Detection of tilapia lake virus (TiLV) infection by PCR in farmed and wild Nile tilapia (Oreochromis niloticus) from Lake Victoria
. Journal of Fish Diseases 2018
, 1181 - 1189. Publisher's VersionAbstract
Abstract Tilapia lake virus disease (TiLVD) has emerged to be an important viral disease of farmed Nile tilapia (Oreochromis niloticus) having the potential to impede expansion of aquaculture production. There is a need for rapid diagnostic tools to identify infected fish to limit the spread in individual farms. We report the first detection of TiLV infection by PCR in farmed and wild Nile tilapia from Lake Victoria. There was no difference in prevalence between farmed and wild fish samples (p = .65), and of the 442 samples examined from 191 fish, 28 were positive for TiLV by PCR. In terms of tissue distribution, the head kidney (7.69%, N = 65) and spleen (10.99%, N = 191), samples had the highest prevalence (p < .0028) followed by heart samples (3.45%, N = 29). Conversely, the prevalence was low in the liver (0.71%, N = 140) and absent in brain samples (0.0%, N = 17), which have previously been shown to be target organs during acute infections. Phylogenetic analysis showed homology between our sequences and those from recent outbreaks in Israel and Thailand. Given that these findings were based on nucleic acid detection by PCR, future studies should seek to isolate the virus from fish in Lake Victoria and show its ability to cause disease and virulence in susceptible fish.
Historical and recent reductions in genetic variation of the Sarotherodon galilaeus population in the Sea of Galilee
. Conservation Genetics 2018
, 1323 - 1333. Publisher's VersionAbstract
The Sea of Galilee has great significance as a natural habitat and a freshwater source for Israel. Anthropogenic impacts have been placing significant pressure on the species inhabiting this lake, among which is Sarotherodon galilaeus, an omnivorous fish with a relatively large population and significance for commercial fishing. An alarming decline in annual catch towards 2008 suggested that this unique population might be at risk. With that in mind, we characterized the current genetic variation of this species in Israel with reference to fish from Ghana, based on D-loop and microsatellite markers. Genetic variation and differentiation were found mostly among fish from Ghanaian localities and between fish from Israel and Ghana, whereas fish from all Israeli localities had uniform and limited variation, a signature compatible with historical founder effect followed by local adaptations. Such historical processes could leave a population vulnerable as reflected in the sudden and recent population decline. Comparing genetic variation between archived 30 year-old scales and modern lake fish revealed further reduction in genetic variation coincident with the recent population decline. Thus, a recently occurring genetic bottleneck had placed this unique and isolated population at an even higher risk. We carefully discuss the events leading to the current risk status for S. galilaeus in Israel and highlight the need for vigilant monitoring and active management to support a more sustainable future for this and other fish communities in this important habitat.
Resistance of Leishmania infantum to allopurinol is associated with chromosome and gene copy number variations including decrease in the S-adenosylmethionine synthetase (METK) gene copy number
. Includes articles from the scientific meeting: "Anthelmintics: From Discovery to Resistance III", pp. 494-628 2018
403 - 410. Publisher's VersionAbstract
Leishmania infantum is one of the causative agents of visceral leishmaniasis (VL), a widespread, life-threatening disease. This parasite is responsible for the majority of human VL cases in Brazil, the Middle East, China, Central Asia and the Mediterranean basin. Its main reservoir are domestic dogs which, similar to human patients, may develop severe visceral disease and die if not treated. The drug allopurinol is used for the long-term maintenance of dogs with canine leishmaniasis. Following our report of allopurinol resistance in treated relapsed dogs, we investigated the mechanisms and markers of resistance to this drug. Whole genome sequencing (WGS) of clinical resistant and susceptible strains, and laboratory induced resistant parasites, was carried out in order to detect genetic changes associated with resistance. Significant gene copy number variation (CNV) was found between resistant and susceptible isolates at several loci, including a locus on chromosome 30 containing the genes LinJ.30.3550 through LinJ.30.3580. A reduction in copy number for LinJ.30.3560, encoding the S-adenosylmethionine synthetase (METK) gene, was found in two resistant clinical isolates and four induced resistant clonal strains. Using quantitative real time PCR, this reduction in METK copy number was also found in three additional resistant clinical isolates. Furthermore, inhibition of S-adenosylmethionine synthetase encoded by the METK gene in allopurinol susceptible strains resulted in increased allopurinol resistance, confirming its role in resistance to allopurinol. In conclusion, this study identified genetic changes associated with L. infantum resistance to allopurinol and the reduction in METK copy number identified may serve as a marker for resistance in dogs, and reduced protein activity correlated with increased allopurinol resistance.