High-level resistance to gentamicin: genetic transfer between Enterococcus faecalis isolated from food of animal origin and human microbiota.

AIMS: To investigate the in vivo gene transfer of high-level gentamicin resistance (HLRG) from Enterococcus faecalis isolated from the food of animal origin to a human isolate, using a mouse model of intestinally colonized human microbiota. METHODS AND RESULTS: In vitro study: The presence of plasmids involved in HLRG coding was investigated. After the conjugation experiment, the recipient strain, Ent. faecalis JH2-SS, acquired a plasmid responsible for HLRG [minimal inhibitory concentration (MIC) >800 µg ml(-1) ], in a similar position to the donor cells. In vivo study: Seven BALB/c mice were dosed with ceftriaxone (400 mg kg(-1) ) and then inoculated with a dilution of 1/100 of human faeces (HFc). After 72 h, Ent. faecalis JH2-SS (recipient) was inoculated and then, after a further 72 h, the animals were given Ent. faecalis CS19, isolated from the food of animal origin, involved in HLRG (donor). The presence of transconjugant strains in HFc was subsequently recorded on a daily basis until the end of the experiment. The clonal relationship between Ent. faecalis and Escherichia coli in faeces was assessed by RAPD-PCR. Both the in vitro and in vivo studies showed that the receptor strain acquired a plasmid responsible for HLRG (MICs >800 µg ml(-1) ), which migrated with a similar relative mobility value. Transconjugant strains were detected from 24 h after the donor strain inoculation and persisted until the end of the experiment. CONCLUSIONS: The in vivo gene transfer of HLRG from Ent. faecalis strains, isolated from the food of animal origin, to human microbiota has been demonstrated in a mouse model. SIGNIFICANCE AND IMPACT OF THE STUDY: The complexity found on the therapeutic responses of invasive infectious diseases caused by Ent. faecalis facilitates the assessment of food of animal origin as a resistant pathogen reservoir. In addition, this study may contribute to the understanding of antimicrobials' resistance gene transfer between Ent. faecalis strains from food and human GI tract.

[History of blood platelets: from "molecules" to "cell"]. / Histoire des plaquettes sanguines: des "molécules" à la "cellule".

Historical annotations attached to the discovery of platelets as blood cells throughout the 19th century are reported. The so-called "minute molecules" were first connected with the formation of red and white blood cells, or of fibrin as well. The active role of platelets in coagulation was recognized only 30 years later. During that time, it became clear that these "molecules" were "cells", anatomical and physiological entities.

Discovery of the red blood cell with notes on priorities and credits of discoveries, past, present and future.

A review of the earliest publications and letters of the scientists who have received credit for the first description of red cells illustrates the philosophical and practical difficulties of assigning priorities for discoveries. A knowledge of the scientific and cultural ambience of the day, of reports of scientific contemporaries or predecessors, both partisans and adversaries, and other background information illustrates how the consensus in crediting the discovery originated. However, the broader question remains: what are the proper criteria for assigning priority of discovery, yesterday, today and tomorrow?

Sickle cell shape and structure: images and concepts (1840-1980).

I. First observations of "crescentic particles" in animals. II. The first five descriptions of sickle shaped red cells in man. III. Relationship of sickling to the state of oxygenation of the hemoglobin. a) Forerunners: the sickling is reversible. b) Discoverers: sickling as result of asphyxia. IV. Sickle cell trait ("latent sickling"). V. Presence of hemoglobin rod-like structures in sickle cells. a) Indirect evidence. b) Observation of the surface of the cells by electron-microscope shadow casting technique. c) Electron microscopy of the interior of the cells. VI. Irreversible sickle cells. VII. Heterogeneity of sickling disorders. a) Association with other hemolytic anemias. b) Non-Hb S sickling. c) Factitious sickle cell shapes. VIII. Myelin forms and agglutination of sickle-cells. IX. Sickle cell shapes. a) Drepanocytes: mechanism of formation. b) Discodrepanocytes (holly-leaf forms). c) Echino-drepanocytes. d) Stomato-drepanocytes. e) Sphero-drepanocytes.