Salmonella is a major zoonotic food-borne pathogen that persists on poultry farms, and animals undergo reinfection with endemic strains. The present study aimed to investigate the characteristics and dissemination of antimicrobial-resistant Salmonella within and between broiler farms that used enrofloxacin and those that did not. Cloacal and environmental (litter, feed, and water) samples from two selected flocks in each of 12 farms owned by the same company were collected three times over a 30-day period of two production cycles during 2015–2016. The rate of Salmonella isolation was 7.8% (123/1584). Nine Salmonella serotypes (116 isolates) and seven untypable isolates were identified, and Salmonella Montevideo was the most prevalent serotype. Azithromycin-resistant (17.9%) and colistin-resistant (3.3%) isolates were detected, and multidrug-resistant isolates (43.1%) were also observed. No isolate was resistant to enrofloxacin or ciprofloxacin; however, intermediate resistance to enrofloxacin was significantly higher (P < 0.05) in farms that used enrofloxacin than in those that did not. The rate of multi-drug resistance among litter isolates (25/44, 56.8%) was significantly higher (P < 0.05) than that among cloacal swab (24/67, 35.8%) and feed (4/12, 33.3%) isolates. Pulsed-field gel electrophoresis (PFGE) analysis of strains of the same serotype was conducted to determine their epidemiological relationship. The PFGE types were classified into 31 groups with a 100% correlation cutoff in dendrograms for Salmonella Montevideo isolates, which showed 100% genomic identity based on age, sample type, flock, and production cycle within and between farms. The present study highlights the occurrence of horizontal transmission and cyclic contamination with antimicrobial-resistant Salmonella in broiler farms owned by the same company. Litter may be a good indicator of indoor environmental contamination with antimicrobial-resistant Salmonella on farms. Additionally, enrofloxacin use may be one of the factors promoting resistance towards it in Salmonella.

The aim of the present study was to investigate variation in antimicrobial resistance in Clostridium perfringens (C. perfringens) isolated from chickens after withdrawal of antimicrobial growth promoters (AGPs); and to investigate the correlation between the presence of toxin genes (cpb2, netB, and tpeL) and antimicrobial resistance. Altogether, 162 isolates of C. perfringens were obtained from chickens displaying clinical signs of necrotic enteritis (n = 65) and from healthy chickens (n = 97) in Korea during 2010–2016. Compared to before AGP withdrawal, increased antimicrobial resistance or MIC₅₀/MIC₉₀ value was observed for nine antimicrobials including penicillin, tetracycline, tylosin, erythromycin, florfenicol, enrofloxacin, monensin, salinomycin, and maduramycin. Significantly (p < 0.05) higher resistance to gentamicin, clindamycin, and virginiamycin was found in isolates from chickens with necrotic enteritis compared to those from healthy chickens. tpeL gene was not detected in C. perfringens isolates from healthy chickens. A correlation between toxin gene prevalence and antibiotic resistance was found in the C. perfringens isolates. Because the usage of antimicrobials may contribute to the selection of both resistance and toxin genes, these can potentially make it challenging to control antimicrobial resistance in pathogenic colonies. Therefore, a more complete understanding of the interplay between resistance and virulence genes is required.

Avian reoviruses (ARVs) are ubiquitous in domestic poultry with 80% of them being non-pathogenic and they are frequently found in clinically healthy birds. ARVs have also been known to be the etiological agents of viral arthritis (VA), tenosynovitis, myocarditis, runting-stunting syndrome (RSS), and respiratory and enteric disease in chickens. Significant economic losses during the process of poultry husbandry are due, in part, to unmitigated ARV infections throughout the poultry industry. Recently, many isolates shared genetic similarities between those recovered from wild birds and those recovered from poultry. One explanation may be that there is a degree of spillover and spillback of ARVs between the two groups. However, studies on the role of wild birds in the epidemiology and pathogenicity of ARVs are insufficient. Here, we describe the pathogenicity in specific pathogen-free (SPF) chickens of ARV originating from wild birds. The challenge experiment was conducted in six groups including a negative control group, a positive control group (reference strain of S1133), and four groups (A15-157, A18-13, A18-205, A19-106) infected with ARVs from wild birds. The 7-day-old SPF chickens were inoculated with 10⁶TCID₅₀ ARV to evaluate the clinical signs, changes in weight gain, gross lesions, histological changes, virus replication, and serum antibody levels. The peak of clinical signs was from 3 to 5 days post infection (dpi). In addition, the death of one chicken was found in the group infected with the A18-13 isolate. Reduced body weight was also found in chickens infected with ARVs from wild birds compared to the negative control group. All the ARVs infection groups showed noticeable swelling of the footpad. In addition, ARVs were detected in the bursa, tendon, and hock joint by reverse transcription-polymerase chain reaction (RT-PCR) in all infected groups at 5 and 15 dpi. Histopathological observations revealed acute inflammatory responses on the synovium covering the joint surfaces (arthritis) and tendon sheaths (tenosynovitis), as well as bursa atrophy and lymphocyte depletion. The analysis of the humoral response was performed by ELISA assay, and chickens infected with ARVs showed seroconverted. In conclusion, this study described the typical severe disease of acute VA and tenosynovitis in SPF chickens infected with ARVs derived from wild birds. This study confirmed the pathogenicity of ARVs infection in SPF chickens for the first time, and these results enrich our understanding of the pathogenicity of ARVs derived from wild birds.

We investigated the molecular mechanisms underlying macrolide resistance in 38 strains ofCampylobacterisolated from poultry. Twenty-seven strains were resistant to azithromycin and erythromycin, five showed intermediate azithromycin resistance and erythromycin susceptibility, and six showed azithromycin resistance and erythromycin susceptibility. FourCampylobacter jejuniand sixCampylobacter colistrains had azithromycin MICs which were 8–16 and 2–8-fold greater than those of erythromycin, respectively. The A2075G mutation in the 23S rRNA gene was detected in 11 resistant strains with MICs ranging from 64 to ≥ 512μg/mL. Mutations including V137A, V137S, and a six-amino acid insertion (114-VAKKAP-115) in ribosomal protein L22 were detected in theC. jejunistrains. Erythromycin ribosome methylase B-erm(B) was not detected in any strain. All strains except three showed increased susceptibility to erythromycin with twofold to 256-fold MIC change in the presence of phenylalanine arginine ß-naphthylamide (PAßN); the effects of PAßN on azithromycin MICs were limited in comparison to those on erythromycin MICs, and 13 strains showed no azithromycin MIC change in the presence of PAßN. Differences between azithromycin and erythromycin resistance and macrolide resistance phenotypes and genotypes were observed even in highly resistant strains. Further studies are required to better understand macrolide resistance inCampylobacter.

Positive identification rates of Salmonella enterica in hatcheries and upstream breeder farms were 16.4% (36/220) and 3.0% (6/200), respectively. Among the Salmonella serovars identified in the hatcheries, S. enterica ser. Albany (17/36, 47.2%) was the most prevalent, followed by the serovars S. enterica ser. Montevideo (11/36, 30.6%) and S. enterica ser. Senftenberg (5/36, 13.9%), which were also predominant. Thirty-six isolates showed resistance to at least one antimicrobial tested, of which 52.8% (n = 19) were multidrug resistant (MDR). Thirty-three isolates (enrofloxacin, MIC ≥ 0.25) showed point mutations in the gyrA and parC genes. One isolate, S. enterica ser. Virchow, carrying the bla_CTX-M-15 gene from the breeder farm was ceftiofur resistant. Pulsed-field gel electrophoresis (PFGE) showed that 52.0% S. enterica ser. Montevideo and 29.6% S. enterica ser. Albany isolates sourced from the downstream of hatcheries along the broiler chicken supply chain carried the same PFGE types as those of the hatcheries. Thus, the hatcheries showed a high prevalence of Salmonella isolates with high antimicrobial resistance and no susceptible isolate. The AMR isolates from hatcheries originating from breeder farms could disseminate to the final retail market along the broiler chicken supply chain. The emergence of AMR Salmonella in hatcheries may be due to the horizontal spread of resistant isolates. Therefore, Salmonella control in hatcheries, particularly its horizontal transmission, is important.