Cmv Retinitis

CMV, or cytomegalovirus Retinitis is a contagious infection associated with a condition known as acquired immunodeficiency syndrome (AIDS) that can result in blindness. Prior to the development of antiretroviral medication, CMV retinitis was more frequent, but it has since been declining in industrialized nations while continuing to be a common problem in developing nations. In addition to patients with AIDS who are immune-compromised for additional causes, patients with this viral retinitis may also experience it. A major eye condition connected with AIDS is CMV retinitis.


Introduction to CMV Retinitis:


The infectious condition known as cytomegalovirus (CMV) retinitis, which can be visually disabling and potentially presage adverse systemic effects, including early mortality, is one that defines acquired immunodeficiency syndrome (AIDS). It is the most frequent clinical manifestation of CMV end-organ disease and, in two-thirds of cases, manifests at first as unilateral disease but develops into bilateral disease in the majority of patients in the absence of treatment or immunological recovery. Both acute viral infection and viral reactivation in the setting of immunocompromise can result in CMV retinitis. AIDS is a typical antecedent; however, CMV retinitis is becoming less common in this situation as highly active antiretroviral therapy (HAART) is introduced.

Other affected patient demographics include those who have had organ transplants and those who take immunosuppressants. Approximately forty percent of people globally are infected with the human cytomegalovirus (HCMV or CMV), a DNA virus in the Herpesviridae family that causes enormous cells with nuclear and intracellular inclusions. Cells in the cytomegalovirus-infected areas develop necrosis, though the inflammation in the retina is not severe. Following the development of holes in regions of healed retinitis (retina may be atrophic), rhegmatogenous retinal detachments may take place. Retinal detachment cases have been associated with proliferative vitreoretinopathy.


Symptoms and Causes:


Cytomegalovirus, a virus with double-stranded DNA and belonging to the herpes viridae family, is what causes CMV retinitis. Prior to the AIDS crisis, it was relatively uncommon but is now frequently linked to HIV/AIDS. It is also linked to autoimmune diseases that need immunomodulators and chemotherapy-induced severe immunosuppression. The prevalence of CMV retinitis has dropped by 90% in the AIDS population after the introduction of antiretroviral treatments.

HIV, a CD4 count below 50, and significant systemic immunosuppression are risk factors. Additionally, recent studies have shown that local ocular immunosuppression can increase the chance of developing CMV Retinitis. In the absence of immunosuppression, CMV retinitis has also been documented in case reports. Infected cells have enormous eosinophilic intracellular cytomegalic aggregates that are characteristic of the infection. Using electron microscopy, the characteristic virus particles within the infected cells may be observed. Full-thickness retinal necrosis is visible on histopathology, and this condition is gradually replaced by atrophic tissue that has scarring, coagulative vascular inflammation, and choroiditis.

The majority of individuals with CMV retinitis experience a gradual, asymptomatic onset that starts with temporary visual obscurations (also known as “floaters”), visual indistinctness, and haze and progresses to regional scotoma and, in some cases, total blindness. These are some of the warning manifestations of CMV retinitis:

  • Many patients present without symptoms at first.
  • Acute fulminant hemorrhage retinal whitening and edema
  • Sclerosis and attenuation of the retinal vessels
  • Perivenular retinal opacification, often known as “frosted branch” angiitis
  • symptoms that are persistent
  • Photopsias (or “flashing lights”)
  • “Floaters” are brief, moving obstructions and opacities in both the middle and periphery of the visual field.
  • (“blind spots”) Scotoma
  • (Uncommon) Pain and Photophobia




Ophthalmoscopy screening is used to identify CMV retinitis. Ophthalmoscopy and pupil dilation will reveal CMV retinitis symptoms. Blood or urine tests that check for chemicals specific to the infection can be used to diagnose a CMV infection. Even though a blood or urine test came back negative, an infection may still be present. Blood and urine testing for CMV may come back negative; however, it can harm particular organs like the GI tract or retina. The presence of CMV virus particles can be found through tissue biopsy, but only in certain organs (the GI Tract) and not in others (the eyes).

A medical examination reveals yellow-white in color retinal lesions that frequently begin in the periphery and travel centripetally along the vasculature. It can, however, begin in the back portion. Retinal hemorrhages with a white, granular texture to the retina are the characteristic symptoms. The margins of each lesion are where activity is highest. Due to the substantial immunosuppression that most patients experience, vitreous inflammatory symptoms may be mild.


Treatment for CMV Retinitis:


Treatment aims to stop CMV retinitis from multiplying, stabilize or restore eyesight, and halt blindness from occurring. Frequently, long-term treatment is required. Medicines can be administered orally, intravenously, or intravitreously, which is an injection straight into the eye. Oral valganciclovir, intravenous ganciclovir, intravenous foscarnet, and intravenous cidofovir are all effective treatments for CMV retinitis. Treatment options include oral valganciclovir in addition to intravitreal injections of foscarnet, which are injections of medication into the vitreous close to the retina.

Surgery is frequently required in CMV patients for intravitreal ganciclovir injection or retinal detachment. Up to 29% of damaged eyes develop retinal detachment, and endo-laser and silicone oil endo-tamponade are the most successful treatments. A benefit of an intravitreal ganciclovir implant is less systemic toxicity. Retinal detachment (and vitreous hemorrhage) are side effects of this, and viral organ disease has no systemic positive effects.

Immune recovery uveitis (IRU), the most severe side effect of treatment for CMV, is another side effect in addition to those brought on by the medications mentioned above. It is assumed that responses to CMV antigens generate anterior or intermediate uveitis as CD4 counts increase with HAART. IRU may also result in epiretinal membranes and cystoid macular edema. Additionally, possible side effects include posterior capsular cataracts, proliferative vitreoretinopathy, and optic nerve neovascularization. In addition, HAART therapy has the potential to either promote the deterioration of pre-existing CMV retinitis (paradoxical CMV-IRR) or reveal CMV retinitis in patients who have never had CMV illness.

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