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Molecular epidemiology of camel trypanosomiasis based on ITS1 rDNA and RoTat 1.2 VSG gene in the Sudan
BACKGROUND: Internal transcribed spacer one (ITS1) of the ribosomal DNA is known to be a suitable target for PCR-based detection of trypanosomes. The analysis of this region provides a multi-species-specific diagnosis by a single PCR. Using ITS1 primer-based PCR, a cross sectional study was carried...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2011
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060148/ https://www.ncbi.nlm.nih.gov/pubmed/21375725 http://dx.doi.org/10.1186/1756-3305-4-31 |
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author | Salim, Bashir Bakheit, Mohammed A Kamau, Joseph Nakamura, Ichiro Sugimoto, Chihiro |
author_facet | Salim, Bashir Bakheit, Mohammed A Kamau, Joseph Nakamura, Ichiro Sugimoto, Chihiro |
author_sort | Salim, Bashir |
collection | PubMed |
description | BACKGROUND: Internal transcribed spacer one (ITS1) of the ribosomal DNA is known to be a suitable target for PCR-based detection of trypanosomes. The analysis of this region provides a multi-species-specific diagnosis by a single PCR. Using ITS1 primer-based PCR, a cross sectional study was carried out in the period from September to November 2009 on samples collected from 687 camels from geographically distinct zones in the Sudan to detect all possible African trypanosomes, which can infect camels. RESULTS: The results showed that all PCR-positive camels were infected with a single parasite species; Trypanosoma evansi. The highest prevalence, 57.1% (117/205), was observed in the Butana plains of mid-Eastern Sudan and the lowest, 6.0% (4/67), was in the Umshadeeda eastern part of White Nile State. In another experiment, the RoTat 1.2 gene encoding the variable surface glycoprotein (VSG) of T. evansi was analyzed for its presence or absence by a polymerase chain reaction (PCR) using T. evansi species-specific primers. The study showed that the RoTat 1.2 VSG gene was absent in thirteen out of thirty T. evansi-positive samples. CONCLUSIONS: It is concluded that camel trypanosomiasis in Sudan is apparently caused by a single parasite species T. evansi and there were no other typanosomes species detected. In addition, the disease is highly prevalent in the country, which strengthens the need to change control policies and institute measures that help prevent the spread of the parasite. To our knowledge, this is the first molecular diagnosis report, which gives a picture of camel trypanosomiasis covering large geographical areas in Sudan. |
format | Text |
id | pubmed-3060148 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-30601482011-03-18 Molecular epidemiology of camel trypanosomiasis based on ITS1 rDNA and RoTat 1.2 VSG gene in the Sudan Salim, Bashir Bakheit, Mohammed A Kamau, Joseph Nakamura, Ichiro Sugimoto, Chihiro Parasit Vectors Short Report BACKGROUND: Internal transcribed spacer one (ITS1) of the ribosomal DNA is known to be a suitable target for PCR-based detection of trypanosomes. The analysis of this region provides a multi-species-specific diagnosis by a single PCR. Using ITS1 primer-based PCR, a cross sectional study was carried out in the period from September to November 2009 on samples collected from 687 camels from geographically distinct zones in the Sudan to detect all possible African trypanosomes, which can infect camels. RESULTS: The results showed that all PCR-positive camels were infected with a single parasite species; Trypanosoma evansi. The highest prevalence, 57.1% (117/205), was observed in the Butana plains of mid-Eastern Sudan and the lowest, 6.0% (4/67), was in the Umshadeeda eastern part of White Nile State. In another experiment, the RoTat 1.2 gene encoding the variable surface glycoprotein (VSG) of T. evansi was analyzed for its presence or absence by a polymerase chain reaction (PCR) using T. evansi species-specific primers. The study showed that the RoTat 1.2 VSG gene was absent in thirteen out of thirty T. evansi-positive samples. CONCLUSIONS: It is concluded that camel trypanosomiasis in Sudan is apparently caused by a single parasite species T. evansi and there were no other typanosomes species detected. In addition, the disease is highly prevalent in the country, which strengthens the need to change control policies and institute measures that help prevent the spread of the parasite. To our knowledge, this is the first molecular diagnosis report, which gives a picture of camel trypanosomiasis covering large geographical areas in Sudan. BioMed Central 2011-03-04 /pmc/articles/PMC3060148/ /pubmed/21375725 http://dx.doi.org/10.1186/1756-3305-4-31 Text en Copyright ©2011 Salim et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Short Report Salim, Bashir Bakheit, Mohammed A Kamau, Joseph Nakamura, Ichiro Sugimoto, Chihiro Molecular epidemiology of camel trypanosomiasis based on ITS1 rDNA and RoTat 1.2 VSG gene in the Sudan |
title | Molecular epidemiology of camel trypanosomiasis based on ITS1 rDNA and RoTat 1.2 VSG gene in the Sudan |
title_full | Molecular epidemiology of camel trypanosomiasis based on ITS1 rDNA and RoTat 1.2 VSG gene in the Sudan |
title_fullStr | Molecular epidemiology of camel trypanosomiasis based on ITS1 rDNA and RoTat 1.2 VSG gene in the Sudan |
title_full_unstemmed | Molecular epidemiology of camel trypanosomiasis based on ITS1 rDNA and RoTat 1.2 VSG gene in the Sudan |
title_short | Molecular epidemiology of camel trypanosomiasis based on ITS1 rDNA and RoTat 1.2 VSG gene in the Sudan |
title_sort | molecular epidemiology of camel trypanosomiasis based on its1 rdna and rotat 1.2 vsg gene in the sudan |
topic | Short Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060148/ https://www.ncbi.nlm.nih.gov/pubmed/21375725 http://dx.doi.org/10.1186/1756-3305-4-31 |
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