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Leishmania spp., Trypanosoma cruzi, and Trypanosoma brucei are protozoan parasites that cause a spectrum of fatal human diseases around the world. Recent completion of the genomic sequencing of these parasites has enormous relevance to the study of their biology and the pathogenesis of the diseases they cause because it opens the door to high-throughput proteomic technologies. This review encompasses studies using diverse proteomic approaches with these organisms to describe and catalogue global protein profiles, reveal changes in protein expression during development, elucidate the subcellular localisation of gene products, and evaluate host-parasite interactions.

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Revisões históricas aos avanços científicos para o controle da doença, o Simpósio Internacional Comemorativo do Centenário da Descoberta da Doença de Chagas (1909-2009).

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An entomologic search was carried out to collect intradomicile triatomines in dwellings from rural communities in the western border of the Panama Canal, Panama. Sixty-nine triatomines were collected inside 20 houses of 67 houses investigated. Rhodnius pallescens was the only triatomine species found and included adults of both sexes and nymphs. A significantly high Trypanosoma cruzi (72.7%) and T. rangeli (40%) vector infection rate was detected. Blood meal analysis showed that 68% of R. pallescens had fed on humans. Human serologic analysis and hemoculture performed on inhabitants from triatomine-infested houses showed that 32.1% (18 of 56) of the samples were trypanosome infected. Thirteen samples (23.2%) had antibodies against T. cruzi. Six of these seropositive samples were from children less than 15 years old. Trypanosoma rangeli was isolated in five hemoculture samples, all from children less than 11 years old. The epidemiologic implications of these findings in terms of human infection are discussed.

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Trypanosoma evansi (Trypanosomatidae, Kinetoplastida) is a salivarian trypanosomatid that infects eight mammal orders spread over America, Europe and Asia. In Brazil, T. evansi is the etiological agent of "Mal de Cadeiras", a horse disease very often described in the region known as Pantanal do Mato Grosso. Few data concerning the genetic diversity and biology of subpopulations of T. evansi that circulate in Brazil are available. The factors that modulate the interaction of this parasite with its hosts also remain to be elucidated. Here we evaluated the course of experimental infection of six T. evansi isolates derived from domestic and wild animals in Swiss-Webster mice and three Mus musculus lineages. The follow-up included biological, immunological as well as biochemical and hematological parameters. The same isolates as well as three others were characterized by pulsed-field electrophoresis. Our results showed that T. evansi isolates displayed significant differences regarding behavior and morbidity patterns in the distinct mouse lineages. Nevertheless, these differences could not be correlated with pulsed-field electrophoresis profiles. Indeed, concerning this molecular marker, only microheterogeneity was observed. Moreover, we observed that the outcome of the infection is defined by both host genetic background and peculiarities (virulence factors) of the distinct T. evansi isolates. Anemia and hypoglycemia were the only features that could be observed in all mouse lineages, independently of the inoculated T. evansi subpopulation. In addition, our data also show that Mus musculus is a suitable model host for the study of the different pathogenetic features of T. evansi infection.

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Cerebral tumor-like American trypanosomiasis (CTLAT) is an uncommon complication of Chagas' disease, observed only in immunosuppressed patients. We assessed 10 human immunodeficiency virus-positive patients with Chagas' disease who presented with CTLAT. All patients had neurological involvement and 6 developed intracranial hypertension. Neuroimaging studies showed supratentorial lesions in 9 patients, being single in 8. One case had infratentorial and supratentorial lesions. Low CD4+ cell counts were observed in all the cases and in 6 of them CTLAT was the first manifestation of acquired immunodeficiency syndrome. Serological tests for Chagas' disease were positive in 6 of 8 patients. Trypanosoma cruzi was identified in all brain specimens and in three cerebrospinal fluid samples. CTLAT should be considered in the differential diagnosis of intracranial mass lesions in human immunodeficiency virus-positive patients and should be added to the list of acquired immunodeficiency syndrome-defining illnesses.

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The ultrastructural study of adrenal gland from mice experimentally infected with Trypanosoma evansi, in addition to intravascular and intracellular trypanosomes, showed different degrees of cortical cell alterations and capillary wall modifications. Beside its biological scope, these results suggest a role for the adrenal cortex to partake in Surra's etiopathogenesis and describe for the very first time a T. evansi intracellular stage.

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