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Food-producing animals including bovine species are major reservoirs for different food-borne pathogens. Staphylococcus aureus is among the causes of food-borne diseases globally that can be transmitted mainly through consumption of contaminated foods of animal origin and emergence of multidrug resistant bacteria like methicillin resistant S. aureus (MRSA) become a significant public health concern. A cross-sectional study was conducted from October 2019 to July 2021 to estimate the prevalence, identify associated risk factors and determine antibiogram profiles of S. aureus and MRSA from foods of bovine origin in Dessie and Kombolcha towns. A total of 384 foods of bovine origin samples were collected using random sampling techniques. Isolation and characterization of S. aureus were done according to the standard bacteriological protocols. Agar disc diffusion method was employed to determine the in vitro antimicrobial resistance pattern of S. aureus and MRSA isolates. The collected data were analyzed using descriptive and inferential statistics. The overall prevalence of S. aureus and MRSA were found to be the equal (39.3%). The prevalence of S. aureus was 55.6, 44.0, 41.1, 36.4, 16.7, and 0.0% in yogurt, beef swab, udder milk, carcass swab, tank milk, and cheese samples, respectively. A statistically significant difference was observed in the prevalence of S. aureus among the different sample types (P < 0.05). The prevalence of S. aureus in milk samples from cows with and without treatment history was 47.1 and 26.0%, respectively. The difference in the prevalence of S. aureus among treatment history categories was statistically significant (P < 0.05). Higher prevalence of S. aureus was recorded in carcass swab samples collected from Dessie town (50.0%), municipal abattoirs (46.7%), slaughtering process with poor hygiene (57.1%); and carcasses slaughtered by butchers with poor hygiene (62.1%). 100.0, 97.4, 90.1, and 74.8% of S. aureus isolates were resistant to Cefoxitin, Penicillin G, Ampicillin, and Nalidixic acid, respectively. 97.3% of S. aureus isolates showed multidrug resistance to three and more than three drugs. To reduce the high magnitude of S. aureus contamination of foods of bovine origin, improvement of cattle health and good hygienic procedures along the production chain should be implemented in the study areas. [ABSTRACT FROM AUTHOR]

BACKGROUND:Trypanosoma evansi is mechanically transmitted by biting flies and affects camels, equines, and other domestic and wild animals in which it causes a disease called surra. At least two types of Trypanosoma evansi circulate in Ethiopia: type A, which is present in Africa, Latin America and Asia, and type B, which is prevalent in Eastern Africa. Currently, no information is available about the drug sensitivity of any Ethiopian T. evansi type. METHODOLOGY/PRINCIPAL FINDINGS:This study was conducted with the objective of determining the in vivo drug sensitivity of two T. evansi type A and two type B stocks that were isolated from camels from the Tigray and Afar regions of Northern Ethiopia. We investigated the efficacy of four trypanocidal drugs to cure T. evansi infected mice: melarsamine hydrochloride (Cymelarsan), diminazene diaceturate (Veriben and Sequzene), isometamidium chloride (Veridium) and homidium chloride (Bovidium). Per experimental group, 6 mice were inoculated intraperitoneally with trypanosomes, treated at first peak parasitemia by daily drug injections for 4 consecutive days and followed-up for 60 days. Cymelarsan at 2 mg/kg and Veriben at 20 mg/kg cured all mice infected with any T. evansi stock, while Sequzene at 20 mg/kg caused relapses in all T. evansi stocks. In contrast, Veridium and Bovidium at 1 mg/kg failed to cure any T. evansi infection in mice. CONCLUSIONS/SIGNIFICANCE:We conclude that mice infected with Ethiopian T. evansi can be cured with Cymelarsan and Veriben regardless of T. evansi type. In contrast, Veridium and Bovidium are not efficacious to cure any T. evansi type. Although innate resistance to phenanthridines was previously described for T. evansi type A, this report is the first study to show that this phenomenom also occurs in T. evansi type B infections.

Antibiotic-resistant Staphylococcus aureus isolates pose a severe challenge to both veterinary and health professions and dairy cattle producers. Cross-sectional study was conducted from November 2014 to May 2015 to isolate and identify S. aureus from mastitic cows' milk and estimate the occurrence of MRSA in the dairy farms of Shire. Physical examination and California mastitis test were performed on a total of 220 dairy cows. Bacteriological isolation and identification and antibiogram testing were performed. Furthermore, multiplex polymerase chain reaction (PCR) was done for the detection of mec A and fem A genes. Out of the 220 dairy cows, 64 (29.09%) were positive for bovine mastitis, and of these, 32.81% were coagulase-positive S. aureus (CoPS). Antibiogram test results showed 100% of the isolates were resistant to penicillin G, nalidixic acid, and ampicillin, and 33.33% of the CoPS showed resistance to oxacillin (phenotypically MRSA positive). But 38.09% of the CoPS were found to be resistant and susceptible to vancomycin. PCR amplification of the seven phenotypically MRSA isolates revealed that 42.9% and 71.4% of them were found to carry fem A and mec A genes, respectively. The current study revealed the existence of alarming level of CoPS and development of multidrug resistance. [ABSTRACT FROM AUTHOR]

E2F transcription factors control the oscillating expression pattern of multiple target genes during the cell cycle. Activator E2Fs, E2F1-3, induce an upswing of E2F targets, which is essential for the G1-to-S phase transition, whereas atypical E2Fs, E2F7 and E2F8, mediate a downswing of the same targets during late S, G2, and M phases. Expression of atypical E2Fs is induced by E2F1-3, but it is unknown how atypical E2Fs are inactivated in a timely manner. Here, we demonstrate that E2F7 and E2F8 are substrates of the anaphase-promoting complex/cyclosome ( APC/C). Removal of CDH1, or mutating the CDH1-interacting KEN boxes, stabilized E2F7/8 from anaphase onwards and during G1. Expressing KEN mutant E2F7 during G1 impairs S phase entry and eventually results in cell death. Furthermore, we show that E2F8, but not E2F7, interacts also with APC/ CCdc20. Importantly, atypical E2Fs can activate APC/ CCdh1 by repressing its inhibitors cyclin A, cyclin E, and Emi1. In conclusion, we discovered a feedback loop between atypical E2Fs and APC/ CCdh1, which ensures balanced expression of cell cycle genes and normal cell cycle progression. [ABSTRACT FROM AUTHOR]