Impact of Health Education in Combination with Nutrition Support Nursing on the Nutritional Status and Quality of Life in Patients with Pulmonary Tuberculosis.

This study aimed to ascertain the effects of health education combined with nutrition support nursing on the nutritional status and quality of life of patients with pulmonary tuberculosis. A clinical study was conducted. Sixty-four patients with tuberculosis were selected as the study participants and divided into control and observation groups (n = 32). Both groups received antituberculosis drugs. The control group received standard nursing care, while the observation group received health education in conjunction with nutrition support nursing. After 3 months of intervention, the total effective treatment rate and adherence were compared. Before and after the intervention, the albumin (ALB), prealbumin (PA), transferrin (TF), and hemoglobin (Hb) level, body mass index (BMI), and Short Form-36 (SF-36) scores were compared. The occurrence of adverse reactions during intervention was recorded. Following the intervention, the observation group exhibited a higher treatment total effective rate and increased levels of ALB, PA, TF, Hb, and BMI compared with the control group (p < 0.05). The observation group demonstrated a higher total adherence rate and a lower incidence of adverse reactions compared with the control group (p < 0.05); the SF-36 score of the observation group was higher than that of the control group (p < 0.05). The integration of health education and nutrition support nursing can effectively enhance the therapeutic outcomes of patients with pulmonary tuberculosis. This approach not only improves their nutritional status, treatment adherence, and quality of life, but also reduces the incidence of adverse reactions. The findings of this study lay a solid foundation for further exploration of the combined effects of health education and nutrition support nursing on pulmonary tuberculosis.

The evolution of infectious transmission promotes the persistence of mcr-1 plasmids.

Conjugative plasmids play a vital role in bacterial evolution and promote the spread of antibiotic resistance. They usually cause fitness costs that diminish the growth rates of the host bacteria. Compensatory mutations are known as an effective evolutionary solution to reduce the fitness cost and improve plasmid persistence. However, whether the plasmid transmission by conjugation is sufficient to improve plasmid persistence is debated since it is an inherently costly process. Here, we experimentally evolved an unstable and costly mcr-1 plasmid pHNSHP24 under laboratory conditions and assessed the effects of plasmid cost and transmission on the plasmid maintenance by the plasmid population dynamics model and a plasmid invasion experiment designed to measure the plasmid's ability to invade a plasmid-free bacterial population. The persistence of pHNSHP24 improved after 36 days evolution due to the plasmid-borne mutation A51G in the 5'UTR of gene traJ. This mutation largely increased the infectious transmission of the evolved plasmid, presumably by impairing the inhibitory effect of FinP on the expression of traJ. We showed that increased conjugation rate of the evolved plasmid could compensate for the plasmid loss. Furthermore, we determined that the evolved high transmissibility had little effect on the mcr-1-deficient ancestral plasmid, implying that high conjugation transfer is vital for maintaining the mcr-1-bearing plasmid. Altogether, our findings emphasized that, besides compensatory evolution that reduces fitness costs, the evolution of infectious transmission can improve the persistence of antibiotic-resistant plasmids, indicating that inhibition of the conjugation process could be useful to combat the spread of antibiotic-resistant plasmids. IMPORTANCE Conjugative plasmids play a key role in the spread of antibiotic resistance, and they are well-adapted to the host bacteria. However, the evolutionary adaptation of plasmid-bacteria associations is not well understood. In this study, we experimentally evolved an unstable colistin resistance (mcr-1) plasmid under laboratory conditions and found that increased conjugation rate was crucial for the persistence of this plasmid. Interestingly, the evolved conjugation was caused by a single-base mutation, which could rescue the unstable plasmid from extinction in bacterial populations. Our findings imply that inhibition of the conjugation process could be necessary for combating the persistence of antibiotic-resistance plasmids.