Aporocotyle mariachristinae n. sp., and A. ymakara Villalba & Fernández, 1986 (Digenea: Aporocotylidae) of the pink cusk-eel, Genypterus blacodes (Ophidiiformes: Ophidiidae) from Patagonia, Argentina.

Aporocotyle mariachristinae n. sp. and A. ymakara Villalba & Fernández, 1986 were collected from the bulbus arteriosus and ventral aorta of pink cusk-eels, Genypterus blacodes (Forster, 1801) from Patagonia, Argentina. A. mariachristinae n. sp. can be distinguished from all the species of Aporocotyle by the asymmetrical extension of posterior caeca (right posterior caecum longer, terminating at the area between mid-level of ovary and posterior body end; left posterior caecum shorter, terminating at the area between mid-level of cirrus sac and posterior to reproductive organs), the distribution of spines along the ventro-lateral body margins and the number of testes. The new species clearly differs from A. ymakara, from the same host species, in the esophagus / body length ratio, the absence of distal loops at caeca, the anterior caeca / posterior caeca length ratio, and the number of testes. Additionally, in A. ymakara the left posterior caecum may be longer than right posterior caecum, while in the new species left posterior caecum is always shorter. The specimen of A. ymakara collected from Argentina is also described. We also provide observations of the distribution of spines in different species of Aporocotyle, including new specimens of A. argentinensis Smith, 1969 from Merluccius hubbsi Marini, 1933. Molecular sequence data obtained from partial 18S and 28S rDNA regions were compared between the new species and other two species of Aporocotyle (A. argentinensis and A. spinosicanalis Williams, 1958). This is a new locality record for A. ymakara, extending the known geographical distribution for this species from Chile to Argentina, and the first report of two species of Aporocotyle in the same host species and locality.

Altered vascular reactivity induced by malaria parasites.

OBJECTIVE: In this study, we have examined the possibility that there is altered vascular reactivity due to the direct interaction between parasitized erythrocytes and vascular endothelial cells. METHOD: Ring preparations of rat aorta were studied using standard in vitro techniques, the rings were mounted in 20 ml organ baths containing PSS under an initial load of 1 g, maintained at 37 degrees C at pH 7.4 and isometric contractions were recorded electronically. Rings were allowed 90 minutes to equilibrate before the commencement of the various protocols: Dose responses to phenylephrine (PE) and other vasoactive agents (high-K+). Acetylcholine (Ach)--induced relaxation in phenylephrine-contracted rings (pre-contraction was induced by EC70 concentration of phenylephrine). Ach-induced relaxation in PE-precontracted, endothelium-denuded rings. Also, relaxation responses to acetylcholine was investigated through application of a single. (EC70) concentration of acetylcholine in rings exposed to blood with varying concentrations and dilutions of parasitized blood and varying durations of exposure. RESULTS: Incubation with parasitized blood resulted in a significant increase in maximum contractile response to phenylephrine in the rat aortic rings (p < 0.05) but no effect to the base line. Analysis of the whole dose-response curve (using paired t-test) showed a significant left-ward shift following the addition of parasitized blood (p < 0.05), EC70 (M) values increasing from 7 x 10(-7) to 5 x 10(-6)M. Following exposure to parasitized blood, the magnitude of Ach-induced relaxation responses reduced significantly from 73 +/- 3.6 to 24.75 +/- 7.25% in rat aortic rings (p < 0.05). Ach relaxations were significantly enhanced (p < 0.05) at 5-minute exposure; however at longer durations, Ach-relaxations were variable and inconsistent. The lesser the dilution, due to increased volume of parasitized blood, the lesser the relaxation response. Following endothelium removal, there was a marked impairment in endothelium-dependent relaxation responses to ACh in both the control and incubated vessels. Exposure to parasitized blood did not significantly alter contractile responses induced by potassium depolarization. CONCLUSIONS: This gives evidence in support of an endothelium-dependent action of malaria parasites as vascular effects of malaria parasites are mediated, at least in part, via endothelium-dependent mechanism(s).

Altered vascular reactivity induced by malaria parasites / Reactividad vascular alterada inducida por los parásitos de la malaria

OBJECTIVES: In this study, we have examined the possibility that there is altered vascular reactivity due to the direct interaction between parasitized erythrocytes and vascular endothelial cells. METHOD: Ring preparations of rat aorta were studied using standard in vitro techniques, the rings were mounted in 20 ml organ baths containing PSS under an initial load of 1g, maintained at 37ºC atpH 7.4 and isometric contractions were recorded electronically. Rings were allowed 90 minutes to equilibrate before the commencement of the various protocols: * Dose responses to phenylephrine (PE) and other vasoactive agents (high-K+) * Acetylcholine (Ach) -induced relaxation in phenylephrine-contracted rings (pre-contraction was induced by EC70 concentration of phenylephrine) * Ach-induced relaxation in PE-precontracted, endothelium-denuded rings * Also, relaxation responses to acetylcholine was investigated through application ofa single (EC7o) concentration of acetylcholine in rings exposed to blood with varying concentrations and dilutions ofparasitized blood and varying durations ofexposure. RESULTS: Incubation with parasitized blood resulted in a significant increase in maximum contractile response to phenylephrine in the rat aortic rings (p < 0.05) but no effect to the base line. Analysis of the whole dose-response curve (using paired t-test) showed a significant left-ward shift following the addition of parasitized blood (p < 0.05), EC70 (M) values increasing from 7 x 10-7 to 5 x 10-6M. Following exposure to parasitized blood, the magnitude ofAch-induced relaxation responses reduced signi ficantlyfrom 73 ± 3.6 to 24.75 ± 7.25% in rat aortic rings (p < 0.05). Ach relaxations were significantly enhanced (p < 0.05) at 5-minute exposure; however at longer durations, Ach-relaxations were variable and inconsistent. The lesser the dilution, due to increased volume of parasitized blood, the lesser the relaxation response. Following endothelium removal, there was a marked impairment in endothelium-dependent relaxation responses to ACh in both the control and incubated vessels. Exposure to parasitized blood did not significantly alter contractile responses induced by potassium depolarization. CONCLUSIONS: This gives evidence in support of an endothelium-dependent action of malaria parasites as vascular effects ofmalaria parasites are mediated, at least in part, via endothelium-dependent mechanism(s).

OBJETIVO: En este estudio, hemos examinado la posibilidad de que exista una reactividad vascular alterada debido a la interacción directa entre los eritrocitos parasitados y las células endoteliales vasculares. MÉTODO: Se estudiaron preparaciones de anillo de aorta de rata usando técnicas in vitro estándar. Los anillos fueron montados en baños de órgano de 20 ml que contenían solución salina fisiológica (SSF) con una carga inicial de 1g, mantenida a 37ºC con un pH de 7.4, y las contracciones isométricas fueron registradas electrónicamente. A los anillos se les dio un tiempo de 90 minutos para permitir que se equilibraran, antes del comienzo de los varios protocolos. * Respuestas a la dosis de fenilefrina (FE) y otros agentes vasoactivos (K+ alto) * Relajación inducida mediante acetilcolina (Ac) en los anillos contraídos con fenilefrina (la precontracción fue inducida mediante una concentración EC70 de fenilefrina) * Relajación inducida mediante Ac en anillos despojados de endotelio. Pre-contraídos con FE. * También, se investigaron las respuestas de relajación a la acetilcolina a través de la aplicación de una sola concentración (EC70) de acetilcolina en anillos expuestos a la sangre con diversas concentraciones y diluciones de sangre parasitada y distintas duraciones de exposición. RESULTADOS: La incubación con sangre parasitada tuvo como resultado un aumento significativo en la respuesta contráctil máxima a la fenilefrina en los anillos aórticos de las ratas (p < 0.05) pero ningún efecto a la línea de base. El análisis de toda la curva de respuesta a la dosis (usando la prueba t pareada) mostró un desplazamiento significativo hacia la izquierda tras la adición de sangre parasitada (p < 0.05), EC70 (M), aumentado los valores de 7 x 10-7 a 5 x 10-6M. Tras la exposición a la sangre parasitada, la magnitud de las respuestas a la relajación inducida por Ac se redujo significativamente de 73 ± 3.6 a 24.75 ± 7.25% en los anillos aórticos de ratas (p < 0.05). Las relajaciones por Ac mejoraron significativamente (p < 0.05) a los 5 minutos de exposición. Sin embargo, a duraciones más largas, las relajaciones por Ac fueron variables e inconstantes. Mientras menor era la dilución, debido al aumento de volumen de la sangre parasitada, menor era la respuesta de relajación. Una vez retirado el endotelio, se producía un marcado deterioro en las respuestas de relajación dependiente del endotelio, ante el Ac, tanto en los recipientes de control como en los encubados. La exposición a la sangre parasitada no alteró de manera significativa las respuestas contráctiles inducidas por la despolarización del potasio. CONCLUSIONES: Esto provee evidencias en apoyo a una acción dependiente del epitelio, por parte de los parásitos de la malaria, por cuanto los efectos vasculares de los parásitos de la malaria se hallan mediados, al menos en parte, por los mecanismos dependientes del endotelio.

Aortic distensibility measured by pulse-wave velocity is not modified in patients with Chagas' disease.

BACKGROUND: Experimental studies demonstrate that infection with trypanosoma cruzi causes vasculitis. The inflammatory lesion process could hypothetically lead to decreased distensibility of large and small arteries in advanced Chagas' disease. We tested this hypothesis. METHODS AND RESULTS: We evaluated carotid-femoral pulse-wave velocity (PWV) in 53 Chagas' disease patients compared with 31 healthy volunteers (control group). The 53 patients were classified into 3 groups: 1) 16 with indeterminate form of Chagas' disease; 2) 18 with Chagas' disease, electrocardiographic abnormalities, and normal systolic function; 3) 19 with Chagas' disease, systolic dysfunction, and mild-to-moderate congestive heart failure. No difference was noted between the 4 groups regarding carotid-femoral PWV (8.4 +/- 1.1 vs 8.2 +/- 1.5 vs 8.2 +/- 1.4 vs 8.7 +/- 1.6 m/s, P = 0.6) or pulse pressure (39.5 +/- 7.6 vs 39.3 +/- 8.1 vs 39.5 +/- 7.4 vs 39.7 +/- 6.9 mm Hg, P = 0.9). A positive, significant, similar correlation occurred between PWV and age in patients with Chagas' disease (r = 0.42, P = 0.002), in controls (r = 0.48, P = 0.006), and also between PWV and systolic blood pressure in both groups (patients with Chagas' disease, r = 0.38, P = 0.005; healthy subjects, r = 0.36, P = 0.043). CONCLUSION: Carotid femoral pulse-wave velocity is not modified in patients with Chagas' disease, suggesting that elastic properties of large arteries are not affected in this disorder.

Treatment with mebendazole is not associated with distal migration of adult Angiostrongylus costaricensis in the murine experimental infection.

Abdominal angiostrongyliasis is a zoonotic infection produced by a metastrongylid intra-arterial nematode, Angiostrongylus costaricensis. Human accidental infection may result in abdominal lesions and treatment with anti-helminthics is contra-indicated because of potential higher morbidity with excitement or death of worms inside vessels. To evaluate the effect of mebendazole on localization of the worms, male Swiss mice, 5 week-old, were infected with 10 third stage larvae per animal. Twelve infected mice were treated with oral mebendazol, at 5 mg/kg/day, for 5 consecutive days, begining 22 days after inoculation. As control groups, 12 infected but non-treated mice and other 12 non-infected and non-treated mice were studied. The findings at necropsy were, respectively for the treated (T) and control (C) groups: 92% and 80% of the worms were inside the cecal mesenteric arterial branch; 8% and 10% were located inside the aorta. Only in the group C some worms (10%) were found inside the portal vein or splenic artery. These data indicate that treatment with mebendazole does not lead to distal or ectopic migration of A. costaricensis worms.

Long-term observations on mouse strains experimentally infected with Angiostrongylus costaricensis.

BALB/c and C57BL/6 mice were experimentally infected with Angiostrongylus costaricensis and the parasitic parameters and antibody response during the acute and chronic phases of infection were analyzed. Following administration of six third-stage larvae (L3), there was no significant difference in the mean worm recovery or mean larval output. Coinciding with the maturation of worms in infected animals and with the egg output in mesenteric arteries, a strong increase in the humoral immune response was observed in both mouse strains. This response was characterized by a hypergammaglobulinemia, with a predominance of IgA and IgG1 during the acute phase of infection, and IgG1 and total IgE during the patent and post-patent periods. Significantly higher levels of IgM, IgG and IgG1 were found in BALB/c mice compared with C57BL/6 mice. On the other hand, a significantly higher concentration of IgA was detected at 6 and 7 weeks post-infection in C57BL/6 mice compared with BALB/c mice. Specific IgE could not be detected in any of the mouse strains. Our results suggest that immunoglobulins, mainly IgG1, contribute to the outcome of a primary A. costaricensis infection with respect to the period of patency and to mortality during the chronic phase.

Infection with Toxoplasma gondii increases atherosclerotic lesion in ApoE-deficient mice.

Toxoplasma gondii is an intracellular protozoan that elicits a potent inflammatory response during the acute phase of infection. Herein, we evaluate whether T. gondii infection alters the natural course of aortic lesions. ApoE knockout mice were infected with T. gondii, and at 5 weeks of infection, serum, feces, and liver cholesterol; aortic lesion size, cellularity, and inflammatory cytokines; and levels of serum nitrite and gamma interferon (IFN-gamma) were analyzed. Our results showed that serum cholesterol and atherogenic lipoproteins were reduced after T. gondii infection. The reduction of serum levels of total cholesterol and atherogenic lipoproteins was associated with increases in the aortic lesion area, numbers of inflammatory cells, and expression of monocyte chemoattractant protein 1 and inducible nitric oxide synthase mRNA in the site of lesions as well as elevated concentrations of IFN-gamma and nitrite in sera of T. gondii-infected animals. These results suggest that infection with T. gondii accelerates atherosclerotic development by stimulating the proinflammatory response and oxidative stress, thereby increasing the area of aortic lesion.

Phyllocaulis variegatus--an intermediate host of Angiostrongylus costaricensis in south Brazil.

Molluscs collected in five localities in the State of Rio Grande do Sul (Brazil) were digested and examined. The infected slugs were identified as Phyllocaulis variegatus and the larvae found were inoculated per os into mice. After 50 days, worms with the caracteristics of Angiostrongylus costaricensis were recovered from the mesenteric arterial system. The results establish the role of P. variegatus as intermediate host of A. costaricensis in south Brazil, where many cases of abdominal angiostrongyliasis have been diagnosed.