BackgroundThe prevalence of asthma and allergic diseases has increased in industrialised countries, and it is known that rates vary according whether the area is urban or rural and to socio-economic status. Surveys conducted in some urban settings in Latin America found high prevalence rates, only exceeded by the rates observed in industrialised English-speaking countries. It is likely that the marked changes in the environment, life style and living conditions in Latin America are responsible for these observations. The understanding of the epidemiological and immunological changes that underlie the increase in asthma and allergic diseases in Latin America aimed by SCAALA studies in Brazil and Ecuador will be crucial for the identification of novel preventive interventions.Methods/DesignThe Salvador-SCAALA project described here is a longitudinal study involving children aged 4–11 years living in the city of Salvador, Northeastern Brazil. Data on asthma and allergic diseases (rhinitis and eczema) and potential risk factors will be collected in successive surveys using standardised questionnaire. This will be completed with data on dust collection (to dust mite and endotoxin), skin test to most common allergens, stool examinations to helminth and parasites, blood samples (to infection, total and specific IgE, and immunological makers), formaldehyde, physical inspection to diagnoses of eczema, and anthropometric measures. Data on earlier exposures when these children were 0–3 years old are available from a different project.DiscussionIt is expected that knowledge generated may help identify public health interventions that may enable countries in LA to enjoy the benefits of a "modern" lifestyle while avoiding – or minimising – increases in morbidity caused by asthma and allergies.

SummaryTrans-sialidase and neuraminidase activities have been detected on the surface membrane of trypomastigotes of Trypanosoma cruzi, and both have been implicated in the parasite's invasion of host cells. We show here that these enzymes are structurally related. They are recognized by two independently derived monoclonal antibodies, are anchored to the membrane by glycosylphosphatidylinositol, copurify by ion exchange, molecular sieving, and hydrophobic chromatography, have maximal activities between pH 6.5 and 7.5, and are inactivated by heating at 56~ Furthermore, the neuraminidase and trans-sialidase reactions are coupled. An increase of the concentration of acceptors of the transfer reaction decreases the amount of flee sialic acid released through the neuraminidase reaction. We conclude that a single enzyme can catalyze the transfer or the hydrolysis of macromolecular-bound sialic acid. The predominant direction of the reaction will depend on the availability of appropriate oligosaccharide acceptors of sialic acid.

The mechanisms of malarial anemia induction are poorly understood, but cytokines and autoantibodies are considered to play important roles. This work aimed at evaluating the degree of anemia and the plasmatic profile of the cytokines tumor necrosis factor alpha (TNF-␣), gamma interferon (IFN-␥), interleukin-12 (IL-12), migration inhibitory factor (MIF), and IL-10 and the monocyte chemotactic protein-1 (MCP-1) chemokine, as well as evaluating the presence of antibodies directed to components of the normal erythrocyte membrane and to cardiolipin in individuals with malaria from the Brazilian Amazon. No difference was observed in the frequency of anemia between patients infected by Plasmodium vivax and those infected by Plasmodium falciparum, and there was no relationship between the levels of parasitemia and the manifestations of anemia in P. vivax and P. falciparum patients. Significant increases in the concentrations of TNF-␣, IFN-␥, MIF, and MCP-1 were observed in patients with P. falciparum and P. vivax malaria, whereas the concentrations of IL-10 was increased only in patients with P. vivax infection. Higher concentrations of IL-12 and IL-10 were observed in the P. falciparum anemic patients, while for TNF-␣ this profile was observed in the nonanemic ones. P. vivax-infected and P. falciparum-infected patients with positive immunoglobulin M (IgM) or IgM and IgG responses, respectively, against blood-stage forms of the parasites had significantly lower hemoglobin levels than did those with negative responses. There was no correlation between the presence of anti-erythrocyte and anti-cardiolipin antibodies and the presence or intensity of the anemia. Our data suggest that in areas of low endemicity and unstable transmission of malaria, P. vivax and P. falciparum infections present similar characteristics in terms of the induction of anemia and cytokine responses.Severe malarial anemia and cerebral malaria are the main complications of Plasmodium falciparum infection. They are responsible for most of the estimated one to three million malaria-related deaths every year in the world, mainly among children below 5 years of age in sub-Saharan Africa (49). Severe malarial anemia is reported to be the earliest complication, usually affecting children below 2 years of age (57). Although severe anemia is a major concern in malaria pathology due to its high mortality rates, milder forms of anemia also are important, since this manifestation is responsible for considerable morbidity and is one of the major factors for the high disability-adjusted life years attributed to malaria (50,51,66). Iron deficiency, intestinal helminths, and human immunodeficiency virus infection make significant contributions to the pathogenesis of anemia in many African countries, but now there is substantial evidence suggesting that malaria is indeed a major underlying factor (28, 48).Although it has been estimated, the real impact of malarial anemia on the affected populations is unknown. The few available data mostly are restricted to studies ...

In Brazil, zoonotic visceral leishmaniasis (ZVL) control programs based on the mass elimination of seropositive dogs have failed to reduce the number of leishmaniasis cases. However, these programs have been done under sub-optimal conditions. We studied a cohort of dogs in an urban area in Brazil to determine, whether a dog-culling program optimized with: (i) replacement of a relatively low-sensitivity indirect immune-fluorescent test on blood eluate by a more sensitive enzyme-linked immunosorbent assay on serum blood samples; (ii) shortening of the time interval from serodiagnosis to removal of dogs; (iii) screening a high proportion of the dog population could reduce the incidence of canine Leishmania infection (CLI). The study ran from December 1997 to July 2000, with four follow-up assessments performed at approximately 8-month intervals. All dogs seropositive for anti-Leishmania antibodies were promptly eliminated. A large number of new dogs immigrated to the study area throughout the study period. They comprised 43.8-49.8% of the cohort at each follow-up assessment, and upto 15% of them already had Leishmania infection. Overall, 42 news cases of CLI were identified, for a crude incidence rate of 11.8 cases per 100 dog-years (95% CI 8.6-15.6). In the first, second, third and fourth follow-up assessments the incidence rates were 8.2 (95% CI 3.0-17.9), 12.2 (95% CI 6.3-21.2), 16.4 (95% CI 8.5-28.6) and 13.6 (95% CI 7.1-23.8), respectively. There was no statistically significant change in these rates throughout the study period. Our results suggest that dog-culling programs do not reduce the incidence of CLI, even with an optimized intervention. Possible reasons for this failure include: currently available serologic methods lack sufficient sensitivity and/or specificity to accurately identify all infected dogs warranting removal in order to prevent Leishmania transmission; destroyed dogs are immediately replaced by susceptible puppies, and quite often, by already infected dogs; and other reservoirs may be involved in maintaining canine infection. Further efforts on ZVL control should be directed to developing new strategies or to testing control methods already in place with properly designed trials.

Trypanosoma cruzi trypomastigotes acquire sialic acid (SA) from host glycoconjugates by means of a plasma membrane-associated trans-sialidase (TS). Here we study the substrate specificity of TS, which differs from all known sialyltransferases in that it does not require cytidine monophosphate (CMP)-SA as donor. The T. cruzi TS reversibly transfers SA to saccharides with terminal beta-Gal (but not alpha-Gal) residues. Donors are saccharides with SA linked to terminal beta-Gal residues by (alpha 2-3), but not (alpha 2-6) bonds. The type of beta-linkage of the terminal Gal residue is of minor importance (beta 1-4 and beta 1-6 are slightly better than beta 1-3), whereas chain length and the structure of additional vicinal sugar residues are not relevant. SA on the surface of living trypomastigotes of T. cruzi is transferred back and forth between the parasite surface and acceptor molecules with terminal beta-Gal, either in solution or on the surface of neighbouring mammalian cells. Addition of fucose residue on or close to the terminal galactose impairs TS activity. As a consequence, the enzyme acts poorly on the E-selectin ligand sialyl-Lewisx and its precursor Lewisx, and in vitro adhesion of TS-treated neutrophils to L-cells expressing L-selectin is not affected. Modifications in the structure of the (alpha 2-3)-linked N-acetyl-neuraminic acid (Neu5Ac) (deoxy or methoxy) of the donor molecules do not impair transfer if the changes are at C9, whereas changes at C4, C7 and C8 impair the ability to donate the modified SA.(ABSTRACT TRUNCATED AT 250 WORDS)