Histopathological changes in the liver and stomach of Didelphis virginiana (Didelphimorphia: Didelphidae) during natural infection with Gnathostoma turgidum (Nematoda: Gnathostomidae).

Gnathostoma turgidum is a nematode parasite that exploits the stomach of Virginian opossums, Didelphis virginiana, in Latin America. The opossum is the definitive host of G. turgidum in the wild. Intrahepatic growth and maturation of the parasite, subsequent migration to the stomach and spontaneous expulsion are common. However, the histopathological lesions caused by G. turgidum are poorly described. A better understanding of the life cycle of this parasite and the pathological changes in natural host-parasite interactions could help to clarify the progression of human infections caused by Gnathostoma binucleatum. The aim of this work was to study morphological changes in the liver and stomach of D. virginiana during natural infection and adult worm expulsion. Three opossums naturally infected with G. turgidum were captured from an endemic area of gnathostomosis. Three uninfected opossums captured from a non-endemic area were used as controls. The opossums were sacrificed at different stages of infection (March, May and December), and a histopathological study of their livers and stomachs was conducted. Injuries in livers were observed by histopathology - areas of necrosis and collagen septa were identified. Parasites caused nodules with necrosis on the periphery of lesions, and collagen fibres were also observed in stomachs. Collagen septa may be caused by antigenic remains of the parasite. Further immunological studies are necessary to verify that stimulation is caused by these factors.

Non-typhi Salmonella serovars found in Mexican zoo animals.

The aim of the present study was to determine the bacteriological prevalence of subclinical non-typhi Salmonella infections in zoo animals and to determine the most frequently isolated serovars of the bacteria. A total of 267 samples were analyzed, including fecal samples from zoo animals and rodents, insects (Musca domestica and Periplaneta americana) and samples of the zoo animal's food. Salmonella was detected in 11.6% of the samples analyzed. Characterization of the isolates was performed with serotyping and pulsed-field gel electrophoresis. The following serovars were isolated: S. San Diego, S. Oranienburg, S. Weltevreden, S. Braenderup, S. Derby, S. 6,7, H:en x:- and S. 3,10, H:r:-. The isolates showed seven pulsed-field gel electrophoresis patterns with a Jaccard coefficient≥0.75 indicating a possible common origin. The prevalence of asymptomatic infections caused by Salmonella spp. in zoo animals was high. These findings demonstrate the diversity of Salmonella serovars in several captive wild animal species.

Severe hyperglycemia: a determinant factor for hypofiltration in alloxan diabetic rats.

The relationships among glomerular filtration rate, renal plasma flow and extracellular fluid volume were investigated in control and severely hyperglycemic (442+/-33 mg/dl) untreated, alloxan diabetic ats. Most of diabetic animals showed significant lower values of inulin clearance (diabetics, 0.55+/-0.07 ml/min.100 g; controls, 0.97+/-0.04) and p-aminohippurate clearance (diabetics, 2.11+/-0.39 ml/min.100 g; controls, 3.93+/-0.25). Diabetic rats exhibited reduced efficiency in tubular Na(+) reabsorption, increased urinary Na(+) excretion (diabetics, 3.12+/-0.27 mEq/day; controls, 1.25+/-0.14) and diminished values of plasma renin activity (diabetics, 3.34+/-0.44 ng/ml.h; controls, 8.64+/-0.79). Significant negative correlations were found between glycemia and renal hemodynamic variables. Acute overload with glucose further decreased these variables in both groups: inulin clearance in diabetics vs. controls, 0.26+/-0.04 vs. 0.44+/-0.05 ml/min.100 g; p-aminohippuric acid clearance in diabetics vs. controls, 1.09+/-0.20 vs. 1.55+/-0.21 ml/min.100 g. We conclude that chronically hyperglycemic alloxan diabetic rats showed diminished glomerular filtration rates (inulin clearance), renal plasma flow ( p-aminohippurate clearance) and extracellular fluid volume associated with urinary Na(+) losses and alterations in the renin-angiotensin system. Decreased renin-angiotensin system activity might reduce aldosterone secretion, which in turn could result in (successively) urinary sodium loss, extracellular fluid volume contraction and reductions in glomerular filtration and renal plasma flow.

Identification of CD4+ T cell epitopes of Taenia solium paramyosin.

T cell mediated response is involved in a protective immune response against experimental cysticercosis conferred by immunization with Taenia solium paramyosin (TPmy) to BALB/c mice. In this study, we analysed the TPmy amino acid sequence for predicted CD4+ T cells epitopes. Five different regions of this protein showed that the residues anchor to bind the I-Ad molecule, synthetic peptides containing these epitopes were evaluated for their ability to induce lymphoproliferative responses of spleen cells from TPmy immunized mice. Among them, Tp176 (amino acids 176-192 sequence DDLQRQMADANSAKSRL) was the immunodominant T cell epitope of TPmy. Delineation of this epitope should facilitate analysis of the role of CD4+ T cell response in experimental cysticercosis.

Infection with Trypanosoma cruzi during pregnancy in rats and a decrease in chronic myocardial lesions in their infected offspring.

To ascertain whether maternal infection with Trypanosoma cruzi may influence the course of the parasitic infection in offspring, two groups of female 1 rats were mated with syngeneic sires. One group of females was infected with 10(6) trypomastigotes of T. cruzi three times at weekly intervals. All offspring were nursed by their mothers until weaning and then separated into two groups of young, one to be infected with the same dose of T. cruzi, and the other to remain uninfected. Infection of pregnant rats caused no aggravated disease but resulted in a self-controlled infection that did not cause any deaths or affect their reproductive capacity. The number of young delivered, litter size, fertility coefficient, and offspring weights at weaning were also unaffected by maternal infection; however, the survival coefficient decreased in comparison with values recorded in the offspring of uninfected mothers. The latter finding is likely due to neonatal transmission, since bloodstream forms of T. cruzi were observed in a few offspring of infected mothers. While infected offspring whose mothers had been inoculated with T. cruzi during pregnancy were not protected from acute infection, the occurrence of chronic focal myocarditis was less prevalent when compared with that recorded in chronically infected offspring born to uninfected mothers.

Depressed adjuvant arthritis in rats transferred with spleen cells from Trypanosoma cruzi-infected syngeneic donors.

In the present study we investigated whether the attenuating effect of chronic Trypanosoma cruzi (Tc) infection on adjuvant arthritis (AA) in the rat could be transferred to naive recipients. Transfer of whole spleen cells, but not of serum, from Tc-infected rats reduced AA (means +/- SEM: 11 +/- 0.5) in recipient animals (control values, means +/- SEM: 19 +/- 0.7). Transfer of a T-cell-enriched subpopulation from spleen cells of Tc-infected rats (obtained by filtration through a nylon wool column) resulted in a similar attenuation of AA (means +/- SEM: 7.5 +/- 2.2). The arthritic response of rats intraperitoneally inoculated with 2 x 10(5) Tc 48 h before induction did not differ from that observed in controls. Neither parasites nor specific antibodies were observed in suckling mice inoculated with serum or cell suspensions employed in transfer experiments. Consequently, the depressive effect on AA could not be directly attributed to Tc per se. We hypothesize that a homeostatic immunosuppressor mechanism may be responsible for this phenomenon.

Depressed adjuvant arthritis in rats transferred with spleen cells from Trypanosoma cruzi-infected syngeneic donors

In the present we investigated whether the attenuating effect of chronica Trypanosoma cruzi (Tc) infection on adjuvant arthritis (AA) in the rat could be transferred to naive recipients. Transfer of whole spleen cells, but not of serum, from Tc-infected rats reduced AA (x ñ SEM: 11 ñ 0.5) in recipient animals (control values, x ñ SEM: 19 ñ 0.7). Transfer of a T-cell enriched subpopulation from spleen cells of Tc-infected rats (obtained by filtration through a nylon column) resulted in a similar attenuationb of AA (x ñ SEM: 7.5 ñ 2.2). The arthritic response of rats intraperitoneally inoculated with 2 x 10**5 Tc 48h before induction did not differ from that observed in controls. Neither parasites nor specific antibodies were observed in suckling mice inoculated with serum or cell suspensions employed in transfer experiments. Consequently, the depressive effect on AA could not be directly attributed to Tc per se. We hypothesize that a homeostatic immunosuppressor mechanism may be responsible for this phenomenon