Retinitis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ilan Dock, B.S.

Retinitis is inflammation of the retina in the eye. The disease may be classified according to the underlying cause for the disease. There are two major categories of underlying causes of retinitis, they are genetic disorders and infectious agents. The underlying cause for the disease may be established based on clinical presentation and manifestation of symptoms.^[1][2]Progression of the disease may be defined by the rate of cellular breakdown of cone and rod cells. Further progression is defined by the degradation of pigment epithelium as well as retinal vessel attenuation and dysfunction of the optic nerve. Infectious diseases may also be responsible as bacterial and viral infections may result in scarring and lesions across the retinal tissue.^[1]

From a historical perspective, there is not much information available for retinitis. Although, biotechnology companies have begun to advance development and research on the topic, as ocular technology further develops.

Retinitis may be classified according to the underlying cause for the disease. There are two major categories of underlying causes of retinitis, they are genetic disorders and infectious agents. The underlying cause for the disease may be established based on clinical presentation and manifestation of symptoms.^[1][2]

Retinitis refers to the inflammation of the retina as a result of either genetic disorders or infectious diseases. Genetic disorders are often a due to an underlying defect in one of the 50 genes that are necessary for the proper creation of photoreceptor proteins. ^[2] Progression may therefore be defined by the rate of the cellular breakdown of cone and rod cells. Further progression is defined by the degradation of pigment epithelium as well as retinal vessel attenuation and dysfunction of the optic nerve. Infectious diseases may also be responsible as bacterial and viral infections may result in scarring and lesions across the retinal tissue.^[1]

Retinitis may be caused by multiple infectious agents including cytomegalovirus, taxoplasmosis, tuberculosis, syphilis, and candida. Retinitis Pigmentosa is classified as a genetic eye disease which occurs as a result of an inherited defect. ^[3]

As retinitis manifests in a variety of clinical forms, differentiation must be established in accordance with the particular subtype. Retinitis caused by genetic defects such as retinitis pigmentosa must be differentiated from other diseases that cause visual acuity, cone-rod dystrophy, night blindness, and vision loss. Infectious agents that cause retinitis must be differentiated from other ocular diseases that may cause lesions and retinal scarring.

The prevalence of retinitis pigmentosa is approximately one case per every 2500 to 7000 people. ^[4] Incidence has not drastically changed over the course of the past decade. However, the risk of contracting cytomegalovirus based retinitis within HIV patients has drastically been reduced with the introduction of HAART treatment.^[5] There is no specific race or ethnicity associated with infection, nor is it gender based. Diagnosis usually occurs during a patients childhood or early adulthood.

Multiple risk factors are associated with the potential manifestation of retinitis. The most common risk factor responsible for the manifestation of retinitis is linked to a variety of unmitigated, rare genetic disorders that are vertically inherited from parents to offspring. ^[2] Other mitigated risk factors include infectious agents such as cytomegalovirus, taxoplasmosis, tuberculosis, and candida. Cytomegalovirus remains the number one risk factor for developing a progressive form of retinitis within HIV infected patients.

If left untreated, patients with retinitis may progress to develop limited vision, night blindness, and blindness. Common complications may vary according to the underlying cause of the disease. Retinal genetic disorders, such as retinitis pigmentosa, will often lead to highly restricted tunnel-like vision. Retinitis as a result of an infectious agent may imply far more serious complications including respiratory or central nervous system infections. The prognosis is usually good for individuals with retinitis resulting form an infectious agent. Most often the symptoms and complications will subside with proper treatment. Certain infections, such as tuberculosis and cytomegalovirus, require closer attention during and after treatment. Retinal genetic disorders, unfortunately, lack treatment. Thus individuals suffering from retinal genetic disorders, such as retinitis pigmentosa, will most likely experience mild to severe vision loss.

The hallmark of retinitis is overall vision loss. A positive history of disturbances in color perception and night blindness is suggestive of retinitis. Other symptoms of retinitis include the loss of peripheral vision and cone-rod dystrophy. ^[2] Infectious diseases may cause retinal hemorrhaging or retinal tissue lesions.

Physical signs associated with retinitis will vary according to the underlying condition responsible for the disease. Genetic defects will result in a genetic disorder known as Retinitis pigmentosa. The presentation of this disorder is primarily visible in the degradation of cone and rod cells.^[3] Infectious agents will present physical manifestations according to the underlying cause of infection. These clinical manifestations will range for yellowish infiltrates to inflammation and lesions localized to specific areas of the eye.^[1]

Due to the variability of causes associated with retinitis, there are a variety of tests available to diagnose the underlying cause. Genetic defects such as retinitis pigmentosa is primarily diagnosed with an electroretinogram.^[3] Other underlying causes may be distinguished using a variety of testing procedures. These procedures are usually directly associated with the hypothesized condition causing retinitis. Many of the underlying conditions may range from fungal to bacterial and thus are tested accordingly.^[1]

The optical coherence tomography (OCT) and the fundus autofluorescence (FAF) techniques are most often used when diagnosing a genetic variation of retinitis. OCT may be used to acquire in situ retinal imaging for diagnosis of ocular diseases. FAF imaging is a non-invasive technique, dependent on the presence of lipofuscin pigments (lipofuscin is a by-product of lysosomes during the normal process of photoreceptor degradation.)^[6]

Other diagnostic studies include intraocular fluid analysis, blood tests, and cerebrospinal fluid testing.^[7]

There is no single medical therapy to treat all types of retinitis. Due to the many underlying causes of retinitis, treatment is administered directly according to the underlying cause. These treatments will vary from vitamin therapy and preventative strategies to a long list of potential antimicrobial therapies.

Surgical intervention is not recommended for the management of retinitis. Cataract surgery has been hypothesized to produce positive results within populations suffering from retinitis pigmentosa. However no studies have proven this method to be significantly effective.^[8]

There are no primary preventive measures available for retinitis that results from the genetic disorder, retinitis pigmentosa.^[9] However, retinitis that results from cytomegalovirus may be prevented through upholding specific preventive strategies for cytomegalovirus. These strategies include avoiding the bodily fluids and items that might come in contact with infected individuals. Furthermore, similar strategies and precautions may be taken in order to prevent fungal, bacterial, and parasitic infections that could potentially result in retinitis.^{[10][11] [12] [13]}

Secondary prevention strategies following retinitis depend on the underlying cause of the infection. Severity of genetic disorders may be lessened through vitamin therapy and reduced sunlight exposure.^[14] Meanwhile, prophylactic treatment may be prescribed to stunt the progression of viral, bacterial, fungal, and parasitic variations of retinitis.^{[11] [10] [12][13]}

Future and investigational therapies for retinitis include retinal prosthesis, bionic eyes, artificial vision, and retinal chips. A recently released apparatus, called Argus II, consists of a camera placed along a patients glasses’ frame. The camera then sends information to a processing unit which is transferred to a microchip implanted in a patient’s eye. Other therapies are focused on photoreceptor transplantation or activation of the induction of light sensitivity to retinal cells.^[15]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Jyostna Chouturi, M.B.B.S [2]; Ilan Dock, B.S.

From a historical perspective, there is not much information available for retinitis. Although, biotechnology companies have begun to advance development and research on the topic, as ocular technology further develops.

• 2006: Stem cells: UK Researchers working with mice, transplanted mouse stem cells into mice that had been genetically induced to mimic the human conditions of retinitis pigmentosa and age-related macular degeneration.
  • These photoreceptors developed and made the necessary neural connections to the animal’s retinal nerve cells, a key step in the restoration of sight. Previously it was believed that the mature retina has no regenerative ability. This research may in the future lead to using transplants in humans to relieve blindness.^[1]

• 2008: Scientists at the Osaka Bioscience Institute have identified a protein, named Pikachurin, which they believe could lead to a treatment for retinitis pigmentosa.^[2][3]
• 2008: Retinitis pigmentosa was attempted to be linked to gene expression of FAM46A^[4]
• 2010: A possible gene therapy seems to work in mice.^[5]
• 2012: Scientists at the Columbia University Medical Center showed on an animal model that gene therapy and induced pluripotent stem cell therapy may be viable options for treating Retinitis Pigmentosa in the future.^[6]
• 2012: Scientists at the University of Miami Bascom Palmer Eye Institute presented data showing protection of photoreceptors in an animal model when eyes were injected with mesencephalic astrocyte-derived neurotrophic factor (MANF).^[7]
• Researchers at the University of California, Berkeley were able to restore vision to blind mice by exploiting a “photoswitch” that activates retinal ganglion cells in animals with damaged rod and cone cells.^[8]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ilan Dock, B.S.; Jyostna Chouturi, M.B.B.S [2]

Retinitis refers to the inflammation of the retina as a result of either a genetic disorder or an infectious disease. Genetic disorders are often due to an underlying defect in one of the 50 genes that are necessary for the proper creation of photoreceptor proteins. ^[1] Progression may therefore be defined by the rate of cellular breakdown of cone and rod cells. Further progression is defined by the degradation of pigment epithelium as well as retinal vessel attenuation and dysfunction of the optic nerve. Infectious diseases may also be responsible for retinitis, as bacterial and viral infections may result in scarring and lesions across the retinal tissue.^[2]

• Retinitis pigmentosa is an umbrella term for multiple genetic, retinal disorders.
• Retinal genetic disorders include; night blindness, visual acuity, a fundus appearance, posterior subscapular cataracts, vitreous particle formation, sector retinitis, and pregnancy based retinitis. ^[3]
• The disease is a result of genetic defects in one of 50 genes required for the proper creation of photoreceptor proteins. ^[4]
• Generally the genetic disorder is linked to the inheritance of a recessive gene contributed by both parents. ^[1]
• Other cases have been linked to the inheritance of a dominant gene, defects of the X chromosome, and newly formed mutations caused by diseases.
• Progression of RP causes photoreceptor, cellular breakdown, of both rod and cone cells.
• Ultimately, the progressive breakdown of photoreceptors leads to restricted vision or permanent loss of vision. ^[1]

• Night blindness results from the loss of rod cell function in the early portion of the clinical course.
• Visual acuity refers to the loss of central acuity. Progression of visual acuity may be used as an indicator for the severity of the disease’s progression.
• Central acuity has been connected to the macular lesions present in the early clinical course of the disease.
• A fundus appearance often refers to the clinical stage.
• Fundus appearance in earlier stages will most often include defective rod cell responses.
• Progression of retinitis will result in the narrowing of the arteriolar portion of the fundus, accompanied by intraretinal pigmentation, and disturbances. These disturbances are often characterized by the degradation of pigments in the pigment epithelium.
• Pigment degradation in the pigment epithelium is an indicator of further degeneration of photoreceptors. This interruption will often manifest in clumping of melanin in odd, coarse configurations.
• Further degradation will result in retinal vessel attenuation and dysfunction of the optic nerve. ^[3]

• Progression of retinitis pigmentosa induces changes in the visual axis of the posterior lens cortex.
• These changes are often described as a yellowish crystalline change, accompanied by colorless, dust-like manifestations.
• Macrophage cells, pigment epithelium, uveal melanocytes, and free melanin pigment granules will mass in the area of dysfunction.
• Other manifestations include pigment epithelial degradation in the form of retinitis punctata albescens and the dysfunction of the optic nerve.
• Severe progression is commonly described as Coats-like disease; a severe case of degradation within the telangiectactic vessels. This particular pathway of progression is commonly attributed to an abnormal amount of lipid deposition in the retina.
• The progression of degradation may be attributed to pathogenic types of CRB1.
• Sector retinitis pigmentosa is often linked to pathogenic variants in the p.Pro 23His of RHO as well as an X-linked variable in heterozygous females.
• These issues will manifest in specific quadrants of the fundus.
• Pregnant women who suffer from retinitis pigmentosa may experience worsened symptoms as physiological changes may occur within the lens and the cornea. ^[3]

• A variety of retinal molecular pathway defects have been matched to multiple known RP gene mutations.
• Mutations in the rhodopsin gene (which is responsible for the majority of autosomal, dominant inherited RP cases) disrupts the process of translating light into decipherable electrical signals within the phototransduction cascade of the central nervous system.
• Defects in the activity of this G-protein-coupled receptor are classified into distinct classes that depend on the specific, abnormal folding and the resulting molecular pathway defects.
• The Class I mutant protein’s activity is compromised as specific point mutations in the protein-coding amino acid sequence affect the pigment protein’s transportation into the outer segment of the eye, where the phototransduction cascade is localized.
• Additionally, the misfolding of Class II rhodopsin gene mutations disrupts the protein’s conjunction with 11-cis-retinal to induce proper chromophore formation.
• Additional mutants in this pigment-encoding gene affect protein stability, disrupt mRNA integrity, and affect the activation rates of the optical proteins, transducin and opsin.^[5]

• Retinitis, caused by cytomegalovirus (CMV), involves the infection of all layers of the retinal tissue.
• Spread of the the infection will occur at approximately 24 nanometers per day.
• Primarily infected areas include the RPE and the subjacent choroid.
• Infection will consist of a vast amount of cellular necrosis across the retina; with the enlargement of infected cells, evidently hosting viral inclusions.
• CMV retinitis, post-treatment, will commonly persist on the previously scarred, retinal tissue.
• Progression of infection may result in the development of small holes across previously scarred and healed tissue.
• Formation of these tiny holes may result in rhegmatogenous, retinal detachments. ^[6]

• Retinitis resulting from a syphilitic infection is commonly referred to as a ocular syphilis.
• The infection persists as syphilitic spirochetes, Treponema pallidum, that invade or cause allergic reactions within the surrounding tissue.^[2]

• Two types of retinal infections may occur depending on a mode of fungal infection. These two types our outlined as endogenous or exogenous.
• Endogenous fungal retinitis is primarily a result of a disseminated fungal infection.
• Exogenous fungal infections primarily occur as a result of a recently traumatic event such as physical injury or surgery.
• Exogenous fungal infections are usually a result of Candidal retinitis. An infection commonly associated with candida chorioretinitis.
• Candidas chorioretinitis is typically caused by the species Candida albicans.^[2]

• Extrapulmonary clinical manifestations of tuberculosis include intraocular caseating granulomas.
• Infection of the retina is associated with the spread of the tuberculosis causing bacterial agents.
• Common presentation of tuberculosis in the retina appears as multiple choroidal tubercles.
• These tubercles are best defined as minor nodules with a grayish appearance.^[2]

• Toxoplasma gondii is a parasitic agent found in contaminated meat and egg products.
• Persistence occurs within the vacuoles of cells found within tissues throughout the host.
• Rupturing of tissue cysts within host cells may lead to progression of the disease, ultimately resulting in retinitis. This occurrence is mostly common within individuals who were previously immuno-compromised.^[2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ilan Dock, B.S.;Jyostna Chouturi, M.B.B.S [2]

Retinitis may be caused by multiple infectious agents including cytomegalovirus, toxoplasmosis, tuberculosis, syphilis, and candida. Retinitis Pigmentosa is classified as a genetically predisposed eye disease which occurs as a result of an inherited genetic defect. ^[1]

• Retinitis Pigmentosa is classified as a genetically inherited eye disease, inherited from either one or both of a patient’s parents. ^[2]
• The disease is a result of genetic defects in one of 50 genes required for the proper creation of photoreceptor proteins. ^[1]
• Generally the genetic disorder is linked to the inheritance of a recessive gene contributed by both parents. ^[2]
• Other cases have been linked to the inheritance of a dominant gene, defects of the X chromosome, and newly formed mutations caused by diseases.
• Progression of RP causes photoreceptor, cellular breakdown, of both rods and cones.
• Ultimately, the progressive breakdown of photoreceptors leads to restricted vision or permanent loss of vision. ^[2]

• Retinitis pigmentosa (RP) is one of the most common forms of inherited retinal degeneration.^[3]

• There are multiple genes that, when mutated, can cause the retinitis pigmentosa phenotype.^[4]
• Inheritance patterns of RP have been identified as autosomal dominant, autosomal recessive, X-linked, and maternally (mitochondrially) acquired, and are dependent on the specific RP gene mutations present in the parental generation.^[5]

• The rhodopsin gene encodes a principal protein of photoreceptor outer segments.
• Mutations in this gene most commonly present as missense mutations or improper folding of the rhodopsin protein, and most frequently follow autosomal dominant inheritance patterns.
• Since the discovery of the rhodopsin gene, more than 100 RHO mutations have been identified, accounting for 15% of all types of retinal degeneration, and approximately 25% of autosomal dominant forms of RP.^[3][6]
• Up to 150 mutations have been reported to date in the opsin gene associated with the RP.
• These mutations are found throughout the opsin gene and are distributed along the three domains of the protein (the intradiscal, transmembrane, and cytoplasmic domains).
• Two of the main biochemical causes of RP, in the case of rhodopsin mutations, are improper protein folding and the disruption of molecular chaperones.^[7]
• It was found that the mutation of codon 23 in the rhodopsin gene, in which proline is changed to histidine, accounts for the largest fraction of rhodopsin mutations in the United States.
• Several other studies have reported various codon mutations associated with Retinitis Pigmentosa, including Thr58Arg, Pro347Leu, Pro347Ser, as well as deletion of Ile-255.^{[6][8][9][10][11]}
• In 2000, a rare mutation in codon 23, in which proline changed to alanine, was reported . The mutation resulted in an autosomal dominant form of retinitis pigmentosa. However, this study showed that the retinal dystrophy associated with this mutation was characteristically mild in clinical presentation as well as progression. Furthermore, there was greater preservation in electroretinography amplitudes than the more prevalent Pro23His mutation.^[12]

• Autosomal recessive inheritance patterns of RP have been identified in at least 45 genes.^[5]
• This means that two unaffected individuals who are carriers of the same RP-inducing gene mutation, in a diallelic form, can produce offspring with the RP phenotype.
• A mutation on the USH2A gene is known to cause 10-15% of a form of RP known as Usher’s Syndrome, when inherited in an autosomal recessive fashion.^[13]

• Mutations in four pre-mRNA splicing factors are known to cause autosomal dominant retinitis pigmentosa.
• These are PRPF3 (human PRPF3 is HPRPF3; also PRP3), PRPF8, PRPF31 and PAP1.
• The above factors are ubiquitously expressed.
• Defects in a ubiquitous factor (a protein expressed everywhere) usually cause disease in the retina due to the retinal photoreceptor cells far greater requirement for protein processing (rhodopsin) than any other cell type.^[14]

• The somatic, or X-linked inheritance patterns of RP are currently identified with the mutations of six genes, the most common occurring at specific loci in the RPGR and RP2 genes.^[13]

• Genetic defects and their associated retinitis pigmentosa subtypes are listed in the table below:

• Cytomegalovirus retinitis is a result of a viral, herpes infection of the retina.
• Highly prevalent as a cause of blindness within the AIDS infected population.^[15]

• Retinitis resulting from a syphilitic infection is commonly referred to as a ocular syphilis.
• The infection persists as syphilitic spirochetes, Treponema pallidum, invade or cause allergic reactions within the surrounding tissue.^[15]

• Two types of retina infections may occur depending on the mode of fungal infection. These two types our outlined as endogenous or exogenous.
• Endogenous fungal retinitis is primarily a result of a disseminated fungal infection.
• Exogenous fungal infections primarily occur as a result of a recent event such as physical injury or surgery.
• Exogenous fungal infections are usually a result of Candidal retinitis. An infection commonly associated with candida chorioretinitis.
• Candidas chorioretinitis is typically caused by the species Candida albicans.^[15]

• Extrapulmonary clinical manifestations of tuberculosis include intraocular, caseating granulomas.
• Infection of the retina is associated with the spread of the tuberculosis causing bacterial agents.
• Common presentation of tuberculosis in the retina appears as multiple choroidal tubercles.
• These tubercles are best defined as minor nodules with a grayish appearance.^[15]

• Toxoplasma gondii is a parasitic agent found in contaminated meat and egg products.
• Persistence occurs within the vacuoles of cells found within tissues throughout the host.
• Rupturing of tissue cysts within host cells may lead to the progression of the disease, ultimately resulting in retinitis. This occurrence is mostly common within individuals who were previously immuno-compromised.^[15]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ilan Dock, B.S.

As retinitis manifests in a variety of clinical forms, differentiation must be established in accordance with the particular subtype. Retinitis caused by genetic defects such as retinitis pigmentosa must be differentiated from other diseases that cause visual acuity, cone-rod dystrophy, night blindness, and vision loss. Infectious agents that cause retinitis must be differentiated from other ocular diseases that may cause lesions and retinal scarring.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ilan Dock, B.S.

The prevalence of retinitis pigmentosa is approximately one case per every 2500 to 7000 people. ^[1] Incidence has not drastically changed over the course of the past decade. However, the risk of contracting cytomegalovirus based retinitis within HIV patients has drastically been reduced with the introduction of HAART treatment.^[2] There is no specific race or ethnicity associated with infection, nor is it gender based. Diagnosis usually occurs during a patients childhood or early adulthood.

• Clinically diagnosed cases of retinitis pigmentosa occur at an approximate rate of one case per every 2500 to 7000 people. ^[1]
• CMV affects nearly 20 percent of patients suffering from an HIV infection.
• 50,000-100,000 patients are currently diagnosed with retintis pigmentosa. ^[2]
• Individuals suffering from infection resulting form infectious agents that may cause retintis, will rarely show an progression of retinitis.

• Retinitis is commonly diagnosed within the population of young children and patients in their early adulthood.

• There is no clear disparity between male and female populations affected by retinitis pigmentosa.
• On average men with X-linked retinitis pigmentosa suffer from the worst prognosis.

• There is no ethnic or racial specificity associated with the development of retinitis. ^[3]

• Nearly 50,000 to 100,000 patients are diagnosed with retintis pigmentosa in the United States.
• Retinitis, as a result of an infectious agent, is very rare among patients in Western countries.
• Prior to HAART therapy, nearly one-third of individuals suffering from an HIV infection progressed towards developing a form of retinitis.
• Twenty percent of individuals suffering from HIV in developed countries, where HAART and anti-CMV treatment is available, will develop CMV based retinitis. ^[2]

• A total of 5 to 25 percent of HIV diagnosed patients in developing countries suffer from cytomegalovirus induced retinits.
• There is a high mortality rate associated with infectious agents that cause retinitis in developing countries. Therefore many patients in developing countries, suffering from the aforementioned diseases, may perish prior to the progression of retinitis. ^[2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ilan Dock, B.S.

Multiple risk factors are associated with the potential manifestation of retinitis. The most common risk factor responsible for the manifestation of retinitis is linked to a variety of unmitigated, rare genetic disorders that are vertically inherited from parents to offspring. ^[1] Other mitigated risk factors include infectious agents such as cytomegalovirus, taxoplasmosis, tuberculosis, and candida. Cytomegalovirus remains the number one risk factor for developing a progressive form of retinitis within HIV infected patients.

• Inherited genetic disorders, either autosomal dominant, autosomal recessive, or X-linked. ^[1]
• Infectious agents may cause result in retinitis.
• Diseases that may result in retinitis include, cytomegalovirus, tuberculosis, taxoplasmosis, and candida.^[2]
• Cytomegalovirus (CMV) is the number one recognized condition responsible for causing retinitis within HIV infected populations. ^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ilan Dock, B.S.Jyostna Chouturi, M.B.B.S [2]

If left untreated, patients with retinitis may progress to develop limited vision, night blindness, and blindness. Common complications may vary according to the underlying cause of the disease. Retinal genetic disorders, such as retinitis pigmentosa, will often lead to highly restricted tunnel-like vision. Retinitis as a result of an infectious agent may imply far more serious complications including respiratory or central nervous system infections. The prognosis is usually good for individuals with retinitis resulting form an infectious agent. Most often the symptoms and complication will subside with proper treatment. Certain infections such as tuberculosis and cytomegalovirus require closer attention during and after treatment. Retinal genetic disorders, unfortunately, lack treatment. Thus individuals suffering from retinal genetic disorders, such as retinitis pigmentosa, will most likely experience mild to severe vision loss.

• Retinitis pigmentosa progresses slowly and with much variation.
• There is no way of predicting the exact progression of vision loss with retinitis pigmentosa. However, future severity of the disease may be quantified by the severity of present symptoms.

• Often begins with floaters, progresses into tunnel vision and restriction of the patient’s visual fields.

• As the disease progresses, patient’s will suffer from very small visual fields, due to tunnel vision.
• Patients rarely become fully blind. Legal blindness is usually a result of highly restricted vision or, uncommonly, blurred vision.

• Depending on the infectious agent, retinitis will most often occur in later stages of infection.
• For many of these infections, retinitis is considered a potential complication, rather than the primary area of infection.
• Disease progression in the retinal tissue will begin with lesions, necrotizing granulomas, or infiltrates. Followed by a period of scarring, blindness, or retinal detachment.

• Night blindness or nyctalopia
• Tunnel vision (due to loss of peripheral vision)
• Latticework vision
• Photopsia (blinking/shimmering lights)
• Photophobia (Aversion to glare)
• Development of bone spicules in the fundus
• Slow adjustment from dark to light environments and vice versa
• Blurred vision
• Poor color separation
• Loss of central vision
• Eventual blindness

• Retinitis is often an ocular complication associated with the progression of a disease.
• Possible general complications would include retinal detachment, scarring of the retinal tissue, and potential blindness.
• In the case of tuberculosis, necrotizing granulomas may cause permanent damage to retinal tissue.
• An ocular fungal infection is often a sign of potential complications in the respiratory tract.
• Ocular cytomegalovirus may be an indicator of a CNS-based cytomegalovirus infection.

• The progressive nature and lack of a definitive cure for retinitis pigmentosa contributes to the discouraging outlook for patients with this disease.
• While complete blindness is rare,^[1] the patient’s visual acuity and visual field will continue to decline as initial rod cell photoreceptors and later cone cell photoreceptors degrade.
• While the psychological prognosis can be slightly alleviated with active counseling,^[2] the physical implications and progression of the disease depend largely on the age of initial symptom manifestation and the rate of photoreceptor degradation.

• The prognosis for a retinitis infection caused by an infectious agent can vary depending on the amount of progression of the infection as well as the infection itself.
• Patients suffering from an HIV infection are at risk of retinal detachment when suffering from an ocular cytomegalovirus infection.
• Proper treatment may reduce the symptoms of an ocular CMV infection, however uveitis and chronic inflammation may persist after initial treatment.
• A poor prognosis for a patient with CMV retinitis is often a combination of a compromised immune-system and improper, poorly bioavailable therapy that results in a potential drug resistance.
• The prognosis for toxoplasmosis is usually good in immuno-competent patients.
• A poor prognosis may result from macular involvement in a toxoplasmosis infection of the retina.
• A tuberculosis infection of the retina tends to have a good prognosis.
• Proper treatment of tuberculosis will often lead to a full recovery, yet must be monitored over the course of treatment.
• A poor prognosis is usually the result of multi-drug-resistant tuberculosis.
• The prognosis for ocular syphilis depends on the progression of the disease.
• Since ocular syphilis is usually paired with neurosyphilis, the prognosis can be poor. However with proper, early, and effective treatment, a patient may experience a visual expansion as well as improvements with visual acuity.

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