Classification According To Mode of Movement
1)Rhizopoda: Move by pseudopodia and divide by binary fission during the trophozoite active stage e.g. Entameba histolytica. 2)Ciliata: Move by cilia and divide by transverse division e.g. Balantidium coli. 3)Zoomastigophora: Move by flagella and divide by longitudinal fission e.g. Giardia,
Trichomonas & Trypanosoma. 4)Sporozoasida: No special locomotor apparatus and reproduce sexually and asexually e.g. Malaria, Toxoplasma. Dr.Sameh M.Mohamadi
1)Rhizopoda: Move by pseudopodia and divide by binary fission during the trophozoite active stage e.g. Entameba histolytica.
2)Ciliata: Move by cilia and divide by transverse division e.g. Balantidium coli.
3)Zoomastigophora: Move by flagella and divide by longitudinal fission e.g. Giardia, Trichomonas & Trypanosoma , Leishmania.
4)Sporozoasida: No special locomotor apparatus and reproduce sexually and asexually e.g. Malaria, Toxoplasma.
Balantidium coli (Ciliata)
Giardia lamblia (Zoomastigophora)
Toxoplasma gondii (Sporozoasida)
Malaria Dr.Sameh M.Mohamadi
Trichomonas vaginalis • Disease: Trichomoniasis • Geographic Distribution: Worldwide, • cause vaginitis specially with persons have multiple sexual partners or other venereal diseases.
• Habitat: The Trophozoite inhabits the urogenital tract of male♂ and female♀, particularly female
• Morphology: (no cyst). Trophozoite: with four anterior flagella and a fifth flagellum on the margin of the short undulating متموجةmembrane.
Life cycle Trichomonas vaginalis
Clinical findings • Venereal infection contacts. • The asymptomatic male ♂ is the most important transmitter of the infection. • In female ♀ it cause vaginitis with yellow-green purulent discharge may be accompanied by vulvalar and cervical lesions, abdominal pain, dysuria and dyspareunia (painful sexual intercourse ). • In men sometimes it cause urethritis , accompanied with epididymitis , and prostatitis . Dr.Sameh M.Mohamadi
Laboratory Diagnosis: Microscopic Detecting Trophozoites in •♀ vaginal
and urethral secretions. •♂ anterior urethral or prostatic secretions.
Direct immuno-florescent antibody staining is more sensitive. Culture of the parasite is the most sensitive method, but results are not available for 3 to 7 days.
Treatment • Treatment should include all sexual partners of the (♀ &♂) infected persons. • Metronidazole (flagyl) • Tinidazole.
• In ♀ vaginal douche, insert (vioform) or cream (clotrimazole) are also recommended.
• Distribution: Worldwide • Warm-blooded animals, • Causing Toxoplasmosis. Congenital Toxoplasmosis. Dr.Sameh M.Mohamadi
• Obligate intracellular parasite that invade all cells except RBCs (non-nucleated). • Infection is usually mild, may be chronic or acute. • High risk with immuno-compromised host e.g (malignancies &organ transplants.
Morphology • Trophozoite (tachyzoite): Intracellular, crescent shaped with central nucleus • Pseudocysts: Intracellular collection of trophozoites in macrophages and R.E.S. cells. • Cysts: collection of trophozoites enclosed in a tissue cyst formed in chronic stage or latent infection when immunity develops. • Oocysts: Oval, contain 2 sporocysts each containing four sporozoites and found in stool of infected cats. Dr.Sameh M.Mohamadi
Life cycle Dr.Sameh M.Mohamadi
Clinical findings • Acquired: in immuno-competent persons is generally an asymptomatic infection. – 10% to 20% of patients with acute infection may develop cervical lymphadenopathy and/or a flu-like illness. Serious or fatal infection occurs in immunodeficiency as in AIDS. – Toxoplasmic encephalitis is the most common cause of intracerebral mass lesions and is thought to be caused by reactivation of chronic infection. – Toxoplasmosis in patients being treated with immunosuppressive drugs may be due to either newly acquired or reactivated latent infection.
• Congenital toxoplasmosis: Cause severe, often fatal cerebral damage to a fetus and who recover often show mental defects. In early pregnancy it cause abortion or still birth and in late pregnancy symptoms occur in the infant 23 months after birth. Dr.Sameh M.Mohamadi
Laboratory diagnosis 1. Microscopic examination of aspirates and fluids. 2. ELISA. 3. Animal inoculation (e.g. lymph node biopsy material in mice).
Treatment: â€˘ Treatment is not needed for a healthy person who is not pregnant, as the infection is usually self limiting. â€˘ Sulphadiazine & Pyrimethamine or Trimethoprime, recommended for pregnant women or persons who have weakened immune systems. Dr.Sameh M.Mohamadi
Blood Flagellates (Haemoflagellates) Are Hemoflagellates protozoan belonging to Mastigophora
Trypanosoma gambiense & T. rhodesiense: African trypanosomiasis. Trypanosoma cruzi: American trypanosomiasis (Chagas disease).
Leishmania donovani: Visceral leishmaniasis (kala-azar) Leishmania Tropica: Cutaneous leishmaniasis (oriental sore) Leishmania Braziliensis: Mucocutaneous leishmaniasis (Espundia) Dr.Sameh M.Mohamadi
Trypanosoma African Trypanosomiasis (Sleeping sickness) â€˘ Caused by T. gambiense (west African) and T. rhodesiense (East African).
Habitat The infection is transmitted by Tsetse fly.
• The metacyclic trypanosomal forms in the saliva of the insect are inoculated into human during the bite. •It multiply at site of bite and then in the blood, lymph and tissue fluid. Trypanosoma
Trypanosoma, 18-30 µm in length, in peripheral blood.
appear in the peripheral blood 5 to 21 days after the Giemsa infecting bite. Dr.Sameh M.Mohamadi stain
Clinical findings: Infection occurs in 3 stages. 1-Trypanosomal primary lesion (chancre) develops at the site of bite (the parasite multiply). 2-hemolymphatic early stage where the parasite reach and multiply in blood with fever, sweating, headache, anemia, increased pulse rate, joint and muscle pain and enlarged regional lymph nodes (lymphadenopathy ). 3-Cerebral Late stage where the parasite reach the C.N.S. causing chronic inflammation with ischaemia(cut of blood supply) and hemorrhage leading to meningoencephalitis , with sever headache, mental dullness and Dr.Sameh M.Mohamadi excessive sleeping, finally coma and death.
• Microscopic examination of chancre fluid, blood film, lymph node aspirate, or CSF (in late stage) for demonstration of motile trypanosomes or stain with Giemsa. • ELISA.
Treatment : • Suramin or pentamidine hemolymphatic stage • melarsoprol for late cerebral stage. Dr.Sameh M.Mohamadi
American Trypanosomiasis (Chagas disease).
Habitat The infection is transmitted by bugs
e.g. Triatoma infestans.
â€˘ The bug takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. â€˘ Trypo-mastigotes enter the host through the wound or through intact mucosal membranes. Inside the host, the trypo-mastigotes invade cells, where they differentiate into intracellular a-mastigotes. Dr.Sameh M.Mohamadi
Morphology T. cruzi in blood sample
Clinical findings • A local lesion (chagoma) can appear at the site of inoculation. • Acute phase ( asymptomatic), but can present with manifestations that include fever, anorexia, lymphadenopathy, mild hepatosplenomegaly , and myocarditis . • Most acute cases resolve over a period of 2 to 3 months into an asymptomatic chronic stage. Romana’s sign, Swelling of Eyelids observed in acute case
chronic stage may not occur for years. - Cardiomyopathy (the most serious manifestation); - Megacolon - Weight loss.
Posteroanterior chest radiograph showing Enlarged heart due to T.cruzi infection.
X-ray showing megacolon in Chagas' disease
Chronic Chagas disease and its complications can be fatal. Dr.Sameh M.Mohamadi
Laboratory diagnosis Microscopic examination • blood for motile trypanosomes • ELISA • Culture on diphasic Novy-Nicholle-MacNeal’s (NNN) medium • Xenodiagnosis, where uninfected bugs are fed on the patient's blood, and their gut contents examined for parasites 4 weeks later.
Treatment • Must be initiated early and not delayed for results of isolation of the parasite. • Benznidazole but once the disease has progressed to later stages, no medication has been proven to be effective. Dr.Sameh M.Mohamadi
Leishmaniasis Caused by Sand flies
• L. donovani : visceral Leishmaniasis (Kala-azar) • L. Tropica : Cutaneous Leishmaniasis (Tropical sore) • L. braziliensis: Mucocutaneous Leishmaniasis (Espundia) Dr.Sameh M.Mohamadi
Leishmaniasis is found in parts of about 88 countries. Approximately 350 million people live in these areas. Dr.Sameh M.Mohamadi Cutaneous leishmaniasis is found in Egypt
Habitat â€˘ Infection is transmitted by sand flies
inject the infective stage (promastigotes) during blood meals, which are phagocyted by macrophages and transform into amastigotes, which multiply in infected cells and affect the Internal organs (visceral leishmaniasis) Skin
Mucocutaneous tissue and skin (mucocutaneous leishmaniasis). Dr.Sameh M.Mohamadi
Leishamnia promastigotes having a single flagellum, Giemsa stain
Leishamnia amastigotes, bone marrow aspirate, Giemsa stain
Clinical findings â€˘
The factors determining the form of disease include leishmanial species, geographic location, and immune response of the host.
• is characterized by one or more cutaneous lesions on areas where sand flies have fed, which finally ulcerate and discharge thin, offensive pus. • It heals within months leaving depigmented scare. • Ulcers often end up looking somewhat like a volcano, with a raised edge and central crater.
Mucocutaneous leishmaniasis Shows similar lesion but affect mucus membranes causing destruction of bone & cartilage of nose and mouth
visceral leishmaniasis â€˘ Persons who have (kalaazar) usually have fever, weight loss, and an enlarged spleen and liver. â€˘ Patients usually have dark skin specially forehead, around mouth.
Laboratory diagnosis • Blood or aspirated material from spleen, bone marrow, • Scraping from raised edge of the ulcer examined with Giemsa stain is still the technique most commonly used to detect the leishmanial form. • Culture on NNN medium (agar slant overlaid with defibrinated rabbit blood used to detect the presence of Leishmania or Trypanosoma cruzi.). • ELISA for detection of specific antibodies in kalaazar.
Treatment • Pentavalent antimony compounds or • sodium stibogluconate (under investigation). Dr.Sameh M.Mohamadi
Malaria (Plasmodium) Caused by – – – –
P. Vivax (Benign tertian malaria) P. Ovale (Ovale tertian malaria) P. Malariae (Quartan malaria) P. Falciparum (Malignant tertian malaria)
Habitat â€˘ The malaria parasite life cycle involves two hosts. The infected female Anopheles mosquito The resting position of the adult is characteristic, head and abdomen in a straight line at an angle of about 45 with the surface on which they rest.
â€˘It inoculates sporozoites into the human, which matures to schizonts in liver cells and release merozoites into the blood stream. Dr.Sameh M.Mohamadi
Clinical findings 1- Malarial classical symptoms are associated with the release of merozoites and their toxin from ruptured RBCS in the end of each erythrocytic cycle which complete every 72 hours in P. malariae and every 24 hours in other species: it consists of a- Cold stage or rigor stage (10 min to one hour), the patient suffers from cold sensation and teeth chattering while temp is above normal. b- Hot or fever stage (1-4 hours), due to release of most merozoites. The skin becomes hot and dry and patient suffers from fever, headache and vomiting. c- Sweating stage (1-4 hours), due to rapid drop of temp and is
accompanied by reinfection of RBCs 2- Anemia due to destruction of RBCs, splenomegaly and hepatomegaly due to engulfed pigment by R.E.S. 3- Adhesion and clumping of infected RBCs in capillaries cause their occlusion (thrombocytopenia) with manifestations varying according to the site of lesion e.g. headache, myalgia, convulsions, coma, diarrhea or dysentery and dehydration. Dr.Sameh M.Mohamadi
Laboratory diagnosis • Blood film (thin and thick films) for comparison of Plasmodium species • Serological reaction (ELISA) when detection of the parasite is difficult.
Treatment • Quinine and chloroquine for blood forms. • Primaquine & pyrimethamine for hepatic forms. • Combination for all forms or fansidar or maloprim Dr.Sameh M.Mohamadi