This narrative review seeks to examine the relationships between bacterial microbiomes and infectious disease. This is achieved by detailing how different human host microbiomes develop and function, from the earliest infant acquisitions of maternal and environmental species through to the full development of microbiomes by adulthood. Communication between bacterial species or communities of species within and outside of the microbiome is a factor in both maintenance of homeostasis and management of threats from the external environment. Dysbiosis of this homeostasis is key to understanding the development of disease states. Several microbiomes and the microbiota within are used as prime examples of how changes in species composition, particularly at the phylum level, leads to such diverse conditions as inflammatory bowel disease (IBD), type 2 diabetes, psoriasis, Parkinson’s disease, reflux oesophagitis and others. The review examines spatial relationships between microbiomes to understand how dysbiosis in the gut microbiome in particular can influence diseases in distant host sites via routes such as the gut–lung, gut–skin and gut–brain axes. Microbiome interaction with host processes such as adaptive immunity is increasingly identified as critical to developing the capacity of the immune system to react to pathogens. Dysbiosis of essential bacteria involved in modification of host substrates such as bile acid components can result in development of Crohn’s disease, small intestine bacterial overgrowth, hepatic cancer and obesity. Interactions between microbiomes in distantly located sites are being increasingly being identified, resulting in a ‘whole of body’ effect by the combined host microbiome.

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The Vibrio pathogenicity island (VPI) in epidemic Vibrio cholerae is an essential virulence gene cluster. The VPI can excise from the chromosome and form extrachromosomal circular excision products. The VPI is 41.2-kb in size and encodes 29 potential proteins, several of which have no known function and whose regulation is not well understood. To determine the transcriptional organization of the tagA-orf2-orf3-mop-tagD region located at the 5'-(left) end of the VPI, we used reverse-transcriptase-PCR (RT-PCR), Northern blot analysis and DNA sequencing. RT-PCR primers were designed to transcribe and amplify regions spanning two or more open reading frames so as to establish the transcriptional organization. RT-PCR and Northern blot results demonstrated that the tagA-tagD region is transcribed as a polycistronic message and organized into several potential operons including tagA-orf2, orf3-mop, orf3-mop-tagD and tagD alone. Transcriptional lacZ fusions supported the existence of a promoter upstream of orf3 that was toxT-dependent. Interestingly, our data suggests that the orf3 promoter can drive the expression of either a long transcript (orf3-mop-tagD) or a short transcript (orf3-mop) without tagD. Our data also suggests that tagD can be expressed from two different promoters and that tagD is either transcribed alone or co-expressed with orf3-mop under certain conditions. These studies provide new insight into the genetic structure, transcriptional organization and regulation of a cluster of virulence genes on the VPI of epidemic V. cholerae.

Antibiotic resistance continues to be an ongoing problem in global public health despite interventions to reduce antibiotic overuse. Furthermore, it threatens to undo the achievements and progress of modern medicine. To address these issues, the development of new alternative treatments is needed. Metallic nanoparticles have become an increasingly attractive alternative due to their unique physicochemical properties that allow for different applications and their various mechanisms of action. In this study, gallium nanoparticles (Ga NPs) were tested against several clinical strains of Pseudomonas aeruginosa (DFU53, 364077, and 365707) and multi-drug-resistant Acinetobacter baumannii (MRAB). The results showed that Ga NPs did not inhibit bacterial growth when tested against the bacterial strains using a broth microdilution assay, but they exhibited effects in biofilm production in P. aeruginosa DFU53. Furthermore, as captured by atomic force microscopy imaging, P. aeruginosa DFU53 and MRAB biofilms underwent morphological changes, appearing rough and irregular when they were treated with Ga NPs. Although Ga NPs did not affect planktonic bacterial growth, their effects on both biofilm formation and established biofilm demonstrate their potential role in the race to combat antibiotic resistance, especially in biofilm-related infections.