Scombroid Poisoning: A Practical Approach. / Escombroidosis: abordaje práctico.

Scombroid poisoning is a common cause of food poisoning worldwide. It is caused by ingestion of oily fish contaminated with bacteria that trigger the formation of high concentrations of histamine. Scombroid poisoning manifests mainly as a skin complaint (flushing that spreads downward and/or an erythematous urticarial rash affecting the face and upper trunk). Although the clinical course is usually self-limiting and benign, vascular compromise, bronchospasm, and arrhythmias have been described. It is important to establish a differential diagnosis that includes conditions such as fish allergy. Oral antihistamines are the mainstay of treatment. Scombroid poisoning is best prevented by refrigerating fish properly. The practical review of scombroid poisoning provided here is intended for dermatologists.

Toxicology tailored low density oligonucleotide microarray for the thicklip grey mullets (Chelon labrosus): Biomarker gene transcription profile after caging in a polluted harbour.

In aquatic organisms inhabiting polluted waters genes are activated to build an adaptive/compensatory defence against the possible effects of pollutants. Such responses can be used as biomarkers of exposure to chemical compounds, outlining the molecular mechanisms activated under specific pollution scenarios. With the aim of exploiting such approach in environmental health assessment, toxicologically relevant gene fragments were sequenced in the thicklip grey mullet (Chelon labrosus) and a toxicologically tailored low-density (160 genes) oligonucleotide microarray was customised. The tool was validated comparing organ/sex specific gene expression profiles and characterising responses under laboratory exposure to model chemicals. Finally, juvenile mullets were caged in a polluted harbour and hepatic gene expression profiles analysed after 5 and 21 days of deployment. Cages were deployed in the inner (IH) and outer (OH) Pasaia harbour, Bay of Biscay. Mussels (Mytilus galloprovincialis) were also caged as biological matrix for chemical bioaccumulation analysis and stress biomarkers measurements. Slightly higher concentrations of chemicals (metals, tributyltin, PAHs, phthalates) were quantified in IH than in OH, fish bile metabolites also revealing higher availability of PAHs in IH. Lysosome membrane stability in mussels was reduced, indicating stress condition in both sites. The developed microarray discriminated mullets showing distinctive expression profiles depending on site and deployment time. Genes related to immune and hypoxia responses were regulated comparing IH and OH at day 5. Phase I and II biotransformation genes, such as cyp2, cyp3 and ugt, were up-regulated in IH, together with the aryl hydrocarbon receptor 2 (ahr2) and the ahr repressor. Similarly, TBT-binding proteins and genes involved in lipid metabolism (pparγ, cyp7) were up-regulated with deployment time. Even if nowadays higher throughput approaches for gene expression analyses are available, the developed mullet tool constitutes a comprehensive tool to assess molecular responses of mullets exposed to pollutants, although it remains to be explored whether it can be applied to assess pollutant exposure in active pollution monitorings and in environmental health assessment.

Zonation in the digestive tract of Eisenia fetida: implications in biomarker measurements for toxicity assessment.

Eisenia fetida is a model species for soil health assessment and different biomarkers that detect either the presence of bioavailable contaminants or their biological effect have been developed. These parameters are performed in a target tissue or whole earthworm, without considering the marked zonation in histological organisation, enzyme activities and gene expression pattern existing along the body. Thus, the present work was aimed at (a) characterising the morphofunctional heterogeneity along the digestive tract of E. fetida in tissue morphology and turnover, lysosomal enzyme markers (ß-glucuronidase, ß-GUS; hexosaminidase, HEX), lipofuscin contents (LPF) and metallothionein (MT) and catalase (CAT) gene expression; and (b) determining whether the responsiveness to Cd exposure varies among tissues and along the digestive tract. HEX and ß-GUS exhibited a heterogeneous distribution pattern along and across the digestive tract and Cd exposure caused a marked decrease of HEX and an increase of ß-GUS activity. Likewise, the significant decrease of cell turnover and the induction of MT transcription were was zone-dependent. Therefore, in was concluded that the consideration of the zonation when applying biomarker for toxicity assessment would reduce the intrinsic variability that results from overlooking the marked morphofunctional heterogeneity that exists in annelids along their body axis.

Construction and characterization of a forward subtracted library of blue mussels Mytilus edulis for the identification of gene transcription signatures and biomarkers of styrene exposure.

Transcriptional profiling can elucidate adaptive/toxicity pathways participating in achieving homeostasis or leading to pathogenesis in marine biota exposed to chemical substances. With the aim of analyzing transcriptional responses in the mussel Mytilus edulis exposed to the corrosive and putatively carcinogenic hydrocarbon styrene (3-5 ppm, 3days), a forward subtracted (SSH) cDNA library was produced. Female mussels were selected and digestive gland mRNA was isolated. A library with 1440 clones was produced and a total of 287 clones were sequenced, 53% being identified through BlastN analysis against Mytibase and DeepSeaVent databases. Those genes included GO terms such as 'response to drugs', 'immune defense' and 'cell proliferation'. Furthermore, sequences related to chitin and beta-1-3-glucan metabolism were also up-regulated by styrene. Many of the obtained sequences could not be annotated constituting new mussel sequences. In conclusion, this SSH study reveals novel sequences useful to generate molecular biomarkers of styrene exposure in mussels.

Escombroidosis: abordaje práctico / Scombroid Poisoning: A Practical Approach

La escombroidosis es una causa frecuente de intoxicación alimentaria a nivel mundial que se debe a la ingesta de pescado azul contaminado con bacterias que inducen la formación de grandes cantidades de histamina. Clínicamente se manifiesta sobre todo a nivel cutáneo, en forma de flushing descendente y/o rash eritemato-urticariforme facial y en el tronco superior. Aunque habitualmente tiene un curso autolimitado y benigno, pueden existir casos de compromiso vascular, broncoespasmo y arritmias. Es importante hacer un correcto diagnóstico diferencial, entre otros con la alergia al pescado. El tratamiento se basa en la administración de antihistamínicos orales. Lo más importante es su prevención mediante una correcta refrigeración del pescado. Este trabajo es una revisión práctica de la escombroidosis orientada para su uso por el dermatólogo

Scombroid poisoning is a common cause of food poisoning worldwide. It is caused by ingestion of oily fish contaminated with bacteria that trigger the formation of high concentrations of histamine. Scombroid poisoning manifests mainly as a skin complaint (flushing that spreads downward and/or an erythematous urticarial rash affecting the face and upper trunk). Although the clinical course is usually self-limiting and benign, vascular compromise, bronchospasm, and arrhythmias have been described. It is important to establish a differential diagnosis that includes conditions such as fish allergy. Oral antihistamines are the mainstay of treatment. Scombroid poisoning is best prevented by refrigerating fish properly. The practical review of scombroid poisoning provided here is intended for dermatologists

Father-to-newborn transmission of herpes simplex virus infection: a sweet but bitter kiss / Herpes neonatal tras contacto con herpes labial paterno: dulce y amargo beso

No disponible

FR - Síndrome de Stevens-Johnson y necrólisis epidérmica tóxica. Actualización en el manejo terapéutico / RF - Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: A Treatment Update

No disponible