Abstract
An ~6-mo-old, free-ranging, male, American black bear (Ursus americanus) cub that was observed stumbling, acting disoriented, and falling, was dispatched and sent for postmortem evaluation. Bilaterally, round concretions were present in both the anterior and posterior aspects of the lens, disrupting the lens epithelium. These concretions were continuous with and extended from the inner surface of the lens capsule, as seen with a periodic acid-Schiff–hematoxylin reaction. Immunohistochemistry for alpha A crystallin was inconsistent, with weakly positive immunolabeling indicative of lens fibers. Other findings in this cub included emaciation and ursicoptic mange. Based on histopathologic findings, in conjunction with the clinical signs observed prior to death, we suspect that the bilateral lens lesions in this cub caused visual impairment. Congenital ocular defects are rarely reported in free-ranging wildlife. Developmental anomalies affecting the lens have not been previously described in Ursidae, to our knowledge.
American black bears (Ursus americanus)—large carnivores of great ecologic, recreational, and cultural importance—are widely distributed across North America. 2 Information regarding their visual acuity is limited; however, they reportedly can learn to discriminate colors, distinguish different shapes, and discriminate visual features of real objects from photographs,1,11 suggesting that their eyesight is good. Reports of ocular disease in American black bears are similarly rare and limited to single case reports8,18 or brief mentions within larger studies of black bear morbidity and mortality. 16
Reports of congenital ocular defects in free-ranging wildlife are uncommon. 6 In black bears, one cub with microphthalmia 16 and another with bilateral retinal dysplasia and optic nerve degeneration 8 have been described. Developmental anomalies affecting the lens have not been reported in ursids, 10 to our knowledge. A single case of juvenile cataracts in a free-ranging American black bear cub is described; however, the cause, whether congenital or merely early onset, is unknown. 19 Here, we describe a case of presumed visual impairment associated with a bilateral lens anomaly in a free-ranging black bear cub from North Carolina, USA.
In 2024 August, a private citizen in Avery County, NC, USA, observed an American black bear cub stumbling, falling, and seemingly disoriented. Upon approach, the cub did not respond to close human proximity. Thus, it was dispatched via gunshot to the chest and the carcass was stored frozen. The North Carolina Wildlife Resources Commission later submitted it to the Southeastern Cooperative Wildlife Disease Study (Athens, GA, USA) for postmortem examination.
At autopsy, the cub weighed 14.2 kg, which corresponds to an approximate age of 6 mo. The cub was in poor nutritional condition with mild skeletal muscle atrophy and a gross lack of internal and subcutaneous adipose stores. The pelage was thinned over the base of the right ear, ventral neck and chest, right body wall, and hindquarters. A fragmented air rifle pellet was embedded within the subcutis over the back of the head at the level of the occipital bone. However, this was interpreted as a chronic, incidental finding given the lack of hemorrhage, damage or remodeling in the underlying bone, or evidence of tissue reaction surrounding the injury. The gastrointestinal tract was filled with partially digested plant material. The remainder of the gross examination was unremarkable. No overt gross changes affected the eyes or brain.
A standard set of tissues was collected during autopsy and fixed in 10% neutral-buffered formalin. The eyes were fixed whole in Davidson fixative. Tissue samples were routinely sectioned. The eyes were sectioned sagittally through the optic nerve perpendicular to the long posterior ciliary artery. All formalin- and Davidson-fixed tissue samples were processed routinely, sectioned at 4 µm, and stained with H&E.
Histologically and bilaterally, the internal surface of the anterior and rarely posterior lens capsule was expanded by 75–150-µm, round, eosinophilic, globular but solid concretions (Fig. 1A, 1B). These concretions irregularly highlighted magenta and were continuous with the lens capsule, as seen with a periodic acid-Schiff–hematoxylin (
Lens from a free-ranging American black bear cub.
For alpha A crystallin immunohistochemistry (IHC), 4-µm unstained sections were deparaffinized and rehydrated followed by protein blocking with a commercial reagent (Universal blocking reagent; BioGenex). Rabbit anti–alpha A crystallin polyclonal antibody (PA 1-009; ThermoFisher) was applied at a 1:100 dilution for 1 h, followed by biotinylated goat anti-rabbit (Universal goat; BioGenex), alkaline-phosphatase–labeled streptavidin (BioGenex), and fast red chromogen (ImmPACT; Vector). Slides were counterstained with hematoxylin and coverslipped. All steps were performed at room temperature. Formalin-fixed cat eye with lens was used as the control tissue. For the negative control, isotypic rabbit negative control serum (Bios) replaced the primary antibody. Immunolabeling within the concretions was inconsistent. Some areas were immunonegative, consistent with the lens capsule; whereas other areas were weakly positive, consistent with the lens epithelium and lens fibers ( Fig. 1D ).
Other histologic findings included mild orthokeratotic hyperkeratosis of haired skin with scattered intrafollicular arthropod mite cross-sections, moderate serous atrophy of fat within the bone marrow, and glycogen-type vacuolar degeneration in the liver. The skin changes corresponded to the areas of thinned hair noted grossly. A skin scrape from these regions revealed numerous mites morphologically consistent with Ursicoptes spp. 4 The latter 2 changes were attributed to chronic negative energy balance. No evidence was found to suggest brain disease. Results from routine screening tests for multiple viral pathogens (rabies virus, canine distemper virus, highly pathogenic avian influenza A virus, herpesvirus, parvovirus, and circovirus) were negative.
The crystalline lens is an avascular structure composed of concentrically layered fibers covered anteriorly by a monolayer epithelium and contained within a basement membrane capsule. Lens fibers are oriented to ensure transparency, which is crucial for focusing and transmitting light to the retina; thus, structural lesions affecting the lens can impair vision. In our case, both lenses were distorted by concretions, with a combination of staining and immunolabeling properties that were variably consistent with lens fibers, epithelium, and capsule. Before death, the cub was observed acting disoriented, stumbling, and falling while attempting to ambulate. These signs are compatible with impaired vision, presumably as a result of the bilateral lens abnormalities. Given this bear’s young age, and a lack of evidence supporting other causes of ocular disease, we suspect that these lens concretions were a congenital anomaly, impairing its vision and contributing to its demise.
Embryologic development of the mammalian lens begins when optic vesicles extend from the embryonic forebrain toward the surface ectoderm. 9 Close proximity of the optic vesicles triggers the surface ectoderm, initiating localized thickening that results in formation of the lens placode. The lens placode invaginates into a hollow sphere, the lens vesicle, which is covered by a single layer of cuboidal ectoderm and a basement membrane that eventually gives rise to lens epithelium and lens capsule, respectively. The hyaloid artery grows into the optic fissure and supplies blood to the developing lens, which subsequently separates from the surface ectoderm. Primary lens fibers begin forming and migrate to fill the lens vesicle. An extensive capillary network, the perilenticular vascular tunic, forms and supports the developing lens for the remainder of embryonic development.
The Ursidae lens is not well characterized. It generally is described as round and biconvex, similar to the canine lens.7,10,15 Its embryologic development has not been elucidated but likely is similar to that of other mammals. Among the 8 extant bear species, the most commonly reported diseases affecting the lens are senile cataracts and cataracts secondary to lens luxation. 10
Congenital lens anomalies arise when problems occur during embryonic development. Failure of the lens placode to differentiate from surface ectoderm results in aphakia.
9
Delayed or defective separation of the optic vesicle is one of several mechanisms contributing to the spectrum of lesions collectively described under the umbrella of anterior segment dysgenesis (
Pseudoexfoliation syndrome (
Histologically, PASH reactivity suggested that these concretions arose from the lens capsule. However, the distribution pattern of alpha A crystallin immunolabeling suggests that, in some areas, these concretions may contain material more consistent with lens capsule; whereas in other areas, the material is more consistent with lens epithelium and fibers. Alpha crystallin proteins play a chaperone-like role by binding to unfolded or denatured proteins within the lens to prevent formation of light-scattering protein aggregates. 17 Several alpha A crystallin gene mutations have been described, and some manifest clinically in cataract formation in mice and humans. 5 Whether the concretions in our case are a form of congenital cataracts, possibly attributed to an alpha A crystallin mutation or another cause, is unclear (although they are histologically inconsistent with the prototypical features of cataractous change). Instead, because the lens epithelium gives rise to both lens fibers and the lens capsule, these concretions may represent aberrant lens epithelial cell function, although the underlying cause remains unknown.
Black bear cubs typically remain with the maternal sow for ~18 mo. However, cubs as young as 5 mo can survive on their own if they are in good health. 14 The suspected visual impairment in this bear cub likely interfered with its ability to locate and consume adequate food resources and to respond appropriately to both conspecifics and other animals, predisposing the cub to emaciation as well as conspecific aggression, especially if it became separated from or was orphaned by the maternal sow. Further, ursicoptic mange, which is common in black bears that are concurrently emaciated, 4 is another indicator that this cub was in poor health.
Ultimately, we were unable to identify a suitable diagnosis in either the veterinary or human literature that accurately depicted the lens lesions observed in this black bear cub. The bilateral distribution and lack of evidence of causes of acquired lens disease (e.g., blunt force trauma, intra-ocular infection) suggest the lesions are likely congenital. Thus, we propose that they are a previously unrecognized developmental anomaly. Congenital ocular defects in free-ranging wildlife are rarely reported, although increased recognition is likely as urbanization intensifies human–wildlife contact. 6
Footnotes
Acknowledgements
We thank SCWDS member states and U.S. Fish & Wildlife Service for their continued support, membership, and case submissions and specifically the North Carolina Wildlife Resources Commission for submitting this case. We thank the histology laboratory at the University of Georgia College of Veterinary Medicine for their technical assistance.
Declaration of conflicting interests
The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
Funding was provided by member state wildlife management agencies of the Southeastern Cooperative Wildlife Disease Study through the Federal Aid to Wildlife Restoration Act (50 Stat. 917), the U.S. Fish & Wildlife Service National Wildlife Refuge System, and the U.S. Geological Survey Ecosystems Mission Area.
