• FIV and Uveitis


  • 1. The Anatomy of the Eye and Diseases of the Eye

  • 2. Primary FIV-Associated Uveitis

  • 3. Secondary FIV-Associated Uveitis

  • 4. Diagnosis of Uveitis

  • 5. Treatment of Primary FIV-Associated Uveitis

  • 6. Treatment of Secondary FIV-Associated Uveitis

  • 7. Lessons

  • Click here to open a Glossary of Terms in a separate window.


  • Infectious diseases of the eye are among the most common disorders associated with FIV infection [Nash]. In a study of 54 clinically ill cats infected with FIV, 19 (35%) had ocular disease [Glaze]. Most of these disorders are not caused by the feline immunodeficiency virus itself, but may follow from the condition of immune deficiency that makes infection with secondary pathogens more likely and immune response to them less efficient. This deficiency helps to explain why some cancers of the eye such as intraocular sarcoma and squamous cell carcinoma of the eyelid occur at higher rates in cats with FIV [Willis], even though FIV has not been shown to directly cause cancer. Collectively, these might be thought of as secondary (i.e., indirect) fiv-associated eye disorders. In at least one case, however, the virus itself has been identified as the cause of a disease of the eye , a primary fiv-associated uveitis. That is, in instances where FIV-infected cats suffer from uveitis, where no other secondary pathogen is found to be present, and where characteristic features are found, FIV is considered the cause. Either the direct action of the virus itself or a skewed or exuberant immune response to the presence of the virus is the likely cause of this disorder.

  • 1. The Anatomy of the Eye and Diseases of the Eye

  • The graphic below offers a schematic representation of basic features of the eyeball. The terms used to differentiate inflammatory diseases of the eye generally add the -itis suffix to the particular part of the eye affected by disease. Sometimes more than one part of the eye is diseased. Moving from the exterior of the eye inward, these are:

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  • Conjunctivitis. The “conjunctiva” is the pink membrane that lines the eyelid. Cats with inflammation of the conjunctiva often squint, paw at the affected eye or eyes, or partially cover the eyeball with the third eyelid. The white portion of the eye (the sclera) may become reddened. Conjunctivitis may be caused by external irritants or allergies or by bacterial, viral, or fungal pathogens. Herpesvirus and calicivirus are the most common causes, followed closely by chlamydia, and mycoplasma (M felis) [Hillstrom][Gerriets]. Infectious causes produce a yellow or green discharge. The outermost portions of the eye are those most likely to suffer primary bacterial infection. FIV may predispose to primary bacterial infection (see, for instance, bacterial rhinitis). One study of infection with Chlamydia psittaci found that “FIV infection prolonged the duration of the clinical signs resulting from the infection . . . and led to the development of chronic conjunctivitis.” Clearance of the organism following standard therapy took nearly four times as long [O'Dair].

  • Keratitis. Keratitis is inflammation of the “cornea,” the clear front layer of the eyeball. Although some types of cats, such as Siamese and Persian may be predisposed to a chronic degenerative keratitis, one of the most common causes of keratitis in cats is viral, specifically “herpetic keratitis,” caused by infection with the feline herpesvirus. It has been speculated that the keratitis is caused by a local immune response to the virus and that the cornea, like the trigeminal ganglia, may be a latent site for herpes since its DNA can be found in normal feline corneas [Martin]. Herpesvirus can form a carrier state in the eyes of cats, causing corneal ulcers that come and go with stress. It is suspected that cats with FIV are predisposed to infection with herpes and well established that they suffer more severely from its effects. (See “FIV and Upper Respiratory Infection.”) Bartonella bacteria, which may have an especial clinical impact on FIV+ cats (see discussion of Uveitis below) have also been implicated in keratitis and corneal ulcers. Corneal disease may cause disease to the interior of the eye (particularly the uvea) through stimulation of inflammatory mediators (self-produced proteins) via cranial nerve 5 extending from the cornea [Bentley].

  • Uveitis. The uvea is the layer of the eyeball between the sclera that contains the eye and the retina, the inner layer. It has three parts, the iris (anterior), the ciliary body (intermediate), and the choroid (posterior). Inflammations of the uvea bear the names of those parts or are identified by relative location.

  • Anterior uveitis (also called “iritis”) is the most common type of uveitis. The iris is the pigmented membrane that regulates the amount of light passing through the pupil to the lens. Anterior uveitis is characterized by painful involuntary constriction of the pupil (“miosis”) caused by the influence of inflammatory mediators on the iris sphincter muscle [Townsend] and is generally accompanied by clouding of the aqueous fluid that occupies the “anterior chamber,” the area between the lens and cornea .
  • Intermediate uveitis (also called “pars planitis”) is inflammation of the ciliary body responsible for altering tension on the lens, removing waste, and producing the clear aqueous fluid that occupies the space between the cornea and the lens. The folded forward portion of the ciliary body is called the pars plicata; the flat portion behind it and forming a bridge to the retina is called the pars plana. “Differentiating whether inflammation arises from the iris or the ciliary body can be difficult because of their close anatomic proximity and the similar clinical signs” [Townsend]. Some discussions treat as a subset of anterior uveitis, and ciliary muscle spasm does contributes greatly to the pain associated with anterior uveitis.
  • Posterior uveitis (also called “choroiditis”) is inflammation of the vascular portion of the uvea behind the ciliary body that provides blood and nutrients to the retina. Cellular debris within the vitreous fluid may accumulate as inflammatory cells diffuse backward from the pars plana and pars plicata of the ciliary body [Townsend].
  • Panuveitis is inflammation of the entire uvea.

  • Retinitis is inflammation of the light-sensitive tissue extending from the optic nerve and lining the inner surface of the eye. Concurrent inflammation of the choroid is common, hence the term “choreoretinitis.” Hypertension due to hyperthyroidism can cause retinitis (and subsequent retinal detachment), but the majority of causes are those pathogens listed below for uveitis.

  • 2. Primary FIV-Associated Uveitis

  • Not all uveitis is caused by pathogens. Some results from trauma, some from cancer. Often no clear cause can be found and the occurrence is labeled “idiopathic,” medical shorthand for “We can’t figure out what the cause is.” Retrospective studies have been unable to document a cause in 30% to 62% of cats with anterior uveitis, though an immune-mediated element is thought likely [Glaze]. The evidence for FIV as an independent cause of uveitis in cats is strong. FIV+ cats in the terminal stage of illness studied during the mid ‘90s suffered overwhelmingly (19 of 23 in one study, 13 of 15 in a follow-up study) from uveal inflammation [Loesenbeck1][Loesenbeck2]. This is of course a much higher percentage than in the FIV+ population generally, but indicates that uveitis does have a natural relation to disease course.

  • Causes. There is no consensus as to how precisely FIV infection might lead to uveitis. It is possible that viral replication in cells of the uvea or vascular tissue may have a direct pathogenic impact. However, as with other inflammatory diseases to which cats with FIV are predisposed (e.g., gingivostomatitis, inflammatory bowel), immune dysfunction probably plays a strong role. This role could involve hypersensitivity responses to deposition of antigen-antibody complexes such as is known to happen with glomerular nephritis in FIV+ cats and has also been implicated in FIP-induced uveitis. Other possible scenarios involve autoimmune responses sparked by cross-reactivity between viral and uveal proteins, or exposure of uveal proteins to immune attack because of virally induced disruptions of the blood-ocular barrier, or virally induced alterations in normal suppressor-cell function and self-tolerance (recognition of one’s own tissue)[English], known actions of FIV. Abnormal levels of antibody activity in the eyes of cats with uveitis have frequently been noted. One study found that elevated levels of interleuken 6 (IL-6), an inflammatory immune-signaling protein (“cytokine”) associated with the antibody-producing pathway, occurs intraocularly in many different forms of uveitis with a variety of causes, indicating that it may be a mediator of uveitis generally in cats [Lappin1]. Elevated levels of IL-6 and abnormal skewing of immune response in the direction of antibody (TH2-mediated) activity are known features of retroviral infections such as FIV and HIV.

  • Distinguishing Features. Although there are no features of primary FIV-associated uveitis that absolutely distinguish it from uveitis caused by other pathogens, it does have some characteristic tendencies. Anterior uveitis, for instance, is universally acknowledged to be most common. The incidence of anterior uveitis in cats with FIV is noteworthy because posterior involvement with inflammation of the retinal vasculature is the most common ophthalmological finding in patients with HIV [English]. It is generally acknowledged that primary FIV-associated uveitis is mild to moderate in severity, but more usually chronic than acute in nature. The disease is usually seen in cats older than 5 years with symptoms often unnoted by the owner prior to veterinary examination [Hoskins]

  • In one study of nine FIV+ cats without demonstrable secondary diseases who were referred to a research facility, three had no ocular abnormalities observed by their owners or their vets prior to the referral, but had been referred for other disorders [English], indicating that an ongoing, subtle, sub-acute onset is not atypical. Five of the nine showed the predominant chronic mild to moderate anterior uveitis. Only one of the nine had posterior involvement, and that in one eye only. Four of the nine, however, were diagnosed with pars planitis (intermediate uveitis affecting the ciliary body) of varying severity and progression–an unusually large number. One cat had anterior uveitis in one eye, pars planitis in the other. One corneal change sometimes attributed to FIV+ cats with chronic anterior uveitis -- accumulation of clumps of inflammatory cells on the inside of the cornea (called keratic precipitates) – was not reported. One authority notes, “Interestingly, the accumulation of inflammatory cells in the anterior vitreous humor, in close approximation to the pars plana of the ciliary body, is a common . . . finding. The specificity of this lesion for FIV infection is uncertain, as many cats with this finding test negative for the virus” [Nasisse]. The same source claims that ocular manifestations of FIV often precede systemic expression of the disease by months to years.

  • Characteristic Findings. Again, there is no single feature of primary FIV-associated uveitis that will be found in 100% of instances, but there are findings that are perhaps more likely than not to be seen, particularly because of its tendency to be chronic.

  • Tearing and squinting. Squinting and reflex tearing are usual symptoms of anterior uveitis.
  • Aqueous flare. Aqueous flare is the characteristic mark of anterior uveitis and indicates a breakdown of the blood-aqueous barrier that keeps the aqueous fluid clear by preventing passage of protein into the anterior chamber [Bentley], and increased permeability of the ocular vasculature, leading to presence of inflammatory cells within the aqueous [Townsend]. Normally, the path of a beam of light directed by an examiner into the anterior chamber is invisible or nearly so. With anterior uveitis the beam is well outlined, as dust motes will make light entering a window visible (the "Tyndall effect"). The flare is graded +4 to +1, depending on the level of light scattering produced by the opacity of the fluid.
  • Snowbanking. Intermediate uveitis (pars planitis) is usually marked by white coalescing infiltrates in the anterior vitreous that appear as puffy “snowbanks” visible peripherally along the ora serrata (the area below the end of the the choroid and behind the ciliary body) and frequently extending over the pars plana [Willis]. The incidence of pars planitis in FIV+ cats is unusual enough that some authorities associate it particularly with FIV infection [Whitaker].
  • Periperal iridal hypemia. The iris becomes swollen and engorged with blood along it periphery
  • Dyscoria. The pupil assumes an abnormal shape.
  • Lymphoplasmacytic nodules. Nodules formed by aggregates of lymphocytes and plasma cells and the proliferation of small vessels upon the surface of the iris (“neovascularization”) often accompany chronic uveitis like that associated with FIV. Conversely, the granulomatous (neutrophilic) lesions often observed in uveitis caused by FeLV and FIP are generally absent with FIV [Willis]. There is also a general paucity of retinal lesions by comparison to cats with uveitis from other causes[Loesenbeck2].
  • Posterior synechia. Adhesion of the iris to the envelope covering the lens, a feature of chronic anterior uveitis [Gelatt].
  • Globe hypotomy and secondary glaucoma. Anterior and intermediate uveitis are accompanied by abnormally low pressure (hypotomy) in the aqueous fluid. Because of the generally more chronic nature with FIV-involvement, the inflammation-induced changes in the normal outflow pathway of fluid often lead to glaucoma (elevated pressure in the vitreous fluid).
  • Anterior subcapsular cataracts. Clouding of the lens, particularly the forward-facing portion, another consequence of chronicity [Bentley].

  • 3. Secondary FIV-Associated Uveitis

  • A number of pathogens and diseases associated with them are known to cause uveitis in cats. There is some evidence that most–perhaps all–have a greater liability of occurrence and/or a greater severity of expression in cats infected with FIV. There is considerable overlap among the characteristic features of uveitis caused by different pathogens, but some features do have notable degrees of association with specific pathogens.

  • Feline infectious peritonitis (FIP). FIP is caused by a mutated form of feline enteric coronavirus that induces a fatal inflammation of the blood vessels. At least one study of FIP-FIV coinfected cats concluded, “Immunosuppression caused by chronic FIV infection may have enhanced the creation and selection of FIPV mutants by increasing the rate of FECV replication in the bowel and inhibiting the host’s ability to combat the mutant viruses once they occurred” [Poland]. Poor cell-mediated immunity particularly has been singled out as a potential factor in persistence of the virus, increasing the probability of mutation. FIP occurs in both an effusive and noneffusive form; the noneffusive form is most commonly associated with ocular disease [Chang]. About 40% of cats with FIP will have ocular symptoms [Glaze]. Common Findings. Inflammation may be of either anterior (iritis) or posterior (choroiditis) uvea, and may include the retina. Over time, the inflammatory condition gradually progresses to panuveitis, involving the entire inner eye [Gelatt]. Damage may extend forward to opaque dotting on the rear of the cornea and proteinaceous deposits within the chamber between cornea and lens or backward to immune deposits on the retinal vasculature.[Chang]

  • Feline herpesvirus (FHV-1). Herpes is a common feline upper respiratory virus that produces an infection that is chronic in most cats and can be reactivated periodically, often after periods of stress. Some studies suggest that cats infected with FIV may be prone to herpesvirus infection and may experience more severe symptoms. (See “FIV and Upper Respiratory Infection.”) Involvement of the eye is a characteristic feature of infection. The most common clinical ocular manifestations of FHV-1 are conjunctivitis and keratitis, but anterior uveitis may be another manifestation of the infection [Chang] The virus does not seem to be directly pathogenic intraocularly, but there is a growing suspicion among researchers that much of what is currently classed “idiopathic uveitis” is caused by secondary immune responses to its presence. Herpes DNA has been found in the aqueous fluid of 14% of cats diagnosed with “idiopathic” uveitis, with 50% registering local production of antibody against it [Glaze]. Concluded one study, “Results suggest that FHV-1 can infect intraocular tissues of cats and that intraocular FHV-1 infection may be associated with uveal inflammation in some cats” [Maggs]. Herpes has an affinity for nerve tissue, and it has been proposed that FHV-1 gains entry to the interior of the eye via nerve fibers [Chang]. Common Findings. Herpes-induced uveitis is anterior in character and lacks distinguishing features from idiopathic anterior uveitis: nonspecific signs of ocular discomfort, miosis, corneal precipitates, blood or proteinaceous material in the anterior chamber.

  • Toxoplasmosis. Toxoplasma gondii is a protozoan parasite for whom felines are the natural host species. Infection is chronic with encysting in host tissue that is usually inconsequential following acute infection. It is well-established that FIV-related immunosuppression can reactivate the encysted parasite and that toxoplasmosis is more of a threat to immune-suppressed than to immune-competent cats and humans. (See “FIV and Toxoplasmosis.”) “The seroprevalence of T. gondii infection in cats with uveitis has been reported as high as 80.2%. Both the organism's DNA and antibodies to the organism have been detected in aqueous humor, confirming that T. gondii can directly infect the eye”. Inflammation within the eye may occur as a direct result of organism replication or indirectly through the immune response of intraocular lymphocytes to circulating T. gondii antigen [Chang]. Common findings. Like FIP, toxoplasmosis can cause anterior and posterior uveitis, and retinitis with associated vascular inflammation. In contrast to viral sources of infection, toxoplasmosis causes granulomatous (neutrophilic) inflammation–sometimes visible as large, whiteish “mutton fat” lesions on the surface of the iris. These may also be observed in the posterior uvea. [Lazard].

  • Bartonellosis. Bartonellas are a group of bacteria that chronically infect perhaps 20% of domestic cats. Most infections are asymptomatic, although some clinical conditions such as gingivostomatitis have been linked to chronic bartonella infection. Bartonella henselae has been found to induce several clinical disorders to a greater degree in cats with FIV than those without, notably lymphadenopathy (swollen lymph nodes) and gingivitis [Ueno]. In both natural and experimental situations, Bartonella have been shown to infect the eyes of some cats and may cause uveitis [Lappin2]. It’s reasonable to assume, therefore, that FIV may be a predisposing factor. One report found 27 of 40 cats with anterior uveitis were positive for Bartonella infection [Glaze], but it is likely that a large portion of these cases have more to do with how common infection with the bacteria is than with a true cause-and-effect relationship. Bartonellas are pathogens with zoonotic (cross-species) potential, and are the cause of ocular disease in humans. Common findings. Bartonella-induced uveitis is difficult to distinguish clinically from uveitis due to other pathogens such as toxoplasmosis. Anterior uveitis with lymphoplasmacytic inflammatory infiltrates is most common, though chorioretinitis also occurs [Ketring].

  • Fungal infection. Several common fungi can cause uveitis in cats. Cryptococcus and histoplasma are the most widely disseminated, although blastomyceses and coccidioides are found regionally. Inhalation of spores is the usual mode of infection. In one study, collection with orophangeal swabs found a significantly higher frequency of Cryptococcus neoformans in FIV+ than in FIV- cats. Systemic Cryptococcal infections have likewise been reported in FIV-infected cats at a significantly higher rate [Mancianti]. Although there is no information on the rate of histoplasmosis in FIV+ cats, experience with HIV patients has shown that it represents a significant source of infection for the immune-suppressed. Ocular signs of cryptococcosis may occur as a neurologic symptom or as a result of dissemination in the blood stream and may include both anterior and posterior uveitis and retinitis. With histoplasmosis, ocular disease may spread widely and include conjunctivitis, anterior and posterior uveitis, and retinitis [Chang]. Common findings. Fungal infections more often involve choroiditis, with anterior uveitis characterized by graulomatous lesions [Gelatt] developing secondary to posterior disease in the later stages of the infection [Glaze][Gionfrido]. With cryptococcidiosis, choroidal and retinal lesions vary in appearance from tiny opaque dots to large circular lesions. With histoplasmosis, ocular discharge is frequent, and spasm of the eyelid , and inflammation of the eyelid, the conjunctiva, and the intraocular cavity may occur, with retinal detachment, and secondary glaucoma sometimes following.[Chang].

  • Feline leukemia virus (FeLV). FeLV is an immunosuppressive retrovirus like FIV. Two disease courses occur in cats infected with FeLV: persistent viremia with progressive infection or and self-limiting, regressive infection. It is well established that cats infected with FeLV who are also infected with FIV have a greater likelihood of developing progressive infection and that co-infected cats have a greater liability to secondary diseases than those with either infection alone. Ocular diseases generally have only a small association with FeLV [Glaze], and uveitis in cats with FeLV infection is probably not a direct result of the virus but rather related to secondary invasion of infectious agents caused by immunosuppression or FeLV-related cancer [Chang]. Lymphosarcoma, is the most common cancer in cats with FeLV and is even more common in those coinfected with FIV. (See “FIV and Lymphoma.”) Lymphoma is a significant cause of uveitis in cats generally and in particular in FeLV+ cats, in whom the lymphoma is induced directly by the virus rather than indirectly, as in the case of FIV. In one study, FeLV+ cats with lymphosarcoma of the eye and uveitis had a reduced survival rate compared to cats without concurrent uveitis. FIV+ cats in the former group were more likely to have advanced disease [Willis]; hence both uveitis and FIV may darken the prognosis for ocular lymphosarcoma. Common Findings. Initial presentation is usually a mild, anterior uveitis [Glaze], which may progress to inflammation of all intraocular tissue (panuveitis) or frank tumor formation [Gelatt]. Other findings may include corneal masses, blood in the anterior chamber between cornea and lens, retinal degeneration, and hemorrhage. FeLV-induced lymphosarcoma often presents as thickening of the iris with associated flesh-colored lesions. These lesions are most often bumpy but may be diffuse in a way difficult to distinguish from uveitis from other causes [Chang]

  • 4. Diagnosis of Uveitis

  • The diagnostic protocol that follows is artificial and meant to familiarize with procedures that take place in the course of differential diagnosis of uveitis and perhaps to suggest points of discussion between client and examining vet. It ignores procedures that would normally take place to diagnose or eliminate problems affecting the external eye – e.g., the conjunctiva, the cornea. In most cases, initial diagnostic evaluation would be done by a veterinary generalist, with a more specialized examination done by a veterinary ophthalmologist perhaps occurring at a later point.

  • Physical Exam. Because many significant systemic diseases can induce uveitis, a thorough physical examination is always called for.

  • General. Inspecting of the coat, palpating abdomen and lymph nodes, stethoscopic sounding of the chest cavity. If systemic disease is suspected, thoracic x-rays and abdominal ultrasound may be called for [Townsend].
  • Ocular. Ophthalmoscopic inspection of the anterior chamber, pupillary reflex, lens, and fundus (the rear portion of the eye opposite the lens) for characteristic features of uveitis previously noted.

  • Tests. Diagnostic tests for uveitis are often done incrementally, based on suspicion raised by medical history and exam findings. A mild, unilateral, non-hemorrhagic anterior uveitis in an otherwise healthy cat may justify symptomatic treatment without further investigation. A more thorough systemic investigation is warranted if, for instance, inflammation is moderate to severe in one or both eyes, glaucoma is present or possible, vision is threatened, posterior disease is noted, or systemic illness exists or is suspected [Bentley]. Specifically:

  • CBC. Complete blood cell count with differential for evidence of anemia, infection, immunosuppression, parasitism, or allergy.
  • Chemistry. Biochemistry profile for evidence of organ impairment, hyperglobulinemia as evidence of chronic or acute infection or cancer.
  • Urinalysis. For renal dysfunction (possible hypertension), presence of protein or sugar.
  • Serology or PCR (polymerase chain reaction assay for the presence of DNA) for diseases with a known association with uveitis.

  •    FIV. Testing for infection with feline immunodeficiency virus is characteristically done in practice or at a lab with an ELISA combination test kit that includes an FIV antibody-test, with confirmation by Western Blot or PCR. (See “Understanding and Applying FIV Testing” for discussion of limitations of various testing instruments.)
  •    FeLV. Testing for Feline Leukemia Virus is characteristically done in practice or at a lab with an ELISA combination test kit that includes an FeLV antigen test. Confirmation is done by repeat ELISA four months later to confirm that clearing of the virus has not occurred.
  •    Toxoplasma gondii. Testing usually involves measuring titres of two toxoplasmosis-specific immunoglobulins, IgG and IgM. However, exposure to toxoplasmosis is common, and titres will continue to register after infection is dormant. Serological evidence can be complicated and ambiguous. FIV complicates the process further by causing atypical titers that may or may not indicate ongoing low-level active infection, and reactivation of dormant oocysts is possible. (See “FIV and Toxoplasmosis” for a fuller discussion of issues related to diagnosis.) PCR is rapidly becoming the diagnostic instrument of choice.
  •    FIP-FCoV. Diagnosing FIP has historically been difficult because available serologic tests cannot differentiate the FIP coronavirus (FIP-CoV) from other feline coronaviruses. The ascites of “wet” FIV can be cytologically examined, but “dry” FIP has been diagnosed based on characteristic clinical signs and laboratory findings: elevated corona virus titer (1:160 or greater), elevated globulin (> 5.1 g/dl), lymphopenia (<1.5 x 106/Fl), criteria which nonetheless have naysayers [Wolf]. Recently, Auburn University has claimed a reliable and clinically available RT-PCR demonstrating active replication of coronavirus in peripheral blood cells, which should only occur with systemic (i.e., FIP) coronavirus infection.
  •    FHV-1. Serologic tests for antibody titer to feline herpesvirus are of limited diagnostic value since most cats have been exposed to or vaccinated against it. PCR can identify active infection, but because the virus can lie dormant in nerve tissue and because FHV may gain access to the inner eye by direct nerve transport, a negative PCR of blood serum may not be reliable. Acute ocular FHV-1 infection can be diagnosed with virus isolation from conjunctival cytology samples or fluorescent antibody testing on corneal or conjunctival smears [Chang], but herpes-related uveitis may be unrelated to the more common conjunctivitis and keratitis.
  •    Regional Mycoses. Serologic testing is of varying value in diagnosing systemic fungal diseases. It is useless, for instance, in demonstrating cryptococcal infection. Clinical findings and microscopic demonstration of an organism in affected tissues, lymph nodes, and in the case of cryptococcus bodily fluids such as sputum are preferred means of diagnosis. PCR of feces, sputum, and blood has become more common in diagnosis of cryptococcus.

  • Specialized Testing. Diseases of the eye frequently call for the specialized expertise of a veterinary ophthalmologist, who also has the skill and equipment to do advanced diagnostics that veterinary generalists may lack.

  • Paracentesis. Perhaps the most important procedure best performed by an ophthalmologist in the diagnosis of uveitis is ocular paracentesis, the drawing of fluid from the interior of the eye with a needle: called aqueous centesis or anterior chamber paracentesis when the aqueous fluid is taken from the anterior chamber, vitreous centesis or posterior chamber paracentesis when vitreous fluid is taken from the posterior chamber. The risks of aqueous centesis are low in the hands of an experienced ophthalmologist but do include cataract formation if contact is made with the anterior lens capsule, hyphema, and exacerbation of the uveitis [Townsend]. The technique is not difficult but does require either general anesthesia or very heavy sedation in most cases [Powell]. Although in many cases a diagnosis cannot be made by the results of aqueous fluid analysis, it may be supportive of an overall diagnosis. Centesis of vitreous fluid is also occasionally used for diagnosis of uveitis, especially posterior uveitis. However, the potential for sight-threatening complications, such as ocular hemorrhage and retinal detachment, is significant. Vitreous centesis is usually reserved for blind or nearly blind eyes [Powell].

  •    Aqueous centesis. If a marked cellular infiltrate is noted in the anterior chamber, evaluation of aqueous fluid can may be helpful in identifying cancerous cells. The fluid can also be subjected to the same tests done for diagnosing systemic presence of pathogens: cytology, culture, antibody titer, and PCR. Performing these tests from ocular matter can resolve ambiguities inherent in systemic testing. For instance, with regard to antibody titers, aqueous centesis can be used to determine the level of intraocular antibody production; in turn, the ratio of aqueous antibody titer to serum titer, known as the Goldman-Witmer coefficient, or C value, if greater than 1, shows that an intraocular pathogen is causing plasma cells of the iris to produce antibody, thereby showing that a pathogen is causing the uveitis rather than merely being present in the body [Townsend].
  •    Vitreous centesis. In some cases, aqueous fluid is of no aid in diagnosis. If marked vitreal infiltrates or cellular retinal detachments are noted in visual examination of the posterior segment of the eye, the same testing of those infiltrates is often more rewarding. In one study, a causative agent was identified in 13 of 20 of cases using vitreous centesis and cytologic examination alone [Powell].

  • Slit-lamp biomicroscopy. The slit-lamp biomicroscope includes a binocular microscope with an external, pivoting, and adjustable light source. It enables identification and localization of subtle lesions of the anterior chamber, the lens, and the anterior vitreous [Gelatt].
  • Tonometry. The tonometer measures subtle elevations in intraocular pressure, making much easier the diagnosis and management of glaucomas secondary to chronic uveitis.
  • Ultrasonography. Ultrasonography has become increasingly useful in the diagnosis of intraocular disease in recent years. Echoes from the corneal surfaces, the anterior and posterior lens surfaces, the retina, and any abnormal intraocular material project an image which aids diagnosis. This is especially useful when dense corneal opacity or mature cataract obscures the view of the fundus (the rear portion of the eye opposite the lens). [Brooks].

  • 5. Treatment of Primary FIV-Associated Uveitis

  • Therapy for uveitis is both specific and nonspecific. (Dosages noted within are those recommended by particular sources and may not reflect those used by a particular clinical practitioner.) Nonspecific therapy addresses inflammation, pain, and such effects of chronic uveitis as synechia formation (adhesion of iris to lens). Specific therapy addresses the pathogenic cause of the uveitis, plus any modifications of nonspecific therapy that might be called for with individual pathogens. Another important factor is the location of the uveitis: the closer to the front of the eye the inflammation is, the more likely topical treatment is to be helpful; the more posterior the inflammation, the more likely that systemic medicating will be called for.

  • Nonspecific Therapies. These generally include two classes of drugs, anti-inflammatories and mydriatics to dilate the pupil; NSAIDs may assist dilation by blocking the prostaglandins that cause ciliary spasm.

  • Topical.
  • Glucocorticoids* (i.e., corticosteroids) 2-6x daily (depending on severity of symptoms)
  •    Prednisolone acetate (1% suspension)
  •    Dexamethasone (0.1% solution or 0.05% ointment)

  • NSAIDs (2-4x daily depending on severity of symptoms)
  •    Flurbiprofen (0.3% solution)
  •    Ketorolac (0.5% solution)
  •    Diclofenac (0.1% solution)

  • Mydriatics
  •    Atropine** (0.5% and 1% solution and ointment) 2-4x daily for 3-4 days
  •    Tropicamide (1% solution)

  • Oral
  • Glucocorticoids*
  •    Prednisolone or prednisone (0.5-2.2 mg/kg) 1-2x daily

  • NSAIDs
  •    Aspirin (10 mg/kg) every second day
  •    Ketoprofen (2 mg/kg initially, then 1 mg/kg) 1x daily

  • *Topical glucocorticoids may not be used when the cornea is ulcerated or otherwise not intact; use of systemic steroids requires ruling out of bacterial or fungal diseases.
  • **Atropine drops are used reluctantly in cats, who will salivate profusely as they drain down the nasolacrimal duct; ointment may cause fewer symptoms. Additional caution needed with those with impaired tear production or at risk to develop glaucoma
  • -Bentley; Powell

  • Treatment of ocular lesions caused solely by FIV infection should include nonspecific therapy. Primary FIV-associated uveitis frequently responds favorably to nonspecific therapy with glucocorticoids and topical mydriatics. In a 1990 study of cats with FIV and uveitis, anterior uveitis treated topically with this regimen showed almost uniform improvement [English]. Long term use is probably necessary to control signs [Glaze]. In the same study, cats with intermediate uveitis (pars planitis), despite treatment with both topical and oral steroids, showed only limited improvement. Long-term use of oral steroids, while indicated, is done with caution since their effect on viral replication is unknown [Powell].

  • Specific Therapy. Uveitis directly caused by FIV infection does not usually call for “prophylactic” use of antibiotics to ward off secondary bacterial infections. Remarkably little is known about the effect of specific therapy aimed at controlling the virus itself. Experience in HIV medicine has shown that anterior, intermediate, and posterior uveitis tends to improve with initiation of highly active antiretroviral therapy (HAART, aka the “triple cocktail”) [Cunningham], suggesting that systemic control of viral replication has important therapeutic benefit. Therefore, any agent or combination of agents that has a substantial impact on viral load (see “Bud’s Medications and Supplements” and “Bud’s Therapeutic Guidelines”) has some likelihood of being beneficial for uveitis caused by FIV.

  • What level of impact would be necessary is speculative, but, again, HIV medicine suggests that it need not involve near-total inhibition of viral replication. A 1998 study of six HIV patients with anterior or posterior uveitis that had been unresponsive to prolonged treatment with systemic and topical corticosteroids, responded dramatically to oral antiretroviral therapy with zidovudine (AZT). “In all 10 eyes of six patients, there was resolution of inflammation in 10 to 42 days after commencement of treatment . . . despite no or minimal response to corticosteroids. Cultures of aqueous humor from three eyes of three patients and culture of vitreous humor from one eye of one patient were positive for HIV; no other organism was isolated. Systemic evaluation disclosed no other identifiable cause for the uveitis in any patient” [Rosenberger]. AZT alone, it should be emphasized, does not reduce HIV viral replication to undetectable levels; this can be accomplished only through combination therapy with multiple antiretroviral drugs.

  • Antiviral Drugs. AZT is the only HIV antiretroviral drug in general use as a clinical treatment for FIV in cats. But as noted elsewhere ( “Bud’s Medications and Supplements”), a number of antiretroviral drugs developed for treatment of HIV are also effective against FIV, and often without the side effects that inevitably accompany AZT (most particularly, anemia). Tenofovir, a drug superior to AZT for use in cats in almost every way, is a nucleoside closely related to cidofovir, which, as noted later, has been used successfully in topical treatment of feline herpetic conjunctivitis and keratitis. The combinations of tenofovir or abacavir with either lamivudine or emtrictabine (companion drugs never used alone) would have action suppressing FIV superior to either used alone. What beneficial impact on uveitis supplements with direct antiviral suppressive action would have alone, in combination with one another, or in combination with antiretroviral drugs is purely speculative.

  • Immune Modulators. A number of drugs have been tested for favorable activity in the immune systems of cats with FIV and/or FeLV, including acemannan, staphylococcus protein A (SPA), and (most recently) lymphocyte T cell immunomodulator (LTCI). (See “Bud’s Medications and Supplements.”) None, however, has been assessed specifically as therapy for primary FIV-associated uveitis. One notable exception is interferons, which have both directly antiviral and immunomodulatory activity.

  •    Feline Omega Interferon (Virbagen Omega). Although there have been no full scale studies of feline omega as therapy for uveitis, there is an intriguing one cat study. In it, an elderly FIV+ /FCV+ cat, Pacha, with jaundice, autoimmune hemolytic anemia and acute exudative, unilateral anterior uveitis and retinitis was presented for care. Jaundice and elevated globulin suggested the dry form of FIP, but the autoimmune haemolytic anaemia pointed more towards FIV, as did the age and outdoor lifestyle of the cat. No clinical basis could be found for crediting his ocular symptoms exclusively to either FIV or the initial stages of FIP. “Hence the hypothesis was put forward that this was a condition caused by both viruses, even though this case did not present with lymphadenitis and lymphocytopenia which are classically described with FIV.” Treatment with a single five dose (1 MU/kg) course of subcutaneous feline omega interferon, plus oral dexamethasone at non-immunosuppressive dosage, resulted in a rapid improvement in the animal’s general condition ( which included arthritis and cystitis due to immunocomplexes) and resolution of his uveitis and retinitis. No recurrence was observed during a follow-up period of thirteen months, although Pacha eventually succumbed to the wet form of FIV. During this period the cat was maintained with corticosteroids and and low-dose oral recombinant human alpha interferon on alternate days [Lazard]. Whether the action of the feline interferon was directly antiviral, immunomodulatory, or some combination of the two is an open question, though concurrent administration of corticosteroids argues more strongly for direct antiviral action.
  •    Oral Human Interferon. For some, the effectiveness of low-dose oral interferon as FIV therapy remains unproven; others are proponents. Both schools concede that dosage is too low for directly antiviral action. (See “Interferon and FIV.”) Oral recombinant interferon is typically diluted to 30 IU/ml and administered by distribution on oral tissue once daily for alternating 7-day periods. In Pacha’s case (above) it was either helpful in maintaining ocular and general health or it was only coincidentally present. A 2006 study of Alfaferone, a natural interferon (cultured from human cell lines rather than synthesized by DNA technology) given orally to FIV+ cats at 50 IU/ml once daily for alternating 7-day periods, found significant benefit to general parameters of health. The published study also notes without elaboration, “There was also a rapid regression of uveitis and retinitis . . . .” [Pedretti]. It is legitimate to conclude, therefore, that there is at least some basis for the belief that oral low-dose interferon therapy may be of benefit in the treatment of uveitis caused by FIV.

  • 6. Treatment of Secondary FIV-Associated Uveitis

  • Nonspecific Therapies. Same as described in Part 5.

  • Specific Therapies. With the exception of bartonella, bacterial infection of the inner eye is usually limited to instances of trauma or sepsis (when bacteria from elsewhere in the body gets into the bloodstream). Uveitis does not, therefore, usually call for “prophylactic” use of antibiotics to ward off secondary bacterial infections. Specific therapies may include antibiotic or antiviral medications (and perhaps supplements).

  • FIP. Systemic therapy has aimed at controlling inflammatory immune response with high doses of immunosuppressive and anti-inflammatory drugs. Feline interferon omega is controversial but has demonstrated some effectiveness in concert with glucocorticoids [Ishida]. A polyprenyl immune stimulant has recently had some success against the “dry” form of the disease [Legendre]. Ocular inflammation is treated with topical and systemic glucocorticoids, and mydriatics, depending on the location and severity of the inflammation; posterior inflammation requires oral glucocorticoids [Powell].

  • Herpesvirus. Frank FHV-1 ocular infection is largely a disease of the cornea and conjunctiva. Topical antiviral medications, including trifluridine and idoxuridine solutions, are efficacious against FHV-1 conjunctivitis and keratitis when administered as one drop in the affected eye four to six times a day for two to three weeks [Chang]. Cidofovir (0.5%) has shown promise in treating FHV-1 conjunctivitis and keratitis, is less irritating and effective when administered twice a day [Fontenelle]. Virbagen interferon omega applied topically is effective in treatment of herpetic keratitis (5 MU diluted w/9.5ml .9% NaCl; 2 drops 5x daily for 10 days, 2 drops 3x daily for 10 days or up to 30 days). Glucocorticoids may not be used. When uveitis is concurrently present, no change in therapy is called for. However, there is no accepted antiviral protocol for treatment of “idiopathic” uveitis with herpesvirus demonstrated in intraocular fluid since the extent to which it is responsible for provoking the immune response likely responsible for the condition remains speculative. Standard nonspecific therapy is usual. Famciclovir, an oral antiviral drug, effectively reduces the severity of systemic and ocular clinical signs in cats; however, dosing regimens remain varied and dosing recommendations are uncertain, ranging from 62.5 mg/cat once to twice a day to 125 mg/cat three times a day [Chang]. Feline omega interferon delivered subcutaneously has systemic activity against acute herpes (2.5 MU/kg 3x on alternate days). Dilute oral human interferon alpha (30 IU distributed on oral tissue once daily for alternating 7 day periods) may be beneficial [Brooks]. Oral L-lysine (250 to 500 mg once or twice a day) inhibits herpes replication by arginine inhibition and has also effectively reduced the severity of conjunctivitis [Chang].

  • Toxoplasmosis. The use of antimicrobial therapy for cats with a positive titer toxoplasma and uveitis is controversial [Nasisse] when clinical signs are not evident and the organism has not been demonstrated within the eye. Current protocol requires (1) the ruling out of other causes and (2) nonresponse of the uveitis to nonspecific therapy alone. In addition to non-specific therapy (oral glucocorticoids for posterior involvement), clindamycin (10-12.5 mg/kg PO or IM q 12 hours) for four weeks is the antibiotic of choice [Powell]. Clindamycin slows the replication rate of the organism but is unlikely to clear it from the body [Nasisse]. For backup therapies, see “FIV and Toxoplasmosis.”

  • Bartonella. In addition to nonspecific therapy to control uveitis, treatment for bartonellosis consists of three to four weeks of oral azithromycin (10mg/kg body weight once daily) [Glaze][Nasisse], doxycycline (10 to 22 mg/kg orally twice daily), or enrofloxacin (22.7 mg twice daily) [Powell].

  • Regional Mycoses. Anterior uveitis is treated with topical nonspecific therapy. Oral glucocorticoids are needed with posterior segment disease. Ketaconazole, itraconazole and fluconazole are most often used to treat cryptococcosis in cats. Fluconazole (50 to 100 mg daily) has the fewest side effects, is well tolerated by cats, and penetrates the central nervous system [Powell]. Histoplasmosis has been successfully treated with ketaconazole [Nasisse], and histoplasmosis and blastomycosis have been effectively treated with itraconazole (orally at 5 mg/kg every 12 hours) [Chang]. “Treatment should be for at least 1 month after clinical signs resolve and the Cryptococcus titer has dropped by at least two orders of magnitude”[Powell]. Writes one authority, “The prognosis for uveitis secondary to systemic mycoses is generally poor, however, a positive response to antifungal therapy has been reported in some cases” [Nasisse]

  • FeLV. Since FeLV appears to cause little in the way of ocular disease with the exception of its role in lymphosarcoma, treatment, in addition to combination chemotherapy, is nonspecific, with topical glucocorticoids for anterior uveitis and oral glucocorticoids when there is posterior involvement [Powell].

  • 7. Lessons

  • FIV status is important. Even seemingly healthy cats with FIV have an increased liability to a number of different pathogens capable of causing diseases of the eye, including uveitis. Secondary pathogens can in turn cause secondary problems. “Secondary glaucoma has been reported to occur in up to 50% of cats with uveitis secondary to systemic disease” [Chang].

  • “Wait and see” could mean “Wait and never see.” Prompt treatment of symptoms of eye disease is vital, particularly in an FIV+ cat. Even prompt, aggressive therapy is not a guarantee of successful resolution. “Unfortunately in some cases, despite aggressive medication, we are unable to control the inflammation in the eye. In these cases . . . vision may also be lost” [Whitaker].

  • “Looks fine” doesn’t necessarily mean “is fine.” Uveitis – and particularly uveitis directly caused by FIV infection – often presents few or no evident symptoms. “The accumulation of inflammatory cells in the anterior vitreous humor is sometimes seen in cats with uveitis, particularly if they are feline immunodeficiency virus (FIV) infected. Uveitis is typically accompanied by pain, manifested most commonly by squinting and reflex tearing. These signs, however, tend to be subtle in cats, and often are not noticed by the owner” [Nasisse]. Cats with FIV need regular veterinary check-ups that include examination of the eyes.

  • It takes raindrops to make floods. Uveitis in cats with FIV is often chronic and protracted in character. Glaucoma, cataract formation, lens luxation (displacement) or synechiae (adhesions), scarring, or detachment of the retina are all possible secondary complications of chronic uveitis.

  • It’s not over when it’s over. Care for cats with uveitis does not end when symptoms end. “Careful follow-up of the patient is important to monitor for the onset of complications such as glaucoma. Recurrences of the anterior uveitis are common in cats, especially in those cats in which an underlying etiology was not detected and treated. Re-examinations every 6-12 months to monitor the intraocular pressure is recommended . . . medications may be discontinued too soon or recommendations for follow-up examinations ignored” [Woerdt]. Medications often need to be gradually tapered and may need to be continued for months after cessation of symptoms [Bentley].
  • ____________________________________________________________________

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