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.

Whether virulent human pathogenic coronaviruses (SARS-CoV, MERS-CoV, SARS-CoV-2) are effectively transmitted by aerosols remains contentious. Transmission modes of the novel coronavirus have become a hot topic of research with the importance of airborne transmission controversial due to the many factors that can influence virus transmission. Airborne transmission is an accepted potential route for the spread of some viral infections (measles, chickenpox); however, aerosol features and infectious inoculum vary from one respiratory virus to another. Infectious virus-laden aerosols can be produced by natural human respiratory activities, and their features are vital determinants for virus carriage and transmission. Physicochemical characteristics of infectious respiratory aerosols can influence the efficiency of virus transmission by droplets. This critical review identifies studies reporting instances of infected patients producing airborne human pathogenic coronaviruses, and evidence for the role of physical/chemical characteristics of human-generated droplets in altering embedded viruses’ viability. We also review studies evaluating these viruses in the air, field studies and available evidence about seasonality patterns. Ultimately the literature suggests that a proportion of virulent human coronaviruses can plausibly be transmitted via the air, even though this might vary in different conditions. Evidence exists for respirable-sized airborne droplet nuclei containing viral RNA, although this does not necessarily imply that the virus is transmittable, capable of replicating in a recipient host, or that inoculum is sufficient to initiate infection. However, evidence suggests that coronaviruses can survive in simulated droplet nuclei for a significant time (>24 h). Nevertheless, laboratory nebulized virus-laden aerosols might not accurately model the complexity of human carrier aerosols in studying airborne viral transport. In summary, there is disagreement on whether wild coronaviruses can be transmitted via an airborne path and display seasonal patterns. Further studies are therefore required to provide supporting evidence for the role of airborne transmission and assumed mechanisms underlying seasonality.

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.

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.

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.

This study analyzed fresh feces from three common bird species that live in urban environments and interact with human communities. Antibiotic resistance genes (ARGs) encoding resistance to three major classes of antibiotics (i.e., tetracyclines, β-lactams, and sulfonamides) and the mobile genetic element integrase gene (intI1) were abundant (up to 10⁹, 10⁸, 10⁹, and 10¹⁰ copies/g dry feces for tetW, blaTEM, sul1, and intI1, respectively), with relative concentrations surprisingly comparable to that in poultry and livestock that are occasionally fed antibiotics. Biomarkers for opportunistic pathogens were also abundant (up to 10⁷ copies/g dry feces) and the dominant isolates (i.e., Enterococcus spp. and Pseudomonas aeruginosa) harbored both ARGs and virulence genes. ARGs in bird feces followed first-order attenuation with half-lives ranging from 1.3 to 11.1 days in impacted soil. Although residual antibiotics were detected in the feces, no significant correlation was observed between fecal antibiotic concentrations and ARG relative abundance. Thus, other unaccounted factors likely contributed selective pressure for ARG maintenance. These findings highlight the contribution of wild urban bird feces to the maintenance and dissemination of ARGs, and the associated health risks.

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.

Phytophthora capsici, an economically devastating oomycete pathogen, causes devastating disease epidemics on a wide range of vegetable plants and pose a grave threat to global vegetables production. Heavy metals and acid pH are newly co-occurring stresses to soil micro-organisms, but what can be expected for mycelia growth and virulence and how they injure the oomycetes (especially P. capsici) remains unknown. Here, the effects of different heavy metals (Cu²⁺, Cr²⁺, and Hg²⁺) on mycelia growth and virulence were investigated at different pHs (4.0 vs. 7.0) and the plausible molecular and physiological mechanisms were analyzed. In the present study, we compared the effective inhibition of different heavy metals (Cu²⁺, Cr²⁺, and Hg²⁺) and acid pH on a previously genome sequenced P. capsici virulent strain LT1534. Both stress factors independently affected its mycelia growth and sporulation. Next, we investigated whether ROS participated in the pH-inhibited mycelial growth, finding that the ROS scavenger, catalase (CAT), significantly inhibited the acid pH-induced ROS in mycelia. Additionally, because MAPK specially transmits different stress responsive signals in environment into cells, we employed CAT and a p38-MAPK pathway inhibitor to investigate ROS and p38-MAPK roles in heavy metal-inhibited mycelia growth at different pHs (4.0 vs. 7.0), finding that they significantly inhibited growth. Furthermore, ROS and p38-MAPK influenced the heavy metal-induced TBARS content, total antioxidant capacity (TAC), and CAT activity at different pHs, and also reduced the expression of infection-related laccases (PcLAC2) and an effector-related protein (PcNLP14). We propose that acid pH stress accelerates how heavy metals inhibit mycelium growth, sporulation, and virulence change in P. capsici, and posit that ROS and p38-MAPK function to regulate the molecular and physiological mechanisms underlying this toxicity. Although these stresses induce molecular and physiological challenges to oomycetes, much remains to be known the mechanisms dedicated to resolve these environmental stresses.

The potential impact of exposure to polychlorinated biphenyls (PCBs) on the health and survival of cetaceans continues to be an issue for conservation and management, yet few quantitative approaches for estimating population level effects have been developed. An individual based model (IBM) for assessing effects on both calf survival and immunity was developed and tested. Three case study species (bottlenose dolphin, humpback whale and killer whale) in four populations were taken as examples and the impact of varying levels of PCB uptake on achievable population growth was assessed. The unique aspect of the model is its ability to evaluate likely effects of immunosuppression in addition to calf survival, enabling consequences of PCB exposure on immune function on all age-classes to be explored. By incorporating quantitative tissue concentration-response functions from laboratory animal model species into an IBM framework, population trajectories were generated. Model outputs included estimated concentrations of PCBs in the blubber of females by age, which were then compared to published empirical data. Achievable population growth rates were more affected by the inclusion of effects of PCBs on immunity than on calf survival, but the magnitude depended on the virulence of any subsequent encounter with a pathogen and the proportion of the population exposed. Since the starting population parameters were from historic studies, which may already be impacted by PCBs, the results should be interpreted on a relative rather than an absolute basis. The framework will assist in providing quantitative risk assessments for populations of concern.