A de novo variant in the bovine ADAMTSL4 gene in an Original Braunvieh calf with congenital cataract.

Inherited forms of cataract are a heterogeneous group of eye disorders known in livestock species. Clinicopathological analysis of a single case of impaired vision in a newborn Original Braunvieh calf revealed nuclear cataract. Whole-genome sequencing of the parent-offspring trio revealed a de novo mutation of ADAMTSL4 in this case. The heterozygous p.Arg776His missense variant affects a conserved residue of the ADAMTSL4 gene that encodes a secreted glycoprotein expressed in the lens throughout embryonic development. In humans, ADAMTSL4 genetic variants cause recessively inherited forms of subluxation of the lens. Given that ADAMTSL4 is a functional candidate gene for inherited disorders of the lens, we suggest that heterozygosity for the identified missense variant may have caused the congenital cataract in the affected calf. Cattle populations should be monitored for unexplained cataract cases, with subsequent DNA sequencing a hypothesized pathogenic effect of heterozygous ADAMTSL4 variants could be confirmed.

Bacterial contamination of slit lamps in veterinary ophthalmology.

PURPOSE: Healthcare-associated infection (HAI) is a well-known problem in human medicine. The contamination of medical devices with pathogenic organisms is less studied in veterinary medicine. The purpose of this multicenter study was to evaluate the bacterial contamination of slit lamps throughout Europe and part of the United States. The efficacy of standard cleaning was additionally investigated. METHODS: Samples from adjustment wheels of slit lamps were taken by different veterinary ophthalmologists and submitted for culture (n = 29). The efficacy of cleaning protocols was evaluated by taking a second sample after routine cleaning (n = 29). Sensitivity testing was performed for pathogenic bacteria using the minimum inhibitory concentration (MIC) or disc diffusion (Kirby-Bauer) method. Statistical analysis was performed using Fisher's exact test. RESULTS: Seventeen of 29 slit lamps were contaminated before cleaning. The most frequently cultured bacteria were Staphylococcus spp. and coliform bacteria. Twelve of 29 slit lamps showed no bacterial growth before and after cleaning. There was a significant difference before and after cleaning (P = 0.0008), with only 4/29 contaminated samples after cleaning. CONCLUSION: Contamination with pathogenic bacterial species is frequent in slit lamps used by veterinary ophthalmologists. A risk of cross-contamination in clinical patients has to be considered. Routine cleaning reduces bacterial contamination significantly.

HSP27 immunization reinforces AII amacrine cell and synapse damage induced by S100 in an autoimmune glaucoma model.

Previous studies have revealed a loss of retinal ganglion cells (RGCs) and optic nerve fibers after immunization with the S100B protein. Addition of heat shock protein 27 (HSP27) also leads to a decrease of RGCs. Our present aim has been to analyze various retinal cell types after immunization with S100B or S100B + HSP27 (S100 + HSP). After 28 days, retinas were processed for immunohistology and Western blot. RGCs, immunostained for NeuN, were significantly decreased in the S100 and the S100 + HSP groups. Significantly fewer ChAT+ cells were noted in both groups, whereas parvalbumin+ cells were only affected in the S100 + HSP group. Western blot results also revealed fewer ChAT signals in both immunized groups. No changes were noted with regard to PKCα+ rod bipolar cells, whereas a significant loss of recoverin+ cone bipolar cells was observed in both groups via immunohistology and Western blot. The presynaptic marker Bassoon and the postsynaptic marker PSD95 were significantly reduced in the S100 + HSP group. Opsin+ and rhodopsin+ photoreceptors revealed no changes in either group. Thus, the inner retinal layers are affected by immunization. However, the combination of S100 and HSP27 has a stronger additive effect on the retinal synapses and AII amacrine cells.

Corneal cross-linking as a treatment for corneal dystrophy with secondary bacterial infection in a Friesian horse.

Corneal cross-linking should be considered as treatment option in Friesian horses with infectious keratitis and corneal dystrophy. Optical coherence tomography, giving information of corneal structure, can help for diagnosis and monitoring.

Specific Inner Retinal Layer Cell Damage in an Autoimmune Glaucoma Model Is Induced by GDNF With or Without HSP27.

PURPOSE: Previously, immunization of rats with ocular antigens induced retinal ganglion cell (RGC) degeneration. We investigated the effect of immunization with glial cell line-derived neurotrophic factor (GDNF) or GDNF in combination with heat shock protein 27 (GDNF+HSP) on RGCs and other retinal cells. METHODS: Rats were immunized with GDNF or GDNF+HSP. After 4 weeks, retinas were stained with Brn-3a and NeuN to quantify RGCs. GFAP and vimentin staining were used to investigate macroglia. Microglia were marked with Iba1 and ED1. Amacrine cells were labeled with parvalbumin and ChAT. Photoreceptors were evaluated with rhodopsin and opsin staining and bipolar cells with PKCα and recoverin. For these cell types, Western blotting was also performed. RESULTS: Retinas of immunized animals showed a significant loss of Brn-3a+ and NeuN+ RGCs. No significant changes could be observed in regard to macroglia. An increase in Iba1+ microglia was detected in both groups, but little change in regard to activated microglia. A loss of cholinergic amacrine cells was seen in the GDNF+HSP group by immunohistochemistry and in both groups via Western blot analysis. AII amacrine cells, bipolar cells, and photoreceptors were not affected. CONCLUSIONS: Immunizations led to loss of RGCs and cholinergic amacrine cells and a strong increase in microglial cells. Our data suggest that RGC loss is the consequence of immunization with GDNF. Astrocyte activity and its neuroprotective effects seem to be inhibited by GDNF immunization. We presume more complex interactions between GDNF and HSP27 because no additive effects could be observed.

S100 alone has the same destructive effect on retinal ganglion cells as in combination with HSP 27 in an autoimmune glaucoma model.

As previously shown, immunization with ocular antigens, like heat shock protein 27 (HSP 27), leads to retinal ganglion cell loss in an autoimmune glaucoma model. Aim of this study was to assess how immunization with S100 alone and in combination with HSP 27 affects retinal ganglion and macroglia cells. Rats were immunized with S100 or S100 plus HSP 27 (COMB). Neuronal cell density was evaluated on Nissl-stained flatmounts. Immunized groups showed a significant neuronal cell loss (S100, p = 0.005; COMB, p = 0.0005). A significant loss of retinal ganglion cells was also observed in both immunized groups on Brn-3a stained retinal cross-sections (S100, p = 0.003; COMB, p = 0.001). An increase in GFAP(+) area was noted in both groups (S100, p = 0.01; COMB, p = 0.001). In contrary, vimentin staining was not altered (S100/COMB, p > 0.05). In summary, immunization with solely S100 leads to retinal ganglion cell damage and reactive gliosis. While the combination of S100 plus HSP 27 also caused retinal ganglion cell loss and a glia response, the combination of the two antigens did not cause additional damage or more severe cell loss. We assume that both antigens might interact, possibly having inhibitory effects on each other and thus preventing additional damage to the retina.