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Appendix J: Pathogenicity Acquisition
Pages 181-192

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From page 181...
... Mobile genetic elements, including transposons, plasmids, and bacteriophage, are the most common sources of acquired antibiotic resistance in MRSA. In addition, spontaneous mutations in chromosomally encoded genes can confer resistance to antibiotics (e.g., rpsL and streptomycin)
From page 182...
... Toxins Protein toxins in bacteria are often associated with mobile genetic elements such as phages and plasmid DNA. For this reason many toxin genes have spread between species by horizontal gene transfer.
From page 183...
... Once CTXΦ is internalized into the bacterial cell, it integrates into the host genome using host machinery. Transcription of phage genes required for phage replication and virion production is repressed during lysogeny.
From page 184...
... pneumoniae to evade host defenses. The regions flanking the capsule loci are very similar among capsular serotypes, and this sequence characteristic facilitates homologous recombination of capsule genes acquired through horizontal gene transfer in this naturally competent organism.
From page 185...
... GENE LOSS Shigella spp The evolution of a non-pathogenic bacterial species into a genetically related but pathogenic species typically occurs as a result of the acquisition of genes encoding virulence factors, often via transfer of pathogenicity islands. However, loss of a gene or genes can also be critical to the capacity of a nonpathogenic organism to be converted to one that causes serious disease.
From page 186...
... . provided an opportunity to identify mutation sets that are responsible for high virulence and cross species adaptation, although the approach is often limited by the isogenic host background as compared with outbred populations in natural settings.
From page 187...
... Thus, age, genetic background of the host and immune status likely facilitate crossspecies transmission and adaptation potential of zoonotic RNA viruses. Se quence analysis of young-mouse-adapted strains revealed mutations in common genes sets, notably nsp5, nsp9, the M glycoprotein genes, including changes within the RBD of S
From page 188...
... Although mutation sets targeted key genes essential for efficient virus-host interaction,
From page 189...
... In turn, most pathogens sense iron availability and induce or repress various iron acquisition systems accordingly. Indeed, many microorganisms possess toxins that are regulated by iron such that low iron concentrations trigger toxin biosynthesis.
From page 190...
... One common mechanism for bacterial transduction of environmental signals involves two-component regulatory systems that act on gene expression, usually at the transcriptional level. Such systems make use of similar pairs of proteins; one protein of the pair spans the cytoplasmic membrane, contains a transmitter domain, and may act as a sensor of environmental stimuli, whereas the other is a cytoplasmic protein ("response regulator")
From page 191...
... pestis strains that are unable to block the flea proventriculus, but, as an ticipated, has no effect on pathogenesis in mammalian hosts because the genes are expressed only at low temperature (in the flea)


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