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The infectivities of 66 Listeria monocytogenes isolates were assessed by intragastric inoculation of mice. Eight were poorly infective. Serovars 4b and 1/2 were more infective than serovars 3 and 4nonb. A noninfective isolate was cleared more rapidly from the cecum than were infective isolates, suggesting that survival in the gut may relate to infectivity.

The emergence of bacterial pathogens resistant to all known antibiotics is a global health crisis. Adding to this problem is that major pharmaceutical companies have shifted away from antibiotic discovery due to low profitability. As a result, the pipeline of new antibiotics is essentially dry and many bacteria now resist the effects of most commonly used drugs. To address this global health concern, citizen science through the Small World Initiative (SWI) was formed in 2012. As part of SWI, students isolate bacteria from their local environments, characterize the strains, and assay for antibiotic production. During the 2015 fall semester at Bowling Green State University, students isolated 77 soil‐derived bacteria and genetically characterized strains using the 16S rRNA gene, identified strains exhibiting antagonistic activity, and performed an expanded SWI workflow using transposon mutagenesis to identify a biosynthetic gene cluster involved in toxigenic compound production. We identified one mutant with loss of antagonistic activity and through subsequent whole‐genome sequencing and linker‐mediated PCR identified a 24.9 kb biosynthetic gene locus likely involved in inhibitory activity in that mutant. Further assessment against human pathogens demonstrated the inhibition of Bacillus cereus, Listeria monocytogenes, and methicillin‐resistant Staphylococcus aureus in the presence of this compound, thus supporting our molecular strategy as an effective research pipeline for SWI antibiotic discovery and genetic characterization.

Nodal deposits of melanoma may present many years after resection of the primary tumour, implying initial suppression of tumour growth with subsequent immune escape. Using immunocytochemical techniques on frozen sections, the cellular types and activation status of infiltrating cells within a series of 19 clinically apparent nodal metastases of melanoma were studied. Infiltrating cells were assessed using a semiquantitative grading system. Macrophages (CD68+) and T-lymphocytes (CD3+) (including both CD8+ and probably also CD4+ T-cells) were the predominant cells infiltrating the tumours. B-lymphocytes (CD20+) were generally present in low numbers. CD1a+ putative dendritic cell density and expression of the early lymphocyte activation markers interleukin-2 receptor alpha (IL2Ralpha) and CD69 was low. However, greater evidence of intermediate lymphocyte activation (CD38) was identified. Expression of interleukin-2 (IL2) by tumour-infiltrating cells was not detected. The paucity of staining for IL2 and IL2Ralpha, with greater expression of CD38 by infiltrating cells, suggests that the usual pathways of lymphocyte activation via IL2 were bypassed or impaired within the lymph node metastases. Low numbers of CD1a+ putative dendritic cells may result in reduced effector cell activation. These findings provide evidence to support the hypothesis that antitumour immune responses within clinically involved lymph nodes are reduced in metastatic melanoma. This also has possible implications for micrometastases to the sentinel lymph node.

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