First detection and phylogenetic analysis of lumpy skin disease virus from Kinmen Island, Taiwan in 2020.

Lumpy skin disease is an arthropod-borne bovine disease caused by lumpy skin disease virus. A suspect lumpy skin disease case in a breeding cattle farm on Kinmen Island, Taiwan was reported on July 8, 2020 and later confirmed the first occurrence of lumpy skin disease in the country by molecular biological detections, electron microscopy, and sequence comparison. Implementation of control measures including blanket vaccination on the island effectively ceased the outbreaks. Phylogenetic analyses revealed that the virus discovered in the outbreaks was most similar to those identified in China in 2019. Identifying this virus in the coastal areas in East Asia indicated the rapid eastward spread of lumpy skin disease in Asia.

Fatal canine parvovirus-2 (CPV-2) infection in a rescued free-ranging Taiwanese pangolin (Manis pentadactyla pentadactyla).

Carnivore protoparvovirus 1 includes feline parvovirus (FPV), variants of canine parvovirus-2 (CPV-2), mink enteritis virus, and raccoon parvovirus, important pathogens affecting both wild and domestic carnivores. In this report, we described a fatal CPV-2 infection in a rescued Taiwanese pangolin, which provides the first evidence of CPV-2 infection in a non-carnivore. Post-rescue, the Taiwanese pangolin died from complications resulting from a severe panleucocytopenia and bloody diarrhoea. A full autopsy was performed and microscopic examination of the tissues revealed ulcerative, necrotizing, and haemorrhagic glossitis, esophagitis and enteritis. The results of transmission electronic microscopy, polymerase chain reaction and in situ hybridization provided confirmatory evidence that the lesions in the tongue, oesophagus and intestine were associated with a protoparvovirus. Phylogenetic comparison of the whole VP2 gene from the current pangolin protoparvovirus strain showed close clustering with the CPV-2c strains from domestic dogs in Taiwan, China and Singapore. The amino acid sequence of the pangolin protoparvovirus showed 100% identity to the CPV-2c strains from domestic dogs in China, Italy, and Singapore. The current findings highlight that pangolins are susceptible to protoparvoviruses. The potential of cross-species transmission of protoparvoviruses between Carnivora and Pholidota should be considered when housing pangolins in close proximity to carnivores and adopting strict biosecurity measures to avoid cross-species transmission in rescue facilities and zoos.

Lyssavirus in Japanese Pipistrelle, Taiwan.

A putative new lyssavirus was found in 2 Japanese pipistrelles (Pipistrellus abramus) in Taiwan in 2016 and 2017. The concatenated coding regions of the virus showed 62.9%-75.1% nucleotide identities to the other 16 species of lyssavirus, suggesting that it may be representative of a new species of this virus.

Kidney stone distribution caused by melamine and cyanuric acid in rats.

BACKGROUND: Melamine (M), which is composed of multi-amine, has been used as a food additive to falsely increase protein contents. Furthermore, cyanuric acid (CA) is a derivative of melamine. It is known that these mixtures can cause renal toxicity. METHODS: The objective of this study was to investigate the possible target cells during acute renal toxicity of melamine and cyanuric acid (MCA) mixture crystals in vivo. Rats were provided with a lethal dose of MCA (1:1; 400mg/kg) and observed after 0.5, 1, 3, 12, 24, and 48-h intervals. RESULTS: MCA caused degeneration/necrosis in the proximal tubules starting at 12h and increased at 24 and 48 h. A small number of yellow-green crystals were observed in the dilated distal renal tubules at 48 h post-treatment. Ultrastructurally, pyknosis, mitochondrial vesicles, and cellular swelling were found in the proximal tubular cells at 0.5h. Small needle-like crystals in the cytoplasm and large crystals in the lumen of tubules indicated physical damage to the renal cells. CONCLUSION: These results clearly reveal that in the MCA-induced renal toxicity model, crystals are distributed to both the proximal and distal tubules in rats. The proximal tubular cells may be initially injured and subsequently block the distal tubules with MCA crystals during early acute intoxication.

Mutation of the gene encoding a major outer-membrane protein in Xanthomonas campestris pv. campestris causes pleiotropic effects, including loss of pathogenicity.

Xanthomonas campestris pv. campestris (Xcc) is the phytopathogen that causes black rot in crucifers. The xanthan polysaccharide and extracellular enzymes produced by this organism are virulence factors, the expression of which is upregulated by Clp (CRP-like protein) and DSF (diffusible signal factor), which is synthesized by RpfF. It is also known that biofilm formation/dispersal, regulated by the effect of controlled synthesis of DSF on cell-cell signalling, is required for virulence. Furthermore, a deficiency in DSF causes cell aggregation with concomitant production of a gum-like substance that can be dispersed by addition of DSF or digested by exogenous endo-beta-1,4-mannanase expressed by Xcc. In this study, Western blotting of proteins from a mopB mutant (XcMopB) showed Xcc MopB to be the major outer-membrane protein (OMP); Xcc MopB shared over 97 % identity with homologues from other members of Xanthomonas. Similarly to the rpfF mutant, XcMopB formed aggregates with simultaneous production of a gummy substance, but these aggregates could not be dispersed by DSF or endo-beta-1,4-mannanase, indicating that different mechanisms were involved in aggregation. In addition, XcMopB showed surface deformation, altered OMP composition, impaired xanthan production, increased sensitivity to stressful conditions including SDS, elevated temperature and changes in pH, reduced adhesion and motility and defects in pathogenesis. The finding that the major OMP is required for pathogenicity is unprecedented in phytopathogenic bacteria.