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Sent on Friday, 2011 Dec 16Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | Bull Soc Pathol Exot. 2011 Dec 14. [Epub ahead of print][Spread of Leishmania major to the north of Algeria.] [Article in French] Boudrissa A, Cherif K, Kherrachi I, Benbetka S, Bouiba L, Boubidi SC, Benikhlef R, Arrar L, Hamrioui B, Harrat Z.SourceInstitut Pasteur d'Algérie, route du Petit-Staouèli, Dely-Ibrahim, Alger, Algérie, boudrissakarim@yahoo.fr. AbstractSince a long time, Leishmania major and L. infantum foci in Algeria were geographically separated by the mountains of the Tell Atlas which represent a natural barrier. Recently, a new focus of cutaneous leishmaniasis (CL) has emerged in the village of El M'hir, located on the north side of the chain of the Tell Atlas, in the basin of the Soummam. During the period 2004-2010, 152 CL cases have been registered and 12 isolates were obtained from patients who declared never having been outside the village the last years. The identification of the parasites showed that all strains belonged to L major MON-25. Investigations on the reservoir hosts showed the presence of the sand rat (Psammomys obesus), for the first time, in this locality. Five strains isolated from this rodent belonged to L. major MON-25. The sand rat, which is usually observed around the chotts in the Saharan and steppe areas, acts as the main reservoir of L. major in Algeria. Its presence in the new focus of ElM'hir is reported for the first time. Entomological surveys carried out in 2009 showed the predominance of two sandfly species: Phlebotomus papatasi and P. perniciosus. The first one is known as a vector of L major in the Algerian Sahara. This study highlights the spread of L. major from the arid zones towards the semi arid areas, particularly in the Soummam valley. Climate changes and desertification observed in the steppe area northern Sahara could play a role in the extension of the disease. |
| 2. | Tidsskr Nor Laegeforen. 2011 des 13;131(24):2482-2486.A 15-month-old girl with fever and pancytopaenia. [Article in English, Norwegian] Skram MK, Bjering S, Hermansen NO, Dini L, Hellebostad M.AbstractBackground. Haemophagocytic lymphohistiocytosis (HLH) is a severe immune dysregulation characterised by fever, splenomegaly, cytopaenias, hyperferritinaemia, hypertriglyceridaemia and/or hypofibrinogenaemia, and haemophagocytosis. HLH may be primary familial or secondary to infections, malignancies or rheumatic disorders. Material and method. A previously healthy 15-month-old girl was admitted because of remitting fever, reduced general condition and increasing pallor. She had been treated with oral antibiotics before admission without improvement, and the family doctor had found anaemia. We present the diagnostic evaluation and interpretation and the clinical course. Results and interpretation. On admission the patient was febrile, pale and had a palpably enlarged liver and spleen. Blood test results showed pancytopaenia, elevated CRP, hyperferritinaemia and hypertriglyceridaemia. Bone marrow examination showed a hypercellular bone marrow with an essentially normal, active trilinear haematopoiesis without increased immature forms. Haemophagocytosis in macrophages was demonstrated as well as the presence of initially unidentified inclusions, which were later recognised as leishmania amastigotes. Serological tests demonstrated antibodies against leishmania, and microbiological culture of bone marrow and spleen aspirates showed leishmania promastigotes. She met six out of the eight criteria for HLH, and the diagnosis was secondary HLH caused by visceral leishmaniasis contracted during a stay on the Mediterranian coast of Spain. The patient was treated with liposomal amphotericin B and recovered without the need for HLH treatment. |
| 3. | J Cutan Pathol. 2011 Dec 15. doi: 10.1111/j.1600-0560.2011.01844.x. [Epub ahead of print]Cutaneous leishmaniasis mimicking inflammatory and neoplastic processes: a clinical, histopathological and molecular study of 57 cases.Saab J, Fedda F, Khattab R, Yahya L, Loya A, Satti M, Kibbi AG, Houreih MA, Raslan W, El-Sabban M, Khalifeh I.SourceDepartment of Pathology and Laboratory Medicine, American University of Beirut Medical Center, Beirut, Lebanon. Department of Human Morphology, American University of Beirut, Beirut, Lebanon. Department of Pathology, Shaukat Khanum Memorial Cancer Hospital and Research Center, Lahore, Pakistan. Department of Pathology, King Abdulaziz Medical City, Jeddah, Saudi Arabia. Department of Dermatology, American University of Beirut Medical Center, Beirut, Lebanon. Department of Pathology, Tishreen University, Lattakia, Syrian Arab Republic. Department of Pathology, Dhahran Health Center, Dhahran, Saudi Arabia. AbstractBackground: Cutaneous leishmaniasis displays considerable variation in its histopathological and clinical presentation. Clinically, it progresses from a papule into a painless ulcerated and crusted nodule/papule. Microscopically, it progresses from sheets of amastigote-filled histiocytes to granulomatous inflammation. Methods: The study was conducted on 145 skin biopsies from untreated patients with histopathological and/or clinical suspicion of cutaneous leishmaniasis in Lebanon, Syria and Saudi Arabia (1992-2010). The pre-biopsy clinical diagnosis and demographic data were collected. Biopsies were evaluated for the major microscopic pattern, and the parasitic index (PI) was also determined. Diagnosis was confirmed by polymerase chain reaction (PCR) followed by molecular sub-speciation. Results: Of the 145 patients, 125 were confirmed as cutaneous leishmaniasis by PCR. Eighteen cases presented with a pre-biopsy clinical diagnosis other than cutaneous leishmaniasis that ranged from dermatitis to neoplasm. Of the 125 cases, 57 showed a major histopathological pattern other than cutaneous leishmaniasis. Identification of amastigotes was equivocal (PI ≤1) in 38 of the 57 cases. Of interest, all the 18 cases with a pre-biopsy clinical diagnosis other than cutaneous leishmaniasis also showed atypical histopathology for cutaneous leishmaniasis. Conclusions: The manifestations of cutaneous leishmaniasis are broad and may mimic other inflammatory and neoplastic diseases. Pathologists and dermatologists should be aware of such pitfalls and can utilize PCR to confirm the diagnosis of leishmaniasis. Saab J, Fedda F, Khattab R, Yahya L, Loya A, Satti M, A-G Kibbi, Houreih MA, Raslan W, El-Sabban M, Khalifeh I. Cutaneous leishmaniasis mimicking inflammatory and neoplastic processes: a clinical, histopathological and molecular study of 57 cases. Copyright © 2011 John Wiley & Sons A/S. |
| 4. | Mol Microbiol. 2011 Dec 14. doi: 10.1111/j.1365-2958.2011.07951.x. [Epub ahead of print]A kinetoplastid-specific kinesin is required for cytokinesis and for maintenance of cell morphology in Trypanosoma brucei.Hu L, Hu H, Li Z.SourceDepartment of Microbiology & Molecular Genetics, University of Texas Medical School at Houston, Houston, TX 77030. AbstractKinesins are motor-based transport proteins that play diverse roles in various cellular processes. The trypanosome genome lacks the homologs of many conserved mitotic kinesins, but encodes a number of trypanosome-specific kinesins with unknown function. Here, we report the biochemical and functional characterization of TbKIN-C, a trypanosome-specific kinesin, which was initially identified through an RNAi screen for cytokinesis genes in T. brucei. TbKIN-C possesses in vitro ATPase activity and associates with cytoskeletal tubulin microtubules in vivo. It is distributed throughout the cytoskeleton with a focal enrichment at the posterior end of the cell during early cell cycle stages. RNAi of TbKIN-C resulted in distorted cell shape with an elongated posterior filled with tyrosinated tubulin microtubules. Silencing of TbKIN-C impaired the segregation of organelles and cytoskeletal structures and led to detachment of the new flagellum and a small portion of the cytoplasm. We also show that RNAi of TbKIN-C compromised cytokinesis and abolished the trans-localization of TbCPC1, a subunit of the chromosomal passenger complex, from the central spindle to the initiation site of cytokinesis. Our results suggest an essential role of TbKIN-C in maintaining cell morphology, likely through regulating microtubule dynamics at the posterior end of the cell. © 2011 Blackwell Publishing Ltd. |
| 5. | Mol Microbiol. 2011 Dec 14. doi: 10.1111/j.1365-2958.2011.07950.x. [Epub ahead of print]Identification of a protein kinase A regulatory subunit from Leishmania having importance in metacyclogenesis through induction of autophagy.Bhattacharya A, Biswas A, Das PK.SourceDepartment of Biotechnology, Presidency University, Kolkata 700073, India. Molecular Cell Biology Laboratory, Infectious Diseases and Immunology Division, Indian Institute of Chemical Biology, Kolkata 700032, India. AbstractcAMP-mediated responses act as modulators of environmental sensing and cellular differentiation of many kinetoplastidae parasites including Leishmania. Though, cAMP synthesizing (adenylate cyclase) and degrading (phosphodiesterase) enzymes have been cloned and characterized from Leishmania, no cAMP-binding effector molecule has yet been identified from this parasite. In this study, a regulatory subunit of cAMP-dependent protein kinase (Ldpkar1), homologous to mammalian class I cAMP-dependent protein kinase regulatory subunit, has been identified from L. donovani. Further characterization suggested possible interaction of LdPKAR1 with PKA catalytic subunits and inhibition of PKA activity. This PKA regulatory subunit is expressed in all lifecycle stages and its expression attained maximum level in stationary phase promastigotes, which are biochemically similar to the infective metacyclic promastigotes. Starvation condition, the trigger for metacyclogenesis in the parasite, elevates LdPKAR1 expression and under starvation condition promastigotes overexpressing Ldpkar1 attained metacyclic features earlier than normal cells. Furthermore, Ldpkar1 over expression accelerates autophagy, a starvation-induced cytological event necessary for metacyclogenesis and amastigote formation. Conditional silencing of Ldpkar1 delays the induction of autophagy in the parasite. The study, for the first time, reports the identification of a functional cAMP-binding effector molecule from Leishmania that may modulate important cytological events affecting metacyclogenesis. © 2011 Blackwell Publishing Ltd. |
| 6. | Rev Med Inst Mex Seguro Soc. 2011 Jul-Aug;49(4):367-72.Trypanosoma cruzi antibodies in blood donors in Yucatan state, Mexico.García-Montalvo B.SourceBanco Central de Sangre, Hospital de Especialidades, Centro Médico Nacional Ignacio García Téllez, Instituto Mexicano del Seguro Social, Mérida, Yucatán, México. bgarciam04@yahoo.com.mx AbstractBACKGROUND:Blood transfusion is the second most frequent way of Trypanosoma cruzi (T. cruzi) transmission in Latin American countries. Few data exists on the geographic distribution and prevalence of T. cruzi seropositive blood donors in Mexico. The objective was to document T. cruzi antibody distribution, and identify the regions with the highest prevalence of seropositive blood donors. METHODS:the analyzed data was collected over a six-year period during blood donations made at the Central Blood Bank and at the transfusion services and donation modules of the Instituto Mexicano del Seguro Social (IMSS) located in the Yucatan state. RESULTS:Trypanosoma cruzi antibody reactivity was determined in 86343 blood donors. Overall seroprevalence was 0.70 % (607/86 343). Since 2002 to 2004, the majority (58 %) of seropositive donors were rural residents, but since 2005 to 2007 the majority (56.6 %) were urban residents. The two highest seroprevalences by region were in the Metropolitan area (0.42 %) and in rural south Yucatan (0.09 %). Most seropositive donors resided in the municipality of Merida (60.3 %). CONCLUSIONS:seroprevalence distribution was heterogeneous during the study period but urban transmission has apparently surpassed rural transmission in recent years. |
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| 7. | Mol Biochem Parasitol. 2011 Oct;179(2):51-8. Epub 2011 Jul 7.Specializations in a successful parasite: what makes the bloodstream-form African trypanosome so deadly?Gadelha C, Holden JM, Allison HC, Field MC.SourceDepartment of Pathology, University of Cambridge, Cambridge, UK. AbstractMost trypanosomatid parasites have both arthropod and mammalian or plant hosts, and the ability to survive and complete a developmental program in each of these very different environments is essential for life cycle progression and hence being a successful pathogen. For African trypanosomes, where the mammalian stage is exclusively extracellular, this presents specific challenges and requires evasion of both the acquired and innate immune systems, together with adaptation to a specific nutritional environment and resistance to mechanical and biochemical stresses. Here we consider the basis for these adaptations, the specific features of the mammalian infective trypanosome that are required to meet these challenges, and how these processes both inform on basic parasite biology and present potential therapeutic targets. Copyright © 2011 Elsevier B.V. All rights reserved. |
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