective stage: Metacyclic trypomastigote.• Diagnostic stage: Trypomastigote.

Raed Z. Ahmed, Medical Parasitology Lab.,2012

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ContinueContinue…… ……

Raed Z. Ahmed, Medical Parasitology Lab.,2012

• Diagnosis:o Detection of Trypanosoma chancer after biteo Blood smear within 21 days from the bite, it will show the

parasites.o Lymph node aspiration (most reliable).o Lumber puncture if brain affected.

Undulating membrane

Flagellum Nucleus

kinetoblast

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Trypanosoma TrypomastigotesTrypanosoma Trypomastigotes

Raed Z. Ahmed, Medical Parasitology Lab.,2012

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Trypansoma brucei ssp. in thick blood smears stained with Giemsa

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Trypansoma brucei ssp. in thin blood smears stained with Giemsa

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Life cycleLife cycleRaed Z. Ahmed, Medical Parasitology Lab.,2012

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Leishmania sppLeishmania spp..• There is many species affect man:

– Leishmania tropica : cause skin lesion ( cutaneous )

– Leishmania braziliense : cause muco-cutaneous lesion.

– Leishmania donovani : cause visceral lesion.(kala azar)

• Leishmania have two stages:

– Amastigote (Leishmania stage), in man (reticuloendothelial cell).

– Promastigote (Leptomonas stage), the infective stage and present in the lumen gut of the sand fly.

• Reservoir host: dogs and rodents.

• Intermediate host: Sand fly (Phlebotomus).

• Definitive host: Human.

Raed Z. Ahmed, Medical Parasitology Lab.,2012

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Cutaneous leishmaniasis

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ContinueContinue…… ……

• Diagnosis:

– Thick and thin blood film

– Skin scraping

– Blood culture on N.N.N media*

(Novy-MacNeal-Nicolle) – Serological tests

Raed Z. Ahmed, Medical Parasitology Lab.,2012

Nucleus

Flagellum

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Leishmania promastigotesLeishmania promastigotes

Raed Z. Ahmed, Medical Parasitology Lab.,2012

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Malaria

• Blood parasites of the genus Plasmodium. 

• There are approximately 156 named species of Plasmodium which infect various species of vertebrates.  Four species are considered true parasites of humans, as they utilize humans almost exclusively as a natural intermediate host: P. falciparum, P. vivax, P. ovale  and P. malariae. 

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Clinical features

• fever and chills, which can be accompanied by headache, myalgias, arthralgias, weakness, vomiting, and diarrhea. 

• Other clinical features include splenomegaly, anemia, thrombocytopenia, hypoglycemia, pulmonary or renal dysfunction, and neurologic changes.

• The clinical presentation can vary substantially depending on the infecting species, the level of parasitemia, and the immune status of the patient

•   Infections caused by P. falciparum can progress to severe, potentially fatal forms with central nervous system involvement (cerebral malaria), acute renal failure, severe anemia, or adult respiratory distress syndrome.

•   Complications of P. vivax malaria include splenomegaly (with, rarely, splenic rupture), and those of P. malariae include nephrotic syndrome.

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Laboratory Diagnosis

• Microscopic identification is the method most frequently used to demonstrate an active infection.

• Morphological comparison and images of Plasmodium species

• Molecular diagnosis techniques can complement microscopy, especially in species identification.

• Antibody Detection can detect past (not necessarily active) infections.

• Immunologic/Biochemical detection of malaria parasite products are available and under evaluation.

• Bench aids for Malaria

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Life cycleLife cycleRaed Z. Ahmed, Medical Parasitology Lab.,2012

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Plasmodium sppPlasmodium spp..• Four species of Plasmodium are the causative agent of malaria, these are:

– P. vivax, P. malariae, P. falciparum, and P. ovale.

• Intermediate host: Human.

• Definitive host: Anopheles mosquitoes.

• Plasmodium spp. have 4 stages:

– Ring form (young trophozoite.)

– Late ( old ) trophozoite

– Schizonts

– Gametocyte.

• Infective stage: Sporozoites.

• Diagnosis:

– Thick and stained thin blood film to detect parasites.

Raed Z. Ahmed, Medical Parasitology Lab.,2012

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Ring formRing form

P. vivax P. ovale

P. malariae P. falciparumRaed Z. Ahmed, Medical Parasitology Lab.,2012

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Trophozoite formTrophozoite form

P. vivax P. ovale

P. malariae P. falciparumRaed Z. Ahmed, Medical Parasitology Lab.,2012

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Schizonts formSchizonts form

P. vivax P. ovale

P. malariae P. falciparumRaed Z. Ahmed, Medical Parasitology Lab.,2012

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Gametocyte formGametocyte form

P. vivax P. ovale

P. malariae P. falciparumRaed Z. Ahmed, Medical Parasitology Lab.,2012

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Raed Z. Ahmed, Medical Parasitology Lab.,2012