Revised from 6th edition of Veterinary Ophthalmology, Chapter 37, Parts 1 (Canine), 2 (Feline), 3 (Equine), and 4 (Food Animals): Ocular Manifestations of Systemic Disease, by Aubrey A. Webb and Cheryl L. Cullen Ocular examination of animals with systemic disease is an essential diagnostic component of a complete physical examination that can help reduce the list of probable differential diagnoses and can assist in organizing such a differential diagnostic list from most to least likely. In addition, the visual prognosis for the animal may be crucial to owners when deciding how aggressively they wish to pursue diagnostic and therapeutic alternatives. Often, the changes in the disease can be monitored by ophthalmic examination and assist in adjustments in medications as the animal recovers. Diseases affecting the vascular and nervous systems are particularly prone to ocular manifestation. Inspection of the uvea and retina, and optic disc of the animal through the transparent cornea, lens, and neurosensory retina permits evaluation of both the peripheral vasculature and central nervous system (CNS), respectively. Since the rate of ocular blood flow is very high, there is increased likelihood that the uveal and retinal vasculature will be exposed to, and possibly filter out, hematogenously spread neoplastic cells and/or infectious organisms. For the purposes of this chapter, ocular manifestations of systemic disease include any disorder not of primary ocular origin that manifests as ocular clinical signs. Selected systemic diseases have been categorized according to species (dog, cat, horse, and food animals), stage of onset (congenital, developmental, or acquired), and have been alphabetically arranged according to the mechanism and/or cause of the systemic disease. Complete albinism (complete lack of pigmentation) or partial or localized albinism (an absence or reduction in the degree of pigmentation) is associated with not only the phenotypic appearance of an animal’s coat and skin color, but also conditions affecting the ear and eye (Table 19.1). Albinism or partial albinism may result from the failure of migration of neural crest cells (precursors to melanocytes) and hence results in reduced numbers of melanocytes in a nonpigmented area, or may result because of impaired production of pigment due to some intrinsic deficiency in melanin production (e.g., tyrosinase deficiency), but where the number of melanocytes in nonpigmented or hypopigmented areas is normal. Table 19.1 Coat color‐related diseases/conditions in dogs. Inherited sensorineural deafness and ocular abnormalities have been linked to coat color genes in many breeds of dogs. Hearing loss related to coat color in dogs typically results from cochleosaccular degeneration and can be associated with the absence of pigment within the stria vascularis of the cochlea. Coat color is often associated, not only with deafness, but also with heterochromia irides, blue irides, and lack of retinal pigment. Coat color genetics soon becomes complicated when one considers all of the combinations and permutations of coat colors seen in the numerous breeds of dogs that have been developed. The blue and red merle Australian Shepherd has been studied rather extensively, and the mode of inheritance for the ocular lesions in the merle dog has been demonstrated to be a recessive trait with incomplete penetrance. Figure 19.1 Clinical presentation associated with oculoskeletal dysplasia, including forelimb varus defects. Inset demonstrates hyphema secondary to retinal detachment. These forms of skeletal dysplasia have been described in several breeds of dogs as a syndrome of short appendages with a normal axial skeleton (i.e., short‐limbed dwarfism) and ocular lesions, so‐called ocular–skeletal dysplasia, have been recorded as being inherited in the Labrador Retriever and the Samoyed (Figure 19.1). The complete phenotype in both breeds is transmitted as an autosomal recessive trait, while ophthalmoscopic findings have indicated a semidominant mode of inheritance in which skeletally normal, heterozygous dogs can have no ophthalmoscopic abnormalities or multiple retinal folds, vitreal membranes, or vitreous degeneration. Syndrome in the Labrador Retriever was felt to be recessive for the skeletal lesions and incomplete dominant trait for the ocular lesions. The causative locus in ocular–skeletal dysplasia of the Labrador Retriever has been termed drd1 and it is mapped to canine chromosome 24, and an insertional mutation in exon 1 of the gene COL9A3 cosegregates with the disease. The Samoyed syndrome of ocular–skeletal dysplasia is an autosomal recessive trait. In particular, the causative locus in ocular–skeletal dysplasia of the Samoyed has been termed drd2 and it is mapped to canine chromosome 15 and cosegregates with a 1267‐bp deletion mutation in the 5′ end of COL9A2. Hydrocephalus in dogs is defined as increased amount of cerebrospinal fluid (CSF) within the cranial vault (Table 19.2). Most common cause of congenital hydrocephalus is a primary congenital stenosis or aplasia of the mesencephalic aqueduct associated with fused rostral colliculi. Congenital hydrocephalus may produce enlargement of the calvarium and failure of closure of the suture lines of the skull (Figure 19.2). Consequently, affected puppies may have a persistently open fontanelle. Table 19.2 Hydrocephalus in dogs. Myasthenia gravis affects the neuromuscular junction, and may be either congenital or acquired. Congenital myasthenia gravis occurs when there is a functional disorder or depletion of nicotinic acetylcholine receptors. Congenital myasthenia gravis has rarely been reported in dogs. Congenital myasthenia gravis is inherited as an autosomal recessive trait in Smooth Fox Terriers, Jack Russell Terriers, and English Springer Spaniels. Clinical signs associated with congenital myasthenia gravis include generalized muscle weakness that worsens with exercise, possible megaesophagus, facial weakness, and tendon reflexes that weaken with repeated testing. A syndrome of decreased vision with nystagmus, ataxia, and tremors has been described in the Irish Setter. This syndrome is thought to be inherited as a postnatally lethal, autosomal recessive trait. Most animals, however, are unable to stand at birth, though walking movements are made that propel them in a “seal‐like” manner when prone. Vision is difficult to evaluate in a very young animal, but those affected lack fixation responses as well as menace responses and dazzle reflexes. The pupillary light reflexes (PLRs) are normal. The ocular fundus is normal on fundic examination. CNS lesions include degeneration and necrosis of the cerebellar cortex, with severe loss of Purkinje cells. Figure 19.2 Congenital hydrocephalus in a toy breed with “sunset eyes.” The calvarium is pushing the globes ventrolaterally. Several inborn defects have been reported in the dog. They are relatively rare, but offer models for similar metabolic errors in man. These include (i) tyrosinemia from a deficiency in hepatic tyrosine aminotransferase and (ii) storage diseases characterized by an accumulation of metabolic by‐products within lysosomes, the cellular organelles that degrade complex macromolecules (see Appendix E). Lysosomal storage diseases, with known mode of inheritance, are inherited as an autosomal recessive trait. When homozygous, the syndromes are usually severe, thus resulting in neurological disease and, eventually, death. Ceroid lipofuscinosis has been described in many species, including cats, cattle, dogs, goats, humans, mice, and sheep (Figure 19.3). Fucosidosis is an autosomal recessive glycoproteinosis in the English Springer Spaniel. The disease is produced by a deficiency of the lysosomal enzyme α‐L‐fucosidase. Deficiency of lysosomal α‐L‐fucosidase causes the accumulation of these glycolipids and oligosaccharides. Galactocerebrosidosis, or globoid cell leukodystrophy or Krabbe’s disease, is an autosomal recessive trait in West Highland White and Cairn Terriers, Australian Kelpies, and Irish Setters. Galactocerebrosidosis in Irish Setters has been characterized by an insertion mutation of 78 bp in the sequence of the galactocerebrosidase (GALC) cDNA consisting of 16 bp of insertion site duplication and 62 bp of sequence derived from the U4 small nuclear RNA. Figure 19.3 Fundus photograph of NCL‐affected Polish Owczarek Nizinny dog at 18 months of age. Note the generalized grayish to brown spots, the hyperreflective areas, and the severely attenuated retinal vessels. GM1 gangliosidosis is a member of the sphingolipidoses. A deficiency of lysosomal hydrolase, β‐galactosidase, produces an accumulation of GM1 ganglioside in the cerebral cortex and visceral organs. GM2 gangliosidosis is caused by a deficiency of hexosaminidase. Variant forms of GM2 gangliosidosis have been reported in the Japanese Spaniel (AB variant gangliosidosis), the German Shorthair Pointer (Tay–Sachs disease), and also in the Golden Retriever and Toy Poodle (Sandhoff disease). The mucopolysaccharidoses (MPSs) are a group of diseases characterized by defective metabolism of mucopolysaccharides (glycosaminoglycans). Five types of MPSs have been identified in dogs (MPSs I, II, III, VI, and VII). MPS I (Hurler syndrome) has been described in the Plott Hound, and other breeds of dogs, as a deficiency of α‐L-iduronidase. Affected dogs have stunted growth, excessive joint laxity, multiple degenerative joint disease and cardiac valvular disease, and develop diffuse corneal opacities from the accumulation of substrate in the keratocytes. Cerebrovascular accidents occur much less frequently in dogs than in people. Although with the ever‐increasing access to magnetic resonance imaging, cerebrovascular disease in dogs is being recognized more frequently. Because cerebrovascular accidents are acute, clinical signs are acute ± progressive in nature. Systemic arterial blood pressure is the product of cardiac output (CO) (CO = heart rate × stroke volume) and total peripheral resistance. Primary (essential) hypertension has been described, although rarely, in dogs. Secondary hypertension is now recognized as being a common complication of renal disease (60–80% of cases), hyperadrenocorticism (59–86% of cases), pheochromocytoma (>50% of cases), diabetes mellitus, primary aldosteronism, hypothyroidism, and hyperthyroidism. Ocular lesions associated with canine hypertension include tortuous retinal vessels, variable‐sized retinal and preretinal hemorrhages, papilledema, variable degrees of retinal detachment (Figure 19.4), and tapetal reflectivity changes. Figure 19.4 Multiple retinal hemorrhages and possible papilledema associated with hypertension in a dog. Anemia is the reduction in red blood cells (RBCs) per volume of whole blood. Severe anemia often manifests systemically as varying pallor of mucous membranes, cool mucous membranes, tachycardia, polypnea, weakness, as well as signs specific to the underlying primary condition. Conjunctival pallor is even used as an indicator of anemia due to gastrointestinal parasitism in sheep and goats. Ocular manifestations of severe anemia include pale retinal vasculature, varying degrees of retinal hemorrhage, and subtle changes in tapetal reflectivity. Retinal hemorrhages are more likely to be observed, however, and are more dramatic if accompanied by thrombocytopenia. Hyperlipidemia refers to an elevation in plasma concentrations of cholesterol and/or triglycerides, and arises due to a disturbance in plasma lipoprotein metabolism. Hyperlipidemia represents an abnormal finding in fasted dogs and, when present, is indicative of either increased production or reduced degradation of lipoproteins. Primary hyperlipidemia/hypercholesterolemia has been described in various breeds, including the Beagle, Briard, Collie, Miniature Schnauzer, and Shetland Sheepdog. Hyperlipidemia is seen in variety of systemic diseases, including hypothyroidism, diabetes mellitus, hyperadrenocorticism, pancreatitis, and renal (e.g., nephrotic syndrome) as well as hepatic (e.g., cholestasis) diseases. Common diseases associated with secondary hypercholesterolemia in the dog are hypothyroidism, diabetes mellitus, and pancreatitis. Visible lipemia in the dog is produced by elevations of triglyceride levels, and it can be detected in the ocular vessels of the conjunctiva and retina (i.e., lipemia retinalis) as pink, engorged vessels. It is most easily observed in the retinal vessels over the nontapetal region. Hyperlipidemia may also manifest with lipids in the anterior chamber. A prerequisite for gaining access to the anterior chamber by the large, lipid‐laden molecules is alteration of the blood–aqueous barrier, presumably resulting from preexisting uveitis. Figure 19.5 Fundus photographs of a dog with multiple myeloma. (a) Left fundus. Note the retinal detachment dorsal to the optic disc and the focal retinal hemorrhage in the medial fundus at the tapetal–nontapetal junction. (b) Right fundus. Note the multifocal retinal and subretinal hemorrhages and the retinal detachment in the dorsal tapetal region. Hyperviscosity syndrome comprises single or multiple clinicopathological abnormalities resulting from increased serum viscosity. The severity of hyperviscosity syndrome is linked to the size, shape, type, and concentration of large molecules (e.g., immunoglobulins [Ig]) in the bloodstream. This syndrome is seen with IgA, IgG, or IgM macroglobulinemia. The underlying cause is usually a malignancy, such as lymphoma, chronic lymphocytic leukemia, plasmacytoma, or multiple myeloma, but infectious diseases such as ehrlichiosis may also produce the syndrome. The ocular lesions most frequently noted include dilated, tortuous retinal vessels, which may develop kinking or “box carring,” or venous dilatation and sacculation; papilledema; retinal hemorrhages; intraretinal cysts; and bullous retinal detachments (Figure 19.5). Anterior segment complications such as anterior uveitis and glaucoma may develop as well. Icterus or jaundice is a condition characterized by hyperbilirubinemia and deposition of bile pigments in the skin, sclera, and mucous membranes causing them to appear a shade of yellow. The sclera is the classic location for detection of icterus given its relative lack of pigmentation. The yellow appearance of icterus may be detected in the intraocular structures as well (e.g., blue irides may turn green [Figure 19.6] and yellow hues may be imparted on the tapetal fundus). Figure 19.6 Yellow‐appearing iris in a dog with icterus. The clinically normal appearing iris in this dog was blue. Polycythemia is classified as relative or absolute (primary and secondary forms). Relative polycythemia is an increased packed cell volume with normal RBC mass occurring as a result of a reduction in plasma volume as may arise from external losses of body fluids (e.g., diarrhea and burns). Thrombocytopenia results from decreased platelet production, increased removal, sequestration, or any combination of these. The most common causes of thrombocytopenia include infectious diseases, neoplasia, drug‐induced reactions, and immune‐mediated disease. In particular, the numerous pathogens implicated in causing infectious thrombocytopenia in dogs include arthropod‐borne agents (e.g., Babesia, Borrelia, Cytauxzoon, Dirofilaria spp., Ehrlichia spp., Leishmania, and Rickettsia), viral agents (e.g., canine distemper virus [CDV], herpesvirus, parvovirus, and adenovirus), and fungal and bacterial organisms (e.g., Candida, Histoplasma, and Leptospira spp.). Thrombocytopenia is also seen in association with (i) many forms of neoplasia, including lymphoma, leukemia, and multiple myeloma and (ii) medications that impair platelet production or cause secondary immune destruction of the platelets (e.g., chloramphenicol, azathioprine, cyclophosphamide, and doxorubicin); or (iii) it may develop as an idiopathic or primary immune‐mediated condition. In particular, of the 36 dogs with thrombocytopenia alone, 9/36 had mild ocular lesions, including conjunctival (n = 3), iridal (n = 1), or retinal petechiae (n = 3), or focal retinal edema (n = 2), and 6/36 had severe ocular lesions, including hyphema (n = 5) and retinal hemorrhage (n = 1). Idiopathic granulomatous disease in the dog is thought to be immune‐mediated because of the absence of any demonstrable infectious agent and because favorable responses to immunosuppressive doses of corticosteroids or other immunosuppressive drugs have been reported. Syndromes of sterile granulomatous inflammation are poorly defined and relatively rare. Multiple sterile granulomas of the eyelids, conjunctiva, and sclera that accompanied dermal granulomas have been described in another case. Bilateral orbital granulomatous disease that was very responsive to corticosteroids and required therapy indefinitely for remission has been noted. Eventually, while this animal was off therapy, massive granulomatous disease developed in the chest and abdomen. Necropsy and histopathology did not reveal the cause of the granulomas. A case of idiopathic ocular and nasal granulomatous disease in a dog without dermatological lesions has been described and may be a different form of the classically described canine idiopathic granulomatous disease. In this case, bilateral limbal and intranasal granulomatous masses were observed. These masses were predominantly T‐cell‐rich granulomatous reactions and the dog responded favorably to immunosuppressive doses of oral prednisolone, topical prednisolone acetate, and azathioprine. Canine dysautonomia is an idiopathic disease resulting from a generalized loss of autonomic function. Dogs affected are typically young adults of medium to large physical stature that typically live in rural areas. It is important to note, however, that animals ranging in age from 5 weeks to 15 years of age and of a variety of breeds can be affected. Canine dysautonomia has been reported in Europe and the United States. The disease is prevalent in dogs living in the midwestern United States, specifically Kansas and Missouri. Affected dogs present with an acute (days) or subacute (two to three weeks) history of clinical signs referable to loss of autonomic (sympathetic and parasympathetic) function. Common nonocular clinical signs include regurgitation, vomiting, diarrhea, anorexia, weight loss, dry mucous membranes, and purulent nasal discharge. Ocular signs include ocular discharge, protruding third eyelid, mydriasis, and a reduction in Schirmer tear test (STT) values. Ocular pharmacological testing with topical 0.05% pilocarpine in dogs with mydriatic pupils, and signalment, history, and clinical signs consistent with dysautonomia provides useful information supporting a diagnosis of dysautonomia. In affected dogs, instillation of 0.05% pilocarpine will cause rapid (<45 min) miosis compared to unaffected animals. Severe neuronal degeneration has been reported in a variety of autonomic ganglia, including the cranial cervical and ciliary ganglia. In addition, neuronal degeneration of various brainstem nuclei, including the facial, oculomotor, and motor nucleus of the trigeminal nerve, has also been reported. At least 85% of dogs affected with dysautonomia succumb to the disease and are euthanized. Granulomatous meningoencephalitis (GME) is an idiopathic nonsuppurative meningoencephalomyelitis seen in dogs. Histopathologically, GME is characterized by perivascular cuffing with mononuclear cells. One study has demonstrated that perivascular cuffs were composed of a heterogeneous population of major histocompatibility complex class II antigen‐positive macrophages and mainly CD3 antigen‐positive lymphocytes, supporting a hypothesis of T‐cell‐mediated, delayed‐type hypersensitivity of an organ‐specific autoimmune disease. Proposed pathogeneses for GME have included a primary immune‐mediated phenomenon, precancerous form of lymphoma, and various infectious etiologies. Studies have failed to identify an infectious etiology from the brains of dogs affected by GME. GME is typically seen in young small breeds, although any breed or age of dog may be affected. GME is characterized typically by neurological signs suggestive of multifocal CNS lesions that, at least temporarily, are responsive to systemic corticosteroids or other immunosuppressive therapies. GME is divided into three types, namely (i) disseminated, (ii) focal, or (iii) ocular. Any combination or permutation of these forms can occur. In the last form, GME may involve the optic nerves, thus producing a syndrome of acute blindness, papilledema, retinal and peripapillary hemorrhages, and, occasionally, extension into the globe, which in turn produces retinal detachments and retinal infiltrates. Confinement to the retrobulbar optic nerves may limit ocular lesions to blindness and dilated pupils. A definitive antemortem diagnosis is difficult to make, but multifocal CNS deficits, increased CSF protein levels, pleocytosis with mononuclear cells, and a response to corticosteroids are suggestive. Definitive antemortem diagnosis can be made based on the above in concert with brain. Treatment involves aggressive use of immunosuppressive corticosteroids with or without radiation therapy or immunosuppression using a combination of corticosteroids with one or more of cytosine arabinoside, azathioprine, leflunomide, or cyclosporine A. Prognosis for survival varies from weeks to years, but clinical signs progress and dogs will succumb to the disease. Sudden acquired retinal degeneration syndrome (SARDS) is an idiopathic blinding condition consisting of acute blindness in the absence of funduscopic disease (early in disease), and clinical signs suggestive of an underlying metabolic disease. The cause of SARDS is unknown, and epidemiological questionnaires have not been suggestive of any common thread for an environmental toxin. Preliminary investigations into excitotoxins (e.g., glutamate) have found increased levels in the vitreous of affected animals, but the significance of this is unknown. Recently, analysis of tissues from SARDS‐affected dogs revealed the presence of Ig‐producing plasma cells in affected retinas that may account for localized intraretinal production of autoantibodies and subsequent development of an antibody‐mediated retinopathy. Animals are characteristically presented with acute blindness and a normal to near‐normal ocular fundus. Because of the acute onset, most dogs are quite disoriented. In most patients, vision loss occurs over the course of one to two weeks, and nyctalopia may be observed. The mean age of affliction is 8.5–10 years. The syndrome occurs predominantly in neutered females, in both pure and mixed breeds, and with a predisposition for Dachshunds. A seasonal incidence has been reported as well, with 46% of cases occurring in December and January. Laboratory values are variable, but lymphopenia (30% of cases), lymphopenia with neutrophilia (21%), and abnormal biochemical profiles (68%) may be present. Elevated levels of alkaline phosphatase (30–40% of cases) and cholesterol (42%) are the most common biochemical changes. Overall, 12–17% of patients have adrenal profile changes compatible with those of Cushing’s disease, but these changes may be adaptations to other diseases as well. Most recently, serum cortisol and sex hormone concentrations were measured prior to and following adrenocorticotropic hormone (ACTH) stimulation in 13 dogs with SARDS. Serum cortisol was elevated in 9 of 13 dogs; elevations in one or more sex hormones were found in 11 of 13 patients with SARDS, while only 1 dog had normal ACTH stimulation results. On ophthalmic examination, dogs with SARDS appear blind and lack a menace response, while they tend to blink in response to bright light (positive dazzle reflex). The pupils are usually dilated at rest and demonstrate sluggish PLRs. In the early stages, all dogs with SARDS have a characteristic pale optic disc due to the presence of vascular attenuation of the optic nerve head. In patients with SARDS of typically greater than two months in duration, subtle tapetal hyperreflective spots may be observed with these hyperreflective spots having been detected in some affected dogs only seven days following the onset of acute blindness. After several weeks to months, more advanced retinal vascular attenuation and tapetal hyperreflectivity become apparent. The funduscopic appearance in chronic SARDS is similar to that of inherited retinal degeneration (progressive retinal atrophy). Electroretinography (ERG) is considered essential for establishing a diagnosis of SARDS. The ERG response is extinguished with SARDS. A recent study documented the spectral properties of the PLR in eyes of healthy dogs compared to eyes of SARDS‐affected dog. Dogs that have SARDS have complete pupillary constriction in response to blue light of a narrow wavelength (480 nm) and high light intensity (200 kcd/m2) most likely due to stimulation of a photosensitive pigment, melanopsin, located in a subpopulation of retinal ganglion cells that can drive PLRs in the absence of photoreceptor activity. When red light of a given wavelength (630 nm) and high light intensity (200 kcd/m2) was used to evaluate PLRs in SARDS‐affected patients, the pupils remained fixed and dilated as this wavelength of red light does not activate the melanopsin pathway but rather activates the photoreceptor‐mediated pathway that is absent in dogs with SARDS. A portable, diode‐based light source with narrow wavelengths for blue and red light that matches the spectral properties of canine visual pigments is available for colorimetric PLR testing (Melan‐100 unit; BioMed Vision Technologies, Inc., Ames, IA, USA). SARDS has long been considered an untreatable, irreversible blinding disease of dogs. Most dogs with SARDS still make acceptable house pets provided they adjust well to being blind. Immune‐mediated and allergic skin diseases often produce a facial dermatitis involving the eyelids and conjunctiva. Immune‐mediated skin diseases are divided into two main categories: primary autoimmune diseases, in which the disease results from an attack against self‐antigens, and secondary immune‐mediated disease, in which the disease results from exogenous material, inducing autoimmune disease. Such causes of secondary immune‐mediated diseases include bacteria, drugs, and viruses. The pemphigus complex consists of five autoimmune skin diseases: (i) pemphigus vulgaris, (ii) pemphigus vegetans, (iii) pemphigus foliaceus, (iv) pemphigus erythematosus, and (v) bullous pemphigoid. The pemphigus complex is characterized by autoantibodies directed against intercellular substances. In most cases, facial lesions involve the mucocutaneous regions and are characterized by pustules and vesicles that eventually rupture, thereby leaving erosions and ulcers, crusting, scaling, and hypopigmentation. Juvenile sterile granulomatous dermatitis (i.e., pyoderma/cellulitis) and lymphadenitis is a syndrome of dogs that usually manifests in animals less than eight months of age. Adult dogs, however, may become affected by this condition. Predisposed breeds include the Dachshund, Golden Retriever, Labrador Retriever, Gordon Setter, and Lhasa Apso. Acute pyoderma affecting mainly the head manifests as pustules that then fistulate and drain, thereby creating several moist, crusty lesions of the pinna, muzzle, and periocular skin (Figure 19.7). Though the lesions appear caused by bacteria, they are actually sterile and cannot be transmitted. Bacterial hypersensitivity has been postulated to explain the response to corticosteroids and the explosive course of the disease. Without systemic therapy, the lesions will progress to involve other typical areas. Immunosuppressive doses of systemic corticosteroids, tapered following three to four weeks after resolution of the clinical signs, and systemic broad‐spectrum antibiotics to treat the secondary bacterial pyoderma, are indicated. Dermatomyositis is an idiopathic, hereditary condition resulting from a suspected immune‐mediated inflammation involving skeletal muscle, skin, and vasculature. The disease is typically described in Collies and Shetland Sheepdogs. Other breeds affected include the American Cocker Spaniel, Jack Russell Terrier, Samoyed, and Welsh Corgi. The condition is thought to be inherited as an autosomal dominant condition with incomplete penetrance in the Collie. Dermatomyositis in the Shetland Sheepdog has been linked to a microsatellite marker, FH3570, on chromosome 35. Dermatological lesions are seen around the face (especially the periocular region), digits, footpads, and tail. Characteristic dermatological findings include alopecia, vesicles, ulceration, erythema, scaling, and crusting. Clinical signs of myositis occur after the development of the skin lesions and include dysphagia, megaesophagus, generalized weakness, stiff gait, and muscle atrophy. Figure 19.7 Juvenile pyoderma in a young Saint Bernard. Treatment of dermatomyositis includes the use of oral vitamin E or fatty acid supplements. Pentoxifylline is also recommended to help improve microvascular blood flow. Prognosis is variable depending on the severity of the disease. Masticatory myositis (masseter, temporalis, pterygoid muscles) and extraocular myositis are two forms of focal inflammatory myopathies. Masticatory myositis typically affects young to middle‐aged adult dogs and predominantly medium to large breeds. Signs include spasm of the masticatory muscles and difficulty in opening the mouth, pain on palpation of the muscles, muscle swelling, or muscle atrophy. Muscular atrophy is a more common clinical sign (72% of cases) than muscle swelling (14% of cases). Ocular signs occur in 45% of cases and are variable depending on the chronicity of the disease. Ocular manifestations of acute masticatory myositis include exophthalmos and prolapse of the third eyelid due to swelling of the pterygoid muscle, and possible optic nerve tension/compression causing blindness. In chronic masticatory myositis, enophthalmos includes bilateral clinical signs, ±peripheral eosinophilia, ±elevated levels of serum creatinine kinase, ±abnormal electromyograms, and ±presence of circulating antibodies for type 2 M fibers, and positive muscle immunohistochemistry for antibodies against type 2M fibers is used to provide a diagnosis of masticatory myositis (Table 19.3). Immunosuppressive doses of systemic corticosteroids (prednisone 1–2 mg/kg p.o. b.i.d.) for a minimum of one month before tapering are recommended at any stage of the disease. Prognosis is good for dogs treated appropriately with immunosuppressive dosages of corticosteroids, although some dogs may require lifelong therapy with these drugs. Table 19.3 Histopathological lesions in masticatory myositis. Extraocular myositis seems to be a different disease affecting the extraocular myositis and affects predominantly young large breed dogs (Figure 19.8). Bilateral exophthalmos is the predominant clinical sign in the acute form of the disease. Chronic extraocular myositis can result in restrictive strabismus and is due to chronic fibrosis of the extraocular muscles. As opposed to masticatory myositis, circulating antibodies to type 2M muscle fibers are not present. Inflammatory infiltrate of affected muscles includes lymphocytes and macrophages and fibrosis may be present depending on the chronicity of the disease. Immunosuppressive corticosteroid therapy is indicated in cases of extraocular myositis (as for masticatory myositis). Adjunctive corrective strabismus surgery may be useful in some cases of chronic extraocular myositis where the disease is in remission. Figure 19.8 Extraocular myositis. (a) Golden Retriever, 1‐year‐old male, with left ventral strabismus at initial presentation. (b) Close‐up of the left eye, only sclera visible due to severe globe deviation. Vogt–Koyanagi–Harada (VKH) syndrome is an idiopathic condition in humans characterized by uveitis, poliosis, vitiligo, ±changes in hearing ability, and meningitis. A similar syndrome is recognized in the dog, except that meningitis is rarely reported, hence the terms uveodermatologic or VKH‐like syndrome have been applied. A relatively recent study examining ocular and dermatological tissue from two dogs with VKH‐like syndrome has suggested that skin lesions are the result of a Th1‐mediated inflammatory response, while ocular lesions are the result of a Th2‐mediated inflammatory response. Further, the role of certain dog leukocyte antigen class II gene alleles may be important. Several other breeds, including the Australian Shepherd, Beagle, Brazilian Fila, Chow Chow, Dachshund, Golden Retriever, Irish Setter, Old English Sheepdog, Saint Bernard, Samoyed, Shetland Sheepdog, and Siberian Husky, are affected. Animals are typically affected in adulthood and ocular lesions usually precede the dermatological lesions. Patients are presented for a complaint of sudden blindness or gradual vision loss. Ocular lesions vary from bilateral anterior uveitis to severe panuveitis. Bullous retinal detachments may occur, and secondary cataracts and glaucoma are common. The iris and retinal pigment epithelium develop progressive depigmentation (Figure 19.9). As the depigmentation progresses, the tapetal fundus becomes hyperreflective, and retinal vascular attenuation as well as optic nerve atrophy may develop. Dermal and hair depigmentation (vitiligo and poliosis, respectively) develop either gradually or rapidly, and they may be ulcerative in nature. No specific diagnostic tests are available for the uveodermatologic syndrome. The diagnosis is made on the basis of clinical signs and histopathological examination of skin biopsies. Routine laboratory tests, including bloodwork, are typically unremarkable. Skin biopsy specimens have lichenoid dermatitis, histiocytes, and small mononuclear cell as well as giant cell infiltrations. The prognosis for dogs affected with uveodermatologic syndrome is guarded, and therapy should be considered to be lifelong. Relapses are frequent if therapy is stopped or tapered. Because of the immunosuppressive therapy, periodic rechecks as well as blood and liver evaluations are necessary. Initial therapy involves immunosuppressive doses of oral prednisone ± azathioprine or cyclophosphamide. Maintenance therapy may require one or both drugs at a markedly reduced dose. Topical corticosteroids may be used for anterior segment lesions. Figure 19.9 Multifocal, depigmented lesions in the nontapetal fundus of a dog with VKH syndrome. Protothecosis is a rare disease in humans and a variety of animals caused by a colorless, ubiquitous, saprophytic alga of the genus Prototheca. Prototheca spp. have a wide geographic distribution and are found in soil, water, sewage, and some vegetable matter. Prototheca spp. are thought to be achlorophyllous mutants of green algae. Three species have been recognized, but only Prototheca wickerhamii and Prototheca zopfii are known to be pathogens. Prototheca zopfii is usually isolated from disseminated cases, whereas P. wickerhamii produces a cutaneous syndrome. Prototheca spp. appear in tissue as thick‐walled, nonbudding, round to ovoid, yeast‐like cells. The disease is not considered to be transmissible and the large breeds of dogs are overrepresented, and ≥50% of animals with protothecosis may have ocular involvement. Tissues most commonly affected include the eyes, digestive tract, kidney, heart, bone, and brain. Ocular lesions include a granulomatous, posterior uveitis or panuveitis that is often bilateral and blinding (Figure 19.10). Exudative retinal detachments are the usual cause for blindness. Chorioretinal lesions may be either diffuse or focal, and they will need to be differentiated from the more common causes of granulomatous uveitis. A definitive diagnosis is usually made on the basis of finding the organism in ocular aspirates, tissue exudates, excretions (i.e., urine sediment), or biopsy specimens. Figure 19.10 Gross image of a sectioned globe infected with Prototheca. There is diffuse retinal detachment with associated retinal exudate and hyphema. The most commonly attempted therapy has been amphotericin B, an imidazole antifungal drug, or both. A recent review of systemic protothecosis in 17 Australian dogs revealed that combination therapy with amphotericin B and itraconazole was effective in only two cases, although one of these dogs should have had treatment for longer duration. Prognosis for dogs with protothecosis is grave. Any sporadic bacteremia may result in seeding of the uveal tract and create various degrees of inflammation, but only a few bacterial syndromes are relatively consistent regarding involvement of the eye (Table 19.4). Table 19.4 Canine infectious diseases with ophthalmic signs. Canine bartonellosis results from infection with the Gram‐negative, intracellular bacilli or coccobacilli bacterium, Bartonella spp. There are numerous species of Bartonella. Bartonella henselae (causative agent of cat scratch disease [CSD]), Bartonella vinsonii (berkhoffii), Bartonella clarridgeiae, and Bartonella elizabethae are known or likely to cause naturally occurring disease in dogs and B. vinsonii (berkhoffii) appears to be an important species to cause clinical disease in dogs. Canine bartonellosis has been associated with numerous pathological conditions, including anterior uveitis, hyphema, retinal detachment due to systemic hypertension, and choroiditis (Figure 19.11), endocarditis, cutaneous vasculitis, granulomatous lymphadenitis, myocarditis, and polyarthritis. Treatment of canine bartonellosis consists of systemic antimicrobial therapy. That include macrolides (e.g., azithromycin), fluoroquinolones (e.g., enrofloxacin), and doxycycline (recommended to be used at high dosages 10 mg/kg q 12 h for four to six weeks). Lyme disease, or borreliosis, is a tick‐borne spirochetosis produced by Borrelia burgdorferi, which comprises several species that affect humans and dogs worldwide. Borrelia organisms, like most spirochetes, are small, 25 μm long and 0.2 μm in diameter, corkscrew‐shaped, motile microaerophilic bacteria of the order Spirochaetales. Successful transmission of the agent relates directly to contact time of the tick on the host, requiring 48–72 h for a 38–92% transmission rate. In the dog, the horse, and humans, B. burgdorferi can produce ocular lesions. Documented ocular lesions included conjunctivitis, corneal edema, anterior uveitis, retinal petechia, chorioretinitis, retinal detachment, and sometimes orbital disease. Figure 19.11 Bartonellosis in a dog. Fundus photograph demonstrating multifocal, gray, hyporeflective areas in the tapetal fundus. Because of the limitations of current tests that measure antibody response, other confirmatory tests must be performed including the Western blot assay and the C6 ELISA. A presumptive diagnosis of borreliosis can be made on the basis of compatible signs (usually lameness, joint pain, pyrexia, and lymphadenopathy of lymph nodes of the limbs), ruling out other causes of systemic disease in endemic areas, and on the basis of response to antibiotic therapy. Vaccination and tick control, both in the environment and on the animal, are important for preventing infection. Various antimicrobials including tetracyclines, some cephalosporins (e.g., ceftriaxone), and macrolides are useful for treating borreliosis. Doxycycline is one of the first‐line antimicrobials of choice. Canine brucellosis is caused by Brucella canis. Brucella canis is a zoonotic aerobic, Gram‐negative coccobacillus. Brucella canis naturally infects dogs by penetrating mucous membranes such as occurs via coitus. Aside from venereal transmission, Brucella spp. can be transmitted via fomites such as cages or equipment, and can persist for extended periods in mononuclear phagocytes and produce a prolonged bacteremia. Brucella canis has been isolated from the eye and is recognized as a cause of uveitis or endophthalmitis in both experimental and naturally occurring brucellosis (Figures 19.12 and 19.13). Infected dogs are often times not systemically ill. Because of the insidious nature of the systemic disease, infected dogs are often presented for ocular disease rather than for systemic signs. Before treatment is recommended, the zoonotic potential and difficulty in clearing the organism from the animal should be carefully explained to the owner. Because brucella can be harbored in reproductive organs, neutering of intact affected animals should be encouraged to decrease any risk of transmission to humans. Currently, there is no effective vaccine against brucellosis. Figure 19.12 Photograph of the left eye (OS) of a dog with Brucella canis endophthalmitis. Numerous punctate, yellow and white opacities are suspended in the peripheral anterior vitreous. Generalized vitreal haze is present. Figure 19.13 Fundus photograph of the OS of a dog with Brucella canis endophthalmitis. Irregular zones of hyporeflectivity with indistinct margins are visible in the peripheral tapetal fundus and adjacent to the optic disc endophthalmitis. Irregular zones of hyporeflectivity with indistinct margins are visible in the peripheral tapetal fundus and adjacent to the optic disk. Canine leptospirosis is caused by Leptospira interrogans sensu lato. It appears, however, that the disease causing serovars, namely grippotyphosa, pomona, and bratislava, are becoming more prevalent. The bacterium is maintained in host‐adapted species that act as reservoir hosts and is shed in the urine. Direct transmission can occur through contact with infected urine, bites, ingestion of infected material, and contact with contaminated water. Leptospirosis is a significant zoonotic disease with worldwide distribution that causes human disease and death, mostly in regions of Asia and South America. In the acute phase of infection, conjunctivitis, scleritis, and anterior uveitis may be present in concert with other systemic signs. Diagnosis of leptospirosis is dependent on consistent clinical signs and detection of antibodies using the microscopic agglutination test or ELISA and/or evidence of the presence of the organism in urine using dark‐field microscopy, or by visualizing the organism in histological preparations. Treatment of leptospirosis is directed at (i) eliminating the bacteremia by initially using penicillins, specifically ampicillin and amoxicillin, and (ii) eliminating the carrier state by administering tetracyclines. Tetanus is caused by the neurotoxin produced by the bacterium Clostridium tetani. Clostridium tetani is a motile, Gram‐positive, nonencapsulated, anaerobic, rod‐shaped, spore‐forming bacterium. Dogs and cats are naturally resistant when compared to other species such as humans and horses. Clinical signs of tetanus develop when spores of C. tetani enter the body through skin wounds or during surgical procedures. Clinical signs may be localized or generalized. In the localized form, increases in stiffness of specific muscle groups or a given limb may be noted. In the generalized form, affected dogs will initially have a characteristic smiling/sneering appearance (risus sardonicus) and a stiff gait that may progress to megaesophagus ± hiatal hernia, and complete rigid paralysis with the appearance of periodic generalized convulsive‐type behavior. Ocular signs seen in a tetanic animal include protrusion of the third eyelid and enophthalmos resulting from globe retraction due to the hypertonicity of the extraocular muscles. Acremoniosis is a systemic mycotic infection caused by Acremonium spp. Systemic signs in this dog were similar to those seen in cases of disseminated aspergillosis. Clinical signs include various general malaise, weight loss and anorexia, lymphomegaly, neurological signs (depending on the neuroanatomic focus of the principle pathological process), and various ocular signs. Ophthalmological signs include chemosis, corneal edema, anterior uveitis, focal chorioretinitis, and bullous retinal detachments. Diagnosis is made based on detection of the organism on histopathological examination of tissues and by culturing the organism from tissues and urine. Aspergillosis is caused by the filamentous fungus Aspergillus spp. Aspergillus spp. are considered ubiquitous in the environment, and animals are infected opportunistically after inhaling Aspergillus spores. Localized aspergillosis involves colonization of the respiratory sinuses and nasal mucosa. Secondary CNS involvement may result from erosion of the cribriform plate. Disseminated infection occurs typically in the immunocompromised patient and involves a whole host of organ systems. Disseminated aspergillosis occurs frequently in German Shepherd dogs. In general, the most common clinical signs relate to multiple organ system involvement, and include general malaise, pyrexia, anorexia and weight loss, and bone pain. Disseminated aspergillosis has been reported to cause panuveitis, chorioretinitis, exudative retinal detachments, and endophthalmitis. Diagnosis is made based on identification and culture of urine sediment, serum, synovial fluid, vitreous, lymph node, or intervertebral disc centesis specimens. Treatment is directed at eliminating the organism by administering amphotericin B, itraconazole, or fluconazole intravenously. Regardless, the prognosis for recovery from disseminated aspergillosis is poor. Blastomycosis is a systemic mycotic infection caused by the dimorphic fungus, Blastomyces dermatitidis. Blastomyces dermatitidis is a thick‐walled yeast that reproduces by budding in infected tissues (i.e., yeast phase), and in nature, it is most likely a soil saprophyte that produces infective spores called conidia (i.e., mycelial phase). The tissue budding yeast form is 5–20 μm in size, with a thick, double‐contoured wall. Young, large breed sporting dogs and hounds living near water are at increased risk of blastomycosis, presumably because of outdoor exposure. Blastomycosis is not a contagious or zoonotic disease but has been transmitted to a person through an accidental needlestick with a syringe and needle. Clinical signs in dogs with blastomycosis vary significantly due to the multisystemic nature of the disease. Pulmonary signs are seen in 43–88% of dogs affected with blastomycosis, ranging from mild respiratory distress during physical exertion to severe dyspnea at rest. Nearly 60% of dogs with blastomycosis develop lymphadenopathy, while cutaneous lesions are reported in approximately 30% of affected dogs. Ocular involvement has been reported in as many as 48% of dogs with blastomycosis. Ocular signs have been reported as the sole indicator of B. dermatitidis infection in up to 3.0% of diagnosed cases. Approximately 50% of the ocular lesions caused by B. dermatitidis are bilateral. For prognostic purposes, the ocular lesions have been divided into anterior segment only (5–30%), anterior and posterior segment lesions (endophthalmitis, 26–72%), and posterior segment (22–43%). Though anterior segment inflammation may be severe, B. dermatitidis is infrequently found in the anterior uvea, and this anterior uveal inflammation has been attributed to a diffusible substance from the posterior segment. Additional ocular lesions of canine blastomycosis are optic neuritis, retinal and vitreal hemorrhages, and orbital cellulitis. Therapy for systemic mycoses, no matter what etiology, is a financial dilemma. Therapy becomes prohibitively expensive for many owners because most of the affected dogs are large breeds, therapy may be very protracted, and imidazole medications are very costly. Currently, itraconazole is considered the drug of choice for the treatment of blastomycosis. Coccidioidomycosis is caused by the dimorphic fungus Coccidioides immitis. The organism is found in sandy, alkaline soils of the dry regions of the southwestern United States, western Mexico, and Central and South America. Coccidioides spp. produce mycelia during seasonal rainfall. The major route of Coccidioides spp. infection is via inhalation. Cutaneous entry of the organism through a penetrating skin wound is possible but occurs rarely. Coccidioidomycosis may produce a wide variety of clinical diseases, depending on the immunocompetence of the host, ranging from a mild, subclinical respiratory disease to a severe multisystemic disseminated disease. Clinical signs are variable and include pyrexia, lymphadenomegaly, coughing, neck pain, chronic lameness, swollen joints, back pain, muscle wasting, and signs of uveitis. In one study, 42% of patients with ocular lesions had no systemic clinical signs, and 80% of the ocular lesions were unilateral. Clinical ocular manifestations were most frequent in the anterior segment, but they were also difficult to classify because of use of the redundant terms of iritis, uveitis, and chorioretinitis. Ocular signs included keratitis in 49%, anterior uveitis in 43%, and glaucoma in 31% of cases. The typical histopathological change in ocular coccidioidomycosis is granulomatous inflammation in the filtration angle, ciliary body, choroid, and retina. Diagnosis of coccidioidomycosis requires the visualization of the organism, or determining the presence of antibodies specific for the organism in light of consistent travel. Treatment of coccidioidomycosis is similar to that for other systemic mycoses (i.e., extended azole therapy or amphotericin B, or these drugs used in combination or in succession). Response to treatment may also be monitored by evaluating radiographs of the lesions in the thorax and bone (if involved). Relapses are common. Cryptococcosis is caused by Cryptococcus neoformans or Cryptococcus gattii (previously C. neoformans var. gattii). Cryptococcus neoformans is associated with high nitrogen‐containing environments such as avian feces or soil enriched with avian feces. Cryptococcus neoformans is a variably sized yeast‐like organism (3.5–7 μm) that typically contains a thick capsule. Cryptococcosis has been described in a variety of mammals as well as in humans. Importantly, cryptococcosis is not contagious. Rather, inhalation of the yeast‐like organism is the likely mode of infection. Canine cryptococcosis is uncommonly reported in comparison to other systemic mycotic infections such as blastomycosis and in comparison to feline cryptococcosis. Clinical manifestations of canine cryptococcosis pertain mainly to CNS involvement, and ocular, upper respiratory, or cutaneous lesions. Common, nonspecific clinical signs of canine cryptococcosis include anorexia, lethargy, and depression. Fever is not a common clinical finding in dogs with C. neoformans infection. Twenty to forty percent of dogs with cryptococcosis have ocular and/or periorbital involvement, including granulomatous to pyogranulomatous chorioretinitis with or without exudative retinal detachment (Figure 19.14). Although less common than posterior segment disease, mild to moderate anterior uveitis may occur as well. Identification of the causative agent permits confirmation of the diagnosis of cryptococcosis. The thin wall and large capsule of Cryptococcus allow ready differentiation from Blastomyces. Cryptococcal organisms can also be readily cultured on Sabouraud’s agar from infected tissue, CSF, exudate, blood, urine, and joint fluid. Treatment of cryptococcosis involves subcutaneous, diluted amphotericin B in combination with oral flucytosine (especially helpful for treating CNS‐infected cases) or azole therapy. Fluconazole is recommended for cases of ocular or CNS cryptococcosis. Figure 19.14 Labrador Retriever with tetraparesis and Cryptococcus in the CSF. Optic neuritis and multiple retinal hemorrhages are present, and a granuloma adjacent to the disc is obscured by a hemorrhage. Vasculitis is evident, with multiple hemorrhages, perivascular infiltrate around smaller vessels, and marked hyperemia. Ophthalmomyiasis interna has been observed in the dog and the cat, and refers to either the intraocular (ophthalmomyiasis interna) or external (ophthalmomyiasis externa) migration of fly (Diptera) larvae. The three forms are named according to location of the larvae and include (i) ophthalmomyiasis externa, where the larvae are found in the orbital and extraocular tissues; (ii) ophthalmomyiasis interna anterior, where the larvae are found in the anterior chamber of the eye; and (iii) ophthalmomyiasis interna posterior, where larvae are found in the posterior segment of the eye. The point of entry of the fly larvae is unknown, but it is postulated that fly larvae cross the conjunctival surfaces. The characteristic ophthalmoscopic lesions are wandering, curvilinear tracts that frequently intersect and are associated with retinal and preretinal hemorrhages in the acute stage. If the larva is observed, it is typically photosensitive, moving away from a strong light. Manual removal of externally located organisms with appropriate anti‐inflammatory and antimicrobial therapy, along with correcting any extraocular conformational defects, has shown positive outcomes. Angiostrongylosis is caused by the nematode, Angiostrongylus vasorum. Angiostrongylus vasorum inhabits the pulmonary arteries and right heart of dogs and wild carnivores in parts of Europe, Africa, and Asia. A case of A. vasorum infection in a dog from northeastern Canada has been described. Dogs are infected by eating intermediate hosts such as snails and slugs. Migrating larvae may become aberrant and may be found in the eye. Severe granulomatous uveitis and secondary glaucoma have been observed with chronic involvement. Dirofilariasis, canine heartworm infection, caused by Dirofilaria immitis, is the most commonly reported intraocular nematode among dogs in North America. Heartworm disease is widely distributed. Dirofilariasis is recognized in dogs worldwide. Approximately 240 000 cases of heartworm disease were diagnosed in 2001 in the United States. In Canada, dirofilariasis is relatively infrequent and limited to the southern‐most portions of the country. Transmission of D. immitis is by mosquitoes. The life cycle of D. immitis is complex; thus, readers are referred to current internal medicine or infectious disease textbooks for further details. Adult heartworms are known to live up to five years, while microfilaria live up to 30 months in dogs. Ocular involvement with D. immitis is postulated to arise as a result of aberrant migration of fourth‐stage larvae from the subconjunctival space into the eye, with subsequent development to immature adults or fifth‐stage larvae. The worm is usually in the anterior chamber, but it may also be found in the vitreous. Anterior uveitis was a consistent ocular manifestation, and ocular discomfort was exacerbated by examination of the affected eye with a light, which stimulated parasitic movement. The diagnosis of intraocular dirofilariasis is established by finding the worm, usually present in the anterior chamber of dogs in areas endemic for heartworm. Severe corneal edema, however, may preclude visualization of the parasite. Therapy has involved removal of the D. immitis worm through a limbal incision, and has been successful in 90% of patients so treated. Ocular onchocerciasis is caused by the nematode, Onchocerca spp. The exact species of Onchocerca causing canine ocular onchocerciasis is still speculative, and consensus has yet to be reached. The life cycle of Onchocerca lupi is not completely understood, but is likely similar to that of other Onchocerca spp. To date, canine ocular onchocerciasis has only been reported in dogs from Germany, Greece, Hungary, Portugal, and the western United States. Clinically, there are two forms of ocular onchocerciasis, namely acute and chronic ocular onchocerciasis. In acute cases, ocular onchocerciasis is characterized by conjunctivitis, chemosis, and periorbital swelling. In some cases, parts of the parasite are observed on the conjunctival surface or other periocular tissues. In chronic cases, parasite‐containing granulomatous nodules are found in various parts of the eye and periocular tissues. Diagnosis is made based on consistent clinical examination findings and, in acute cases, by identifying the presence of worm fragments on the conjunctiva or in periocular tissues. In chronic cases, diagnosis is made by grossly and/or histopathologically identifying Onchocerca spp. within the granulomatous nodules or within the periocular tissues. Therapy for ocular onchocerciasis involves, in part, surgical removal of the granulomatous nodules and other tissues containing the worm. Administration of antimicrobials effective against the endosymbiont (tetracyclines) may be useful at eliminating the parasite. Antiparasitic agents such as ivermectin and diethylcarbamazine are not effective against adult worms but are effective against dirofilaria. Strongyloidiasis is caused by the aberrant migration of strongyles (order Strongylida). The most common routes of infection of a common strongyle of dogs, Ancylostoma sp., is through ingestion of larvae or direct penetration of larvae through intact skin. Toxocariasis is caused by the nematode Toxocara canis. Toxocara canis is an extremely common roundworm or ascarid of the dog, and is thought to be responsible for migrating larvae that may, occasionally, aberrantly migrate to the eye of humans and dogs. Both visceral and ocular larval migrans as a result of T. canis pose a public health problem. Ocular larval migrans is migration of nematode larvae through the eye. Aberrant migration of T. canis to the canine eye has been described as an incidental finding manifesting as small (one‐fourth to one‐sixth disc diameter), solitary focal granulomas in the posterior segment in four dogs. Canine demodicosis is caused by the parasitic mite Demodex canis. Demodex spp. live as commensals in the skin of most mammals, including dogs. Predisposing factors contributing to overgrowth of Demodex include poor nutrition, concurrent parasites/infectious disease, short hair coat, nonenrolment into preventive wellness plan, stress, and immunosuppressive drug therapy. Localized demodicosis typically develops in young dogs (three to six months of age), starting preferentially around the eyes, lips, and forelegs. Skin scrapings are the main method of establishing a diagnosis, and the mites are typically easy to find. All forms of blepharitis should indicate the need for skin scrapings, and demodicosis should be an important differential diagnosis in young dogs with blepharitis. Treatment of canine demodicosis involves the use of amitraz dips and/or oral ivermectin or milbemycin administration. Use of avermectin drugs should be limited to animals lacking mutation for the P‐glycoprotein gene (MDR1). Sarcoptic mange is caused by the mite Sarcoptes scabiei var. canis. Although sarcoptic mites have host species preference, they are able to cause disease in nonpreferred hosts. Consequently, sarcoptes can be transmitted from dogs to people, and vice versa. Clinical signs of sarcoptic mange include intense pruritis, alopecia, and reddish papulocrustus eruptions of infected areas. Commonly affected sites include the ventral ears, abdomen, chest, and legs, and in severe cases the entire body, including periocular regions. Diagnosis of sarcoptic mange is dependent upon visualizing the mite, eggs, or mite feces via microscopic examination of skin scrapings. It should be noted, however, that skin scrapings are oftentimes negative in affected animals. Treatment of sarcoptic mange involves the use of amitraz (monoamine oxidase inhibitor), fipronil (GABA receptor inhibitor), or avermectin drugs (i.e., ivermectin, milbemycin oxime, moxidectin, and selamectin). Leishmania spp. are diphasic protozoal parasites that infect a wide range of vertebrates, including dogs and humans. Dogs and other are primary reservoirs of Leishmania spp., and sandflies (Phlebotomus spp. or Lutzomyia spp.) are the vectors. Leishmania infantum is the species responsible for endemic leishmaniasis in dogs from Greece, Spain, Portugal, Turkey, parts of Africa, Central and South America, and India. Alterations in socioeconomic and possible climate factors have resulted in changes in the distribution in L. infantum in Europe. Leishmania spp. cause cutaneous, mucocutaneous, and visceral diseases. Dogs will typically develop a combination of these forms of leishmaniasis. The disseminated disease produces emaciation with muscular weakness, chronic renal failure, and chronic, nonpruritic skin lesions. The cutaneous lesions begin on the head, thereby producing a blepharitis characterized by scaliness and loss of hair that begin at the medial canthus. Focal granulomatous blepharitis is also a typical eyelid reaction. Ocular manifestations of leishmaniasis occur in up to 81% of dogs with the disease (Figure 19.15). Ocular manifestations of leishmaniasis consist of blepharitis, simple or granulomatous conjunctivitis, scleritis, superficial or deep keratitis, anterior uveitis, keratoconjunctivitis sicca (KCS), and secondary glaucoma; signs are typically bilateral. The anterior vitreous may have an inflammatory reaction, but the posterior choroid and retina are usually spared. The inflammation is mononuclear, and the organism can be found in histiocytes. Leishmania spp. and associated granulomatous inflammatory infiltrates have been recently described in intraocular, extraocular, and adnexal smooth and striated muscles in affected dogs.
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Ocular Manifestations of Systemic Disease
Introduction
Section I: Dogs
Congenital
Coat Color‐Related Diseases/Conditions in Dogs
Dwarfism (Skeletal Dysplasia–Osteochondrodysplasia)
Hydrocephalus in Dogs
Myasthenia Gravis
Quadriplegia and Amblyopia
Developmental
Inborn Errors of Intermediary Metabolism
Acquired
Cardiovascular Diseases
Hematological Diseases
Idiopathic Systemic Diseases
Canine Idiopathic Granulomatous Disease
Dysautonomia
Granulomatous Meningoencephalitis
Sudden Acquired Retinal Degeneration Syndrome
Immune‐Mediated Diseases
Dermatological Diseases
Juvenile Pyoderma/Cellulitis (Puppy Strangles)
Myositides
Dermatomyositis
Masticatory Myositis and Extraocular Myositis
Masticatory myositis:
Uveodermatologic Syndrome (Vogt–Koyanagi–Harada‐Like Syndrome)
Infectious Diseases
Algal Diseases
Protothecosis
Bacterial
Algal diseases:
Protothecosis
Bacterial:
Bartonellosis
Borreliosis (Lyme disease)
Brucellosis
Leptospirosis
Tetanus
Mycotic:
Aspergillosis
Blastomycosis
Coccidioidomycosis (valley fever; San Joaquin Valley fever)
Cryptococcosis
Virus:
Canine distemper virus
Herpesviruses
Canine herpesvirus
Infectious canine hepatitis (CAV‐1)
Papillomavirus
Tick‐borne encephalitis virus
Bartonellosis
Borreliosis (Lyme Disease)
Brucellosis
Leptospirosis
Tetanus
Mycotic
Acremoniosis
Aspergillosis
Blastomycosis
Coccidioidomycosis (Valley Fever; San Joaquin Valley Fever)
Cryptococcosis
Parasitic – Dipteric Larvae
Ophthalmomyiasis
Parasitic – Nematodes
Angiostrongylosis (Heartworm of France; French Heartworm)
Dirofilariasis (Canine Heartworm Disease)
Onchocerciasis (Onchocercosis)
Strongyloidiasis (Hookworms)
Toxocariasis (Roundworm Ascarids)
Parasitic – Mites
Demodicosis
Sarcoptic Acariasis (Sarcoptic Mange, Canine Scabies)
Leishmaniasis
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