lishmania.pdf

Practical Parasitology Lab 3: -amoeba -Blood and tissue flagellates Amebic ulcer NONPATHOGENIC INTESTINAL AMEBA Entamoeba coli It is worldwide in distribution and a nonpathogenic comensal intestinal ameba. It is larger than histolytica about 20-50 μm with sluggish motility and contains ingested bact...

Practical Parasitology Lab 3: -amoeba -Blood and tissue flagellates Amebic ulcer NONPATHOGENIC INTESTINAL AMEBA Entamoeba coli It is worldwide in distribution and a nonpathogenic comensal intestinal ameba. It is larger than histolytica about 20-50 μm with sluggish motility and contains ingested bacteria but no red cells. The nucleus is clearly visible in unstained films and has a large eccentric karyosome and thick nuclear membrane lined with coarse granules of chromatin Cysts are large, 10- 30 μm in size, with a prominent glycogen mass in the early stage. The chromatoid bodies are splinter-Like and irregular. The mature cyst has eight nuclei The life cycle is the same as in E. histolytica except that it remains a luminal commensal without tissue invasion and is nonpathogenic. Endolimax nana This common commensal ameba is widely distributed. It lives in the human intestine. The trophozoite is small (nana: small), less than 10 μmin size with a sluggish motility The nucleus has conspicuous karyosome connected to nuclear membrane by one or none coarse strands. The cyst is small, oval and quadrinucleate with glycogen mass and chromidial bars which are inconspicuous or absent It is nonpathogenic. lodamoeba butschlii This is widely distributed, though less common than E. coli and E. nana. The trophozoite is small, 6- 12 μm, with conspicuous nucleus The prominent karyosome is half the size of the nucleus, having bull 's eye appearance. Keywords Hemoflagellates Leishmania Species Trypanosomiasis Hemoflagellates these can be in different forms according to the position of their Kinetoplast and flagellum. Leishmania Species Clinical diseases Leishmania tropica / Cutaneous leishmaniasis (Baghdad boil or Oriental sore) Leishmania donovani / Visceral leishmaniasis (Dum-Dum fever or Kalazar) Leishmania braziliensis / Mucocutaneous leishmaniasis (Uta, Chiclero ulcer, Espundia) Leishmania Species The species of leishmania exist in two forms, amastigote (aflagellar) and promastigote (flagellated) in their life cycle. Leishmania They are transmitted by certain species of sand flies (vector) Leishmania donovani - (DumDum fever or Kalazar) Location The natural habitat of L. donovani in man is the reticuloendothelial system of the viscera, in which the amastigote multiplies. Pathogenesis in visceral leishmaniasis, the organs of the reticuloendothelial system (liver, spleen and bone marrow) are the most severely affected organs. The spleen and liver become markedly enlarged, and hypersplenism contributes to the development of anemia and lymphadenopathy also occurs. L. donovani infection of the classic kala- Epidemiology azar (“black sickness”) or dumdum fever type occurs in many parts of Asia, Africa and Southeast Asia. Laboratory diagnosis Examination of tissue biopsy, spleen aspiration, bone marrow aspiration or lymph node aspiration in properly stained smear. The amastigotes appear as intercellular & extra cellular L. donovani (LD) bodies. Serologic testing is also available. Leishmania tropica (Baghdad boil) Location These are parasites of the skin found in: endothelial cells of the capillaries of the infected site, nearby lymph nodes, within large mononuclear cells, in neutrophilic leukocytes, and free in the serum exuding from the ulcerative site. Metastasis to other site or invasion of the viscera is rare. Pathogenesis In neutrophilic leukocytes, phagocytosis is usually successful, but in macrophages the introduced parasites round up to form amastigote and multiply. There is a variable infiltration of lymphocytes and plasma cell. The overlying epithelium shows acanthosis and hyperkeratosis, which is usually followed by necrosis and ulceration. Epidemiology Cutaneous leishmaniasis produced by L. tropica complex is present in many parts of Asia, Africa, Mediterranean Europe and the southern region of the former Soviet Union. Leishmania braziliensis mucocutaneous leishmaniasis Location Mucocutaneous leishmaniasis is the same as oriental sore. But some of the strains tend to invade the mucous membranes of the mouth, nose, pharynx, and larynx. Pathogenesis The lesions are confined to the skin in cutaneous leishmaniasis and to the mucous membranes, cartilage, and skin in mucocutaneous leishmaniasis. A granulomatous response occurs, and a necrotic ulcer forms at the bite site. The lesions tend to become superinfected with bacteria. Secondary lesions occur on the skin as well as in mucous membranes. Nasal, oral, and pharyngeal lesions may be polypoid initially, and then erode to form ulcers that expand to destroy the soft tissue and cartilage about the face and larynx. Epidemiology The mucocutaneous leishmaniasis is seen from: the Yucatan peninsula into Central & South America, especially in rain forests where workers are exposed to sand fly bites while invading the habitat of the forest rodents. There are many jungle reservoir hosts, and domesticated dogs serve as reservoirs as well. Laboratory diagnosis Demonstration of the amastigotes in properly stained smears from touch preparations of ulcer biopsy specimen. Serological tests based on fluorescent antibody tests. Trypanosomiasis Etiologic agents Trypanosoma brucei Disease: African trypanosomiasis (sleeping sickness). Location: Blood. Forms: Epimastigote, trypomastigote. Vector: Tse tse fly. Important features Typical trypanosome structure is an elongated spindleshaped body that more or less tapers at both ends, a centrally situated nucleus, a kinetoplast posterior to nucleus, an undulating membrane arising from the kinetoplast and proceeding forward along the margin of the cell membrane and a single free flagellum at the anterior end. Pathogenesis The trypomastigotes spread from the skin through the blood to the lymph node and the brain. The typical somnolence (sleeping sickness) usually progresses to coma as a result of demyelinating encephalitis. Epidemiology T. brucei is limited to tropical west and central Africa, correlating with the range of the tsetse fly vector. The tsetse flies transmitting T. brucei prefer shaded stream banks for reproduction and proximity to human dwellings. People who work in such areas are at greatest risk of infection. Laboratory diagnosis Examination of thin and thick films, in concentrated anticoagulated blood preparations, and in aspiration from lymph nodes and concentrated spinal fluid. Methods for concentrating parasites in blood may be helpful approaches including centrifugation of heparinized samples and an ion–exchange chromatography. Trypanosomiasis Trypanosoma cruzi Disease: American trypanosomiasis (Chagas’ disease). Location: Heart muscle. Forms: Amastigote, promastigote, epimastigote, trypomastigote. Vector: Triatomid bug. Pathogenesis During the acute phase, the organism occurs in blood as a typical trypomastigote and in the reticuloendothelial cells as a typical amastigote. Cardiac muscle is the most frequently and severely affected tissue. Epidemiology T. cruzi occurs widely in both Triatomid bugs and a broad spectrum of reservoir animals in North, Central, and South America. Human disease is found most often among children in South and Central America, where there is direct correlation between infected wild animal reservoir hosts and the presence of infected bugs whose nests are found in human dwellings. Examine thin or thick stained preparations for trypomastigotes. Laboratory diagnosis Biopsy of lymph nodes, liver, spleen, or bone marrow may demonstrate organisms in amastigote stage. Xenodiagnosis - which consists of allowing an uninfected, laboratory-raised triatomid bug to feed on the patient and, after several weeks, examining the intestinal contents of the bug for the organism. Thanks for listening