AEGiS-GMHC: CMV ABCs Gay Men's Health CrisisImportant note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.
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CMV ABCs

Treatment Issues, Vol 11, No. 4/5; April 1997
Jill Cadman


CMV (cytomegalovirus) is a prevalent virus from the herpes family which can cause opportunistic infections in immune-compromised persons. It is estimated by the Centers for Disease Control (CDC) that one-third of all Americans are infected with CMV. The virus is transmitted through body fluids or transfusions. It is common for infected people to show no symptoms while CMV is inactive. There is a CMV antibody test commercially available for those wishing to know if they are infected. The risk of developing active CMV disease increases in persons with AIDS as CD4 counts decrease. Those with CD4 counts below 100 are at greatest risk and should begin ophthalmologic screenings for CMV retinitis. As CD4 cells drop below 50, screening should become more frequent. Screenings should continue even if CD4 cell counts increase due to antiviral therapy.

CMV is a systemic infection that can cause disease in many parts of the body in addition to the eye, including the brain, colon, esophagus and other organs. The most common manifestation is CMV retinitis, which causes lesions on the retina. Severity depends on the location of the lesion. Zone 1 disease causes damage in the highly sensitive central retina (the macula) and is most sight-threatening. Zone 2 includes the periphery of the retina.

Infection there is less dangerous to vision, although it may spread to the central retina. CMV retinitis is frequently associated with CMV encephalitis, a severe brain disorder with multiple neurological complications (see Treatment Issues article Responding to CMV Neurologic Infections , November 1996, pages 5-10).

Treatment for CMV retinitis is given in two phases. An initial induction therapy consists of twice a day intravenous ganciclovir or foscarnet (or once weekly cidofovir) administered for two to three weeks. The purpose of induction therapy is to halt disease progression and prevent blindness. Induction is followed by maintenance therapy which consists of daily ganciclovir or foscarnet infusions, biweekly cidofovor infusions, or other treatments (see Ganciclovir Implants: One Year Later) to prevent or delay reactivation of viral replication. It is difficult to completely suppress CMV, and if there is a reactivation, the patient will need "reinduction" via intravenous infusions.

Systemic medication can also be used as prophylaxis for persons with low CD4 counts who have never developed active CMV disease. There are indications that the choice of such therapy depends on a patient's CMV viral load. Those with very high plasma CMV burdens (over 50,000) may require preemptive intravenous (high dose) therapy, even when there is no evidence of active disease, while those with low CMV viral loads (below 50,000) may receive satisfactory results from a course of daily oral ganciclovir. (See Treatment Issues article Opportunistic Infections In Vancouver, September 1996, page 4).

Retinal detachment is a frequent complication of CMV infection. It occurs when a hole in the retina allows ocular fluid to seep behind, causing the retina to separate from the back of the eye (the choroid). The first symptom is often the appearance of small moving spots known as floaters. Surgery may be necessary to repair the hole and reattach the retina. The injection of silicone oil may also be used in the treatment of retinal detachments. Whatever the treatment, some loss of visual acuity can result.


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