Region 7, harbouring 6 out of 17 genes of the eut operon, is absent in 1 pre-epidemic (31/88) and 2 non-human
epidemic (32/00 and 49/98) S. Enteritidis isolates. These genes encode ATM/ATR activation alcohol dehydrogenase, aldehyde dehydrogenase and enzymes required for ethanolamine utilization (eutG, J, E, N, M, D). S. Enteritidis 32/00 also lacks the pduS gene, a ferredoxin involved in propanediol utilization (part of the pdu operon). In Salmonella both 1, 2-propanediol degradation and ethanolamine degradation require vitamin B12. Many Enterobacteriaceae have lost the capacity to synthesize cobalamine and therefore to degrade 1, 2-propanediol and ethanolamine but a few genera, including Salmonella and Yersinia, re-acquired a 40 kb metabolic island encoding both the ability to synthesise cobalamine and degrade 1, 2-propanediol, whilst retaining the eut operon [36–39]. Although 1, 2-propanediol is an important source of 17DMAG in vitro energy for S. Typhimurium and cbi mutants are significantly attenuated in their ability learn more to grow in macrophages  it is apparent that genes within these pathways are lost in the host-adapted S. enterica serovars including Gallinarum, Typhi and Paratyphi A . Region 8 (SEN2761-SEN2763)
comprises three genes (rpoS and two unknown genes) which are absent/divergent in S. Enteritidis 47/03 isolated from human disease. RpoS is inducible in stationary phase, is the master regulator of the general stress response in Salmonella and is required for virulence in mice [41, 42]. There are previous reports of S. Typhi, S. Typhimurium and S. Enteritidis clinical and environmental isolates carrying mutations in rpoS that result in impaired RpoS functionality [42, 43]. A test of catalase activity in stationary phase is used as a method to detect RpoS function , thus we performed the test in all 29 isolates and found a negative result only in S. Enteritidis isolate 47/03. This strongly suggest that RpoS function is impaired in this isolate. Region 6 harbouring genes encoding nitrate reductases, cytochrome C and ferredoxin-type proteins (napC, B, H, G, A, D), was also absent in 3 S. Enteritidis (31/88, 48/98 and 92/05) isolates
from different periods of the Uruguayan epidemic. Variation in S. Enteritidis Genomic Uroporphyrinogen III synthase Islands Although there is a large number of genomic islands in S. Enteritidis PT4 P125109  which carry the hallmarks of having been laterally acquired, and maintain mobility functions, surprisingly our data show that most are ubiquitous in the S. Enteritidis isolates tested here. The exceptions are Region 5 (or ROD21) and Region 9. Region 5 is one of the largest genomic islands identified in S. Enteritidis PT4 P125109 (26.5 kb; SEN1970-SEN1999), and it encodes the global transcriptional silencers H-NS (hnsB) and the H-NS antagonist (hnsT) [44–46]. This region was undetected using the microarray in the Kenyan S. Enteritidis isolate AF3353 but it is present in all other strains.