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Rainbow trout (Oncorhynchus mykiss) is the principal species of inland-farmed fish in the Western hemisphere. Recently, we diagnosed in farmed rainbow trout a disease in which the hallmark is granulomatous-like hepatitis. No biotic agents could be isolated from lesions. Still, unbiased high-throughput sequencing and bioinformatics analyses revealed the presence of a novel piscine nidovirus that we named “Trout Granulomatous Virus” (TGV). TGV genome (28,767 nucleotides long) is predicted to encode non-structural (1a and 1 ab) and structural (S, M, and N) proteins that resemble proteins of other known piscine nidoviruses. High loads of TGV transcripts were detected by quantitative RT-PCR in diseased fish and visualized in hepatic granulomatous sites by fluorescence in situ hybridization. Transmission electron microscopy (TEM) revealed coronavirus-like particles in these lesions. Together, these analyses corroborated the association of TGV with the lesions. The identification and detection of TGV provide means to control TGV spread in trout populations.

Over 100 years ago, Ramon y Cajal hypothesized that two forces played a role in the evolution of mammalian brain connectivity: minimizing wiring costs and maximizing conductivity speed. Using diffusion MRI, we reconstructed the brain connectomes of 123 mammalian species. Network analysis revealed that both connectivity and the wiring cost are conserved across mammals. We describe a conservation principle that maintains the overall connectivity: species with fewer interhemispheric connections exhibit better intrahemispheric connectivity.

Over 100 years ago, Ramon y Cajal hypothesized that two forces played a role in the evolution of mammalian brain connectivity: minimizing wiring costs and maximizing conductivity speed. Using diffusion MRI, we reconstructed the brain connectomes of 123 mammalian species. Network analysis revealed that both connectivity and the wiring cost are conserved across mammals. We describe a conservation principle that maintains the overall connectivity: species with fewer interhemispheric connections exhibit better intrahemispheric connectivity.

Streptococcus agalactiae is one of the most important fish pathogenic bacteria as it is responsible for epizootic mortalities in both wild and farmed species. S. agalactiae is also known as a zoonotic agent. In July 2018, a stranded wild sandbar shark (Carcharhinus plumbeus), one of the most common shark species in the Mediterranean Sea, was found moribund on the seashore next to Netanya, Israel, and died a few hours later. A post-mortem examination, histopathology, classical bacteriology and advanced molecular techniques revealed a bacterial infection caused by S. agalactiae, type Ia-ST7. Available sequences publicly accessible databases and phylogenetic analysis suggest that the S. agalactiae isolated in this case is closely related to fish and human isolates. To the best of our knowledge, this is the first description of a fatal streptococcosis in sandbar sharks.

Peste des petits ruminants (PPR) is a devastating disease that generally affects sheep and goats, mostly in Asia, the Middle East and Africa. The disease has been declared a target for global eradication. Despite its high prevalence in domestic flocks and its high seroprevalence among wildlife, it is rarely reported as a fulminant disease in wild ruminant species (with the exception of Central Asia). In this report, we describe a severe PPR outbreak in a zoo herd of Nubian ibex (Capra nubiana), causing the deaths of 2/3 of the herd. The clinical onset was acute with morbid animals exhibiting lethargy and watery-to-bloody diarrhea and death usually within 48 h. The most consistent gross pathologic findings were hemorrhagic abomasitis and enteritis. Oral lesions and pulmonary lesions were rare. Histology revealed necrohemorrhagic enteritis and abomasitis with myriad nuclear and cytoplasmic viral inclusion bodies. Molecular examinations confirmed the diagnosis of PPR and determined that the causative agent belongs to lineage IV. Further molecular examination showed that the virus belongs to the Asian clade of lineage IV and is closely related to a virus described in Turkey.

In this report we describe for the first time the detection of Sarcoptes scabiei type suis mites on domestic pigs in Israel and examine its genetic variation compared with S. sabiei from other hosts. Microscopic examination of skin samples from S. scabiei-infested pigs (Sus scrofa domesticus) revealed all developmental stages of S. scabiei. To detect genetic differences between S. scabiei from different hosts, samples obtained from pig, rabbits (Orictolagus cuniculus), fox (Vulpes vulpes), jackal (Canis aureus) and hedgehog (Erinaceus concolor) were compared with GenBank-annotated sequences of three genetic markers. Segments from the following genes were examined: cytochrome C oxidase subunit 1 (COX1), glutathione-S-transferase 1 (GST1), and voltage-sensitive sodium channel (VSSC). COX1 analysis did not show correlation between host preference and genetic identity. However, GST1 and VSSC had a higher percentage of identical sites within S. scabiei type suis sequences, compared with samples from other hosts. Taking into account the limited numbers of GST1 and VSSC sequences available for comparison, this high similarity between sequences of geographically-distant, but host-related populations, may suggest that different host preference is at least partially correlated with genetic differences. This finding may help in future studies of the factors that drive host preferences in this parasite.

Pyrrolizidine alkaloids (PAs) are carcinogenic and genotoxic phytochemicals found exclusively in angiosperms. The ingestion of PA-containing plants often results in acute and chronic toxicities in man and livestock, targeting mainly the liver. During February 2014, a herd of 15-18-month-old mixed-breed beef cattle (n = 73) from the Galilee region in Israel was accidently fed hay contaminated with 12% Heliotropium europaeum (average total PA intake was 33 mg PA/kg body weight/d). After 42 d of feed ingestion, sudden death occurred over a time period of 63 d with a mortality rate of 33%. Necropsy and histopathological examination revealed fibrotic livers and moderate ascites, as well as various degrees of hyperplasia and fibrosis of bile duct epithelial cells. Elevated γ-glutamyl-transferase and alkaline phosphatase levels were indicative of severe liver damage. Comprehensive PA profile determination of the contaminated hay and of native H. europaeum by LC-MS/MS revealed the presence of 30 PAs and PA-N-oxides, including several newly reported PAs and PA-N-oxides of the rinderine and heliosupine class. Heliotrine- and lasiocarpine-type PAs constituted 80% and 18% of the total PAs, respectively, with the N-oxides being the most abundant form (92%). The PA profile of the contaminated hay showed very strong resemblance to that of H. europaeum.

Ionophores are used as feed additives for the control of coccidiosis and growth promotion in farm animals. Reports of maduramicin toxicosis in farm animals are scarce. The present work describes an acute maduramicin toxicosis affecting 22 pregnant gilts, 2 pregnant sows and 2 boars, resulting in a total mortality of 65% within 2 days. The clinical and histopathological findings observed shared similar characteristics to acute ionophore toxicosis in pigs, being characterized by severe myodegeneration in skeletal muscle and degenerative changes in the myocardium. Important clinical pathology indices found were elevated levels of CPK and ALT. In contrast to the pregnant gilts, the two pregnant sows completely recovered after 1 month and farrowed 2 months after the intoxication event healthy piglets. The lack of effect of maduramicin on the fetuses might be indicative of poor placental penetration of maduramicin. Moreover, the present work reports for the first time maduramicin levels in livers (0.5 mg/kg) of gilts exposed to lethal concentrations of maduramicin (18.5 mg/kg) in the feed. As the average feed intake of the gilts was estimated to be 3.5 kg feed/day, the mean maduramicin intake leading to the observed high mortality rate was 0.4 mg/kg body weight/day.