Justice where justice is due: A posthumous Nobel Prize to Carlos Chagas (1879-1934), the discoverer of American Trypanosomiasis (Chagas' disease).

Working in the Brazilian backland, Chagas described a new disease. He discovered the etiologic agent, the vector, the reservoir, the acute stage, the several clinical aspects of the chronic stage (particularly the heart disease), role of autoimmunity in its pathogenesis, and anticipated the social impact of the disease. Chagas was nominated to Nobel Prize twice: in 1913, and in 1921. In 1913, Richet won the prize because his work on anaphylaxis. In 1921, no one received the Nobel Prize. It is believed that detraction of Chagas' work at the National Academy of Medicine, made by jealousy, mediocrity, and political rivalries can be maculated the image of the scientist. Furthermore, misperception of Chagas' work may also have led the Nobel Committee not to award him. One-hundred years after the discovery, we can appreciate the greatness of the discovery of Carlos Chagas, never seem in the realm of biological research. Time to make justice, therefore, has finally come.

The loss of PSP toxin production in a formerly toxic Alexandrium lusitanicum clone.

Toxin production has always been considered a constitutive characteristic of dinoflagellates in the genus Alexandrium. Here we demonstrate that saxitoxin production can be lost by an Alexandrium species during routine culture maintenance. This is the first report of any marine saxitoxin-producing alga ever to have completely lost the ability to produce toxins. A clonal toxic isolate of Alexandrium lusitanicum from Portugal has been maintained in culture since 1962. In 1992, a subculture was established and sent to a different laboratory. Recent comparisons of the parental strain and the subculture revealed that the former had lost its toxicity, whereas the latter still produces saxitoxins. This loss of toxicity was confirmed by three independent toxin detection methods: mouse bioassay, mouse neuroblastoma assay and HPLC. Sequence analyses of different rRNA domains demonstrated that the toxic and non-toxic cultures are genetically identical for those markers. Morphological analysis showed that both cultures have the same plate tabulation and are A. lusitanicum. These results strongly argue that the loss of toxicity is not a result of a culturing artifact or mistake, such as mislabeling or contamination. The clonal cultures also show a significant difference in growth. Possible explanations for the change include genetic mutations or the effects of prolonged treatment of the non-toxic culture with antibiotics.

Reevaluation of production of paralytic shellfish toxin by bacteria associated with dinoflagellates of the Portuguese coast.

Paralytic shellfish toxins (PSTs) are potent neurotoxins produced by certain dinoflagellate and cyanobacterial species. The autonomous production of PSTs by bacteria remains controversial. In this study, PST production by two bacterial strains, isolated previously from toxic dinoflagellates, was evaluated using biological and analytical methods. Analyses were performed under conditions determined previously to be optimal for toxin production and detection. Our data are inconsistent with autonomous bacterial PST production under these conditions, thereby challenging previous findings for the same strains.