Giant grouper, Epinephelus lanceolatus in Taiwan are affected by diseases caused mainly by the members of the iridovirus and nervous necrosis virus; consequently, the increase in mortality rate of the groupers has resulted in major losses in their production, consequently threatening the commercial grouper industry. Antrodia camphorate—containing several bioactive compounds—is used for medicinal purposes including cancer prevention and treatment. In this study, the effects of A. camphorata extract (ACE) on the innate immune responses and disease resistance in giant groupers against grouper iridovirus (GIV) were examined after subjecting the groupers to diets with different levels of ACE for 14 days. After GIV infection, groupers that were fed diets with ACE doses higher than 1.5 g/kg revealed higher survival rates than that of control groupers that did not receive any ACE. The innate immune parameter values—determined after 14 days of ACE administration—were also significantly higher in groupers fed ACE-supplemented diets compared to those of the control groupers. The enhanced disease resistance of the giant groupers to GIV may be attributable to the ACE-induced innate immunity, whereas ACE showed significant anti-GIV infection activities in a dose-dependent manner, thus emphasizing the significance of ACE as a potential therapeutic for giant groupers against GIV infection.
This study aimed to elucidate the genetic characteristics of lincomycin (LCM) resistance in the absence of erythromycin (EM) resistance in fish pathogenic Lactococcus garvieae serotype I. Two novel lsa(D) variants were found in clinically LCM-sensitive and resistant strains. The amino acid sequences of the two Lsa(D) variants shared 94.77% identity with that of Lsa(D) in L. garvieae serotype II. One of the lsa(D) variants, designated as lsa(D)36A, conferred cross-resistance to lincosamides, streptogramins A, and pleuromutilin, which was defined as the LSAP-resistant phenotype. This phenotype was confirmed by the minimum inhibitory concentrations of the lsa(D)36A-disruption mutant Δlsa(D)36A, and its complementation strain. However, a single-point mutation, which led to an amino acid substitution, was found in lsa(D)36D in clinically LSAP-sensitive strains. In addition, single-nucleotide replacement of lsa(D)36D alleles was identified in laboratory-induced LCM-resistant mutants. Meanwhile, the lsa(D)36D or lsa(D)36A was also detected in EM-resistant strains carrying erm(B). These strains carried lsa(D)36D with erm(B) or lsa(D)36A with erm(B), which conferred the EM- and LCM-resistant (ML-resistant) or MLSAP-resistant phenotype, respectively. In conclusion, lsa(D)36D was an intrinsic in the LSAP-sensitive L. garvieae serotype I, and its mutated allelic variant was named as lsa(D)36A, which explains the characteristic resistance of this strain to the LSAP-resistance phenotype.
A recently described microsporidian Inodosporus fujiokai demonstrated trophic transmission from common prawn Palaemon paucidens to rainbow trout Oncorhynchus mykiss. Some of the infected trout showed petechiae-like red spots containing microsporidian spores in the trunk muscle beneath the skin and many died with hypoxia symptoms. However, it remained unclear whether the red spots are the typical sign of the disease, and the causal link between the infection and host death has not been determined. Furthermore, the identity of a similar microsporidian observed in Biwa trout Oncorhynchus masou subsp. in our previous study was not conclusive. We conducted two prawn-feeding trials using the two trout species, O. mykiss and O. masou subsp., in order to determine the pathology of I. fujiokai infection and for deeper understanding of the disease. The infections of I. fujiokai associated with high mortalities with hypoxia symptoms (opened mouth and operculum) were confirmed in both trout species that have been fed with P. paucidens. Whitish microsporidian cysts were detected in the heart as well as trunk muscle at around 20 days after feeding the infected prawns. Red spots beneath the skin were rarely observed and considered resulting from fish processing, or a post-mortem symptom. Histological analyses suggested that the cyst formation in the heart caused myocarditis which reduced cardiac function, leading to hypoxia.
A dead nematode was recovered from the swimbladder of a one-year old cultured Japanese amberjack Seriola quinqueradiata. Microscopically, the nematode had many bosses on the body surface and contained mass of larval nematodes inside the body, suggesting the parasite was a mature Philometroides seriolae. Molecular analysis of its body part confirmed the identity of the parasite. This is the first record of infection site of this nematode beside the skeletal muscle from the fish host. The amberjack had most likely been infected with the nematode before introduced to the farm. The possibility of errant parasitism in this case is discussed.