Spontaneous B-cell lymphoma in hamster

Durante estudo anatomopatológico, incluindo imunoistoquímica, sobre pancreatite chagásica, experimentalmente induzida em hamsters machos, não-isogênicos, com quatro meses de idade, pesando 107,8 ± 10,9g, infiltração por linfoma foi observada em um animalcontrole normal, com 15 meses de idade. A neoplasia foi notada na ocasião da necropsia, 330 dias após o início do experimento. Lirifoma similar não foi achado nos demais controles normais (n=73), nem nos hamsters do grupo infectado, pareados para peso e idade (n=94). As alterações histopatológicas e imunoistoquímicas foram consistentes com linfoma difuso, não-Hodgkin, de grandes céiulas-B; porém, a hipótese de eventual origem leucêmica não foi inteiramente excluída. Linfomas experimentalmente induzidos têm sido relatados em animais de laboratório; entretanto, relatos de caso de linfoma, ocorrendo espontaneamente em hamsters, não têm sido freqüentes. No presente caso, o desenvolvimento da doença poderia ter alguma relação com o processo de envelhecimento.During anatomopathologic study, including immunohistochemistry, about chagasic pancreatitis experimentally induced in four month aged male non-isogenic hamsters, weighing 107.8 ± 10.9g, lymphoma infiltration was observed in a 15 month-aged normal control animal. The neoplasia was disclosed on the occasion of necropsy studies, 330 days after the beginning of experiment. Similar lymphoma was not found in the remainder normal controls (n=73), nor in the group of infected hamsters age and weight matched (n=94). The neoplasia histopathologic and immunohistochemical changes were consistent with non-Hodgkin diffuse large B-ceIl lymphoma; nevertheless, the hypothesis of eventual leukemic origin was not entirely excluded. Experimentally induced lymphomas have been related in laboratory animais; however, cases of spontaneously occurring lymphoma have been infrequently described in hamsters. In the present case, the development of the disease could have some relation with the animal aging process

Genome of the Avirulent Human-Infective Trypanosome—Trypanosoma rangeli

Background: Trypanosoma rangeli is a hemoflagellate protozoan parasite infecting humans and other wild and domestic mammals across Central and South America. It does not cause human disease, but it can be mistaken for the etiologic agent of Chagas disease, Trypanosoma cruzi. We have sequenced the T. rangeli genome to provide new tools for elucidating the distinct and intriguing biology of this species and the key pathways related to interaction with its arthropod and mammalian hosts.  Methodology/Principal Findings: The T. rangeli haploid genome is ,24 Mb in length, and is the smallest and least repetitive trypanosomatid genome sequenced thus far. This parasite genome has shorter subtelomeric sequences compared to those of T. cruzi and T. brucei; displays intraspecific karyotype variability and lacks minichromosomes. Of the predicted 7,613 protein coding sequences, functional annotations could be determined for 2,415, while 5,043 are hypothetical proteins, some with evidence of protein expression. 7,101 genes (93%) are shared with other trypanosomatids that infect humans. An ortholog of the dcl2 gene involved in the T. brucei RNAi pathway was found in T. rangeli, but the RNAi machinery is non-functional since the other genes in this pathway are pseudogenized. T. rangeli is highly susceptible to oxidative stress, a phenotype that may be explained by a smaller number of anti-oxidant defense enzymes and heatshock proteins.  Conclusions/Significance: Phylogenetic comparison of nuclear and mitochondrial genes indicates that T. rangeli and T. cruzi are equidistant from T. brucei. In addition to revealing new aspects of trypanosome co-evolution within the vertebrate and invertebrate hosts, comparative genomic analysis with pathogenic trypanosomatids provides valuable new information that can be further explored with the aim of developing better diagnostic tools and/or therapeutic targets

Karyotype variability in KP1(+) and KP1(-) strains of Trypanosoma rangeli isolated in Brazil and Colombia

In the present study, the molecular karyotypes of 12 KP1(+) and KP1(-) Trypanosoma rangeli strains were determined and 10 different molecular markers were hybridized to the chromosomes of the parasite, including seven obtained from T. rangeli [ubiquitin hydrolase (UH), a predicted serine/threonine protein kinase (STK), hexose transporter, hypothetical protein, three anonymous sequences] and three from Trypanosoma cruzi [ubiquitin-conjugating enzyme E2 (UBE2), ribosomal RNA methyltransferase (rRNAmtr), proteasome non-ATPase regulatory subunit 6 (PSMD6)]. Despite intraspecific variation, analysis of the karyotype profiles permitted the division of the T rangeli strains into two groups coinciding with the KP1(+) and KP1(-) genotypes. Southern blot hybridization showed that, except for the hexose transporter probe, all other probes produced distinct patterns able to differentiate the KP1(+) and KP1(-) genotypes. The UH, STK and An-1A04 probes exclusively hybridized to the chromosomes of KP1(+) strains and can be used as markers of this group. In addition, the UBE2, rRNAmtr and PSMD6 markers, which are present in a conserved region in all trypanosomatid species sequenced so far, co-hybridized to the same T. rangeli chromosomal bands, suggesting the occurrence of gene synteny in these species. The finding of distinct molecular karyotypes in KP1(+) and KP1 (-) strains of T rangeli is noteworthy and might be used as a new approach to the study of genetic variability in this parasite. Together with the Southern blot hybridization results, these findings demonstrate that differences at the kDNA level might be associated with variations in nuclear DNA. (c) 2009 Elsevier BY. All rights reserved.Funda ao de Amparo a Pesquisa do Estado de Minas Gerais (FAPEMIG)[APQ 00135-08]CNPq Conselho Nacional de Desenvolvimento Cientifico a Tecnologico[301375/2005-4]CNPq Conselho Nacional de Desenvolvimento Cientifico a Tecnologico[479184/2008-9