MICs of all tested antibiotics to Av. S5 Table. MICs of all tested antibiotics to S. S6 Table. RT-PCR primer sets in this study. S1 Fig. Mapped IC cases in China. S2 Fig. Genetic Characteristics of Av. S3 Fig. The radii of satellitism. S4 Fig. Antimicrobial phenotype and genotype of Av. S5 Fig. Virulence genes carried by S. S6 Fig. Growth curves of Av. S7 Fig.
Different Staphylococcus species promote the survival of Av. S8 Fig. Water intake is greatly reduced when birds are coinfected with S. S9 Fig. Monoinfection of S. S10 Fig. S11 Fig. E -Daporinad exhibits no cytotoxicity to respiratory cells. S12 Fig. The extracellular growth of Av. S13 Fig. S14 Fig. References 1. Kamada N, Nunez G. Regulation of the immune system by the resident intestinal bacteria. The microbiota of the respiratory tract: gatekeeper to respiratory health.
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NAD metabolic dependency in cancer is shaped by gene amplification and enhancer remodelling. Elevation of cellular NAD levels by nicotinic acid and involvement of nicotinic acid phosphoribosyltransferase in human cells. J Biol Chem. Chang HC, Guarente L. Sex-based differences in myocardial infarction-induced kidney damage following cigarette smoking exposure: more renal protection in premenopausal female mice. Opportunistic pathogens are a group of microorganisms that do not usually infect healthy hosts but produce infections in hospitals, to immunodepressed persons or those patients presenting underlying diseases as cystic fibrosis, which favors infection Koch and Hoiby, Commensal bacteria are among the most prevalent opportunistic pathogens.
However, the use of antibiotics, which usually kill commensals besides pathogens, increased the incidence of infections due to environmental microorganisms presenting reduced susceptibility to antibiotics Bergogne-Berezin et al. The evolution of non-pathogenic bacteria towards virulence has been deciphered in occasions. The best studied among these evolution processes is that of Yersinia pestis , the causal agent of plague Achtman et al.
The genus Yersinia is formed by 15 different species among which only Y. Phylogenetic reconstruction of the evolution of this genus indicates that Y. The ancestor of these pathogenic Yersiniae evolved towards virulence, from a non-pathogenic environmental Yersiniae , by acquiring a virulence plasmid named pCD1 Wren, This plasmid contains genes coding for a Type III secretion system, which activity allows subversion of the immune system, and is required for the virulence of this pathogen.
It is worth mentioning that the acquisition of this plasmid occurred before the divergence between Y. This means that the evolution of human pathogens is not exclusively driven by the infection of humans Martinez, As stated before, the speciation of Y. The loss of genes has been frequently associated to genome reduction evolution mostly in the case of endosymbionts Perez-Brocal et al. For these microorganisms, several metabolic functions can be covered by the host and un-needed genes are lost just by gene drift.
The situation concerning Yersinia is not the same. In its process of evolution Y. Consequently, the evolved organism does not kill insects, a property that allowed its improved transmission by beats of colonized insects Chouikha and Hinnebusch, Since this may mean that Y. As described in this example, evolution towards virulence involves the acquisition of some elements and the loss of other ones.
This process leads to speciation from non-virulent towards virulent microorganisms. As above stated, these organisms do not infect healthy people and the main factor allowing infection is the patient predisposition for being infected.
This may mean that any organism may infect an immunocompromised patient, something that is not fully true. The human body can be considered as an extreme environment. Actually, when we talk about human microbiota we refer to microorganisms colonizing the surfaces of human body; the body itself is an sterile environment unless an infection occurs.
The entrance in this ecosystems requires either the acquisition of virulence determinants to cope with the human defences, as happens with the aforementioned example of Y. However, even in this last case, to colonize the human host a microorganism requires to survive under the physicochemical conditions of human body: a narrow range of temperature oxygen tension and pH; some specific nutrients and low iron availability.
In the case of opportunistic pathogens infecting immunocompetent patients as those suffering cystic fibrosis, mechanisms to cope with the immune response are also needed.
In addition, and since patients at hospitals are frequently under antibiotic therapy, these opportunistic pathogens frequently display low susceptibility to antibiotics Martinez and Baquero, Indeed, antibiotic treatment is a risk factor for being infected by some environmental opportunistic pathogens presenting low susceptibility to antibiotics as Stenotrophomonas maltophilia Alonso and Martinez, ; Sanchez et al.
One of the best studied bacterial opportunistic pathogens is Pseudomonas aeruginosa. This microorganism is currently among the most prevalent causes of infection at hospitals and is the major cause of chronic infections in cystic fibrosis patients. These patients are frequently infected by a single P. Since P. Nevertheless, molecular epidemiology has shown that the same clonal complexes present in non-clinical ecosystems are the ones producing infections Morales et al.
Further, the comparison of clinical and non-clinical isolates showed that they were functionally equivalent. All of them extruded the synthetic antibiotics quinolones, presented the genes encoding the elements of the Type III secretion system and of the quorum sensing regulation response and were capable to invade epithelial cells; all these characteristics typical of virulent strains.
In addition, all strains were able of use oil hydrocarbons as carbon sources, a feature characteristic of environmental biodegradative microorganisms, which is not required for producing an infection Alonso et al.
Together with the aforementioned epidemiological evidences, this indicates that P. Rather, several if not all of the strains have the capability of infecting patients presenting underlying diseases. The reason for this situation resides likely in the ability of P. Since the same virulence determinants serve to infect all these host it is worth thinking that such determinants evolved during the interaction with the oldest organisms in this phylogenetic tree. In this respect, it is worth mentioning that P.
It is then possible that a major force in the evolution of P. All these studies reinforce the idea P. Rather, this bacterial species can infect humans by using elements that evolved for its interaction with other hosts Rahme et al. Nevertheless, once a strain enters inside the human host, it can evolve to improve its adaptation to this new environment Folkesson et al.
The evolution of P. It has been found that strains producing chronic infection carry mutations in global regulation factors that regulate expression of P. As a consequence, expression of these elements, which are of relevance in P. This in-host evolution process is favored by the increased prevalence of strains presenting high mutation rates found in chronic infections Oliver et al.
It can be thought that these adaptive mutations could be fixed in the population, hence constituting the beginning of a speciation process towards virulence. However, with the exception of some epidemic clones causing infections in cystic fibrosis patients, mainly at Denmark and England see below , most patients are infected by independent P. This evolution process by which an organism follows the same pattern of evolution that is not fixed afterwards each time it enters in a given ecosystem has been dubbed as short-sighted evolution Levin and Bull, This process is likely fundamental for the adaption of microorganisms producing chronic infections with low inter-patient transmission rates.
Although each bacterial isolate colonizes the lung of an independent patient, all lungs are quite similar habitats. It is then expected that the evolutionary landscapes of each of this chronic strains may be similar. However, once bacteria are released, these adaptations are of no use unless the microorganism colonize another cystic fibrosis patient.
This is likely the situation of countries as Denmark in which patients have been usually in contact for treatment and in occasions even on holiday camps Ojeniyi et al. Similarly, it has been shown that the acquisition of novel prophage islands is a critical event in increasing the competitiveness of epidemic P. It could be predicted that under those circumstances epidemic clones, presenting cystic fibrosis adaptive mutations spread, a situation that has been already described in occasions Jelsbak et al.
Whether or not these epidemic clones are in the route of speciation remains to be established. However, the fact that the implementation of strict cohort-based patients segregation policy has halted the epidemic of the Liverpool strain, with an increase in the percentage of patients with unique P. In other cases in which inter-host transmission is low, the evolved isolates are released into natural ecosystems.
In other words, without an open wound, this sexually transmitted disease would be unable to use the human body as a host. It takes advantage of the opportunity to infect the lymphocytes, macrophages and granulocytes as soon as it enters the area of broken skin. Learning Objectives Describe the traits of an opportunistic microorganism.
Key Points A microorganism is a microscopic organism that can either be a single cell, cell cluster, or multicellular. Haemophilus ducreyi, a microorganism, infects its host through broken skin or epidermis.
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