Background Streptococcus anginosus group (SAG) strains are common pathogens causing abscesses and bacteraemia. They are generally susceptible to β-lactams, which constitute first-line treatment. EUCAST recommends testing penicillin G susceptibility to screen for β-lactam resistance. Isolates categorized as susceptible (negative screening) can be reported as susceptible to aminopenicillins and third-generation cephalosporins. Objectives To assess the reliability of penicillin G resistance screening in predicting β-lactam resistance in SAG blood culture isolates, and to investigate isolates for which this test would be unreliable. Methods We determined the susceptibility to penicillin G, amoxicillin and ceftriaxone of 90 SAG blood culture isolates, all with negative penicillin G resistance screening. β-Lactam-resistant strains were sequenced and compared with susceptible reference SAG strains. Results We detected two isolates displaying β-lactam resistance, especially to third-generation cephalosporins, despite negative screening for penicillin G resistance. For these isolates, amino acid substitutions were identified next to the essential PBP motifs SxxK, SxN and/or KS/TGS/T. Changes in these motifs have been previously linked to β-lactam resistance in Streptococcus pneumoniae. Conclusions Our study suggests that aminopenicillin and third-generation cephalosporin susceptibility should be determined for SAG strains in the event of severe infection as screening for penicillin G resistance might not be sufficient to detect resistance mechanisms that predominantly affect cephalosporins. The PBP sequencing of resistant SAG strains allowed us to detect amino acid changes potentially linked to β-lactam resistance.

Double-hit multiple myeloma with atypical "faggot" cellsA 60-year-old woman was diagnosed with kappa light chain multiple myeloma following the investigation of proteinuria and deteriorating general health. There was no cytopenia but rare dystrophic plasma cells (2%) with Auer rod-like inclusions in faggots were present in the blood film (images, May-Gr€ unwald-Giemsa, 9100 objective, left). The same morphology was found in a bone marrow aspirate at diagnosis, displaying 38% of myeloma cells (right). Targeted next generation sequencing of sorted plasma cells revealed a bi-allelic inactivation of TP53 (deletion 17p and TP53 mutation) and the presence of a t(11;14)(q13;q32) translocation. Considering this to be ultra high-risk myeloma, intensive treatment is planned.The presence of Auer rod-like inclusions in myeloma cells has been described previously, particularly in patients with kappa light chain myeloma and adverse cytogenetic abnormalities. The unusual feature of faggots of such inclusions should not lead to confusion with other cells, such as atypical lymphoid cells or the abnormal promyelocytes of acute promyelocytic leukaemia. This easily recognised, rare morphological feature is likely to be a marker of aggressive disease.