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Streptococcus agalactiae is an important bacterial pathogen in intensive Nile tilapia production, causing high mortality rates and great economic losses. This work aimed to evaluate the Nile tilapia vaccination against S. agalactiae and fed with ration containing probiotic AQUA PHOTO® composed of Bacillus subtilis and Lactobacillus plantarum, on the immune response action and gut microbiota. The experimental design was completely randomized with five treatments (CON = control; ADJ = adjuvant; PRO = probiotic; VAC = vaccine; PRO + VAC = probiotic + vaccine) and five replicates. The vaccine (bacterin + adjuvant) was injected after 21 days (21d) of probiotic feeding and the vaccine was booster 14 days post-vaccination (35d). After 14 days of the booster (49d), the fish were challenged with S. agalactiae and observed for more than 14 days, completing 63 days. The immunized group showed a better survival rate (CON 40%; ADJ 57%; PRO 67%; VAC 87%; PRO + VAC 97%). The treatments VAC and PRO + VAC, after booster produced higher levels of IgM antibodies compared with the control from the same time. The combination of probiotic and vaccination provided better protection against S. agalactiae infection, directly affecting the gut microbiological profile. These results indicated the contribution of probiotic to the adaptive immune response through the modulation of the intestinal microbiota, improving the effect of the vaccination. In conclusion, AQUA PHOTO®, composed of B. subtilis and L. plantarum, orally administered to Nile tilapia vaccinated against and challenged with S. agalactiae increases protection from infection and modifies the intestinal microbiota profile of the host, promoting the microbiota balance and improving adaptive immune response.

Introduction: Marfan syndrome (OMIM #154700) was described for the first time in 1896 by Antoine Bernard-Jean Marfan. It is characterized by its autosomal dominant inheritance pattern, affects 1:5000 of those born alive, and involves the gene that codifies the structural protein fribrillin-1. Fibrillin-1 is critical for the formation of the elastic system backbone and for the negative regulation of the cytokine transforming growth factor beta 1 (TGF-β1). In the syndrome this fibrillar component causes the degeneration of the fibers of the elastic system, which no longer sequesters matrix TGF-β, causing disorganization of the collagen fibers and vascular smooth muscles. The disease affects mainly the cardiovascular system, cardiovascular problems being the main cause of death. This is because arteries have large amounts of elastic fibers that rupture in an adverse process, causing mainly dissections and aneurisms, which have been better clarified in experimental studies with mice. Objective: The objective of this study was to conduct an etiopathogenic and molecular review to describe the advances in the understanding of blood vessel dysmorphism in the syndrome, especially of the aorta. Materials and Methods: For this purpose the literature of the last 35 years was extensively reviewed. Conclusion:The origin of the aortic dysmorphism in the syndrome stems from a number of events that begin with the mutation of the gene fibrillin-1, causing fragmentation of the aortic elastic fibers. Excess cytokine TGF-β increases the amount of metalloproteinases and of vascular smooth muscle cell apoptosis, leading to matrix remodeling and increasing the susceptibility of the vessel to an aneurysm or dissecting process.

Fibrillin-1 is a pivotal structural component of the kidney’s glomerulus and peritubular tissue. Mutations in the fibrillin-1 gene result in Marfan syndrome (MFS), an autosomal dominant disease of the connective tissue. Although the kidney is not considered a classically affected organ in MFS, several case reports describe glomerular disease in patients. Therefore, this study aimed to characterize the kidney in the mgΔlpn-mouse model of MFS. Affected animals presented a significant reduction of glomerulus, glomerulus-capillary, and urinary space, and a significant reduction of fibrillin-1 and fibronectin in the glomerulus. Transmission electron microscopy and 3D-ultrastructure analysis revealed decreased amounts of microfibrils which also appeared fragmented in the MFS mice. Increased collagen fibers types I and III, MMP-9, and α-actin were also observed in affected animals, suggesting a tissue-remodeling process in the kidney. Video microscopy analysis showed an increase of microvessel distribution coupled with reduction of blood-flow velocity, while ultrasound flow analysis revealed significantly lower blood flow in the kidney artery and vein of the MFS mice. The structural and hemodynamic changes of the kidney indicate the presence of kidney remodeling and vascular resistance in this MFS model. Both processes are associated with hypertension which is expected to worsen the cardiovascular phenotype in MFS.

An alarming number of global warnings concerning amphibian mortality outbreaks have been released in recent years. Emerging diseases stand out as the main potential causes. Ranavirus is a worldwide-spread highly infectious disease capable of affecting even other ectothermic animals such as fish and reptiles. One major issue regarding this pathology is the lack of clinical signs before it leads up to death. Aiming at having a better understanding of anurans susceptibility, this study analyzed bullfrog (Lithobates catesbeianus) survival rate, when challenged with three doses of a Brazilian strain of Frog Virus 3 (FV3). The qPCR analysis indicated a low infectivity rate in these animals both as larvae and as adults. To elucidate the results, the following hypothesis was performed: 1) The amount of inoculum used on the frogs was insufficient to trigger an infection; 2) For the FV3 to produce clinical signs in this species, there is the need for a cofactor; 3) The animals did undergo FV3 infection but recovered in the course of the experiment, and 4) The inoculum utilized might have been low-virulence. Finally, the presence of actual clinical signs of ranavirus is discussed, with the more likely hypothesis.