The Antibacterial Activity of Thymol Against Drug-Resistant Streptococcus iniae and Its Protective Effect on Channel Catfish (Ictalurus punctatus)

Abstract

Streptococcus iniae is a zoonotic pathogen, which seriously threatens aquaculture and human health worldwide. Antibiotics are the preferred way to treat S. iniae infection. However, the unreasonable use of antibiotics leads to the enhancement of bacterial resistance, which is not conducive to the prevention and treatment of this disease. Therefore, it is urgent to find new efficient and environmentally friendly antibacterial agents to replace traditional antibiotics. In this study, the antibacterial activity and potential mechanism of thymol against S. iniae were evaluated by electron microscopy, lactate dehydrogenase, DNA and protein leakage and transcriptomic analysis. Thymol exhibited potent antibacterial activity against S. iniae in vitro, and the MIC and MBC were 128 and 256μg/mL, respectively. SEM and TEM images showed that the cell membrane and cell wall were damaged, and the cells were abnormally enlarged and divided. 2MIC thymol disrupted the integrity of cell walls and membranes, resulting in the release of intracellular macromolecules including nucleotides, proteins and inorganic ions. The results of transcriptomic analysis indicated that thymol interfered with energy metabolism and membrane transport, affected DNA replication, repair and transcription in S. iniae. In vivo studies showed that thymol had a protective effect on experimental S. iniae infection in channel catfish. It could reduce the cumulative mortality of channel catfish and the number of S. iniae colonization in tissues, and increase the activities of non-specific immune enzymes in serum, including catalase, superoxide dismutase, lysozyme and acid phosphatase. Taken together, these findings suggested that thymol may be a candidate plant agent to replace traditional antibiotics for the prevention and treatment of S. iniae infection.

Activity of the botanical compound thymol against kiwifruit rot caused by Fusarium tricinctum and the underlying mechanisms

“…Therefore, the mode of action of this compound to F. tricinctum was investigated. It was found that the cell wall structure of F. tricinctum was not or only slightly affected by the treatment of thymol, which is in contrast to a recent study claiming that thymol could damage the cell wall of the bacterium Streptococcus iniae 43 . This may be resulted from the distinct difference of cell wall structure between fungi and bacteria.…”

“…It was found that the cell wall structure of F. tricinctum was not or only slightly affected by the treatment of thymol, which is in contrast to a recent study claiming that thymol could damage the cell wall of the bacterium Streptococcus iniae. 43 This may be resulted from the distinct difference of cell wall structure between fungi and bacteria. However, thymol could rapidly cause the damage of plasma membrane and increase membrane permeability.…”

Evaluation of the Antibacterial Activity of Essential Oil of Dysphania ambrosioides (L.) Mosyakin and Clemants Against Clinical Multidrug-Resistant Bacteria

“…Thymol is involved in the up-regulation of genes coding for outer membrane protein synthesis. It also interacts with membrane proteins which disrupt outer and inner membrane and intracellular targets 42,43 . Carvacrol is responsible for the inhibition of flagellin which damages bacterial motility 34 .…”

Protective Effects of Natural Antioxidants on Inflammatory Bowel Disease: Thymol and Its Pharmacological Properties

“…Thymol enhances anti-oxidative capacity to alleviate OS in different tissues [ 33 ]. As a spectrum anti-bacterial agent, thymol reduces the activities of microorganisms belonging to the Enterobacteriaceae, Streptococcus, and Saccharomycetaceae families, involving membrane rupture, inhibition of biofilm formation, and other pathways [ 34 , 35 ]. Thymol shows anti-viral potential to inhibit virus colonization, such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-298), by docking with the S1 receptor-binding domain of spike glycoprotein [ 36 ].…”