Campylobacter is a leading foodborne bacterial pathogen, which causes gastroenteritis in humans. This pathogenic organism is increasingly resistant to antibiotics, especially fluoroquinolones and macrolides, which are the most frequently used antimicrobials for the treatment of campylobacteriosis when clinical therapy is warranted. As a zoonotic pathogen, Campylobacter has a broad animal reservoir and infects humans via contaminated food, water or milk. Antibiotic usage in both animal agriculture and human medicine, can influence the development of antibiotic-resistant Campylobacter. This review will describe the trend in fluoroquinolone and macrolide resistance in Campylobacter, summarize the mechanisms underlying the resistance to various antibiotics and discuss the unique features associated with the emergence, transmission and persistence of antibioticresistant Campylobacter. Special attention will be given to recent findings and emphasis will be placed on Campylobacter resistance to fluoroquinolones and macrolides. A future perspective on antibiotic resistance and potential approaches for the control of antibiotic-resistant Campylobacter, will also be discussed.
Escherichia coli strains causing avian colibacillosis and human neonatal meningitis, urinary tract infections, and septicemia are collectively known as extraintestinal pathogenic E. coli (ExPEC). Characterization of ExPEC strains using various typing techniques has shown that they harbor many similarities, despite their isolation from different host species, leading to the hypothesis that ExPEC may have zoonotic potential. The present study examined a subset of ExPEC strains: neonatal meningitis E. coli (NMEC) strains and avianpathogenic E. coli (APEC) strains belonging to the O18 serogroup. The study found that they were not easily differentiated on the basis of multilocus sequence typing, phylogenetic typing, or carriage of large virulence plasmids. Among the APEC strains examined, one strain was found to be an outlier, based on the results of these typing methods, and demonstrated reduced virulence in murine and avian pathogenicity models. Some of the APEC strains tested in a rat model of human neonatal meningitis were able to cause meningitis, demonstrating APEC's ability to cause disease in mammals, lending support to the hypothesis that APEC strains have zoonotic potential. In addition, some NMEC strains were able to cause avian colisepticemia, providing further support for this hypothesis. However, not all of the NMEC and APEC strains tested were able to cause disease in avian and murine hosts, despite the apparent similarities in their known virulence attributes. Thus, it appears that a subset of NMEC and APEC strains harbors zoonotic potential, while other strains do not, suggesting that unknown mechanisms underlie host specificity in some ExPEC strains.
The purpose of this study was to develop a multiplex polymerase chain reaction (PCR) protocol useful in the virulence genotyping of Salmonella spp. with the idea that genotyping could augment current Salmonella characterization and typing methods. Seventeen genes associated with Salmonella invasion, fimbrial production, toxin production, iron transport, and intramacrophage survival were targeted by three PCR reactions. Most of these genes are required for full Salmonella virulence in a murine model, and many are also located onSalmonella pathogenicity islands (PAIs) and are associated with type III secretion systems (TTSSs). Once the success of procedures that used positive and negative control strains was verified, the genotypes of 78 Salmonella isolates incriminated in avian salmonellosis (primarily from sick, commercially reared chickens and turkeys) and 80 Salmonella isolates from apparently healthy chickens or turkeys were compared. Eleven of the 17 genes tested (invA, orgA, prgH, tolC, spaN [invJ], sipB, sitC, pagC, msgA, spiA, and iroN) were found in all of the isolates. Another (sopB) was present in all isolates from sick birds and all but one isolate from healthy birds. The remaining five genes (lpfC, cdtB, sifA, pefA, and spvB) were found in 10%-90% of the isolates from sick birds and 3.75%-90% of the healthy birds. No significant differences in the occurrence of these genes between the two groups of isolates were detected. These results suggest that these virulence genes, and presumably the PAIs and TTSSs with which they are associated, are widely distributed among Salmonella isolates of birds, regardless of whether their hosts of origin have been identified as having salmonellosis. SUMMARY. The purpose of this study was to develop a multiplex polymerase chain reaction (PCR) protocol useful in the virulence genotyping of Salmonella spp. with the idea that genotyping could augment current Salmonella characterization and typing methods. Seventeen genes associated with Salmonella invasion, fimbrial production, toxin production, iron transport, and intramacrophage survival were targeted by three PCR reactions. Most of these genes are required for full Salmonella virulence in a murine model, and many are also located on Salmonella pathogenicity islands (PAIs) and are associated with type III secretion systems (TTSSs). Once the success of procedures that used positive and negative control strains was verified, the genotypes of 78 Salmonella isolates incriminated in avian salmonellosis (primarily from sick, commercially reared chickens and turkeys) and 80 Salmonella isolates from apparently healthy chickens or turkeys were compared. Eleven of the 17 genes tested (invA, orgA, prgH, tolC, spaN [invJ], sipB, sitC, pagC, msgA, spiA, and iroN) were found in all of the isolates. Another (sopB) was present in all isolates from sick birds and all but one isolate from healthy birds. The remaining five genes (lpfC, cdtB, sifA, pefA, and spvB) were found in 10%-90% of the isolates from sick birds and 3.75%-90...
Avian pathogenic Escherichia coli (APEC) strains belong to a category that is associated with colibacillosis, a serious illness in the poultry industry worldwide. Additionally, some APEC groups have recently been described as potential zoonotic agents. In this work, we compared APEC strains with extraintestinal pathogenic E. coli (ExPEC) strains isolated from clinical cases of humans with extra-intestinal diseases such as urinary tract infections (UTI) and bacteremia. PCR results showed that genes usually found in the ColV plasmid (tsh, iucA, iss, and hlyF) were associated with APEC strains while fyuA, irp-2, fepC sitDchrom, fimH, crl, csgA, afa, iha, sat, hlyA, hra, cnf1, kpsMTII, clpV Sakai and malX were associated with human ExPEC. Both categories shared nine serogroups (O2, O6, O7, O8, O11, O19, O25, O73 and O153) and seven sequence types (ST10, ST88, ST93, ST117, ST131, ST155, ST359, ST648 and ST1011). Interestingly, ST95, which is associated with the zoonotic potential of APEC and is spread in avian E. coli of North America and Europe, was not detected among 76 APEC strains. When the strains were clustered based on the presence of virulence genes, most ExPEC strains (71.7%) were contained in one cluster while most APEC strains (63.2%) segregated to another. In general, the strains showed distinct genetic and fingerprint patterns, but avian and human strains of ST359, or ST23 clonal complex (CC), presented more than 70% of similarity by PFGE. The results demonstrate that some “zoonotic-related” STs (ST117, ST131, ST10CC, ST23CC) are present in Brazil. Also, the presence of moderate fingerprint similarities between ST359 E. coli of avian and human origin indicates that strains of this ST are candidates for having zoonotic potential.
Because of concerns related to the use of antibiotics in animal agriculture, antibiotic-free alternatives are greatly needed to prevent disease and promote animal growth. One of the current challenges facing commercial turkey production in Minnesota is difficulty obtaining flock average weights typical of the industry standard, and this condition has been coined “Light Turkey Syndrome” or LTS. This condition has been identified in Minnesota turkey flocks for at least five years, and it has been observed that average flock body weights never approach their genetic potential. However, a single causative agent responsible for these weight reductions has not been identified despite numerous efforts to do so. The purpose of this study was to identify the bacterial community composition within the small intestines of heavy and light turkey flocks using 16S rRNA sequencing, and to identify possible correlations between microbiome and average flock weight. This study also sought to define the temporal succession of bacteria occurring in the turkey ileum. Based upon 2.7 million sequences across nine different turkey flocks, dominant operational taxonomic units (OTUs) were identified and compared between the flocks studied. OTUs that were associated with heavier weight flocks included those with similarity to Candidatus division Arthromitus and Clostridium bartlettii, while these flocks had decreased counts of several Lactobacillus species compared to lighter weight flocks. The core bacterial microbiome succession in commercial turkeys was also defined. Several defining markers of microbiome succession were identified, including the presence or abundance of Candidatus division Arthromitus, Lactobacillus aviarius, Lactobacillus ingluviei, Lactobacillus salivarius, and Clostridium bartlettii. Overall, the succession of the ileum bacterial microbiome in commercial turkeys proceeds in a predictable manner. Efforts to prevent disease and promote growth in the absence of antibiotics could involve target dominant bacteria identified in the turkey ileum that are associated with increased weight gain.
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