In the previous publication “Can atmospheric pollution be considered a co-factor in extremely high level of SARS-CoV-2 lethality in Northern Italy?” Conticini et al. hypothesized that the surplus of lethality of the novel SARS-CoV-2 in Northern Italy may be at least in part explained by the evidence of highest pollution reported in this area, as both severe COVID-19 and smog exposure are correlated to an innate immune system hyper-activation with subsequent lung inflammation and injury. Since this hypothesis alone does not fully explain why specific subgroups of patients are at major risk, we hypothesized that obesity may be one of the links between COVID-19 severity and high level of air pollution. First, obesity is a predisposing factor for SARS-Cov-2 infection and worse COVID-19 outcomes, and unequivocal evidence demonstrated that fat mass excess is independently associated with several pulmonary diseases and lung inflammation. Moreover, it has been shown that obesity may intensify the detrimental effects of air pollution on the lungs, and this is not surprising if we consider that these conditions share an excessive activation of the immune system and a lung inflammatory infiltrate. Finally, fat mass excess has also been speculated to be itself a consequence of air pollutants exposure, which has been proved to induce metabolic disruption and weight gain in murine models. In conclusion, although many variables must be taken into account in the analysis of the pandemic, our observations suggest that obesity may act as effect modifier of smog-induced lung-injury, and the concomitant presence of these two factors could better explain the higher virulence, faster spread and greater mortality of SARS-CoV-2 in Northern Italy compared to the rest of the country.

Antibiotic resistance among gram-negative bacteria is increasingly becoming a problem of global concern. Particularly problematic is the emergence of resistance to last-resort antibiotics such as carbapenems and colistin. The increasing number of reports on the plasmid-mediated colistin resistance gene mcr-1 in isolates worldwide is raising concerns for the future usefulness of this class of antibiotics. Dissemination of mcr-1 is believed to have originated mainly from animal breeding, however, the role of the environment as a transmission source is not yet fully understood. In the current study, 89 extended-spectrum β-lactamase-producing Escherichia coli isolated from 231 samples from different environmental sources in 12 villages in a rural area of Shandong, China, were screened for mcr-1. 17 (19.1%) mcr-1-positive isolates were found from different environmental sources, aggregated in 6 villages. Plasmids of three different Inc-groups carrying mcr-1 were confirmed, indicating that the widespread geographical distribution of mcr-1 in the local area is due to a number of different plasmids. Additionally, almost a third (29.4%) of the isolates carried virulence factors associated to intestinal pathogenic E. coli. These results illustrate the high complexity of the transmission patterns of mcr-1 among different environmental matrices on a local scale and the potential for the environment to facilitate dissemination and emergence of antibiotic-resistant and virulent strains of bacteria.

The aim was to determine the prevalence of E. coli and coliform bacteria in playground sand of all public children's sandpits in Graz (n = 45), Austria, and to assess the frequency of antimicrobial resistance in E. coli. Molecular characterization included the discrimination of O-serotypes and H-antigens and the determination of virulence and resistance genes, using a microarray technology. E. coli isolates were tested for susceptibility to a set of antibiotics by VITEK2 system and disk diffusion method. In total, 22 (49%) and 44 (98%) sandpits were positive for E. coli and coliform bacteria. Median concentrations of E. coli and coliform bacteria in the sand samples were: 2.6 × 104 CFU/100 g and 3.0 × 105 CFU/100 g. Resistance rates were: ampicillin, 12.5%; piperacillin, 10.4%; amoxicillin/clavulanic acid, 9.4%; cotrimoxazole, 6.3%; tetracycline, 6.3%; piperacillin/tazobactam, 5.2%. No ESBL- or carbapenemase-producing isolates were found. The most prevalent serogroups were O15, O6 and O4. Isolates harbored 0 up to 16 different virulence genes.

Antibiotic resistance genes (ARGs) and virulence factors (VFs) are critical threats to human health. Their abundance in aquatic ecosystems is maintained and enhanced via selection driven by environmental xenobiotics. However, their activity and expression in these environments under xenobiotic stress remains unknown. Here ARG and VF expression profiles were examined in aquatic microcosms under ciprofloxacin, glyphosate and sertraline hydrochloride treatment. Ciprofloxacin increased total expression of ARGs, particularly multidrug resistance genes. Total expression of ARGs and VFs decreased significantly under glyphosate and sertraline treatments. However, in opportunistic human pathogens, these agents increased expression of both ARGs and VFs. Xenobiotic pollutants, such as the compounds we tested here, have the potential to disrupt microbial ecology, promote resistance, and increase risk to human health. This study systematically evaluated the effects of environmental xenobiotics on transcription of ARGs and VFs, both of which have direct relevance to human health. Transcription of such genes has been overlooked in previous studies.

The abuse or misuse of antibiotics is directly linked to the emergence of antibiotic-resistant bacteria and antibiotic resistance genes (ARGs) in the environment. Most fish farms located on Jeju Island operate a flow-through system that pumps in seawater for fish farming and discharges it back to the ocean. To investigate the amount of ARGs that these fish farm effluents discharge into the marine environment, we conducted a metagenomic-based resistome analysis. We observed higher levels of ARGs in fish farm effluents than in seawater at beach and residential areas. A greater proportion of ARGs was found on plasmid rather than on chromosomal DNA, especially for sulfonamide and phenicol classes. The distribution of ARGs did not differ between summer and winter, but the microbial community did. In addition, fish farm samples contained significantly more opportunistic pathogens (i.e., Vibrio, Photobacterium, Aliivibrio, and Tenacibaculum) and virulence factors than non-fish farm samples. Vibrio was the most frequently identified host of ARGs and virulence factors. The presence of Vibrio in the coastal area has been increasing owing to the recent rise in the temperature of seawater. This study suggests the need for actions to treat or monitor ARGs in the coastal areas where fish farms operating a flow-through system are located.

Mycotoxins are increasingly considered as micropollutants in the environment. Fumonisins, as one of the most important mycotoxins, cause potential health threats to humans and animals due to their ubiquitous contamination on cereals, fruit, vegetables and other environmental samples around the world. However, the contribution of fumonisins to the interaction of fungi with plant hosts is not still fully understood. Here, we investigated the effect of fumonisin B1 (FB1) on the infection of Fusarium proliferatum on banana fruit and the underlying mechanisms from the host perspective. Our results found that FB1 treatment increased the aggressiveness of F. proliferatum on banana fruit and inhibited the defense ability of banana fruit via decreasing phenylalanine ammonia lyase (PAL), β-1,3-glucanase (GLU) and chitinase (CHI) activities. Meanwhile, FB1 accelerated cell death, indicated by higher relative conductivity, MDA content and higher transcripts of cell death-related genes. FB1 treatment resulted in higher hydrogen peroxide (H₂O₂) content possibly due to MaRBOHs induction. These consequences accelerated the ROS-dependent cell death, which subsequently result in reduction of disease resistance of banana fruit. Additionally, energy metabolism and MaDORN1s-mediated eATP signaling might involve in FB1-meidiated suppression of banana defense responses. Collectively, results of the current study indicated that FB1 contamination triggered the cell death of banana peel, subsequently instigating the invasion and growth of F. proliferatum on banana fruit. In summary, for the first time, we demonstrated a previously unidentified role of fumonisins as a potential virulence factor of F. proliferatum in modulating fruit defense response, which provides new insight on the biological roles of fumonisins.

In soils, the presence of clinically relevant bacteria carrying ARGs, including extended-spectrum β-lactamase- and plasmid-mediated AmpC β-lactamase-encoding genes, is an underestimated public health problem that requires more attention. For this investigation, 300 samples from agricultural and non-agricultural soils were used to obtain 41 MDR E. coli isolates, standing out the resistance to β-lactams, fluoroquinolones and colistin. Virulence genes related to diarrheagenic E. coli and extraintestinal pathogenic E. coli were detected. Several ARGs were found, highlighting the presence of at least one β-lactamase-encoding gene (blaTEM, blaCMY, blaSHV, blaOXA₋₁₋ₗᵢₖₑ, blaCTX₋M₋₂, and/or blaCTX₋M₋₁₅) in each isolate. Among the fluoroquinolone-resistant E. coli isolates, the plasmid-mediated quinolone resistance genes (qnrB and oqxA) and substitutions in the quinolone resistance-determining regions were detected. Some isolates were resistant to colistin (MICs of 4–8 mg/L) and, although no mcr-like gene was detected, substitutions in the two-component systems involving PhoP/PhoQ and PmrA/PmrB were found. Furthermore, the E. coli isolates presented plasmids and class 1 integrons, the last one detected in all isolates. The ARGs blaTEM, aadA and dfrA and the lpfA virulence-associated gene presented statistically significant differences (P < 0.05) in agricultural soils, while the blaOXA₋₁₋ₗᵢₖₑ gene presented a statistically significant difference in non-agricultural soils. Thirty-eight sequence types (STs) were identified among the isolates, spotlighting the 20 different STs that carried blaCMY and blaCTX₋M₋ₜyₚₑ genes and those commonly reported in infections worldwide. The occurrence of virulent, multidrug- and colistin-resistant E. coli isolates in soils could lead to contamination of surrounding environments and food, increasing the risk of human and animal exposure. Therefore, this study contributes to a better understanding of E. coli in soils and reinforces the importance of the One Health approach to antimicrobial resistance surveillance.

As zoned areas of industries, industrial parks have great impacts on the environment. Several studies have demonstrated that chemical compounds and heavy metals released from industrial parks can contaminate soil, water, and air. However, as an emerging pollutant, antimicrobial resistance genes (ARGs) in industrial parks have not yet been investigated. Here, we collected soil samples from 35 sites in an industrial park in China and applied a metagenomics strategy to profile the ARGs and virulence factors (VFs). We further compared the relative abundance of ARGs between the sites (TZ_31–35) located in a beta-lactam antimicrobial-producing factory and other sites (TZ_1–30) in this industrial park. Metagenomic sequencing and assembly generated 14, 383, 065 contigs and 17, 631, 051 open reading frames (ORFs). Taxonomy annotation revealed Proteobacteria and Actinobacteria as the most abundant phylum and class, respectively. The 32 pathogenic bacterial genera listed in the virulence factor database (VFDB) were all identified from the soil metagenomes in this industrial park. In total, 685,354 ARGs (3.89% of the ORFs) and 272,694 virulence factors (VFs) (1.55% of the ORFs) were annotated. These ARGs exhibited resistance to several critically important antimicrobials, such as rifampins, fluroquinolones, and beta-lactams. In addition, no significant difference in the relative abundance of ARGs was observed between sites TZ_31–35 and TZ_1–30, indicating that ARGs have already disseminated widely in this industrial park. The present study gave us a better understanding of the whole picture of the resistome and virulome in the soil of the industrial park and suggested that we should treat the industrial park as a whole in the surveillance and maintenance of ARGs.

Infections caused by carbapenem-resistant Enterobacteriaceae are a growing concern worldwide. Raoultella ornithinolytica is a species in the Enterobacteriaceae family which can cause hospital-acquired infections and is sporadically reported as carbapenem-resistant from human and environmental sources. In this study, we firstly report on an NDM-1-producing R. ornithinolytica, Rao166, isolated from drinking water in an animal cultivation area in China. In addition to carbapenem-resistance, Rao166 was resistant to several other antibiotics including gentamicin, sulfamethoxazole-trimethoprim, tetracycline and fosfomycin. Rao166 carried a novel IncFIC-type megaplasmid, 382,325 bp in length (pRAO166a). A multidrug resistance region, 60,600 bp in length, was identified in the plasmid containing an aac(3)-IId-like gene, aac(6′)-Ib-cr, blaDHA₋₁, blaTEM₋₁B, blaCTX₋M₋₃, blaOXA₋₁, blaNDM₋₁, qnrB4, catB3, arr-3, sul1, and tet(D). Results from virulence assays implied that Rao166 has considerable pathogenic potential. Although pRAO166a was found to be non-transmissible, dissemination of the NDM-1 producing strain may occur from well water to humans or animals through cross-contamination during food preparation or directly via drinking water, and potentially lead to difficult-to-treat infections. Thus, contamination of well water by this carbapenem-resistant and presumptively virulent strain of R. ornithinolytica should be considered a potential public health risk.

Per- and Poly-fluoroalkyl substances (PFAS) are one of the major persistent environmental contaminants. Epidemiological studies have linked PFAS exposures to altered immunity and increased occurrence of infections in children. However, the mechanisms leading to immune susceptibility to bacterial infections remains unclear. To elucidate the mechanism, transcriptional alteration in the Caenorhabditis elegans model caused by a PFAS contaminated environmental water and two reconstituted PFAS solutions were evaluated using RNA-sequencing. PFAS affected the expression of several genes involved in C. elegans immune surveillance to Gram-positive bacteria (cpr-2, tag-38, spp-1, spp-5, clec-7, clec-172). The combined exposure to PFAS and Staphylococcus aureus significantly reduced C. elegans survival and increased intestinal membrane permeability. Furthermore, the growth of S. aureus in the presence of PFAS increased the expression of virulence genes, specifically, the virulence gene regulator saeR and α-hemolysin, hla, which resulted in increased hemolytic activity. The present study demonstrated that PFAS exposure not only increased C. elegans susceptibility to pathogens by reducing host immunity and increasing intestinal membrane permeability, but also increased bacteria virulence. This presents a broader implication for humans and other animals, where environmental contaminants simultaneously reduce host resilience, while, increasing microbial pathogenicity.