Pathophysiology to Risk Factor and Therapeutics to Treatment Strategies on Epilepsy.

Epilepsy represents a condition in which abnormal neuronal discharges or the hyperexcitability of neurons occur with synchronicity, presenting a significant public health challenge. Prognostic factors, such as etiology, electroencephalogram (EEG) abnormalities, the type and number of seizures before treatment, as well as the initial unsatisfactory effects of medications, are important considerations. Although there are several third-generation antiepileptic drugs currently available, their multiple side effects can negatively affect patient quality of life. The inheritance and etiology of epilepsy are complex, involving multiple underlying genetic and epigenetic mechanisms. Different neurotransmitters play crucial roles in maintaining the normal physiology of different neurons. Dysregulations in neurotransmission, due to abnormal transmitter levels or changes in their receptors, can result in seizures. In this review, we address the roles played by various neurotransmitters and their receptors in the pathophysiology of epilepsy. Furthermore, we extensively explore the neurological mechanisms involved in the development and progression of epilepsy, along with its risk factors. Furthermore, we highlight the new therapeutic targets, along with pharmacological and non-pharmacological strategies currently employed in the treatment of epileptic syndromes, including drug interventions employed in clinical trials related to epilepsy.

Evaluation of a Novel Synthetic Peptide Derived from Cytolytic Mycotoxin Candidalysin.

The importance of neuroinflammation in neurology is becoming increasingly apparent. In addition to neuroinflammatory diseases such as multiple sclerosis, the role of neuroinflammation has been identified in many non-inflammatory neurological disorders such as stroke, epilepsy, and cancer. The immune response within the brain involves the presence of CNS resident cells; mainly glial cells, such as microglia, the CNS resident macrophages. We evaluated the peptide Ca-MAP1 bioinspired on the C. albicans immature cytolytic toxin candidalysin to develop a less hemolytic peptide with anti-neuroinflammatory, antibacterial, and cytotoxic activity against tumor cells. In silico and in vitro studies were performed at various concentrations. Ca-MAP1 exhibits low hemolytic activity at lower concentrations and was not cytotoxic to MRC-5 and BV-2 cells. Ca-MAP1 showed activity against Acinetobacter baumannii, Escherichia coli ATCC, E. coli KPC, Klebsiella pneumoniae ATCC, Pseudomonas aeruginosa, and Staphylococcus aureus ATCC. Furthermore, Ca-MAP1 exhibits anti-neuroinflammatory activity in the BV-2 microglia model, with 93.78% inhibition of nitrate production at 18.1 µM. Ca-MAP1 presents cytotoxic activity against tumor cell line NCI-H292 at 36.3 µM, with an IC50 of 38.4 µM. Ca-MAP1 demonstrates results that qualify it to be evaluated in the next steps to promote the control of infections and provide an alternative antitumor therapy.

Purification, Characterization and Evaluation of the Antitumoral Activity of a Phospholipase A2 from the Snake Bothrops moojeni.

Nature presents a wide range of biomolecules with pharmacological potential, including venomous animal proteins. Among the protein components from snake venoms, phospholipases (PLA2) are of great importance for the development of new anticancer compounds. Thus, we aimed to evaluate the PLA2 anticancer properties from Bothrops moojeni venom. The crude venom was purified through three chromatographic steps, monitored by enzymatic activity and SDS-PAGE (12%). The purified PLA2 denominated BmPLA2 had its molecular mass and N-terminal sequence identified by mass spectrometry and Edman degradation, respectively. BmPLA2 was assayed against human epithelial colorectal adenocarcinoma cells (Caco-2), human rhabdomyosarcoma cells (RD) and mucoepidermoid carcinoma of the lung (NCI-H292), using human fibroblast cells (MRC-5) and microglia cells (BV-2) as a cytotoxicity control. BmPLA2 presented 13,836 Da and a 24 amino acid-residue homologue with snake PLA2, which showed a 90% similarity with other Bothrops moojeni PLA2. BmPLA2 displayed an IC50 of 0.6 µM against Caco-2, and demonstrated a selectivity index of 1.85 (compared to MRC-5) and 6.33 (compared to BV-2), supporting its selectivity for cancer cells. In conclusion, we describe a new acidic phospholipase, which showed antitumor activity and is a potential candidate in the development of new biotechnological tools.

Relationship between intestinal microbiota, diet and biological systems: an integrated view.

The health-disease process can be influenced by the intestinal microbiota. As this plays a fundamental role in protecting the organism, the importance of studying the composition and diversity of this community becomes increasingly evident. Changes in the composition of the intestinal bacterial community may result in dysbiosis, and this process may contribute to triggering various diseases in all biological systems. This imbalance of intestinal microbiota homeostasis may alter commensal bacteria and the host metabolism, as well as immune function. Dysbiosis also causes an increase in intestinal permeability due to exposure to molecular patterns associated with the pathogen and lipopolysaccharides, leading to a chronic inflammatory process that can result in diseases for all biological systems. In this context, dietary intervention through the use of probiotics, prebiotics and antioxidant foods can be considered a contribution to the modulation of intestinal microbiota. Probiotics have been used to provide up to 10 billion colony forming units, and probiotic foods, Kefir and fermented natural yogurt are also used. Prebiotics, in turn, are found in supplemental formulations of processed foods and in functional foods that are also sources of phenolic compounds, such as flavonoids, antioxidant and anti-inflammatory substances, polyunsaturated fatty acids, vitamins, and minerals. In this review, we will discuss the relationship between an imbalance in the intestinal microbiota with the development of diseases, besides indicating the need for future studies that can establish bacterial parameters for the gastrointestinal tract by modulating the intestinal microbiota, associated with the adoption of healthy habits during all life cycles.

Do Bioactive Food Compound with Avena sativa L., Linum usitatissimum L. and Glycine max L. Supplementation with Moringa oleifera Lam. Have a Role against Nutritional Disorders? An Overview of the In Vitro and In Vivo Evidence.

Functional clinical nutrition is an integrative science; it uses dietary strategies, functional foods and medicinal plants, as well as combinations thereof. Both functional foods and medicinal plants, whether associated or not, form nutraceuticals, which can bring benefits to health, in addition to being included in the prevention and treatment of diseases. Some functional food effects from Avena sativa L. (oats), Linum usitatissimum L. (brown flaxseed), Glycine max L. (soya) and Moringa oleifera have been proposed for nutritional disorders through in vitro and in vivo tests. A formulation called a bioactive food compound (BFC) showed efficiency in the association of oats, flaxseed and soy for dyslipidemia and obesity. In this review, we discuss the effects of BFC in other nutritional disorders, as well as the beneficial effects of M. oleifera in obesity, cardiovascular disease, diabetes mellitus type 2, metabolic syndrome, intestinal inflammatory diseases/colorectal carcinogenesis and malnutrition. In addition, we hypothesized that a BFC enriched with M. oleifera could present a synergistic effect and play a potential benefit in nutritional disorders. The traditional consumption of M. oleifera preparations can allow associations with other formulations, such as BFC. These nutraceutical formulations can be easily accepted and can be used in sweet preparations (fruit and/or vegetable juices, fruit and/or vegetable vitamins, porridges, yogurt, cream, mousses or fruit salads, cakes and cookies) or savory (vegetable purees, soups, broths and various sauces), cooked or not. These formulations can be low-cost and easy-to-use. The association of bioactive food substances in dietary formulations can facilitate adherence to consumption and, thus, contribute to the planning of future nutritional interventions for the prevention and adjuvant treatment of the clinical conditions presented in this study. This can be extended to the general population. However, an investigation through clinical studies is needed to prove applicability in humans.

Potential role of zinc in the visceromegaly regression and recovery of hematological parameters during treatment of visceral leishmaniasis in children from an endemic area.

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.

Intake of Polydextrose Alters Hematology and the Profile of Short Chain Fatty Acids in Partially Gastrectomized Rats.

Polydextrose (PDX) ingestion may increase the intestinal absorption of iron. This study evaluated the effects of 7.5% polydextrose supplementation on markers of iron uptake, transport and storage in partially gastrectomized rats. Half of a batch of 40 male Wistar rats (250 g) underwent Billroth II partial gastrectomy with anterior truncal vagotomy (GXT), while the other half underwent sham gastrectomy (SHAM). At 7 postoperative days, the animals were subdivided into four groups (n = 10): Sham Control and GXT Control (no polydextrose); Sham PDX and GXT PDX (with 7.5% PDX). The animals were euthanized after 60 day of PDX treatment. Organ weight, cecal pH, the characterization and quantification of short-chain fatty acids (SCFA), hematological parameters, hepatic iron content and the expression of ferroportin (FPT) in the jejunum, cecum, colon and liver were evaluated. PDX caused changes in the cecum of the supplemented animals, where there was a decrease in pH, increase in cecal wall and marked production of SCFA, especially acetic and propionic acids (p < 0.05). Hepatic iron levels were lower in GXT animals. PDX increased hemoglobin (HGB) values by 29.2% and hematocrit (HCT) by 55.8% in the GXT PDX group compared to the GXT Control group. The GXT PDX group had lower hepatic FPT expression (p < 0.05). PDX led to increased SCFA concentration in the supplemented animals. Considering that SCFAs play a central role in the increasing nutrients uptake, this mechanism may be involved in altering the hematology profile observed in these animals but not enough to reverse iron deficiency anemia in post-gastrectomy rats.

Renal histopathological findings in dogs with visceral leishmaniasis.

Visceral leishmaniasis affects various organs including the kidneys; which can lead to renal failure and death. In order to verify this renal involvement, material was evaluated from 100 dogs naturally infected and with serological diagnosis of canine visceral leishmaniasis (CVL). Inflammatory changes were present in 25.3% of the tubules, in 67.0% of interstitium and in 52.0% of glomeruli. There was no significant difference (p > 0.05) between the presence of glomerulonephritis in symptomatic and oligosymptomatic dogs. The membranous and membranoproliferative glomerulonephritis were the most frequent, both with 18.0% frequency, followed by focal segmental glomerulosclerosis with 14.0%. Changes such as cylindruria, tubular and fibrosis hypertrophy, periglomerular inflammatory infiltrate, and multifocal and diffuse peritubular inflammatory infiltrate were observed. The findings are consistent with those of other authors indicating that renal involvement is common in CVL and the standards of membranous and membranoploriferative glomerulonephritis, as well as the tubulointerstitial involvement, are frequent.

Renal histopathllogical findings in dogs with visceral leishmaniasis / Achados histopatológicos renais em cães com leishmaniose visceral

Visceral leishmaniasis affects various organs including the kidneys; which can lead to renal failure and death. In order to verify this renal involvement, material was evaluated from 100 dogs naturally infected and with serological diagnosis of canine visceral leishmaniasis (CVL). Inflammatory changes were present in 25.3% of the tubules, in 67.0% of interstitium and in 52.0% of glomeruli. There was no significant difference (p > 0.05) between the presence of glomerulonephritis in symptomatic and oligosymptomatic dogs. The membranous and membranoproliferative glomerulonephritis were the most frequent, both with 18.0% frequency, followed by focal segmental glomerulosclerosis with 14.0%. Changes such as cylindruria, tubular and fibrosis hypertrophy, periglomerular inflammatory infiltrate, and multifocal and diffuse peritubular inflammatory infiltrate were observed. The findings are consistent with those of other authors indicating that renal involvement is common in CVL and the standards of membranous and membranoploriferative glomerulonephritis, as well as the tubulointerstitial involvement, are frequent.

A leishmaniose visceral acomete vários órgãos entre eles os rins; o que pode levar a insuficiência renal e a morte. Com o objetivo de verificar este acometimento renal foram avaliados materiais de 100 cães naturalmente infectados e com diagnósticos sorológicos de leishmaniose visceral canina - LVC. As alterações inflamatórias estavam presentes em 25,3% dos túbulos, em 67,0% do interstício e em 52,0% dos glomérulos. Não houve diferença significativa (p > 0,05) entre a presença de glomerulonefrite em cães sintomáticos e oligossintomáticos. As glomerulonefrites membranosa e membrano proliferativa foram as mais freqüentes, ambas com 18,0% de freqüência seguidas da glomeruloesclerose segmentar e focal com 14,0%. Foram observadas alterações como cilindrúria, hipertrofia tubular e fibrose e infiltrados inflamatórios periglomerulares e peritubulares multifocais e difusos. Os achados concordam com os de outros autores indicando que o acometimento renal é comum na LVC e que os padrões de glomerulonefrites membranoploriferativa e membranosa; assim como o acometimento tubulointersticial são freqüentes.

Inducible nitric oxide synthase in heart tissue and nitric oxide in serum of Trypanosoma cruzi-infected rhesus monkeys: association with heart injury.

BACKGROUND: The factors contributing to chronic Chagas' heart disease remain unknown. High nitric oxide (NO) levels have been shown to be associated with cardiomyopathy severity in patients. Further, NO produced via inducible nitric oxide synthase (iNOS/NOS2) is proposed to play a role in Trypanosoma cruzi control. However, the participation of iNOS/NOS2 and NO in T. cruzi control and heart injury has been questioned. Here, using chronically infected rhesus monkeys and iNOS/NOS2-deficient (Nos2(-/-)) mice we explored the participation of iNOS/NOS2-derived NO in heart injury in T. cruzi infection. METHODOLOGY: Rhesus monkeys and C57BL/6 and Nos2(-/-) mice were infected with the Colombian T. cruzi strain. Parasite DNA was detected by polymerase chain reaction, T. cruzi antigens and iNOS/NOS2(+) cells were immunohistochemically detected in heart sections and NO levels in serum were determined by Griess reagent. Heart injury was assessed by electrocardiogram (ECG), echocardiogram (ECHO), creatine kinase heart isoenzyme (CK-MB) activity levels in serum and connexin 43 (Cx43) expression in the cardiac tissue. RESULTS: Chronically infected monkeys presented conduction abnormalities, cardiac inflammation and fibrosis, which resembled the spectrum of human chronic chagasic cardiomyopathy (CCC). Importantly, chronic myocarditis was associated with parasite persistence. Moreover, Cx43 loss and increased CK-MB activity levels were primarily correlated with iNOS/NOS2(+) cells infiltrating the cardiac tissue and NO levels in serum. Studies in Nos2(-/-) mice reinforced that the iNOS/NOS2-NO pathway plays a pivotal role in T. cruzi-elicited cardiomyocyte injury and in conduction abnormalities that were associated with Cx43 loss in the cardiac tissue. CONCLUSION: T. cruzi-infected rhesus monkeys reproduce features of CCC. Moreover, our data support that in T. cruzi infection persistent parasite-triggered iNOS/NOS2 in the cardiac tissue and NO overproduction might contribute to CCC severity, mainly disturbing of the molecular pathway involved in electrical synchrony. These findings open a new avenue for therapeutic tools in Chagas' heart disease.

Chronic Trypanosoma cruzi-elicited cardiomyopathy: from the discovery to the proposal of rational therapeutic interventions targeting cell adhesion molecules and chemokine receptors--how to make a dream come true.

One hundred years ago, Carlos Chagas discovered a new disease, the American trypanosomiasis. Chagas and co-workers later characterised the disease's common manifestation, chronic cardiomyopathy, and suggested that parasitic persistence coupled with inflammation was the key underlying pathogenic mechanism. Better comprehension of the molecular mechanisms leading to clinical heart afflictions is a prerequisite to developing new therapies that ameliorate inflammation and improve heart function without hampering parasite control. Here, we review recent data showing that distinct cell adhesion molecules, chemokines and chemokine receptors participate in anti-parasite immunity and/or detrimental leukocyte trafficking to the heart. Moreover, we offer evidence that CC-chemokine receptors may be attractive therapeutic targets aiming to regain homeostatic balance in parasite/host interaction thereby improving prognosis, supporting that it is becoming a non-phantasious proposal.

Chronic Trypanosoma cruzi-elicited cardiomyopathy: from the discovery to the proposal of rational therapeutic interventions targeting cell adhesion molecules and chemokine receptors: how to make a dream come true

One hundred years ago, Carlos Chagas discovered a new disease, the American trypanosomiasis. Chagas and co-workers later characterised the disease's common manifestation, chronic cardiomyopathy, and suggested that parasitic persistence coupled with inflammation was the key underlying pathogenic mechanism. Better comprehension of the molecular mechanisms leading to clinical heart afflictions is a prerequisite to developing new therapies that ameliorate inflammation and improve heart function without hampering parasite control. Here, we review recent data showing that distinct cell adhesion molecules, chemokines and chemokine receptors participate in anti-parasite immunity and/or detrimental leukocyte trafficking to the heart. Moreover, we offer evidence that CC-chemokine receptors may be attractive therapeutic targets aiming to regain homeostatic balance in parasite/host interaction thereby improving prognosis, supporting that it is becoming a non-phantasious proposal.

TNF/TNFR1 signaling up-regulates CCR5 expression by CD8+ T lymphocytes and promotes heart tissue damage during Trypanosoma cruzi infection: beneficial effects of TNF-alpha blockade.

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-alpha) is important for resistance to acute Trypanosoma cruzi infection; however, in patients suffering from chronic T. cruzi infection, plasma TNF-alpha levels correlate with cardiomyopathy. Recent data suggest that CD8-enriched chagasic myocarditis formation involves CCR1/CCR5-mediated cell migration. Herein, the contribution of TNF-alpha, 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-alpha+ 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-alpha 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-alpha-treated infected mice showed regular expression of connexin-43 and reduced fibronectin deposition, respectively. Furthermore, anti-TNF-alpha 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.

TNF/TNFR1 signaling up-regulates CCR5 expression by CD8+ T lymphocytes and promotes heart tissue damage during Trypanosoma cruzi infection: beneficial effects of TNF-á blockade

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-á) is important for resistance to acute Trypanosoma cruzi infection; however, in patients suffering from chronic T. cruzi infection, plasma TNF-á levels correlate with cardiomyopathy. Recent data suggest that CD8-enriched chagasic myocarditis formation involves CCR1/CCR5-mediated cell migration. Herein, the contribution of TNF-á, 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-á+ 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-á 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-á-treated infected mice showed regular expression of connexin-43 and reduced fibronectin deposition, respectively. Furthermore, anti-TNF-á 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.

Infecção crônica experimental de macacos rhesus (Macaca mulatta) pelo Trypanosoma cruzi: caracterização do modelo e imunopatogênese da cardiomiopatia / Rhesus model in the experimental chronic infection for the Trypanosoma cruzi: molecular mechanisms involved in the myocarditis

A doença de Chagas permanece um importante problema de saúde pública em países da América Latina.Modelos experimentais que reproduzam aspectos clínicos e histopatológicos desta doença são essenciais para pesquisas pré-clínicas.Previamente,foi mostrado que a infecção experimental de macacos rhesus com a cepa Colombiana do Trypanosoma cruzi reproduz manifestações clínicas características da fase aguda da doença humana. Assim,em nosso trabalho buscamos caracterizar o modelo de infecção crônica estudando o perfil clínico, parasitológico e alguns aspectos da resposta imune,assim como mecanismos envolvidos na imunopatogênese da cardiomiopatia chagásica.De modo interessante,3 dos 6 animais infectados avaliados desenvolveram alterações eletrocardiográficas 16 anos após a infecção.A persistência do parasito foi detectada no sangue e no tecido em 6 dos 7 animais infectados,nos quais também detectou-se resposta imune celular e anticorpos específicos para o parasito.A caracterização do perfil de ativação imunológica dos animais infectados em relação ao grupo controle mostrou níveis séricos aumentados de metabólitos do óxido nítrico,IL-6 e CCL3/MIP-1α.Quando células mononucleares do sangue periférico(PBMC)foram estimuladas com PMA e ionomicina observou-se no sobrenadante maior produção de IL-1β,IL-4,IL-6,IL-10,TNF-α e IFN-y,CCL2/MCP-1,CCL3/MIP-1α e CXCL8/IL-8 nos macacos infectados.Objetivando caracterizar os mecanismos moleculares envolvidos na imunopatogênese da miocardite chagásica crônica,investigou-se a participação de moléculas de adesão celular,quimiocinas e citocinas. Observou-se o predomínio das células CD3+CD8+ entre as PBMC dos animais cronicamente infectados.Também,estes animais apresentavam maior freqüência de células CD4+CD28-e CD8+CD28-circulantes,comparados aos animais controle. De modo...Assim,no modelo rhesus...parecem estar envolvidas na imunopatogênese da miocardite chagásica crônica,com predomínio de células T CD8+.As citocinas...

Chronic Chagas' disease in rhesus monkeys (Macaca mulatta): evaluation of parasitemia, serology, electrocardiography, echocardiography, and radiology.

Severe chronic damage to the heart and gastrointestinal tract in patients with Chagas' disease are often observed 10-20 years after the acute phase. The course of long-lasting infection with the Colombian strain of Trypanosoma cruzi was studied in seven rhesus monkeys infected for 15-19 years. Subpatent parasitemia was detected in all studied animals, using hemoculture (two of seven), artificial xenodiagnosis (three of seven), and a polymerase chain reaction PCR (six of six). High titers of specific IgG antibody to T. cruzi persisted throughout the chronic phase of infection. Abnormal electrocardiographic (three of six) and echocardiographic (one of six) patterns detected in the T. cruzi-infected monkeys were possibly related to parasite-triggered myocardial damage. The results suggest that rhesus monkeys experimentally infected with T. cruzi, besides reproducing the acute phase of Chagas' disease, also develop chronic chagasic cardiomyopathy.

Anticorpos contra Toxoplasma gondii em estudantes de Medicina Veterinária de Campo Grande, MS, Brasil / Antibodies to Toxoplasma gondii in veterinary medicine students of Campo Grande, MS, Brazil

Amostras de soro obtidas de estudantes do curso de Medicina Veterinária da Universidade para o desenvolvimento do Estado e da Regiäo do Pantanal, Campo Grande, MS, Brasil, foram examinadas para a presença de anticorpos contra Toxoplasma gondii. Dos 145 soros testados, 44 (30,34 por cento) foram positivos na hemaglutinaçäo, com título igual ou superior a 1:16. Näo foram observadas associaçöes entre as características epidemiológicas examinadas tais como hábitos alimentares (ingestäo de carne bovina crua ou malpassada, vegetais crus/näo lavados, produtos lácteos näo pasteurizados) ou contato constante com cäes 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).