Hydrolytic bacteria associated with natural helminth infection in the midgut of Red Sea marbled spinefoot rabbit fish Siganus rivulatus.

Fish infected with intestinal helminths or pathogenic bacteria can pose a serious risk of foodborne disease, threatening human and animal health, and require high attention. The current study investigates the diversity and composition of the microbiota in the midgut of rabbit fish Siganus rivulatus naturally infected with helminths. Six species of helminth parasites, including the digeneans Hexangium sigani and Gyliauchen volubilis, the acanthocephalans Sclerocollum rubrimaris and Neorhadinorhynchus macrospinosus, and the nematodes Procammalanus elatensis, and Ascaridoid larvae were recorded in the fish intestine. P. elatensis had the highest prevalence, occurring in 65% of infected fish; 72.2% of infected fish had concurrent infection with two or more helminth species. The total count of aerobic bacteria ranged from 1 to 305 colony-forming units (CFU)/g midgut contents. Four hydrolytic bacteria were recovered from the infected samples: Escherichia coli (ASU 31), Bacillus cereus (ASU 36) MN955553, Bacillus thuringiensis (ASU 34) MN955550, and Novosphingobium aromaticivorans (ASU 35) MN955552, which were identified using 16S rRNA genes. Bacterial richness was significantly correlated with concurrent parasitic infection and high content of extracellular hydrolytic amylases, proteases, cellulases, and lipases. The present results showed that the composition of the microbiota was affected by natural helminth infections in Siganus rivulatus, and the significant interaction between parasitic load and intestinal pathogenic bacteria, which may be primary in fish diseases etiology.

Animal models of primary biliary cirrhosis.

Within the last decade, several mouse models that manifest characteristic features of primary biliary cirrhosis (PBC) with antimitochondrial antibodies (AMAs) and immune-mediated biliary duct pathology have been reported. Here, the authors discuss the current findings on two spontaneous (nonobese diabetic autoimmune biliary disease [NOD.ABD] and dominant negative transforming growth factor-ß receptor II [dnTGFßRII]) and two induced (chemical xenobiotics and microbial immunization) models of PBC. These models exhibit the serological, immunological, and histopathological features of human PBC. From these animal models, it is evident that the etiology of PBC is multifactorial and requires both specific genetic predispositions and environmental insults (either xenobiotic chemicals or microbial), which lead to the breaking of tolerance and eventually liver pathology. Human PBC is likely orchestrated by multiple factors and hence no single model can fully mimic the immunopathophysiology of human PBC. Nevertheless, knowledge gained from these models has greatly advanced our understanding of the major immunological pathways as well as the etiology of PBC.