CANINE DISTEMPER.

Distemper is a disease of wo rldwide prevalence afflicting many canids, including the dog. It is caused by a paramyxovirus (Morbillivirus) designated canine distemper virus (CDV) that is spread by aerosol and droplet exposure.

Table 18-1 Systemic Causes of Eyelid Disorders in the Dog and Cat

* The signs of blepharitis are generalized (i.e., not cause-specific); they include dermatitis, alopecia, scales, crusts, ulcers of the skin, and conjunctivitis, chemosis, and congestion of the palpebral conjunctiva.

Table 18-2 Systemic Causes of Conjunctivitis^* in the Dog and Cat

* Associated ocular signs include ocular discharge/secretion, chemosis, congestion, and follicular hyperplasia.

Table 18-3 Systemic Causes of Miscellaneous Conjunctival Disorders in the Dog

Table 18-4 Systemic Causes of Corneal Diseases in the Dog and Cat

* Associated ocular signs include epiphora and discharge, blepharospasm, conjunctival congestion, corneal edema, vascularization, infiltration, ulceration, and pigmentation.

† Associated signs include corneal opacity, bullous keratopathy, keratoconus, and impairment of vision.

Table 18-5 Systemic Causes of Scleral and Episcleral Diseases in the Dog and Cat

Table 18-6 Systemic Causes of Uveitis in the Dog and Cat^*

* Associated ocular signs include corneal edema, flare, keratic precipitates, hypopyon and/or hyphema, hypotony, miosis, ciliary injection, blepharospasm, iris congestion, and photophobia. Secondary glaucoma and lens luxation are possible sequelae.

† Has been reported to cause secondary glaucoma.

Table 18-7 Systemic Causes of Cataract in the Dog and Cat

Table 18-8 Systemic Diseases Causing Posterior Uveitis^* in the Dog and Cat

* Includes chorioretinitis and choroiditis. Associated signs include diffuse or multifocal retinal edema and hemorrhage, subretinal effusion and hemorrhage, vascular cuffing, and loss of vision. Retinal detachment and retinal atrophy are possible sequelae. Retinochoroiditis, which has a similar clinical presentation, is caused by canine distemper virus.

Table 18-9 Systemic Noninfectious Causes of Retinal/Chorioretinal Scarring and Atrophy in the Dog and Cat^*

* Associated signs include multifocal scarring, pigment clumping, depigmentation, tapetal hyperreflectivity, and attenuation of retinal blood vessels.

† May be caused by any systemic disease causing posterior uveitis.

Table 18-10 Systemic Causes of Lipemia Retinalis in the Dog and Cat

Table 18-11 Systemic Causes of Retinal Hemorrhage in the Dog and Cat

* Has also been associated with increased tortuosity and/or dilatation of retinal blood vessels.

Table 18-12 Systemic Causes of Retinal Detachment in the Dog and Cat^*

* Associated signs include anterior displacement of the retina and its vessels, loss of vision and pupillary light reaction, and focal/multifocal/diffuse retinal folds. Retinal detachment may also be caused by any disease causing retinal hemorrhage, as listed in Table 18-11.

Table 18-13 Systemic Causes of Optic Neuritis in the Dog and Cat^*

* Associated signs include papillary edema, optic nerve head congestion, hemorrhage of optic nerve vessels, and loss of vision and pupillary light reaction.

Table 18-14 Systemic Causes of Disorders of the Globe in the Dog and Cat

Table 18-15 Systemic Causes of Endophthalmitis/Panuveitis in the Dog and Cat

Table 18-16 Systemic Disorders Causing Blindness in the Dog and Cat

The systemic and ocular clinical signs vary with the stages of the disease and depend on the immune status of the dog (i.e., age, vaccination status, individual variation), the virulence of the virus, and environmental conditions. Most (50% to 70%) of the infections are subclinical.

The ocular signs are the earliest manifestations of the systemic disease; they include acute, mild to severe, bilateral, serous to mucopurulent conjunctivitis, mostly with involvement of the palpebral conjunctiva. With the progression of disease, respiratory and/or gastrointestinal signs appear. CDV may also cause lacrimal gland adenitis with decreased tear production leading to blepharospasm, keratoconjunctivitis sicca (KCS), and possible corneal ulceration. Corneal ulceration may be severe and may not respond well to routine therapy. KCS may resolve after recovery from the systemic disease.

Anterior and posterior uveitis often accompany distemper encephalomyelitis and may be observed even if the dog is clinically asymptomatic for the latter. A high incidence (41%) of multifocal, nongranulomatous chorioretinitis has been found in the neurologic forms of canine distemper. Choroidal exudation may induce retinal detachment. Retinal atrophy and scarring are the chronic sequelae of chorioretinitis. In the tapetal fundus they are characteristically observed as circumscribed, hyperreflective areas with clumps of pigment in the center, whereas the nontapetal lesions are characterized by depigmentation (see Chapter 15, Figure 15-34).

CDV has a predilection for the central nervous system (CNS), including the central visual pathways. It may cause inflammation or demyelinization of the optic nerve and tract, lateral geniculate nucleus, optic radiations, and visual cortex. Patients may present with actue, bilateral blindness and fixed, dilated pupils due to severe optic neuritis (Figure 18-1). The inflammation may be isolated, prodromal, or concurrent with other neurologic signs of canine distemper.

Figure 18-1 Optic neuritis in a dog. Note the blurry disc margins, hemorrhages, and loss of detail on the disc surface caused by edema of the nerve head.

(Courtesy University of California, Davis, Veterinary Ophthalmology Service Collection.)

The diagnosis of canine distemper is complicated because many dogs are infected but not clinically ill. Cytoplasmic inclusion bodies may be present in conjunctival epithelial cells 5 to 21 days after exposure and may be demonstrated in cytologic smears. Immunofluorescence (IF) techniques for the detection of these inclusion bodies may be used on different cytologic smears, including conjunctival epithelial smears. Recently, CDV amplicons were detected by reverse transcriptase– polymerase chain reaction (RT-PCR) of conjunctival swabs of all dogs experimentally with CDV, from day 3 to 14 after infection. The detection rate of these amplicons in conjunctival swabs was significantly higher during most of the experimental period compared to other tissue samples. Ocular treatment, which is essentially symptomatic, consists of topical ophthalmic antibacterial preparations for conjunctivitis and corneal ulcers. Cases of KCS may be treated with artificial tears, topical antibiotics, and lacromimetics. Treatment of severe corneal ulceration may require surgical intervention. Systemic and topical steroids as well as topical atropine are indicated in cases of uveitis. However, atropine should be used with extreme caution if the animal is also suffering from KCS, and steroids may not be used if the cornea is ulcerated. Systemic administration of antiinflammatory dosages of glucocorticosteroids is indicated in an animal with acute optic neuritis following confirming diagnosis of distemper, even if there is no other sign of clinical disease.

INFECTIOUS CANINE HEPATITIS.

Caused by canine adenovirus 1 (CAV-1), infectious canine hepatitis affects dogs and foxes. The virus is shed in the feces and urine of infected animals, and dogs are exposed through the oronasal route. After an incubation period of 4 to 7 days, seronegative animals infected by CAV-1 exhibit systemic clinical signs that range from those of a mild upper respiratory disease to those of a severe systemic disease, including hepatomegaly, icterus, and bleeding that may progress to disseminated intravascular coagulation. The prevalence of the disease has been dramatically reduced with the introduction of vaccination. Immunization with attenuated CAV-1 and, to a lesser extent, CAV-2 strains led to ocular signs of anterior uveitis and corneal edema in some animals. Dogs are currently vaccinated mostly with attenuated strains of CAV-2.

Ocular signs of infectious canine hepatitis are seen within 7 to 21 days of infection or vaccination. The signs are due to the presence of immune complexes in the eye and occur during convalescence. The initial signs include blepharospasm, miosis, hypotonicity, and anterior chamber flare (Figure 18-2) due to anterior uveitis. Corneal edema (“blue eye”) may develop within 1 to 2 days, although it is bilateral in only 12% to 28% of cases. The edema may be severe and lead to formation of keratoconus. Such cases may progress and cause corneal scarring and pigmentation. Persistent or long-lasting corneal edema may also occur, and the Afghan hound has been described as predisposed to chronic edema and glaucoma. However, in most cases the edema is transient, and animals recover spontaneously within a few days to 2 to 3 weeks.

Figure 18-2 Slit-lamp photography is used to illustrate aqueous flare characteristic of uveitis. A, Two beams of light, on the corneal and anterior lens surfaces, are visible. B, The aqueous humor between these two beams is translucent owing to the presence of inflammatory material. This results in light scattering similar to that observed while driving on a foggy night.

(Courtesy Paul E. Miller.)

The diagnosis of the ocular disease is based on the signalment, history, and clinical signs. Treatment is symptomatic, including topical glucocorticoids or nonsteroidal antiinflammatory drugs (NSAIDs) and atropine. Hypertonic solutions and ointments may be used to resolve severe corneal edema.

FELINE HERPESVIRUS INFECTION.

Feline herpesvirus 1 (FHV-1) infection, also called feline rhinotracheitis (FRV), is caused by a member of the Alphaherpesvirinae subfamily that affects all members of the Felidae, and all isolates belong to the same serotype. The virus is widespread in the domestic cat population, especially in colonies and catteries. Cats are infected after direct and indirect contact with sick and carrier animals; the infection occurs through the oronasal and conjunctival routes. Cats that recover from the disease probably remain persistent carriers, a state characterized by latent infection and intermittent periods of virus shedding.

Secondary bacterial infections are common complications, especially with Chlamydophila felis. Unilateral or bilateral conjunctivitis with hyperemia, ocular discharge, chemosis, and blepharospasm are the most common lesions in adult cats with no respiratory disease. Other ocular signs are dendritic (Figure 18-3) or geographic corneal ulcers, KCS, and stromal keratitis. Symblepharon is a common sequel of infection (Figure 18-4), and FHV-1 may also play a role in the pathogenesis of corneal sequestration and eosinophilic keratitis. Vascularization of the cornea and pain may be severe or absent.

Figure 18-3 Rose bengal staining used to demonstrate dendritic corneal ulceration, typical of feline herpesvirus 1 infection.

(Courtesy Mark Nasisse.)

Figure 18-4 Symblepharon (adhesions of the conjunctiva to the cornea) following feline herpesvirus 1 infection in a cat. Note that the dorsotemporal part of the cornea (and inner ocular structures) is obscured by the adherent conjunctiva and its blood vessels.

(Courtesy David J. Maggs.)

Confirmatory diagnosis of FHV-1 can be made through virus isolation in feline cell cultures. Serology is not very useful owing to the presence of antibodies from vaccination; however, immunofluorescent antibody (IFA) techniques can be used on cytologic and histologic specimens. PCR analysis has been used successfully to identify infected cats, but it is of limited use in a clinical setting because of the high prevalence of the infection in the general feline population.

In vitro sensitivity studies have identified several effective antiviral drugs—in decreasing order of potency, they are trifluridine, 5-iododeoxyuridine, and vidarabine. However, treatment is hampered by drug irritancy and availability. Trifluridine is commercially available but is topically irritating and needs to be administered at high frequency. The other two drugs are less irritating and administered less frequently but are difficult to obtain because they are not available commercially. Bromovinyl-deoxyuridine and acyclovir are not effective against FHV-1, whereas valacyclovir is toxic in felines. Promising in vitro results have been reported with ganciclovir, cidofovir, and penciclovir, but large-scale clinical studies with these drugs are still lacking.

Use of human recombinant interferon, administered topically or orally, has shown synergism in vitro and has decreased the severity of clinical signs in experimentally infected cats when given 1 to 2 days after inoculation. l-Lysine, administered orally, may also inhibit viral replication. Treatment of deep corneal ulcers and necrosis includes surgical intervention. The use of glucocorticoids is contraindicated, as it may induce shedding of viral particles in the latent stage. Topical tetracycline is frequently added because coinfections with Mycoplasma spp. and/or Chlamydophila felis (formerly Chlamydia psittaci) are common. Topical treatments are frequently continued for several weeks after resolution of clinical signs to prevent recurrence.

Stress is a very important factor in the pathogenesis of the clinical disease, and events such as the introduction of a new animal to the household or traveling to cat shows may exacerbate the symptoms. For this reason, frequent treatment with multiple drugs may sometimes aggravate the clinical signs of the disease. If worsening of signs is noted, the clinician is advised to carefully consider reducing treatment rather than increasing it.

FELINE CALICIVIRUS INFECTION.

Feline calicivirus (FCV), which belongs to the family of caliciviruses, affects only members of the Felidae family. The genus consists of one serotype and many different strains varying in antigenicity and pathogenicity. It is widespread in the domestic cat population, especially in crowded conditions. The epidemiology is very similar to that of FHV-1, and despite extensive vaccinations, many cats are carriers of FCV. Some of these cats remain carriers for life and shed the virus continuously. Feline immunodeficiency virus (FIV) infection may potentiate FCV shedding from carriers. Infection by FCV occurs through the oronasal and conjunctival routes. The clinical signs may vary owing to differences in virulence and tropism of the different virus strains. They include fever, anorexia, oral and tongue ulceration, and mild respiratory signs (sneezing, nasal discharge). Certain FCV infections may manifest as shifting lameness and pyrexia for 24 to 48 hours, and oral and respiratory signs may be absent. FCV is also involved in chronic gingivitis. Recently, highly virulent strains of FCV have emerged that are associated with high mortality and a new range of clinical signs (FCV-associated virulent systemic disease). The ocular lesions of FCV include mainly conjunctivitis, but the disease is milder than that induced by FHV-1.

The diagnosis of FCV infection is based mostly on the clinical signs. The virus can be isolated in feline cell cultures from oropharyngeal swabs. These samples may serve for PCR analysis that allows identification of the virus and its strains. Conjunctivitis should be treated symptomatically.

FELINE LEUKEMIA VIRUS INFECTION.

A retrovirus with worldwide distribution, feline leukemia virus (FeLV) is transmitted primarily through the saliva, although it can be present in any body secretion. Infected cats become viremic and may be persistently infected or clear the infection. Latent infections and carrier states are common. The virus is responsible for a third of feline cancer-related deaths through cell transformation and may also lead to anemia and immunosuppression. The prevalence of FeLV-related diseases has been declining over the past 10 years owing to the introduction of a protective vaccine. The clinical signs of FeLV infection vary with the virus subtype and the body system involved.

The ocular disease in FeLV-infected cats may relate to lymphoma, and transformed lymphocytes invade the globe through the uvea, leading initially to a mild uveitis characterized by corneal precipitates. Small masses may be observed on the iris (Figure 18-5), and with progression they will lead to thickening and distortion of the iris. Secondary glaucoma is a common complication because of infiltration and obstruction of the iridocorneal angle by tumor cells.

Figure 18-5 Multifocal gray masses on the surface of the iris of a 12-year-old male cat seropositive for feline leukemia virus. Histopathology confirmed the diagnosis of lymphoma.

The diagnosis of FeLV infection in cats can be made by serologic testing (enzyme-linked immunosorbent assay [ELISA], IFA) and PCR analysis. The latter can be used to detect viral material in tissues, including the cornea, when blood samples and immunohistochemistry of tissues are negative.

The treatment of lymphoma in cats usually requires a multidrug chemotherapy protocol. FeLV-positive cats with lymphoma treated chemotherapeutically were found to have significantly shorter remission and survival times compared with FeLV-negative cats with lymphoma treated with the same chemotherapeutic protocols. Other systemic conditions, including the ocular disease, are treated symptomatically. However, frequently the uveitis may be unresponsive to treatment or may cause secondary glaucoma, thus necessitating enucleation.

FELINE IMMUNODEFICIENCY VIRUS INFECTION.

Feline immunodeficiency virus is a lentivirus with worldwide distribution. At least four subtypes (A to D) have been isolated in different regions of the world, and cats can be concurrently infected with more than one subtype. The seroprevalence of FIV varies among countries, approaching 30% where the free-roaming cat population is large. It is higher in sick than in healthy cats. The virus is known to infect other Felidae. The primary mode of transmission is through bite wounds, because the virus is present in the blood and saliva of infected cats. Thus, intact outdoor male cats are at the highest risk of infection. Other important modes of transmission are the in utero route and through infected queens’ milk to suckling kittens.

The disease has three main phases—acute, asymptomatic, and terminal. With the beginning of the terminal phase consisting of the acquired immunodeficiency syndrome (AIDS)– related complex (ARC), cats exhibit nonspecific signs that reflect opportunistic infections (e.g., toxoplasmosis, feline infectious peritonitis virus, systemic mycoses, exacerbation of FHV-1) in different body systems.

The ocular disease manifests mainly as conjunctivitis and anterior uveitis. Pars planitis has been observed in four of nine cats with natural FIV infection. Many FIV-positive cats may exhibit a concurrent FIV- and Toxoplasma-induced ocular disease that manifests mainly as an anterior uveitis and chorioretinitis. Other ocular abnormalities reported are glaucoma (Figure 18-6) with or without uveitis, focal retinal degeneration, and retinal hemorrhages.

Figure 18-6 Glaucoma (secondary to posterior synechia) in domestic shorthair cat positive for feline immunodeficiency virus. Note swelling of the iris due to increased aqueous pressure in the posterior chamber, typical of the iris bombè syndrome. Color changes in the iris and ciliary congestion are indicative of uveitis.

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