Leishmania and Trichomonas PDF

Haemoflagelates They have 4 life stages “according to presence of flagella”. Blood flagellates (Haemoflagellates) Amastigotes : It is Roundish to oval in shape ,Consist of a nucleus and kinetoplast. The large single nucleus is typically located off- center.The dotlike blepha...

Haemoflagelates They have 4 life stages “according to presence of flagella”. Blood flagellates (Haemoflagellates) Amastigotes : It is Roundish to oval in shape ,Consist of a nucleus and kinetoplast. The large single nucleus is typically located off- center.The dotlike blepharoplast is attached to a small axoneme, this axoneme extends to the edge of the organism.The single parabasal body is located adjacent to the blepharoplast. Promastigotes : It is Long and slender in appearance.The large single nucleus is located in or near the center.The kinetoplast is located in the anterior end of the organism.A single free flagellum extends anteriorly from the axoneme. Epimastigotes : It is Long and slightly wider than promastigote form.The large single nucleus is located in posterior end.The kinetoplast located anterior to the nucleus.Undulating membrane extending half of the body length.A single free flagellum extends anteriorly from the axoneme. Trypomastigotes : It is C or U shape in stained blood films.Long and slender in appearance.One nucleus located anterior to the kinetoplast.The kinetoplast is located in the posterior end of the organism.Undulating membrane extending entire body length.A single free flagellum extends anteriorly from the axoneme when present. Clinical classification: - Visceral leishmaniasis (cause by Leishmania donovani, Leishmania infantum ,Leishmania chagasi)  - Cutaneous leishmaniasis (Leishmania tropica, Leishmania major, Leishmania mexicana, Leishmania aethiopica) - Mucocutaneous leishmaniasis (Leishmania brazillenesis) Old classification: Old world leishmaniasis - Leishmania tropica, - Leishmania major, - Leishmania aethiopica New world leishmaniasis: Leishmania chagasi , Leishmania mexicana, Leishmania brazillenesis The species of leishmania exist in two forms, amastigote (aflagellar) and promastigote (flagellated) in their life cycle. They are transmitted by certain species of sand flies )(Phlebotomus & Lutzomyia.. Old World Cutaneous Leishmaniasis (Oriental. sore) Clinical disease L.tropica minor - dry or urban cutaneous leishmaniasis L.tropica major - wet or rural cutaneous leishmaniasis L.aethiopica - cutaneous leishmaniasis Important features 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. In the early stage, the lesion is characterized by the proliferation of macrophages that contain numerous amastigotes. There is a variable infiltration of lymphocytes and plasma cell. The overlying epithelium shows acanthosis(lose of nuclei) 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. The urban Cutaneous leishmaniasis is thought to be an anthroponosis while the rural cutaneous leishmaniasis is zoonosis with human infections occurring only sporadically. The reservoir hosts in L. major are rodents. L.aethopica is endemic in Ethiopia and Kenya. The disease is a zoonosis with rock & tree hyraxes serving as reservoir hosts. The vector for the old world cutaneous.leishmaniasis is the Phlebotomus sand fly Clinical features The first sign, a red papule, appears at the site of the fly’s bite. This lesion becomes irritated, with intense itching, and begins to enlarge & ulcerate. Gradually the ulcer becomes hard and crusted and exudes a thin, serous material. At this stage, secondary bacterial infection may complicate the disease. In the case of the Ethiopian cutaneous leishmaniasis, there are similar developments of lesions, but they may also give rise to diffuse cutaneous leishmaniasis (DCL) in patients who produce little or no cell mediated immunity against the parasite. This leads to the formation of disfiguring nodules over the surface of the.body Immunity Both humoral and cell mediated immunity (CMI) are involved Treatment The drug of choice is sodium stibogluconate, with an alternative treatment of applying heat directly to the lesion. Treatment of L.aethopica remains to be a problem as.there is no safe and effective drug Prevention - Prompt treatment & eradication of ulcers -.Control of sand flies & reservoir hosts New World Cutaneous and Mucocutaneous. Leishmaniasis )American cutaneous leishmaniasis( Clinical disease: Leishmania mexicana complex- Cutaneous leishmaniasis. Leishmania braziliensis complex- mucocutaneous or cutaneous leishmaniasis :Important features The American cutaneous leishmeniasis is the same as oriental sore. But some of the strains tend to invade the mucous membranes of the mouth, nose, pharynx, and larynx either initially by direct extension or by metastasis. The metastasis is usually via lymphatic channels but.occasionally may be the bloodstream Pathogenesis The lesions are confined to the skin in cutaneous leishmaiasis 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. Regional.lymphadenopathy is common Epidemiology Most of the cutaneous & mucocutaneous leishmaniasis of the new world exist in enzootic cycles of infection involving wild animals, especially forest rodents. Leishmania mexicana occurs in south & Central America, especially in the Amazon basin, with sloths, rodents, monkeys, and raccoons as reservoir hosts. 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. The vector.is the Lutzomyia sand fly Clinical features The types of lesions are more varied than those of oriental sore and include Chiclero ulcer, Uta,.Espundia, and Disseminated Cutaneous Leishmaniasis Laboratory diagnosis Demonstration of the amastigotes in properly stained smears from touch preparations of ulcer biopsy specimen. Serological tests based on fluorescent antibody tests. Leishman skin test in some.species Immunity The humoral and cellular immune systems are involved.Treatment The drug of choice is sodium stibogluconate Prevention Avoiding endemic areas especially during times when local vectors are most active. Prompt treatment of infected individuals Visceral leishmaniasis Leishmania donovani Important features- the natural habitat of L.donovani in man is the reticuloendothelial system of the viscera, in which the amastigote multiplies by simple binary fission until the host cells are destroyed, whereupon new macrophages are parasitized. In the digestive tract of appropriate insects, the developmental cycle is also simple by longitudinal fission of promastigote forms. The amastigote stage appears as an ovoidal or μm in length; and the 3-2rounded body, measuring about μm 3.5-1.5μm lengths by 25-15promastigotes are.breadths Pathogenesis In visceral leishmaniasis, the organs of the reticuloendothelial system (liver, spleen and bone marrow) are the most severely affected organs. Reduced bone marrow activity, coupled with cellular distraction in the spleen, results in anaemia, leukopenia and thrombocytopenia(pancytopnea). This leads to secondary infections and a tendency to bleed. The spleen and liver become markedly enlarged, and hypersplenism contributes to the development of anaemia and lymphadenopathy also occurs. Increased production of globulin results in hyperglobulinemia, and reversal of the.albumin-to-globulin ratio Epidemiology L. donovani donovani, infection of the classic kala-azar (“black sickness”) or dumdum fever type occurs in many parts of Asia, Africa and Southeast Asia. Kala-azar occurs in three distinct epidemiologic patterns. In Mediterranean basin (European, Near Eastern, and Africa) and parts of China and Russia, the reservoir hosts are primarily dogs & foxes; in sub-Saharan Africa, rats & small carnivores are believed to be the main reservoirs. In India and neighboring countries (and Kenya), kala-azar is anthroponosis, i.e. there is no other mammalian reservoir host other than human. The vector is the Phlebotomus sand fly. Other variants of L. donovani are also recognized: L. donovani infantum with similar geographical distribution, reservoir host and vector; with L. donovani donovani. L. donovani chagasi is found in South America, Central America, especially Mexico, and the West Indies. Reservoir hosts are dogs, foxes, and cats,.and the vector is the Lutzomiya sand fly Clinical features Symptoms begin with intermittent fever, weakness, and diarrhea; chills and sweating that may resemble malaria symptoms are also common early in the infection. As organisms proliferate & invade cells of the liver and spleen, marked enlargement of the organs, weight loss, anemia, and emaciation occurs. With persistence of the disease, deeply pigmented, granulomatous lesion of skin, referred to as post-kala-azar dermal leishmaniasis, occurs. Untreated visceral leishmaniasis is nearly always fatal as.a result of secondary infection Immunity Host cellular and humoral defence mechanisms.are stimulated Laboratory diagnosis Examination of tissue biopsy, spleen aspiration, bone marrow aspiration or lymph node aspiration in properly stained smear (e.g. Giemsa stain). The amastigotes appear as intracellular & extra cellular L. donovan (LD).bodies ); Giemsa-stained amastigotes (LD bodies9Figure Culture of blood, bone marrow, and other tissue often demonstrates the promastigote stage of the organisms..Serologic testing is also available Treatment The drug of choice is sodium stibogluconate, a pentavalent antimonial compound. Alternative approaches include the addition of allopurinol and the use.of pentamidine or amphotercin B Prevention Prompt treatment of human infections and control of reservoir hosts. Protection from sand flies by screening and insect repellents Trichomonas vaginalis Important features- it is a pear-shaped organism with a central nucleus and four anterior flagella; and undulating membrane extends about two-thirds of its length. It exists only as a trophozoite form and measured7-23μm long & 5- 15μm wide., Transmission is by sexual intercourse. Pathogenesis The trophozoite is found in the urethra & vagina of women and the urethra & prostate gland of men. After introduction by sexual intercourse, proliferation begins which results in inflammation & large numbers of trophozoites in the tissues and the secretions. The onset of symptoms such as vaginal or vulval pruritus and discharge is often sudden and occurs during or after menstruation as a result of the increased vaginal acidity. The vaginal secretions are liquors, greenish or yellowish, sometimes frothy, and foul smelling. Infection in the male may be latent, with no symptoms, or may be present as.self limited, persistent, or recurring urethritis Epidemiology This parasite has worldwide distribution, and sexual intercourse is the primary mode of transmission. Occasionally, infections can be transmitted by fomites (toilet articles, clothing), although this transmission is limited by liability of the trophozoite. Rarely Infants may be infected by passage through the mother’s infected birth canal. The prevalence of this flagellate in developing countries is reported to be 2% –10% in men5% –20% in women. Clinical features Clinical disease - trichomoniasis. Most infected women at the acute stage are asymptomatic or have a scanty, watery vaginal discharge. In symptomatic cases vaginitis occurs with more extensive inflammation, along with erosion of epithelial lining, and painful urination, and results in symptomatic vaginal discharge, vulvitis and.dysuria Immunity The infection may induce humoral, secretory, and cellular immune reactions, but they are of little diagnostic help and.do not appear to produce clinically significant immunity Laboratory diagnosis In females, T.vaginalis may be found in urine sediment, wet preparations of vaginal secretions or vaginal scrapings. In males it may be found in urine, wet preparations of prostatic secretions or following massage of the prostate gland. Contamination of the specimen with faeces may confuse T.vaginalis with.T.hominis Treatment Metronidazole is the drug of choice. If resistant cases.occur, re-treatment with higher doses is required Prevention Both male & female sex partners must be treated to - avoid reinfection - Good personal hygiene, avoidance of.shared toilet articles & clothing. - Safe sexual practice Dientamoeba fragilis Dientamoeba fragilis was initially classified as an amoeba; however, the internal structures of the trophoziote are typical of a flagellate. No cyst stage has been described. The life cycle and mode of transmission of D. fragilis are not known. It has worldwide distribution. The transmission is postulated, via helminthes egg such as those of Ascaris and Enterobius species. Transmission by faecal- oral routes does occur. Most infection with D. fragilis is asymptomatic, with colonization of the cecum and upper colon. However, some patients may develop symptomatic disease, consisting of abdominal discomfort, flatulence, intermittent diarrhea, anorexia, and weight loss. The therapeutic agent of choice for this infection is iodoquinol, with tetracycline and parmomycine as acceptable alternatives. The reservoir for this flagellate and lifecycle are unknown. Thus, specific recommendation for prevention is difficult. However, infection can be avoided.by maintenance of adequate sanitary conditions Other flagellates inhabiting the alimentary canal. Trichomonas hominis – The trophozoites live in the caecal area of the large intestine and feed on bacteria. It is considered to be non-pathogenic, although it is often recovered from diarrheic stools. Since there is no known cyst stage, transmission probably occurs in the trophic.form. There is no indication of treatment Trichomanas tenax – was first recovered from the mouth, specifically in tartar from the teeth. There is no known cyst stage. The trophozoite has a pyriform shape and is smaller and more slender than that of T.hominis. Diagnosis is based on the recovery of the organism from the teeth, gums, or tonsillar crypts, and no therapy is.indicated