Abstract

Salmonella enterica serovar Heidelberg is a human pathogen also found in broilers. A strain (UFPR1) has been associated with field reports of resistance to short-chain organic acids (SCOA) in broilers in the South of Brazil, but was susceptible to a Bacillus subtilis-based probiotic added in feed in a related study. This work aimed to (i) report clinical symptoms caused by SH UFPR1 in broilers, (ii) study its susceptibility to some antibiotics in vitro, and (iii) SCOA in vivo; and (iv) relate these phenotypic observations with its genome characteristics. Two in vivo trials used 1-day-old chicks housed for 21 days in 8 sterilized isolated negative pressure rooms with 4 battery cages of 12 birds each. Birds were challenged or not with 107 CFU/bird of SH UFPR1 orally and exposed or not to SCOA in a 2 × 2 factorial design. Zootechnical parameters were unaffected (P > 0.05), no clinical signs were observed, and few cecal and hepatic histologic and immune-related alterations were seen, in birds challenged with SH. Formic and propionic acids added together in drinking water, fumaric and benzoic acid in feed (Trial 1), and coated calcium butyrate in feed (Trial 2) did not reduce the SH isolation frequencies seen in cecum and liver in broilers after SH challenge (P > 0.05). SH UFPR1 was susceptible to amikacin, amoxicillin + clavulanate, ceftiofur, cephalexin, doxycycline and oxytetracycline; and mildly susceptible to ampicillin + sulbactam, cephalothin, ciprofloxacin, enrofloxacin, and gentamycin in an in vitro minimum inhibitory concentration model using Mueller–Hinton agar. The whole genome of SH UFPR1 was sequenced and consisted of a circular chromosome, spanning 4,760,321 bp with 52.18% of GC-content encoding 84 tRNA, 22 rRNA, and 4,427 protein-coding genes. The comparison between SH UFPR1 genome and a multidrug-resistant SL476 strain revealed 11 missing genomic fragments and 5 insertions related to bgt, bgr, and rpoS genes. The deleted genes codify proteins associated with cell cycle regulation, virulence, drug resistance, cellular adhesion, and salt efflux which collectively reveal key aspects of the evolution and adaptation of SH strains such as organic acids resistance and antibiotic sensitivity and provide information relevant to the control of SH in poultry.

Highlights

  • Despite recent advances in the treatment of infectious diseases, pathogenic microorganisms, including Salmonella, remain an important threat to human and animal health worldwide [1]

  • At the in vivo trails, short-chain organic acids (SCOA) were offered to the birds during the early days of life to allow the gut to adapt to the treatment before the SH challenge

  • No effect in zootechnical parameters was observed at any time in both trials (P > 0.05) either from the adding SCOA in drinking water and/or feed, from challenging birds with SH UFPR1 strain, or from the interaction between these factors (Table 2)

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Summary

Introduction

Despite recent advances in the treatment of infectious diseases, pathogenic microorganisms, including Salmonella, remain an important threat to human and animal health worldwide [1]. Non-typhoid Salmonella serovars are well-known pathogens but they silently infect animals, poultry, as transient members of the intestinal microbial population without causing disease [2, 3]. Kogut et al [4] described that the infection in chickens caused by Salmonella Enteritidis leads to immune tolerance beginning around 3–4 days post-primary infection. This decreases the host immune responsiveness resulting in the establishment of Salmonella and persistent colonization. This asymptomatic infection could increase the probability of transmission to humans via contaminated food [5]

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