Wednesday, December 9, 2009

What's new for 'Trypanosomatids' in PubMed

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Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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PubMed Results
Items 1 -4 of 4

1. Int J Infect Dis. 2009 Dec 5. [Epub ahead of print]

Leishmaniasis of the eyelid mimicking an infundibular cyst and review of the literature on ocular leishmaniasis.

Veraldi S, Bottini S, Currò N, Gianotti R.

Dipartimento di Anestesiologia, Terapia Intensiva e Scienze Dermatologiche, Università degli Studi di Milano, Fondazione I.R.C.C.S., Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Milan, Italy.

Cutaneous leishmaniasis is an infection caused by protozoa belonging to the genus Leishmania. The disease is transmitted by sandflies. Reservoirs are represented by dogs, mice, rats, and wild rodents. Cutaneous leishmaniasis is usually characterized by a single, polymorphous lesion located in an uncovered area. We report a case of cutaneous leishmaniasis localized on the left upper eyelid in a 36-year-old woman. The disease was characterized by a single, asymptomatic nodule, which was clinically diagnosed as an inflammatory infundibular cyst. The lesion was excised surgically. Histopathological examination showed an inflammatory infiltrate consisting of lymphocytes, histiocytes, and plasma cells. Several Leishmania spp amastigotes were observed in the cytoplasm of macrophages. Culture examination on Novy-MacNeal-Nicolle medium was positive for Leishmania spp. PCR was positive for Leishmania infantum. No relapses were observed during follow-up (17 months). The purpose of this report is to emphasize the changeability of clinical presentation in cutaneous leishmaniasis.

PMID: 19969498 [PubMed - as supplied by publisher]
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2. Int J Parasitol. 2009 Dec 4. [Epub ahead of print]

Evolution of the heme synthetic pathway in kinetoplastid flagellates: An essential pathway that is not essential after all?

Kořený L, Lukeš J, Oborník M.

Biology Centre, Institute of Parasitology, Czech Academy of Sciences and Faculty of Science, University of South Bohemia, Ceské Budejovice, Czech Republic.

For a vast majority of living organisms, heme is an essential compound that is synthesized through a conserved biosynthetic pathway. However, certain organisms are heme auxotrophs and need to obtain this molecule from exogenous sources. Kinetoplastid flagellates represent an interesting group of species, as some of them lost the complete pathway while others possess only the last three biosynthetic steps. We decided to supplement a current view on the phylogeny of these important pathogens with the expected state of heme synthesis in representative species. We propose a scenario in which the ancestor of all trypanosomatids was completely deficient of the synthesis of heme. In trypanosomatids other than members of the genus Trypanosoma, the pathway was partially rescued by genes encoding enzymes for the last three steps, supposedly obtained by horizontal transfer from a gamma-proteobacterium. This event preceded the diversification of the non-Trypanosoma trypanosomatids. Later, some flagellates acquired a beta-proteobacterial endosymbiont which supplied them with heme precursors. On the other hand, the medically important trypanosomes have remained fully deficient of heme synthesis and obtain this compound from the host.

PMID: 19968994 [PubMed - as supplied by publisher]
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3. Int J Parasitol. 2009 Dec 4. [Epub ahead of print]

Investigations into human serum sensitivity expressed by stocks of Trypan osoma brucei evansi.

Lai DH, Wang QP, Li Z, Lukins AG, Reid SA, Lun ZR.

Center for Parasitic Organisms, State Key Laboratory of Biocontrol, School of Life Sciences, and Key Laboratory of Tropical Diseases Control (the Ministry of Education), Zhongshan College of Medicine, Sun Yat-Sen (Zhongshan) University, Guangzhou 510275, China.

Trypanosoma bruceievansi, a widely distributed species of trypanosome infecting different livestock species in many countries in Africa, Asia and South America, has recently been reported as a pathogen causing a case of human trypanosomiasis in India. To date, there is little information regarding the natural resistance of animal-infective stocks of T. b. evansi to normal human serum (NHS). In this study, we investigated the degree of sensitivity to NHS of 15 stocks of T. b. evansi from different geographical origins and found that 10 of the stocks were completely susceptible to the action of NHS; parasites disappeared from the blood of infected mice within a few hours and the mice remained free from infection for more than 1 month. The remaining five stocks were partially resistant to NHS; although parasites initially disappeared from the circulation more than 50% of the mice showed relapse infection 10 -18 days later. Studies on one stock, T. b. evansi STIB 810, showed that the changes in parasitaemia in the infected mice were correlated with the amount of NHS inoculated (correlation factor -0.584 and P = 0.001). When this stock was passaged 25 times in mice in the presence of NHS it was found that the trypanosomes' serum resistance increased compared with the parent stock from which they were derived; 40% of the passaged parasites survived after in vitro incubation with 50% NHS for 7 h, while only 1% of individual trypanosomes of the parent stock survived under the same conditions. These findings show, to our knowledge for the first time, that human serum sensitivity varies amongst stocks of T. b. evansi, that some of them naturally display resistance to NHS and that, furthermore, T. b. evansi serum resistance can be increased by sub-passage in the presence of NHS.

PMID: 19968993 [PubMed - as supplied by publisher]
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4. FEBS J. 2009 Dec 7. [Epub ahead of print]

Functions and cellular localization of cysteine desulfurase and selenocysteine lyase in Trypanosoma brucei.

Poliak P, Van Hoewyk D, Oborník M, Zíková A, Stuart KD, Tachezy J, Pilon M, Lukeš J.

Biology Centre, Institute of Parasitology and Faculty of Natural Science, University of South Bohemia, Ceské Budejovice (Budweis), Czech Republic.

Nfs-like proteins have cysteine desulfurase (CysD) activity, which removes sulfur (S) from cysteine, and provides S for iron-sulfur cluster assembly and the thiolation of tRNAs. These proteins also have selenocysteine lyase activity in vitro, and cleave selenocysteine into alanine and elemental selenium (Se). It was shown previously that the Nfs-like protein called Nfs from the parasitic protist Trypanosoma brucei is a genuine CysD. A second Nfs-like protein is encoded in the nuclear genome of T. brucei. We called this protein selenocysteine lyase (SCL) because phylogenetic analysis reveals that it is monophyletic with known eukaryotic selenocysteine lyases. The Nfs protein is located in the mitochondrion, whereas the SCL protein seems to be present in the nucleus and cytoplasm. Unexpectedly, downregulation of either Nfs or SCL protein leads to a dramatic decrease in both CysD and selenocysteine lyase activities concurrently in the mitochondrion and the cytosolic fractions. Because loss of Nfs causes a growth phenotype but loss of SCL does not, we propose that Nfs can fully complement SCL, whereas SCL can only partially replace Nfs under our growth conditions. Structured digital abstract * MINT-7298305: NFS (uniprotkb:Q386Y7) and PHB1 (uniprotkb:Q57UX1) colocalize (MI:0403) by cosedimentation through density gradients (MI:0029) * MINT-7298357: SCL (uniprotkb:Q38DC4) and Enolase (uniprotkb:Q38BV6) colocalize (MI:0403) by cosedimentation through density gradients (MI:0029).

PMID: 19968861 [PubMed - as supplied by publisher]
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