Ehlers-Danlos syndrome (EDS) is a group of heritable connective tissue disorders caused by defective collagen synthesis or incorrect assembly of the collagen triple helical structure. EDS is characterised by joint hypermobility, skin hyperextensibility, abnormal scarring, poor wound healing and tissue friability. Human EDS may be caused by variants in several different genes including COL5A1, which encodes the collagen type V alpha 1 chain. For the present study we investigated a 1.5-year-old, spayed female, domestic shorthair cat with EDS. The affected cat showed multiple recurrent skin tears, hyperextensibility of the skin and joint abnormalities. We obtained whole genome sequencing data from the affected cat and searched for variants in candidate genes known to cause EDS. We detected a heterozygous single base-pair deletion in exon 43 of the COL5A1 gene, namely c.3420delG. The deletion was predicted to result in a frameshift and premature stop codon: p.(Leu1141SerfsTer134). Sanger sequencing confirmed that the variant was present in the affected cat and absent from 103 unaffected cats from different breeds. The variant was also absent from a Burmese cat with EDS. Based on knowledge about the functional impact of COL5A1 variants in other species, COL5A1: c.3420delG represents a compelling candidate causative variant for the observed EDS in the affected cat.

Background The feline counterpart of human inflammatory linear verrucous epidermal nevus (ILVEN) has been described; however, the possible underlying developmental defect has not been investigated. Objective To report a case of multiple ILVEN‐like lesions in a cat with a genetic variant in the NSDHL gene. Animals A 2‐year‐old, female, domestic short hair cat with a history of multiple alopecic, verrucous, hyperpigmented and erythematous skin lesions, following Blaschko's lines on the head, the limbs, the trunk and paw pads. Methods and results According to the clinical and histopathological findings, a diagnosis of multiple ILVEN‐like lesions was made. Genetic investigation revealed a heterozygous missense variant in the X‐chromosomal NSDHL gene predicted to lead to a loss‐of‐function of the NSDHL protein. Conclusions and clinical importance To the best of the authors’ knowledge, this is the first case of feline ILVEN‐like lesions in which a genetic cause has been proposed. Future studies to establish a causal relationship between NSDHL variants and skin lesions might lead to pathogenesis‐directed treatments.

In 16 mongrel dogs bovine xenografts of 4 to 12 cm of length were used for arterial replacement. The grafts were removed after 30 minutes and up to 13 months for electronmicroscopic examination. The graft was shown to be significantly thrombogenic during the first six weeks after implantation. After 8 to 10 weeks an increasing revitalization of the graft is found starting from the ends of the canine artery. A cover of endothelial cells is formed in the graft lumen. The graft wall is enforced by formation of collagen and elastic fibers originating from capillaries and fibroblasts. Revitalization of the graft is limited to a rim of 2 to 3,5 cm next to the anastomoses with the canine artery. The remaining graft segment shows revitalization only on the outside wall. Degenerative changes take place in the inner layer of the graft with time passing.

In 12 mongrel dogs tracheal defects of different size were covered by bovine xenografts. The grafts were subjected to electronmicroscopic examination 2 to 19 months after implantation. Following the ingrowht of fibroblasts and capillaries a basal membrane is formed on the side of the previous graft lumen. After 4 to 5 months this membrane is covered from the tracheal margins by microvillous cells. After 8 months ciliated epithelia and goblet cells are developed by cell metaplasia. Although the graft becomes revitalized and integrated into the tracheal wall, the layer of ciliated epithelia is interrupted by less differentiated cells. The possible causes for this phenomenon are discussed. Thus bovine xenograft used for the repair of tracheal defects has the following advantages: total revitalization, no shrinkage, less prone to infection and formations of ciliated epithelia.

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