Natural antibiotic susceptibility of Listeria species: L. grayi, L. innocua, L. ivanovii, L. monocytogenes, L. seeligeri and L. welshimeri strains

Objective   To investigate the natural susceptibility to 71 antimicrobial agents of 103 Listeria strains belonging to all known Listeria species ( L. monocytogenes ( N  = 21), L. innocua ( N  = 21), L. seeligeri ( N  = 21), L. ivanovii ( N  = 19), L. welshimeri ( N  = 11), and L. grayi ( N  = 10)).
Methods   MICs were determined using a microdilution procedure in H-Medium.
Results   All listeriae were naturally sensitive or intermediate to tetracyclines, aminoglycosides, penicillins (except oxacillin), loracarbef, cefazoline, cefaclor, cefotiam, cefoperazone, carbapenems, macrolides, lincosamides, glycopeptides, dalfopristin/quinupristin, chloramphenicol and rifampicin (probably except L. grayi ). Listeria spp. were naturally resistant or intermediate to most 'modern' cephalosporins (cefetamet, cefixime, ceftibuten, ceftazidime, cefdinir, cefpodoxime, cefotaxime, ceftriaxone, cefuroxime), aztreonam, pipemidic acid, dalfopristin quinupristin and sulfamethoxazole. Significant differences in natural susceptibility among the species were seen with the quinolones, trimethoprim, co-trimoxazole, rifampicin, fosfomycin and fusidic acid. It seems likely that L. grayi is naturally resistant to all antifolates; the species was least susceptible to rifampicin and most susceptible to quinolones, whereas L. ivanovii was naturally resistant to most quinolones. L. ivanovii was naturally sensitive to fosfomycin, whereas L. innocua and L. monocytogenes were naturally resistant. L. ivanovii was also the most susceptible species to fusidic acid.
Conclusions   The present study describes a database on the natural susceptibility of Listeria spp. to a wide range of antibiotics, which can be used to validate susceptibility testing results of these microorganisms.     

Phenotypic spectrum associated with SPECC1L pathogenic variants: new families and critical review of the nosology of Teebi,Opitz GBBB,and Baraitser-Winter syndromes

The SPECC1L protein plays a role in adherens junctions involved in cell adhesion, actin cytoskeleton organization, microtubule stabilization, spindle organization and cytokinesis. It modulates PI3K-AKT signaling and controls cranial neural crest cell delamination during facial morphogenesis. SPECC1L causative variants were first identified in individuals with oblique facial clefts. Recently, causative variants in SPECC1L were reported in a pedigree reported in 1988 as atypical Opitz GBBB syndrome. Six families with SPECC1L variants have been reported thus far. We report here eight further pedigrees with SPECC1L variants, including a three-generation family, and a further individual of a previously published family. We discuss the nosology of Teebi and GBBB, and the syndromes related to SPECC1L variants. Although the phenotype of individuals with SPECC1L mutations shows overlap with Opitz syndrome in its craniofacial anomalies, the canonical laryngeal malformations and male genital anomalies are not observed. Instead, individuals with SPECCL1 variants have branchial fistulae, omphalocele, diaphragmatic hernias, and uterus didelphis. We also point to the clinical overlap of SPECC1L syndrome with mild Baraitser-Winter craniofrontofacial syndrome: they share similar dysmorphic features (wide, short nose with a large tip, cleft lip and palate, blepharoptosis, retrognathia, and craniosynostosis), although intellectual disability, neuronal migration defect, and muscular problems remain largely specific to Baraitser-Winter syndrome. In conclusion, we suggest that patients with pathogenic variants in SPECC1L should not be described as “dominant (or type 2) Opitz GBBB syndrome”, and instead should be referred to as “SPECC1L syndrome” as both disorders show distinctive, non overlapping developmental anomalies beyond facial communalities.     

Lésions thalamiques médianes et effects différentiels dans les apprentissages operants

In the albino rat, lesion of the centrum - medianum - parafascicularis complex of the thalamus (CM/PF) leads to a significant response rate increase in variable interval (VI 2 min) and differential reinforcement of low rates schedules (DRL 20 sec). Furthermore, there is a significant decrease in the number of reinforcements obtained in the DRL schedule. The same lesion remains without effect on a fixed interval schedule (FI 2 min). This differential effect is interpreted on the basis of schedule structure analysis. This analysis, confirmed by studies on the role of stimulations linked to reiforcement distribution, allows a reinterpretation of CM/PF lesion effects on operant or instrumental behavior with both positive and negative reinforcement.