ABSTRACT Leishmaniasis is a disease complex with various clinical symptoms caused by different species of parasites of the genus Leishmania. The visceral form of the disease, characterized by severe symptoms is fatal, if not treated. The high toxicity of current antileishmanial drugs and the need for long-term treatment make the therapy complicated, especially in a large number of infected children. Hence, the search for new therapies must be intensified. Oral administration of the trace element zinc has been considered in alternative treatments against different clinical forms of leishmaniasis. This study revealed that the administration of zinc in children with visceral leishmaniasis, during treatment with amphotericin B or glucantime, accelerates the regression of the spleen enlargement without interfering with the recovery of hematological parameters.

In Chagas disease, understanding how the immune response controls parasite growth but also leads to heart damage may provide insight into the design of new therapeutic strategies. Tumor necrosis factor-alpha (TNF-α) is important for resistance to acute Trypanosoma cruzi infection; however, in patients suffering from chronic T. cruzi infection, plasma TNF-α levels correlate with cardiomyopathy. Recent data suggest that CD8-enriched chagasic myocarditis formation involves CCR1/CCR5-mediated cell migration. Herein, the contribution of TNF-α, especially signaling through the receptor TNFR1/p55, to the pathophysiology of T. cruzi infection was evaluated with a focus on the development of myocarditis and heart dysfunction. Colombian strain-infected C57BL/6 mice had increased frequencies of TNFR1/p55+ and TNF-α+ splenocytes. Although TNFR1-/- mice exhibited reduced myocarditis in the absence of parasite burden, they succumbed to acute infection. Similar to C57BL/6 mice, Benznidazole-treated TNFR1-/- mice survived acute infection. In TNFR1-/- mice, reduced CD8-enriched myocarditis was associated with defective activation of CD44+CD62Llow/- and CCR5+ CD8+ lymphocytes. Also, anti-TNF-α treatment reduced the frequency of CD8+CCR5+ circulating cells and myocarditis, though parasite load was unaltered in infected C3H/HeJ mice. TNFR1-/- and anti-TNF-α-treated infected mice showed regular expression of connexin-43 and reduced fibronectin deposition, respectively. Furthermore, anti-TNF-α treatment resulted in lower levels of CK-MB, a cardiomyocyte lesion marker. Our results suggest that TNF/TNFR1 signaling promotes CD8-enriched myocarditis formation and heart tissue damage, implicating the TNF/TNFR1 signaling pathway as a potential therapeutic target for control of T. cruzi-elicited cardiomyopathy.

Amostras de soro obtidas de estudantes do curso de Medicina Veteriná ria da Universidade para o Desenvolvimento do Estado e da Região do Pantanal, Campo Grande, MS, Brasil, foram examinadas para a presença de anticorpos contra Toxoplasma gondii. Dos 145 soros testados, 44 (30,34%) foram positivos na hemaglutinação, com título igual ou superior a 1:16. Não foram observadas associações entre as caracterí sticas epidemiológicas examinadas, tais como hábitos alimentares (ingestão de carne bovina crua ou malpassada, vegetais crus/não lavados, produtos lácteos não pasteurizados) ou contato constante com cães e a presença de anticorpos contra T. gondii, exceto pelo percentual significativamente maior de estudantes soropositivos que relataram ter contato freqüente com gatos (P=0,03).

Serum samples obtained from students of the School of Veterinary Medicine, Universidade para o Desenvolvimento do Estado e da Região do Pantanal, Campo Grande, MS, Brazil, were examined for Toxoplasma gondii gondii antibodies. Serum samples from 44 (30.34%) of the 145 veterinary students examined were positive on the hemagglutination test, yielding a titer of 1:16 or greater. There were no relations between the epidemiological characteristics examined, such as food habits (eating of raw or rare-cooked cattle meat, raw/uncleaned vegetables, unpasteurized dairy products), frequent contact with dogs and the presence of T. gondii antibodies, except for a significantly higher percentual of seropositive students that reported frequent contact with cats (P=0.03).