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Surveillance study of faecal E. coli isolates producing AmpC and extended spectrum β-lactamases (ESBLs) enzymes in poultry and workers from aviculture around Tehran
2015
Doregiraee, Fatemeh | Nayeri Fasaei, Bahar | Alebouyeh, Masoud
BACKGROUND: AmpC and ESBLs as mediated-plasmid extended spectrum β-lactabases are the main factors of resistance to extended-spectrum cephalosporins in enterobacteriacea especially E. coli and will follow treatment failure, high costs of treatment in human and economic losses in the poultry industry. OBJECTIVES: The purpose of this study was to screen and study the faecal E. coli isolates producing extended spectrum β-lactamases (ESBLs) and AmpC enzymes and related workers. METHODS: A total of 500 cloacal swab samples from broiler chickens and 25 rectal swab samples from workers were collected from five poultry houses around Tehran. All samples were seeded on MacConkey agar and identification of E. coli isolates were performed via biochemical tests. Antibiotic susceptibility was determined against 12 antibiotics using the disk diffusion method as recommended by the clinical and laboratory standard institute (CLSI2012). Ceftazidim / ceftazidim-clavolanic acid and cefoxitin / cefoxitin-EDTA disks were used for the detection of ESBL and AmpC phenotypes, respectively. phonetic analysis of the drug resistances was performed via SPSS software and Chi-square test. ESBL- producing E. coli screened by PCR for the presence of genes encoding beta-lactamases of TEM, CTX-M and SHV. RESULTS: A total 467 E. coli isolates were isolated from 88.9% of the samples as 92% and 72.7% of isolates presenting MDR phenotype among chickens and workers respectively. ESBL phenotype detected in 5.5% (26) of poultry isolates while, none of the workers isolates have this phenotype. Six isolates carried both of TEM and CTX-M whereas, five and one isolates were detected only for TEM and CTX-M, respectively. Eighty-eight and nine-tenths percent of ESBL E. coli displayed AmpC phenotype. CONCLUSIONS: Since cephalosporins are not used in broilers in Iran, isolation of faecal E. coli isolates producing extended spectrum β-lactamases in broilerchickens can indicate transfer of the resistance genes via plasmids and other mobile genetic elements among Enterobacteriaceae.
Show more [+] Less [-]Association of increased rate of condemnation of broiler carcasses due to hepatic abnormalities with immunosuppressive diseases in the broiler chicken industry in Saskatchewan
2015
Amini, Keyvan | Zachar, Tara | Popowich, Shelly | Knezacek, Tennille | Goodhope, Bob | Wilson, Philip | Gomis, Susantha
The objective of this study was to identify the causative agents of hepatitis observed in broiler chickens at processing. Livers of chickens from 16 broiler farms in Saskatchewan with gross lesions of hepatitis were collected at processing. In addition to routine bacterial isolation and histopathological examination, serologic studies for infectious bursal disease virus (IBDV) and Chicken anaemia virus (CAV), calculation of the ratio of the weight of the bursa of Fabricius (BF) to body weight (BBW), and histopathological examination of the BF were done. Of the 264 livers with gross lesions, 83% had multifocal to coalescing necrotizing hepatitis, 16% had perihepatitis, and 1% had hemorrhages. No definitive causative microorganisms were isolated from the hepatic lesions; however, no significant bacterial isolations were made. Bursal atrophy, low BBW ratio, and high titer of antibody against IBDV each correlated with the rate of total condemnations (P = 0.0188, P = 0.0001, and P = 0.0073, respectively). Nucleotide sequencing of IBDV isolated from the BF identified the variant strains Delaware-E and 586. Condemnation because of hepatic lesions was correlated with titer of antibody against IBDV and BBW (P = 0.016 and P = 0.027). The results of this study demonstrate that hepatic lesions in Saskatchewan chickens are not currently caused by a primary bacterial pathogen but are associated with indicators of immunosuppression that is likely due to variant IBDV.
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