ABSTRACT
Guinea pigs (Cavia porcellus) have been reared for centuries in the Andean region for ceremonial purposes or as the main ingredient of traditional foods. The animals are kept in close proximity of households and interact closely with humans; this also occurs in western countries, where guinea pigs are considered pets. Even though it is acknowledged that domestic animals carry pathogenic yeasts in their tissues and organs that can cause human diseases, almost nothing is known in the case of guinea pigs. In this work we used traditional microbiological approaches and molecular biology techniques to isolate, identify, and characterize potentially zoonotic yeasts colonizing the nasal duct of guinea pigs raised as livestock in Southern Ecuador (Cañar Province). Our results show that 44% of the 100 animals studied were colonized in their nasal mucosa by at least eleven yeast species, belonging to eight genera: Wickerhamomyces, Diutina, Meyerozyma, Candida, Pichia, Rhodotorula, Galactomyces, and Cryptococcus. Noticeably, several isolates were insensitive toward several antifungal drugs of therapeutic use, including fluconazole, voriconazole, itraconazole, and caspofungin. Together, our results emphasize the threat posed by these potentially zoonotic yeasts to the farmers, their families, the final consumers, and, in general, to public and animal health.
ABSTRACT
BACKGROUND: Helicobacter pylori is detected by pathogen recognition receptors including toll-like receptors (TLR) and nucleotide-binding oligomerization domain (NOD)-like receptors, eliciting an innate immune response against this bacteria. The aim of this study was to assess if polymorphisms of TLR2, TLR4, TLR5, NOD1 and NOD2 genes are associated with gastric cancer, in particular in individuals infected with H. pylori. RESULTS: A case-control study of 297 gastric cancer patients and 300 controls was performed to assess the association of 17 polymorphisms. Analyses performed under the allele model did not find association with gastric cancer. However, NOD1 rs2075820 (p.E266K) showed association with intestinal-type gastric cancer among H. pylori infected subjects (OR = 2.69, 95% CI 1.41-5.13, p = 0.0026). The association was not statistically significant in diffuse-type gastric cancer cases (OR = 1.26, 95% CI 0.63-2.52, p = 0.51). When the analyses were performed in patients carrying H. pylori strains harboring the cag pathogenicity island (cagPAI), we noticed significant association with NOD1 rs2075820 (OR = 4.90, 95% CI 1.80-3.36, p = 0.0019), in particular for intestinal-type gastric cancer cases (OR = 7.16, 95% CI 2.40-21.33, p = 4.1 × 10- 4) but not among diffuse-type gastric cancer cases (OR = 3.39, 95% CI 1.13-0.10, p = 0.03). CONCLUSIONS: NOD1 rs2075820 increases the risk of intestinal-type gastric cancer among individuals infected with H. pylori, particularly in those harboring the cagPAI.
Subject(s)
Helicobacter Infections , Nod1 Signaling Adaptor Protein/genetics , Stomach Neoplasms , Case-Control Studies , Genomic Islands , Helicobacter Infections/genetics , Helicobacter pylori , Humans , Stomach Neoplasms/geneticsABSTRACT
BACKGROUND: Helicobacter pylori is detected by pathogen recognition receptors including toll-like receptors (TLR) and nucleotide-binding oligomerization domain (NOD)-like receptors, eliciting an innate immune response against this bacteria. The aim of this study was to assess if polymorphisms of TLR2, TLR4, TLR5, NOD1 and NOD2 genes are associated with gastric cancer, in particular in individuals infected with H. pylori. RESULTS: A case-control study of 297 gastric cancer patients and 300 controls was performed to assess the association of 17 polymorphisms. Analyses performed under the allele model did not find association with gastric cancer. However, NOD1 rs2075820 (p.E266K) showed association with intestinal-type gastric cancer among H. pylori infected subjects (OR = 2.69, 95% CI 1.41-5.13, p = 0.0026). The association was not statistically significant in diffuse-type gastric cancer cases (OR = 1.26, 95% CI 0.63-2.52, p = 0.51). When the analyses were performed in patients carrying H. pylori strains harboring the cag pathogenicity island (cagPAI), we noticed significant association with NOD1 rs2075820 (OR = 4.90, 95% CI 1.80-3.36, p = 0.0019), in particular for intestinal-type gastric cancer cases (OR = 7.16, 95% CI 2.40-21.33, p = 4.1 × 10- 4) but not among diffuse-type gastric cancer cases (OR = 3.39, 95% CI 1.13-0.10, p = 0.03). CONCLUSIONS: NOD1 rs2075820 increases the risk of intestinal-type gastric cancer among individuals infected with H. pylori, particularly in those harboring the cagPAI.
Subject(s)
Humans , Stomach Neoplasms/genetics , Helicobacter Infections/genetics , Nod1 Signaling Adaptor Protein/genetics , Case-Control Studies , Helicobacter pylori , Genomic IslandsABSTRACT
Se presentan los resultados del estudio de la secreción de insulina y hormona de crecimiento en 20 niños con antecedentes de DPE y retraso pondoestatual actual de causa nutricional. Se realizó, en pacientes y controles prueba de tolerancia a la glucosa, en la cual se midió: glicemia, insulina, área total de glicemia y de insulina y constante K. al evaluar estos resultados no se encontró alteración en el metabolismo de hidratos de carbono. Se analizó también en estos niños la secreción de GH a través de la prueba de sensibilidad a la insulina. Se concluyó que nuestros pacientes tenían una deficiencia parcial de GH; a su vez se insiste en la necesidad de la evaluación de esta condición en todo niño con antecedentes de DPE y retraso estatural importante (AU)
Subject(s)
Child, Preschool , Child , Adolescent , Humans , Male , Female , Growth Hormone/blood , Insulin/blood , Growth Hormone , Protein-Energy Malnutrition , Body Weight , Body Height , Insulin/metabolism , Growth Hormone/metabolismABSTRACT
Se presentan los resultados del estudio de la secreción de insulina y hormona de crecimiento en 20 niños con antecedentes de DPE y retraso pondoestatual actual de causa nutricional. Se realizó, en pacientes y controles prueba de tolerancia a la glucosa, en la cual se midió: glicemia, insulina, área total de glicemia y de insulina y constante K. al evaluar estos resultados no se encontró alteración en el metabolismo de hidratos de carbono. Se analizó también en estos niños la secreción de GH a través de la prueba de sensibilidad a la insulina. Se concluyó que nuestros pacientes tenían una deficiencia parcial de GH; a su vez se insiste en la necesidad de la evaluación de esta condición en todo niño con antecedentes de DPE y retraso estatural importante
