Natural biocide-assisted ultrasonic disinfection of wastewater effluent following a response surface methodology approach

The increasing prevalence of multidrug-resistant (MDR) bacteria in wastewater poses a significant threat to public health and the environment, necessitating more effective and sustainable disinfection methods. Ozonation and chlorination frequently fall short of eliminating these bacteria and can create toxic byproducts. This study introduces a novel disinfection strategy that combines ultrasonication with tea tree oil to target MDR bacteria in residential wastewater treatment systems, aiming to provide an eco-friendly, efficient, and scalable solution. The method harnesses tea tree oil's natural biocidal properties alongside the physical effects of ultrasonication, particularly acoustic cavitation, to enhance bacterial inactivation. Temperature, biocide dosage, and ultrasonication power were the three main factors that were optimized using response surface methodology. The system achieved a 2.2–2.4 log CFU/mL reduction of total bacteria in secondary effluent within 30 min and complete disinfection of modified effluent inoculated with high-strength MDR bacteria (6-log CFU/mL) in 50 min. Optimal conditions were 698.4 Watt power, 1.234 µl/mL tea tree oil, and 20.64 °C. Nucleic acid release and respiratory chain dehydrogenase inhibition indicated bacterial cell membrane rupture. Regrowth tests showed long-term effectiveness, with no bacterial colonies after three days. Using a natural biocide, the hybrid technique reduces operational costs and time, thus having commercial and environmental benefits. The capacity to remove MDR bacteria makes it an attractive contender for large-scale wastewater treatment. [Display omitted] •Novel hybrid disinfection method integrates ultrasonication and tea tree oil.•Successfully eradicated multi-drug resistant (MDR) bacteria in wastewater effluent.•The response surface methodology was critical in process optimization.•Complete disinfection resulting from cell wall rupture and metabolic inhibition.