Ocular examination in laboratory species presents a number of unique challenges to the examiner. The foremost of these challenges is gaining familiarization with what is normal for a given species. The small size of laboratory rodent eyes renders ophthalmoscopic examination more difficult than in dogs or cats. Slit‐lamp biomicroscopy of the adnexa, cornea, and anterior segment is relatively straightforward, whereas fundoscopy can be difficult, especially in pigmented and nontapetal strains, among which mydriasis may be exceptionally difficult to achieve. In all mammalian laboratory species, pupil dilation is essential for thorough examination of the entire lens and posterior segment and is easily achieved with topical short‐acting antimuscarinics such as 0.5–1.0% tropicamide. While not always necessary, some references advocate use of topical phenylephrine in combination with agents such as tropicamide, particularly pigmented rodents. Examiners must also be mindful of the inverse relationship between a species’ globe dimensions and the lateral and axial magnification of the ocular fundus when viewed ophthalmoscopically. Rodents’ small globes, bearing short optical focal distances, produce considerable magnification. In rodents, for example, this phenomenon makes the normal retinal vasculature appear to “float.” If the examiner is unfamiliar with this artifact, it could be falsely interpreted as a retinal detachment. Indirect ophthalmoscopy is readily performed in lagomorphs and primates and can, with practice, be mastered in rodents. In laboratory species, the range of globe and pupil sizes requires examiners to use condensing lenses of different dioptric strengths. Some examiners prefer a 90‐D lens used in conjunction with a table‐mounted slit lamp; others prefer a 28‐D lens and an indirect headpiece. Still others find a 2.2 Pan Retinal lens to be useful in most rodents. The estimation of intraocular pressure (IOP) is part of essential diagnostics. While the TonoPen® has been favorably evaluated in the small eyes of ferrets and rats, the mouse cornea is too small to accommodate the footplate of even the TonoPen applanation tonometer, and is better suited to a rebound tonometer, which measures the speed of rebound of a small plastic probe fired at the ocular surface, and is small enough to provide accurate measurements of IOP in even these eyes. The majority of animals in many laboratory animal collections are mice and rats, with far fewer rabbits, dogs, and nonhuman primates (NHPs). Mini‐ and miniature pigs are becoming more popular as a replacement for NHPs, so knowledge of swine diseases is now very important. The reported ophthalmic diseases in mice and rats are listed in Table 17.1. Chromodacryorrhea occurs in many laboratory rodents, but particularly rats exhibit red crusting around their eyes in cases of ocular irritation, upper respiratory tract infection, and general stress (Figure 17.1). Porphyrin pigmented and lipid‐laden tears are produced in normal amounts by the Harderian glands in several rodent species. The porphyrin pigments are also autofluorescent, which can be used to differentiate chromodacryorrhea from infections such as mycoplasmosis and sialodacryoadenitis, nutritional deficiencies, and other physiological stresses like restraint and transport may cause chromodacryorrhea. Table 17.1 Reported ophthalmic disorders in mice and rats. Harderian gland pathology can result in exophthalmos in laboratory rodents. Orbital cellulitis with retrobulbar abscessation is most commonly associated with Pasteurella multocida in the rabbit, but similar conditions can occur in chinchillas and other rodents with continually growing molar and incisor teeth. Conjunctivitis may be observed in mice or rats. In both species, clinical signs are generally nonspecific, including serous to mucoid/mucopurulent ocular discharge, conjunctival hyperemia, chemosis, blepharospasm, and chromodacryorrhea. In laboratory rodents, primary conjunctivitis is most commonly of infectious etiology. In both rats and mice, the most common cause of conjunctivitis unrelated to intraocular disease is mycoplasmal respiratory infection, but other agents can also be involved. Numerous bacterial organisms have been implicated in naturally occurring conjunctivitis in mice and rats, including Mycoplasma spp., Pseudomonas aeruginosa, Salmonella spp., Pasteurella spp., Streptobacillus moniliformis, Staphylococcus aureus, and Corynebacterium kutscheri. Viral agents have also been implicated, including lymphocytic choriomeningitis (LCM) virus, ectromelia virus (the causative agent of mousepox, which primarily causes dermatologic disease), and Sendai virus. Figure 17.1 Chromodacryorrhea occurs in many laboratory rodents, but particularly rats. The most devastating adnexal disease in rats in both its acute and chronic forms is sialodacryoadenitis virus infection. This coronavirus infection in rats causes ocular irritation with conjunctivitis and periorbital swelling, followed by sneezing, edematous cervical swelling, and enlarged lymph nodes and salivary glands. This is a highly contagious but self‐limiting disease in rat colonies. The classic epizootic disease has a high morbidity but a low mortality rate. Acute ocular disease is characterized by conjunctivitis or keratoconjunctivitis, often associated with periorbital swelling and exophthalmos, and chromodacryorrhea resulting from swelling and inflammation of the Harderian and lacrimal glands. Primary signs include blepharospasm and photophobia, as well as eye rubbing. Lacrimal gland involvement leads to reduced tear production and hence keratitis, conjunctivitis, periorbital swelling aggravated by self‐mutilation, and chromodacryorrhea. The disease itself usually resolves within one week, whereas resolution of the secondary signs may take as long as one month. Figure 17.2 Microphthalmia and persistent hyaloid artery in the right eye (OD) of a mouse. The normal left eye (OS) is provided for comparison. Note the anterior–posterior diameter of the normal mouse lens and correspondingly narrow anterior and vitreous chambers. (Courtesy of Leandro Teixeira, DVM, DACVP, COPLOW, University of Wisconsin–Madison.) Microphthalmos and anophthalmos have been reported in both mice and rats. Clinically, microphthalmos presents as an abnormally small globe (Figure 17.2), unilaterally or bilaterally, often with concurrent anomalies such as engorged or tortuous episcleral and/or iridal vessels, microcornea, corneal opacities, anterior segment dysgenesis, cataract and/or microphakia, retinal dysplasia and detachment, and colobomas. As with other species, true microphthalmos must be differentiated from acquired phthisis bulbi. Several experimental microphthalmic rodent models exist, but microphthalmos also occurs sporadically as an incidental finding in several standard rat and mouse lines. Though microphthalmos is rare in most strains, the inbred pigmented C57BL/6J mouse carries a higher relative risk, with a reported incidence of up to 12%. Corneal opacification is relatively common in rodents, perhaps more so in mice than in rats. Corneal opacities in rodents may be categorized as traumatic, iatrogenic, toxic, infectious, or heritable (e.g., corneal dystrophy [CD]). Since most mice and rats are group housed, corneal opacities/scars related to trauma are common, and may present with or without concurrent uveitis and/or intraocular findings. Several causes of corneal inflammation exist in this species. Opacities in the nasal part of the cornea are common, and while they may relate to anterior segment inflammation, they can also relate to orbital gland inflammation. More severe keratitis can also occur and is probably caused by reduced tear secretion, although, as noted earlier, evaluation of tear production is rarely undertaken in these rodents, producing a secondary keratitis. Thus, keratitis may occur without any obvious infective or environmental factors. CD is a common, bilateral, opacifying disease in mice and rats with a putatively heritable cause and no association with underlying systemic disease. Corneal opacification has been more frequently reported in mice than rats. In rats, the incidence of CD is variable, depending primarily on the age, sex, and strain of the animal. Incidence in both mice and rats increases with age. CD typically presents as fine or punctate, granular, translucent to opaque white corneal opacities in the anterior subepithelial corneal stroma, often observed in the nasal and/or axial cornea. Lesions of the anterior uvea in rodents can for the most part be divided into congenital anomalies and those secondary to inflammation. The former lesions include keratolenticular adhesions (discussed earlier) and the persistence of the pupillary vasculature. Blood in the anterior segment is more commonly associated with persistent embryonic vasculature around the lens and iris than with active inflammation. Similarly, blood in the vitreous is often associated with persistent hyaloid vessels. Persistent pupillary membranes (PPMs) have been reported in almost every species of laboratory animal, including rats and mice. Naturally occurring glaucomas have been reported in mice and rats. The failure of aqueous drainage is not necessarily because of an abnormality of the iridocorneal angle, as in many inherited glaucomas in the dog or in the bu/bu rabbit. In rats, it often results from PPMs causing pupil‐block glaucoma or from peripheral anterior synechiae causing angle‐closure glaucoma. Clinical descriptions of sporadic primary congenital glaucoma have been reported in F344, Wistar, and RCS (Royal College of Surgeons) rats. Clinically, signs of glaucoma in rodents may be difficult to recognize, as signs like episcleral congestion, corneal edema, mydriasis, or behavioral changes indicating vision deficits may not be as prominent as in other species. In the laboratory setting, buphthalmos is often the first sign observed, possibly developing with little delay in the face of elevated IOP due to the rodent’s comparatively thin sclera. In the rat, cataracts may occur both congenitally and in aging animals. These reports concerned the Sprague–Dawley rat, but other rat strains (e.g., the albino Sherman) and the F344 are also affected. Although occurring at a low incidence, these spontaneous lesions complicate experimental work on cataract induction and toxicological studies. In rats with retinal dystrophy or degeneration, cataracts occur secondarily, probably because of the release of various posterior segment metabolic by‐products. The mouse is one of the most commonly used models for human inherited cataract, with early‐ and late‐onset cataracts described in association with numerous mutations, representing varying modes of genetic inheritance. Inherited cataracts have been documented in mice, such as those occurring in the Scat and Lop‐10 strains, which have autosomal dominant cataracts. Iatrogenic transient lens opacities in rodents have been described in association with prolonged eyelid separation while under anesthesia, putatively a result of changes in the osmotic environment and/or temperature in the AC. Persistence of the hyaloid vasculature is a common spontaneous finding in both mice and rats, typically visible on examination as a white filamentous structure spanning the axial vitreous. This finding is most common among weanling rodents, often regressing as animals age until it is negligible or no longer visible shortly after sexual maturity. Abnormalities of the fundus may be divided into congenital lesions, inherited retinal dystrophies, chorioretinal inflammatory lesions, acquired retinal degenerations, and retinal detachments. Most congenital lesions of the rodent fundus are either abnormalities of the retinal and hyaloid vasculature or colobomatous defects of the retina or optic disc. Vascular anomalies such as preretinal loops have been reported in up to 12% of Sprague–Dawley rats. Other vascular lesions include spontaneous saccular aneurysms of the retinal vessels, observed sporadically in older mice and rats. Nontransitional retinal folds consistent with retinal dysplasia have been described and histologically characterized in adult rats from several strains, including the Sprague–Dawley, RCS, Long–Evans, and Wistar‐derived WAG rats. Retinal degeneration is well characterized in mice and rats, categorized as hereditary, senile (age related), phototoxic, or postinflammatory. In the mouse, there are numerous forms of hereditary retinal degeneration. Perhaps, the most well‐characterized form is one that commonly serves as a phenotypic model for human retinitis pigmentosa. The rd gene, for instance, is seen in C57BL/6J, CBA, C3H, and various outbred albino mouse strains. The RCS rat with its retinal pigment epithelial dystrophy is one such example, as is the Osborne–Mendel rat with its retinal degeneration. In mice, the most common infectious cause of retinal degeneration is LCM. Mice are the natural carrier for this potentially zoonotic arenavirus, shedding the organism in saliva, urine, and/or feces. LCM virus can also be transmitted between animals horizontally via aerosolization and direct contact, or vertically from dam to offspring. Relative to its cranial dimensions, the guinea pig possesses a large, open orbit. In comparison to smaller rodents whose orbits are roughly ovoid in shape, the guinea pig orbit assumes a more spherical conformation. Like mice and rats, the guinea pig possesses intra‐ and extraorbital lacrimal glands, as well as a prominent Harderian gland. The primary lacrimal gland of the guinea pig is intraorbital and resides in the lateral and anteroventral orbit. The presence of a large zygomatic salivary gland has also been reported in guinea pigs, occupying a large portion of the caudal and superior orbit. However, some suggest that this zygomatic gland is instead a portion of the large Harderian gland. The guinea pig is also one of few nonhuman species with a distinguishable Bowman’s layer in the anterior corneal stroma and subtending the epithelial basement membrane. The dynamics of the tear film and ocular surface in the guinea pig appear to differ considerably from other animals. The low blink rate in guinea pigs (2–5 blinks/20 min) suggests the presence of an inherently very stable tear film. The guinea pig fundus is clinically anangiotic, as it lacks a grossly identifiable retinal vasculature. Histologically, blood vessels are present within the guinea pig optic disc; therefore, there is controversy as to whether this species is anangiotic or paurangiotic like equids. There is very little published work on ocular disease in this species; however, a survey of ocular disease in 1000 apparently normal cavies reported 45% had some ocular disorder, ranging from cataracts to heterotopic bone formation. Congenital defects ranging from those as severe as clinical anophthalmos (Figure 17.3) to posterior polar subcapsular cataracts are seen in a significant proportion of guinea pigs, particularly those of roan × roan matings. Congenital cataracts have been reported in a litter of guinea pigs also affected with urogenital abnormalities after treatment of pregnant sows with the antibiotic tylosin. Space‐occupying orbital disease or exophthalmos has been reported in guinea pigs in association with dental disease and/or retrobulbar abscess. Primary retrobulbar neoplasia has not been described in guinea pigs, but bilateral exophthalmos has been reported in association with ocular infiltration due to disseminated lymphoma. Bilateral exophthalmos has also been reported in association with hyperadrenocorticism. Figure 17.3 Clinical anophthalmos in a guinea pig. Eyelid abnormalities are sporadically reported in guinea pigs. Blepharitis may be a manifestation of primary dermatophytosis, but may also develop secondary to the extension of generalized dermatologic disease or conjunctivitis. Conjunctivitis is a common ophthalmic diagnosis in guinea pigs, observed in 3.4% of eyes in a survey of 1000 animals. Infectious conjunctivitis is also reported in guinea pigs, most commonly in young animals. Chlamydia caviae is one of the most commonly implicated bacterial organisms, resulting in a conjunctivitis that is typically self‐limiting within three to four weeks. Some animals have only slight reddening of the eyelid margins, whereas others have thick purulent exudate. Infection in young animals is characterized by inclusion bodies in conjunctival epithelial cells with leukocytic infiltrates. The disease is now recognized to be associated with Chlamydophila psittaci . Other causative bacterial organisms include P. multocida , Listeria monocytogenes , Bordetella bronchiseptica , Streptococcus spp., and both Salmonella and Shigella spp. Conjunctival masses are common in guinea pigs. Smooth, benign conjunctival protrusions typically in the inferior conjunctiva, known by guinea pig breeders and enthusiasts as “fatty eye,” were observed in 1.9% of eyes in the aforementioned survey of 1000 animals. These masses are composed of lipids, and may be associated with diet and increased body condition. Prolapse of lacrimal tissue is the putative cause of “flesh eye” or “pea eye,” a lesion observed in 0.4% of eyes surveyed. This appears as a small pink‐colored mass in the medial canthus (Figure 17.4) and is probably analogous to prolapsed nictitating membrane in the dog or rabbit although histopathological confirmation of this has yet to be reported. In a large survey of 1000 animals, findings attributed to ocular trauma were observed in 25 eyes (1.25%), largely manifesting as corneal lesions. In another investigation of 20 male and female guinea pigs (pigmented and nonpigmented American and Dunkin–Hartleys), fluorescein staining confirmed the presence of punctate and linear superficial corneal erosions in both eyes of all animals examined, despite the absence of clinical discomfort or overt corneal opacification on examination. The authors of both of these studies propose that the relatively high incidence of corneal lesions in guinea pigs is likely due to environmental trauma, particularly contact with hay or straw bedding. Figure 17.4 A small pink‐colored mass (flesh eye) in the medial canthus in guinea pigs may represent prolapsed lacrimal tissue. Figure 17.5 Heterotopic bone formation (osseous metaplasia) in the ciliary body of guinea pigs as a focal lesion (a) or a larger area (b). Corneal lipidosis has been described in guinea pigs and may be observed in association with conjunctival lipid deposits. Such lesions may also represent a bilateral condition with a similar axial‐to‐paraxial distribution and a clinical appearance similar to stromal lipid dystrophies reported in dogs. Formation of bone in the ocular soft tissues is a unique but relatively common and well‐characterized finding in guinea pigs, particularly in older animals. Bony spicules surrounded by a fibrous envelope form most commonly in the ciliary body of guinea pigs (Figure 17.5), but other anterior segment structures (e.g., iris base, iridocorneal angle, and/or peripheral cornea) as well as extraocular sites have also been reported. Lesions are clinically visible when they extend anteriorly, commonly appearing as well‐demarcated white lesions originating at the limbus, and extending into the adjacent cornea. Lesions involving only the ciliary body or iridocorneal angle will not be visible clinically, and may not produce any clinical signs. One report identified an association between osseous metaplasia of the iridocorneal angle and secondary glaucoma on postmortem examination. Cataracts are commonly seen in guinea pigs. In the aforementioned survey of 1000 guinea pigs, cataract was the most commonly observed spontaneous ocular lesion on ophthalmic examination, identified in 16.9% of eyes. In another study, 18% of outbred animals were affected with cataract. The vast majority were observed in older animals, often presenting as an incipient or immature lens opacity (2.2% and 4.9% of eyes, respectively). Congenital cataracts were observed in 3.7% of eyes. Diabetic cataracts, some reaching maturity, have also been reported in guinea pigs. Inherited cataracts have been reported in the N13 strain of guinea pigs. Lens opacities in these latter animals are caused by a single splice‐site mutation in the zeta‐crystallin gene. The scientific literature yields little information regarding diseases of the chinchilla eye. They are nocturnal and crepuscular animals with a vertical pupil that can close to a narrow slit, protecting their scotopically adjusted retina from bright light, which can render fundoscopy somewhat difficult without mydriasis, and an anangiotic fundus with variable vascularization of the optic disc. They have a shallow orbit, a rudimentary nictitating membrane, a large cornea, and a densely pigmented iris in pigmented individuals. A significant problem in this species when kept in captivity is dental disease. The ferret eye is adapted for dim light conditions; predation by ferrets occurs between dawn and dusk, and if in daytime, within the scotopic conditions of rabbit warrens and prairie dog burrows. Thus, the ferret retina is predominantly rod based, although like in the cat there is a cone‐rich strip, the area centralis, allowing a higher acuity to be achieved. The ferret has a large retrobulbar venous sinus that has been suggested as a site for blood collection. Given the ease of blood collection from the ventral tail vein or jugular in this species, however, orbital blood collection cannot be recommended. The depth of the orbit in a ferret renders detection of an orbital space‐occupying lesion difficult until it has reached a considerable size. A large, poorly encapsulated zygomatic salivary gland is located posteroinferior in the orbit in the ferret, and head trauma may result in a salivary mucocele with associated exophthalmos. Congenital ocular disease in ferrets is relatively rare, although persistent hyaloid artery, tunica vasculosa lentis, and hyperplastic primary vitreous occur. The eyelids of ferret kits do not separate until about 20 days postpartum; this late opening may account for the relatively high prevalence of ophthalmia neonatorum in this species. Conjunctivitis in ferrets has been caused by human influenza virus, canine distemper virus, systemic mycobacteriosis, and salmonellosis. Canine distemper in this species may cause photophobia and serous oculonasal discharge, which becomes mucopurulent with associated chemosis and corneal ulceration. Canine distemper infection in ferrets is usually fatal, but with influenza, the almost identical early signs often resolve. Conjunctivitis may be a constant sign in systemic mycoplasmosis. Microphthalmos occurs in ferrets, and as part of an autosomal dominant multiple ocular anomaly syndrome with cataract and retinal dysplasia. Cataracts have been reported several times in ferrets. Lens luxations have been reported in ferrets as primary lens dislocations and as secondary to chronic cataract. Ferrets have a holangiotic retina, with a reflective tapetum in pigmented animals and possibly also in albinos. Anecdotally, retinal degeneration is believed to be common in the ferret, with inherited atrophy and degeneration associated with taurine deficiency in this obligate carnivore suggested in review, but not reported in the primary literature. The majority of rabbits have moved from being a laboratory model to the third most popular pet in small animal practice in the United Kingdom. Ocular disease in rabbits has a significant impact on the welfare of these animals kept as pets, and several diseases, from dacryocystitis to corneal ulceration, cataract, and uveitis, are chronic and can be difficult to manage. The rabbit, as a prey animal, has laterally placed prominent eyes with a large ocular surface relative to the size of the animal, giving a wide field of vision but also potentially an exposed ocular surface prone to traumatic damage or evaporative tear loss (Table 17.2). The optic nerve is unusual with a deep normal physiological pit and it enters the eye above the optic axis, unlike in other domestic animals or humans. The normal physiological appearance of the rabbit optic nerve head can complicate clinical detection of pathological optic disc cupping associated with glaucoma. Table 17.2 Important clinical characteristics of the rabbit eye. Since the 1940s, the laboratory rabbit was the standard animal model for ophthalmic biochemistry, physiology, pharmacology, and toxicology investigations (Table 17.3). Based on those studies, investigations into other species, including humans, were comparative and still useful as reference studies to those today. Today, rabbits are used less frequently, as other avenues are available, and the number of the different breeds of rabbits kept as pets probably exceeds this species currently maintained for research. The indoor house rabbit is becoming a more frequent pet because it can easily be trained to use a litterbox and does not need to be outside daily. Table 17.3 Ocular diseases in the rabbit. Congenital abnormalities of the globe such as microphthalmos or anophthalmos are uncommon in rabbits. A case of colobomatous microphthalmos has been described in a New Zealand white rabbit, suspected to be associated with vitamin E deficiency. An important feature of rabbits, and one that is vital to note during enucleation, is the retrobulbar venous plexus. Perforation of the orbital venous plexus during globe removal can lead to significant blood loss with hemostasis difficult to achieve by digital pressure. Performing this surgery transconjunctivally rather than transpalpebrally, and remaining as close as possible to the globe during dissection, obviates this problem in the vast majority of cases. Another important condition arising from this orbital venous plexus or sinus is that of periodic bilateral exophthalmos when the animal is stroked or picked up. Here, the problem is that venous return from the head is precluded by a mass around the jugular veins, most commonly a thymoma or thymic carcinoma, which fills the orbital sinus and causes a startling exophthalmos, which resolves when the stressful situation ceases. Retrobulbar space‐occupying lesions that can cause exophthalmos can be neoplasms or parasitic cysts, although both of these are much less common than a retrobulbar abscess. Orbital neoplasia is rare, but lymphoma involving the Harderian gland has been reported. Most cases of exophthalmos are caused by retrobulbar abscesses, usually originating from the tooth root retrobulbar abscesses, usually originating from the tooth root (Figure 17.6). These can be very difficult to manage, as can any rabbit abscess, but some groups have reported success with endoscopic curettage after dental extraction Pasteurella is often associated with retrobulbar abscessation in rabbits, and this condition is often linked to a tooth root abscess. Orbital exenteration is one option in such cases, but the orbital venous plexus can yield significant blood loss. Figure 17.6 Exophthalmos is caused by retrobulbar abscesses, usually originating from the tooth root. Three orbital glands present in the rabbit (the lacrimal gland, nictitans gland, and superficial and deep nictitans gland, also known as the Harderian gland) can become hyperplastic, and all but the lacrimal gland can prolapse and protrude from the orbit. These glands are very heavily vascularized. Diseases of these structures include tear deficiency, gland protrusion, hyperplasia, and neoplasia. Blepharitis is rabbits is not an uncommon finding. Traumatic origins are often suspected, especially in group‐housed animals. Most nontraumatic instances are extensions of generally dermatitis or of keratoconjunctivitis or dacryocystitis. While infectious blepharitis without concurrent conjunctivitis and/or keratitis is uncommon in rabbits, blepharitis may be associated with Treponema cuniculi infection, the agent of rabbit syphilis (Figure 17.7) that is transmitted to the neonates by the infected genital tract of the mother. The definitive diagnosis is made on the basis of identifying the spirochete on conjunctival cytology. Treatment is with three injections of penicillin G at 40000 IU/kg at seven‐day intervals. Because prolonged β‐lactam antibiotic therapy can cause fatal dysenteribiosis in rabbits and rodents, this treatment should be given with care and should be stopped if diarrhea is noted. Rabbit poxvirus can also cause blepharitis, primarily due to local extension of cutaneous disease. Figure 17.7 Infectious blepharitis without concurrent conjunctivitis and/or keratitis may be associated with T. cuniculi infection, the agent of rabbit syphilis. Figure 17.8 Annulus of conjunctiva growing over the cornea from the limbus. This may be a narrow band (a) or a sizable ring (b) of tissue with only a small aperture centrally. Entropion is relatively commonly seen in rabbits and can be corrected by the Hotz–Celsus surgical procedure. Often, the lid inversion leads to corneal ulceration with subsequent increased blepharospasm and worsening ocular surface trauma. An unusual and apparently unique abnormality in rabbits is an aberrant overgrowth of the conjunctiva, producing a type of ankyloblepharon involving the conjunctiva covering of the ocular surface. Also referred to as precorneal membranous occlusion, conjunctival centripetalization, epicorneal membrane, or pseudopterygium, the condition is benign and idiopathic and has a classic appearance of an annulus of conjunctiva growing over the cornea from the limbus. This may be a narrow band or a sizable ring of tissue with only a small aperture centrally (Figure 17.8). The conjunctival growth is not adherent to the underlying cornea and is not associated with conjunctivitis or preexisting structural conjunctival abnormalities. Dwarf rabbits are overrepresented. Resection of this tissue merely leads to its regrowth, but surgical techniques to transect and reposition the overgrowth into the conjunctival fornix have met with improved success. Conjunctivitis is seen commonly in pet rabbits and has several causes. In rabbits, it is important to distinguish conjunctivitis from dacryocystitis. Purulent ocular discharge with conjunctival hyperemia often accompanies not only conjunctivitis, but also nasolacrimal duct and lacrimal sac infections (Figure 17.9). The diagnosis of infectious conjunctivitis and dacryocystitis must be approached with appreciation of the normal bacterial flora of the conjunctival sac. Pasteurella spp. are considered by many to be the most common bacterial pathogen in the rabbit, but it is also important to consider S. aureus . In a more recent survey of conjunctival flora in rabbits with conjunctivitis and dacryocystitis, Staphylococcus spp. (78% of swabs) and not Pasteurella (12%) were not the most commonly isolated species. Conjunctival disease in the rabbit can be caused by viral as well as bacterial agents. In rabbits, it is important to remember that conjunctivitis, particularly unilateral conjunctivitis, is a common manifestation of underlying dental disease. Figure 17.9 Rabbit with dacryocystitis with lid swelling and purulent exudate. Clinical keratoconjunctivitis sicca is seen rarely in rabbits, but the species is used as a model for human dry eye and there is extensive literature on the pathology and treatment of aqueous tear deficiency in these animals. Cyclosporine increases tear production in rabbits with such autoimmune lacrimal adenitis. Rabbits treated with oral trimethoprim–sulfamethoxazole twice daily at a dose of 40 mg/kg had significant reductions in Schirmer tear test (STT) readings. Perhaps, the most common and one of the most frustrating ocular conditions in the rabbit is dacryocystitis (see Figure 17.9). While mostly present with a purulent ocular discharge, other rabbits can have a swollen medial canthal area or medial canthal dermatitis that can be severe. In one study, the most common initial treatment was topical antibiotic, but flushing of the nasolacrimal duct was performed in 87% of the rabbits; 80% of animals had dental treatment. As already mentioned, the rabbit is unusual in having only one lacrimal punctum (lower), with a nasolacrimal duct that follows a tortuous route through the lacrimal and maxillary bones. Malocclusion of the molar arcades in particular results in retropulsion of the tooth into the weakened maxillary bone, with subsequent nasolacrimal occlusion; incisor malocclusion may perhaps more commonly produce this same result. Treatment of dacryocystitis in the rabbit is by cannulation of the single lacrimal punctum and flushing of the duct. The copious discharge needs to be flushed out, and this should be done regularly until the condition resolves. If cannulation from the lacrimal punctum is difficult, cannulation of the duct opening at the nasal meatus is possible, but the small diameter of the duct at its nasal end renders this procedure difficult. The most serious corneal condition in rabbits is corneal ulceration. Rabbits have particularly protuberant eyes with a large exposed ocular surface relative to their body mass. Every posttraumatic corneal ulcer, such as this linear erosion (Figure 17.10), should thus heal in under one week. Treatment is similar to that in affected dogs. After topical anesthetic administration, a sterile cotton bud or bacteriology swab is used to debride the nonadherent epithelium at the edge of the ulcer. Diamond burr debridement or a grid keratotomy are useful to facilitate and encourage healing, but use considerable caution because the rabbit cornea is substantially thinner than that in the dog. Protection for the healing ulcer is also important (shield contact lenses). Lipid keratopathy has been documented in rabbits fed a cholesterol‐rich diet, and is seen in Watanabes with heritable hyperlipidemia. It has also been documented in rabbits fed a 10% fish meal maintenance diet, and in one pet rabbit fed a predominantly milk‐based diet. Clinical appearance is variable, with some lesions appearing faint and translucent, and others more opaque and even slightly raised. Some corneal lesions may be associated with secondary vascularization. Figure 17.10 Nonhealing corneal ulcer with devitalizes nonadherent epithelial edge. Corneal epithelial dystrophy in the rabbit has been reported as a peripheral lesion histopathologically characterized by areas of epithelial thinning adjacent to areas of epithelial cell hyperplasia. Another report described a plaque‐like paracentral granular stippling in American Dutch Belted rabbits, which was characterized histopathologically by an irregularly thickened epithelial basement membrane similar to that seen in epithelial basement membrane dystrophy or Reis–Buckler’s dystrophy in humans. Hereditary glaucoma in the New Zealand white rabbit has been studied extensively since the early 1960s (Figure 17.11), but also occurs in pigmented breeds. The inheritance pattern is putatively autosomal recessive with incomplete penetrance. Neonatal bu/bu homozygotes have normal IOP (15–23 mmHg), but after one to three months of age IOP rises to between 26 and 48 mmHg. Clinical signs are typically subtle, often limited to observation of buphthalmos and corneal edema. Exposure secondary to buphthalmos may also result in keratitis and/or corneal ulceration. In chronic cases, eventual atrophy of the ciliary body may result in normalization of IOP, though most affected eyes remain buphthalmic. Histopathological features have shown goniodysgenesis involving the pectinate ligaments and trabecular meshwork in affected eyes. Vision is lost at this stage, but the eyes do not appear painful, probably because of the increase in size of the globe accompanying the raised pressure. Treatment with topical carbonic anhydrase inhibitors such as dorzolamide three times daily reduces the IOP but appears to make no difference to behavior of the affected animal. The bu gene is a recessive trait that is also semilethal, with heterozygotes giving birth to small litters of unthrifty kits. Figure 17.11 Hereditary glaucoma in the New Zealand white rabbit has been studied extensively since the early 1960s. Clinical signs include buphthalmia, mild corneal edema, and dilated pupil. For many years, inflammatory lesions with vascularization in the rabbit iris were ascribed to infection by P. multocida , which produces white, purulent abscesses in other locations in this species. Recent findings are strongly suggestive that many of these lesions are caused by lens‐induced uveitis (Figure 17.12), which occurs secondary to lens capsular rupture caused by intralenticular infection by the protozoan Encephalitozoon cuniculi. Because of the lens‐induced nature of this inflammation, treatment is lens removal by phacoemulsification with concurrent topical anti‐inflammatory medication. The rabbit has a significant postoperative capsule fibrosis response. Figure 17.12 Uveitis in rabbits occurs secondary to lens capsular rupture and intralenticular infection by the protozoan E. cuniculi. Not all anterior uveitis is lens induced. Pasteurella spp.‐associated cases may be encountered with a more classic uveitis characterized by episcleral congestion, miosis, and hypopyon. Some Pasteurella spp. or Staphylococcus‐associated iridal inflammation is difficult to differentiate from lens‐induced inflammatory disease; in other cases, the yellow purulent material in the anterior chamber is characteristic of a more obvious bacterial infection. Congenital, primarily nuclear cataracts and PPMs have been documented in rabbits. Nuclear sclerosis, the aging change in which the continually growing cortex compresses the lens nucleus, occurs in rabbits with an average age of 6.0 years. Many of these cataracts are small opacities with little effect on vision, whereas some may be much more rapidly maturing and hence blinding. One form of cataract unique to the rabbit is that caused by E. cuniculi (Figure 17.13). This remarkable obligate intracellular microsporidian generally infects rabbits through ingestion of contaminated urine and may cause renal or neurological symptoms. If the organism migrates to the developing lens, it may lie dormant for many months, before moving through the lens, causing cataract and then erupting through the anterior lens capsule to liberate lens material into the anterior chamber that elicits lens‐induced uveitis. Phacoemulsification is the method of choice to remove a cataractous lens. However, the rabbit as a species has an unusual propensity to reform lens fibers after removal surgically. When intraocular lens implants have been used, these have sometimes been forced out of the lens capsule by the regrowth of lens tissue. Careful removal of all lens fibers from the lens capsule reduces this risk. Figure 17.13 (a) Sudden‐onset progressive cataract in Netherland dwarf rabbit, and (b) Mature cataract in a 7‐year‐old diabetic rabbit. The fundus of the rabbit is merangiotic with a band of blood vessels and myelinated nerve fibers traversing the retina in a horizontal plane from the optic disc (Figure 17.14a and b). Few reports of retinal disease in rabbits exist. The large physiological cup of the rabbit optic nerve head is often misdiagnosed as an optic nerve coloboma. Spontaneous disease of the retina and posterior segment is rare in laboratory rabbits. In one large survey, the only spontaneous finding involving the posterior segment was choroidal hypoplasia, a typically bilateral lesion affecting 1.2% of examined animals. The orbital sinus or retrobulbar venous plexus is most important to be aware of when performing an enucleation. A transpalpebral approach runs the risk of entering this sinus with the potentially severe side effect of blood loss. The transconjunctival technique, generally preferred in all species by most ophthalmologists yet little used by many general veterinary surgeons, enables one to remove only the globe and not exenterate the orbit and its contents, including the orbital sinus. Figure 17.14 (a) Albino rabbit and (b) pigmented rabbit. Fundus of the rabbit is merangiotic with a band of blood vessels and myelinated nerve fibers traversing the retina in a horizontal plane from the optic disc. The miniature pig (minipig) is increasingly being used as an animal model in vision science and toxicological investigations. This is partially attributable to anatomical and biometric similarities between features of the porcine eye and the human eye. Minipigs are approximately 25% of the size of a regular domestic pig. The Göttingen and Yucatan are the most commonly cited breeds in ocular investigations. Others that may be cited include the Hanford, Sinclair, Ossabaw Island hog, Vietnamese Pot‐bellied pig, and the Chinese Bama minipig. Domestic and miniature pigs both have deep open orbits, with globes that are relatively deep set, particularly in the Yucatan. The pig has a Harderian gland located within the ventromedial orbit, posterior to the globe. An orbital venous sinus has also been identified in the porcine orbit and, as for the rodent, was formerly used as a site for venous blood collection. Microphthalmos (and less commonly anophthalmos) with or without retinal dysplasia and other ocular anomalies has been described in young piglets in association with maternal hypovitaminosis A. While rare, polycoria and suspected anterior uveal colobomas have been described in pigs, and colobomatous lesions involving the optic disc and choroid have been described specifically in minipigs. Entropion is commonly diagnosed in minipig breeds such as the Vietnamese Pot‐bellied pig, related to robust subcutaneous periocular and forehead fat. In some cases, the conformational entropion may be severe enough to impair vision. While this condition is not common in other minipig breeds, it has been reported in the Göttingen. Primary conjunctivitis is uncommon in purpose‐bred minipigs, but a transient, self‐limiting blepharoconjunctivitis has been described in young (six‐ to eight‐week‐old) Göttingens.
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Exotic Animals: Ophthalmic Diseases and Surgery
Considerations for Ophthalmic Examinations in Laboratory Animals
Ocular Diseases in the Mouse and Rat
Chromodacryorrhea
Orbital space‐occupying lesions
Conjunctivitis
Sialodacryoadenitis
Microphthalmos
Corneal opacification and inflammation
Corneal dystrophy
Anterior uvea lesions
Glaucoma
Cataracts
Posterior segment
Persistence of the hyaloid vasculature
Vascular anomalies and saccular aneurysms of the retinal vessels
Retinal degeneration
Infectious lymphocytic choriomeningitis
Orbital Space‐Occupying Lesions
Conjunctivitis
Sialodacryoadenitis
Microphthalmos
Corneal Opacification and Inflammation
Corneal Dystrophy
Anterior Uvea Lesions
Glaucoma
Cataracts
Posterior Segment
Guinea Pig
Congenital/Developmental Anomalies
Retrobulbar Disease
Eyelids and Conjunctiva
Cornea
Heterotopic Bone Formation (Osseous Metaplasia)
Cataracts
Chinchilla
Ferret
Rabbits
Special Characteristics of the Rabbit Eye
Laterally placed prominent eyes
Closed orbit with a large ocular surface relative to the size of the animal
Wide field of vision orbit is closed
Slow blink rate in the rabbit
Large orbital vascular plexus
Third eyelid moves passively, and has no muscles
Orbital glands: the lacrimal, intraorbital, Harderian (largest)
Tear drainage is through a single slit‐like lacrimal lower punctum
Nasolacrimal duct is tortuous and diameter varies along its course
High incidence of tooth root disease
Cornea is large for the size of eye 15 mm (diameter) and radius of curvature approximately 7 m
Anterior chamber is deep at its center, but shallow at the periphery
Iris may be darkly pigmented or devoid of pigment, depending on coat color
Pupil almost circular but very slightly oval in the vertical meridian
Optic nerve head has deep normal physiological pit, and large lateral and medial myelinated nerve fibers
Ocular Diseases in the Rabbit
Orbital diseases
Adnexal diseases
Corneal diseases
Glaucoma
Uveitis
Cataracts
Orbital Diseases
Congenital/Developmental Anomalies
Orbital Gland Diseases
Adnexal Disease
Blepharitis
Entropion
Conjunctival Overgrowth
Conjunctivitis
Keratoconjunctivitis Sicca
Nasolacrimal Duct Abnormalities
Corneal Disease
Glaucoma
Uveitis
Cataracts
Diseases of the Fundus
Surgery – Enucleation
Miniature Pig
Congenital/Developmental Anomalies
Adnexa and Anterior Segment
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