The widespread and indiscriminate use of antimicrobials in food animals is a key contributor to antimicrobial resistance and antimicrobial residue, which have become a growing public and animal health concern in developing countries such as Bangladesh. This study was aimed to assess the knowledge, attitude, and practices (KAP) of large-animal farmers towards antimicrobial use (AMU), antimicrobial resistance (AMR), and antimicrobial residue (AR) with their correlation. A cross-sectional survey was conducted with a structured and pretested questionnaire in the Mymensingh division of Bangladesh. A total of 212 large-animal farmers (dairy, beef fattening, buffalo, sheep, and goat farmers) were surveyed. Results showed that most of the farmers are male (85.8%) and belong to the 18–30 age group (37.3%). About 20.3% had no formal education, and nearly half of the participants (48.1%) received training regarding antibiotic use and resistance. Penicillin is the most common class of antibiotic used (61.8%) in the study area, followed by other antimicrobials. Only 37.7% of the farmers used antimicrobials on the recommendation of their veterinarian. Overall, 41.5%, 42.5%, and 21.7% of farmers possess adequate knowledge and a satisfactory attitude and perform desirable practices, respectively. Farmers in the 31–40 age group have adequate knowledge, attitude, and ability to implement desired practices compared to farmers in the 18–30 age group. Farmers having a graduate or post-graduate degree scored better in relation to knowledge, attitude, and practice than other farmers. Analysis revealed that farmers who received training on AMU and AMR had 10.014 times (OR = 10.014, 95% CIs: 5.252–19.094), 9.409 times (OR = 9.409, 95% CIs: 4.972–17.806), and 25.994 times (OR = 25.994, 95% CIs: 7.73–87.414) better knowledge, attitude, and performance, respectively, compared to their counterparts. A significant proportion of farmers (97.2%) dispose of leftover antibiotics inappropriately. The findings of the present study will be used to intervene in the education and training of the farmers, which will help to limit the indiscriminate and irrational use of antimicrobials, leading to reducing the chances of developing AMR.
Diabetes mellitus comprises a heterogeneous group of metabolic disorders with underlying hyperglycemia and secondary cardiovascular complications. Growing evidence suggests that vascular dysfunction is among the most important causes of diabetic cardiovascular disease. Therefore, we determined whether streptozotocin (STZ)-induced diabetes in mice affects blood pressure and cerebral arterial responsiveness to angiotensin (Ang) II and acetylcholine (ACh), which are important modulators of cerebrovascular autoregulation. Diabetes was induced using a single intraperitoneal injection of STZ (50 mg/kg). Blood pressure was measured in conscious mice using the indirect tail-cuff method. Functional studies of the isolated arteries' response to vasoactive substances were performed using a micro-organ-bath system at 60 days after STZ injection. Systolic, diastolic, and mean blood pressures significantly increased at days 45 and 60 in the STZ-induced diabetic mice. In the isolated basilar arteries, ACh-induced relaxation, which is dependent on nitric oxide (NO) production from endothelial cells, decreased. In contrast, Ang II-induced contraction, mediated via rho-kinase activation in the smooth muscle, increased in the diabetic mice. There was significantly greater relaxation in the precontracted isolated basilar arteries of diabetic mice that had been treated with Y27632, a rho-kinase inhibitor, than in the control mice arteries. Pretreatment with Nω-nitro-L-arginine (L-NAME), an NO synthase inhibitor, significantly enhanced Ang II-induced contraction and Y27632-induced relaxation in the control basilar arteries but not in the STZ-induced diabetic mice arteries. These results suggest that decreased NO bioavailability and enhanced rho-kinase activity in basilar arteries contribute to altered reactivity to ACh and Ang II, respectively, in STZ-induced diabetic mice.
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