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.

BACKGROUND: High grain diets in ruminants increases the risk of digestives disorders such as acidosis which may lead to high economic loss. OBJECTIVES: This experiment was conducted to determine the effects of an unsaturated and polyunsaturated fatty acid and monensin on gene expression of enzymes involved metabolic pathway of cell proliferation and rumen epithelial intracellular pH regulation. METHODS: Twenty two male Afshari lambs with live body weight of 45 ± 8 kg and six month age were used in a completely randomized design with 3 treatments replicates for 77days including 21 days adaptation period. Experimental diets were consisted of a basal high concentrate diet (16% CP and 2.75 Mcal/kg ME) and 1) no additive (control, C= 8 lambs), 2) 30 mg monensin/day/head during the whole experimental period (T1= 8 lambs), and 3) (polyunsaturated fatty acidduring the whole experimental period (T2 = 6 lambs). Lambs were killed after 77 days on the treatment diets. RESULTS: Compared with the C treatment, relative abundance of mRNA of monocarboxylate transporter isoforms MCT1, MCT4 and the ketogenic enzyme 3-hydroxy-3 methyl-glutaryl CoA-synthase (HMGCS2) were higher for the T1 treatment. The expression of cholesterolgenic enzyme HMGCS1 was down-regulated for the T1 treatment and that of HMGCS1 was up- regulated for the T2 treatment. The expression of MCT1 and MCT4 were down-regulated for the T2 treatment. Monensin had an additional impact on the mRNA abundance of epithelial SCFA- and acid-base transporters with concurrent changes in rumen epithelial thickness. CONCLUSIONS: The results suggest that adding monensin and oil as nutritional means to reduce acidosis cause changes in mRNA expression of VFA transferring proteins and limiting enzyme in the synthesis of cholesterol and Ketone bodies in the rumen epithelium.

Diminazene aceturate is one of a limited number of drugs currently being used in animals to treat the tsetse fly-transmitted protozoal disease, African trypanosomiasis. Efficacy of the drug at the recommended single IM administered doses of 3.5 and 7.0 mg/kg of body weight is widely acknowledged. However, resistance to the drug at these dosages has been reported. Although the mechanisms of resistance to diminazene are poorly understood, field and experimental data indicate that it may develop naturally through administration of subcurative doses, or as a result of cross-resistance. Evidence from other experimental studies indicates that there are additional mechanisms by which trypanosomes may develop resistance to diminazene aceturate. For instance, some populations ot Trypanosoma brucei and T. vivax are refractory to treatment because of their ability to invade the CNS, a site that is believed to be poorly accessible to diminazene. Furthermore, in recent studies carried out in goats, it has been documented that the ability of T. Congolense IL 3274 to survive treatment with diminazene depends on the stage of infection when treatment is administered; populations of the parasite reappeared in animals that were treated on day 19 after tsetse fly challenge, whereas all goats were cured when treated on day 1 of infection. Because trypanosomes are confined to the skin on day 1 after infection, but thereafter invade the blood circulation, it is possible that the efficacy of the treatment on day 1 is attributable to exposure of the small number of parasites, relative to later stages of infection, to higher concentrations of drug than those attained in blood. The objective of the study reported here was to determine whether diminazene's pharmacokinetics differ between plasma and lymph draining the skin of goats and therefore account for the variation in therapeutic activity of the drug at different stages of a tsetse fly-transmitted infection. Peripheral lymph was used for this work because it appears to be identical in composition to tissue interstitial fluid, into which trypanosomes are inoculated by infected tsetse flies when feeding.