Sampled strains were extracted from poultry carcass sponges used for cleaning the chopping board used to carve the poultry. The procedures followed were extracted from FSIS/USDA MLG 4.09 Rev. 09. Isolation and Identification of Salmonella from Meat, poultry, Pasteurized Egg, and Siluriformes (Fish) Products and Carcass and Environmental Sponges Briefly, the sponges were washed in 50 mL of buffered peptone water (BPW; Oxoid, Basingstoke, England). Selective enrichment was done using a 500 µl aliquot of enriched bacteriae was re-enriched in 10 mL of Tetrathionate Broth Base, Hajna (BD Cat. 249120) and 100 μl aliquot of enriched bacteriae in 10 ml of Modified Rappaport and Vassiliadis (mRV) broth (BD Cat. 218581). Plating media were made of Brilliant green sulfa agar (BGS; contains 0.1% sodium sulfapyridine) (BD Cat. 271710) and Xylose lysine Tergitol™ 4 agar (XLT4) (BD Cat. 223420). In order to characterize the bacteria strain remaining in the differential bacteria selection step, we grew the isolates in two different screening media: Triple Sugar Iron agar (TSI) (BD Cat. 226540) and Lysine Iron Agar (BD Cat. 284920). The resulting bacterial colony was then sub-cultured in BIH media for a further 18 h at 37˚C.

In Salmonella enterica, the transition between somatic phase and flagellar phase is mediated by a post-transcriptional control mechanism. In order to determine the isolated Salmonella phase, we performed a serological test with polyvalent O antiserum reactive with serogroups A through I + Vi (Statens Serum Institute Cat: 44807) and SSI H (Flagellar) antisera for slide Agglutination flagellar (Statens Serum Institute Cat: 40290) antigen. We performed a biochemical test using a standardized identification system known as API20E (Biomerieux Ref 20 100). This system uses 21 miniaturized biochemical tests and a database. These tests were inoculated with a bacterial suspension and were incubated at 35˚C for 22 hours. The reactions were read according to the Reading table and the Identification was obtained using the identification software (APIWEB).

DNA templates were prepared from the resulting enrichments by boiled cell lysis. Briefly, 1 ml of overnight enrichment was pelleted by centrifugation, re-suspended in 200 µl of sterile distilled water, and boiled for 10 min. The boiled cell suspensions were centrifuged, and the resulting lysate was used for PCR.

Genomic DNA was extracted using the Wizard genomic purification kit (Promega) and used for PCR amplification (Data not shown). DNA fragment libraries were constructed using using Genomic DNA Sample Preparation Kit (illumina ctalog numb. FC-102-1001) according to the manufacturer’s recommendations.

The sequences from the genomes libraries were obtained using 454 FLX pyrosequencing (Roche). The genome was assembled using Newbler version 2.8. Genome sequence annotation was made by RAST [http://rast.nmpdr.org] [5] . This Whole Genome Shotgun project has been deposited at DDBJ/ENA/GenBank under the accession NBXM00000000 and NBXN00000000. The version described in this paper is version NBXM00000000 and NBXN00000000.

We used rpoB and tufA genes (Data not shown) to determine the strains closeness.

A total of 4,811,656 bp, 53 contigs, an N50 of 321,932 bp were obtained for the 103 strain. The 2199 strain sequencing datas consist in 4,907,872 pb, 62 contigs, an N50 of 425,021. The genome size of both strains is nearly identical (a 1.9% size difference) and maintained synteny with the closest strain CT18 (Figure 1).

The resulting genome comprises 4748 coding proteins, 54 rRNAs, 73 tRNAs, and 52% GC content for strain 103. The 2199 strain 4874 coding proteins, 55 rRNAs, 70 tRNAs and 52 GC_content. We found 98.49% identity with S. enterica var. CT18 for the 103 strain and 98.35 for the 2199 strain with high synteny in both cases (Figure 1). CT 18 Salmonella enterica serovar Typhi is a pathogenic, multidrug resistant strain, hence the interest in comparing the isolated salmonella with this particular strain [14] . Interestingly, the genomic sequences of these potentially harmful strains present in 50% more ribosomal proteins coding sequences than the reference CT18 strain, which in Salmonella

enterica is quite variable, from 67 to more than 200 elements (img.jgi.doe.gov, data not show). We could assume that this difference would be reflected in a higher protein synthesis capacity, eventually affecting their pathogenicity.

The resistance genes from the two Salmonella strains isolated from the poultry were characterized. We found that both strains shared seven resistance genes (Table 1). Common genes are the aminoglycoside 6’-N-acetyltransferase (aac and aac1) that acetilates aminoglycoside antibiotics [15], Par E providing fluoroquinolones resistance [16], TetA transporter exporting tetracyclin outside the cell [17], the QRDR Asp87 --> Gly mutation in the DNA gyrase gyrA and GyrB produces bacteria quinolone resistance [18], ParC topoisomerase mutation allowing for ciprofloxacin resistance [19] and TetA mutation allowing this enzyme to produce the oversupercoiling needed for exponential growth even in presence of tetracyclin [20] . Nevertheless, these show individual resistance genes such as cat2, a gene conferring chloramphenicol resistance [21], for the 103 strain and sul2 (sulfonamide resistance through mutation in the enzymes of the folate synthesis pathway [21] ), strA and strB (streptomycin resistance gene) for the 2199 strain.

The pathogenicity of these strains is related to the presence of particular genes. The strains shared 18 virulence genes, while 4 different genes were encountered in 103 and 2 in 2199 (Table 1).

Amongst the virulence genes present only in 103 strain, GipA is a transposase allowing for the recombination of DNA of the enterobacteriae, whose presence in E. coli has been associated to Crohn’s disease [10] . The hinS gene, correlating

to flagellar antigen variation [22], and a gene coding for a putative transposase are also only present in the 103 isolate. These genes could allow for antigen shifting, cloaking the bacteriae from the human immune system. The rhuM is a hypothetical cytoplasmic protein loosely related to STY4036 DNA Binding protein. (oncotarget 07 35169-s003]. The spoE gene, only present in 103 isolate, is a gene associated with DNA segregation and Cell cycle control in Mycobacterium tuberculosis [23] . Conversely, the avrA and orgA genes are only present in the 2199 isolate. The first codes for an inhibitor of the c-Jun N-terminal kinase pathway that provoke intestinal cell tight junction stabilization [24] promoting colonic tumor [25] ; while the second correspond to a gene related to low oxygen environment adaptability, hence to the ability of the bacteria to strive intracellularly [26] .

bcfC genes codes for an outer membrane usher protein, which is sometimes carried in the microbe genome as part of a transposable element. The pore is located in the outer membrane of the microbial pili, allowing a better bacterial protein secretion during the intestine invasion [9] . invA is an internal membrane protein allowing type III secretion required for cell invasion [27] . invE is also related to secretion, allowing retention of secreted substrates within the bacterium rather than the translocation of substrates through the bacterial and/or eukaryotic membranes.

SopE is a protein required for invasion through cytoskeleton reorganization, while SopB is needed for invasion, mediating trans epithelial signaling of the polymorphonuclear leukocyte (PMNs). SopB is required for the inflammation and fluid accumulation and stimulate the recruitment of PMNs to the site of a Salmonella infection [28] . SPi 4 is a secretion protein related to LipC. In addition to invasion, the SPI1 system appears to function in programmed cell death (apoptosis) of infected cultured macrophages [29] . ssaQ S enterica is a SPI2 type III secretion protein involved in cell invasion, giving an enhanced HepG2 cell invasion capacity as well as higher cytotoxicity towards macrophages [30] . spiR is a spire type nucleation factor and pipC is a protein coded in the pathogenicity island five, and is related to sigE, a stress response transcription factor. SigE activation enhances the Salmonella survival in the acidic environment of the phagosomal vacuole [31] . TtrC_S gene is found in the Salmonella LT2 serovar and is an integral membrane protein containing a quinol oxidation site required for anaerobic Salmonella respiration though tetraionate reduction. MisL is a Salmonella auto transporter outer membrane protein binding to collagen IV, thereby favoring epithelial cells invasion and colon invasion [32] . suRgi_S gene is a LT2 coded protein with ATP binding capacity that is related with bacteria virulence [33] .

PhoP/PhoQ, the phoP/phoQ two-component regulatory system, controls the PrgH 45-kDa lipoprotein component of the syringe structures involved in cell secretion system [34] [35] . SlyA is a regulatory DNA binding protein, transcriptional regulator that confers resistance to oxyradicals. [36] . rmbA gi is a transcriptional regulator coded in the SPI-3 pathogenicity Island [37] . iroB gene codes for a protein with homology with bacterial glycosyl transferase and, under iron-limited growth conditions, its expression is regulated by the iron response regulator Fur [38] . MgtC virulence factor has a dual role: when bacteria localize in macrophages a part of the protein permit to withstand the acidic pH, while another part of the protein allow the Salmonella to strive in low Mg (2+) environment [39] .

Specific toxins related to Salmonella symptomatology have been hard to pinpoint, as the host susceptibility factor appears to be central for salmonellosis symptoms development. Comparison of the hereby reported genomes with the DBDiaSNP database failed to provide sequences directly related to diarrhea symptoms [40] . In the reported genome, we encountered SPI-4 pathogenicity island, reported elsewhere to be related to the severity of the diarrhea [41] .