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Background: Salmonella enterica subsp. enterica serovar Indiana (antigenic formula 1,4,12:z:1,7) is a serovar of the O:4 (B) serogroup. Serovar Indiana was first isolated from a 9-month-old child in 1955 in Indiana, US. Infection of this serovar can result in abortion in ewes. In recent years, serovar Indiana has emerged and expanded rapidly in China, frequently identified in patients experiencing diarrhea. 

NCBI PD link for serovar Indiana: https://www.ncbi.nlm.nih.gov/pathogens/isolates/#(taxgroup_name:%22Salmonella%20enterica%22)%20AND%20computed_types:(%22serotype=Indiana%22)

Genetic characteristics: Serovar Indiana has been found to be polyphyletic with one lineage identified and one stand-alone singleton that does not cluster with any other Salmonella Indiana isolates. Luque et al. analyzed 17 Indiana strains isolated from the ewes and wild birds and revealed that 11 (64.7%) were resistant to nalidixic acid (R-Nx), while 6 (35.3%) were sensitive (S-Nx). Sequencing of the gyrA gene identified specific mutations in the R-Nx strains: a substitution of glycine to cysteine at position 81 (Gly81→Cys) was found in 10 strains isolated from wild birds and ovine fetuses, and a substitution of aspartic acid to tyrosine at position 87 (Asp87→Tyr) was identified in one strain isolated from ewe feces. Serovar Indiana was commonly found in raw chicken from the Henan province in China, which have been reported to be resistant to ciprofloxacin, with frequent co-resistance to cefotaxime. A Chinese study indicated that serovar Indiana ST17 is an emerging multidrug-resistant (MDR) superclone found in chickens. ST17 carries a novel cluster of resistance genes, including blaCTX-M, blaOXA-1-like, and/or blaTEM-1-like. Zhang et al. found that ST17 isolates were distributed into four clades (I, II, III and IV), which was likely linked to international clonal dissemination. Hu et al. investigated a total of 224 CIP-CTX co-resistant  resistant Indiana isolates collected from retail chicken samples in China and found the most prevalent amino acid substitutions observed were in GyrA (S83F and D87N/G) and ParC (T57S and S80R). Additionally, the plasmid-mediated quinolone resistance (PMQR) genes genes oqxA, oqxB, and aac(6′)-Ib-cr were frequently identified as key contributors to quinolone resistance.

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