Cytomegalovirus (CMV, or human herpesvirus 5) is another ubiquitous virus with worldwide distribution. It is, like the other members of the herpesvirus family, capable of causing a primary illness and then existing in a latent state in the human host indefinitely with the ability to reactivate at a later time. It is present in approximately 1

percent of newborns and in 40 to 100 percent of adults, depending on geographic location, socioeconomic status, attendance at day care, and sexual behavior. There are two peaks of seroconversion, the first in the perinatal period and the second during young adulthood, presumably related to sexually activity. CMV is not easily spread by casual contact, but requires repeated or prolonged intimate contact for transmission. It is found in milk, saliva, urine, semen, and cervical secretions. CMV is also transmitted via blood transfusions containing viable leukocytes or via solid organs or bone marrow during transplantation.

CMV is one of the TORCH agents [ toxoplasmosis, other (viruses), rubella, CMV, and herpes (simplex viruses)] and is capable of causing intrauterine infection. Fewer than 25 percent of neonates with intrauterine CMV will display symptoms. Those at highest risk are those whose mother acquires primary disease during the first half of the pregnancy. A seropositive mother's antibodies to CMV appear to provide the fetus some protection. Classic intrauterine CMV (congenital cytomegalic inclusion disease) involves multiple organs, including jaundice, hepatosplenomegaly, microcephaly, petechiae, and inner ear problems, as well as CNS defects. Children who are asymptomatic at birth may still have hearing loss that results in lower IQ scores and learning disabilities later in life.

In contrast to intrauterine infection, perinatal infection (presumably acquired from the cervix of the mother during birth or from breast milk) is usually asymptomatic and has no long-term consequences.

In healthy immunocompetent children and adults, CMV infection is also usually asymptomatic. When CMV does cause disease in this setting, it is typically an illness resembling EBV infectious mononucleosis. Typical presenting complaints include fever, chills, myalgia, and headache. Clinical features include a prolonged fever (1 to 5 weeks), an atypical lymphocytosis, lymphadenopathy, splenomegaly, and mild elevations of the liver transaminase levels. Pharyngitis and tonsillitis are not usually present. There are rarely complications or long-term health consequences. The diagnosis of CMV mononucleosis should be considered in individuals who have a mononucleosis-type illness but are heterophil-antibody negative. The complications of CMV in immunocompetent patients include the Guillain-Barre syndrome, viral pneumonitis, hepatitis, hemolytic anemia, and thrombocytopenia.

In patients with HIV, CMV can cause illness with significant morbidity. Symptomatic infections generally do not occur in patients who are simply HIV positive, but in those with more advanced disease, such as ARC (AIDS-related complex) or AIDS. The most common illness is CMV retinitis, which occurs in more than 10 percent of AIDS patients. Typical complaints are of floaters or of decreased vision. Careful funduscopic examination may reveal characteristic retinal hemorrhages and exudates. Progression to blindness will occur without chronic suppressive therapy with IV ganciclovir or foscarnet. CMV may cause gastrointestinal disease as either an esophagitis or as a colitis. Additionally, CMV can cause an adrenalitis resulting in adrenal insufficiency.

CMV causes significant morbidity and mortality in transplant patients. It can infect numerous different organs, causing colitis, hepatitis, pneumonia, and CNS disease. The most serious infection is CMV pneumonia, which is most common in recipients of bone marrow transplants. The CMV seen in transplant patients may represent primary infection after exposure from the transplanted tissue itself or in transfused blood products, or reactivation of latent infection. The primary infections tend to be more severe. CMV infections occur 4 to 8 weeks after transplant typically, and CMV should be included in the differential diagnosis for patients presenting with a febrile illness within the first 3 months after transplant. CMV may also contribute to rejection of the transplanted organ.

The diagnosis of CMV is difficult because most people are seropositive. The presence of IgM antibodies is helpful, but not very sensitive or specific because of false negatives during some acute infections and their persistence beyond the acute infection in others. To make a definitive diagnosis based on serologies, a conversion from seronegative to seropositive or an acute rise in antibody titer should be seen, and this will require samples from before the illness and during the illness. Another method of diagnosis is by viral culture, which, using the "shell" method, takes only 48 h. Children can shed virus in their urine and respiratory secretions for extended periods following infection, but, in healthy adults, virus is not usually shed in the urine or respiratory tract except during acute illness. Healthy adults may shed virus in semen and cervical secretions. In immunocompromised individuals, a biopsy of the organ suspected to be infected with CMV is the preferred method of diagnosis, because of the prevalence of false-positive cultures in immunocompromised patients. Biopsy specimens of infected organs will show characteristic CMV inclusion bodies. In the emergency department, definitive diagnosis is not available, and suspicion of CMV should be based on clinical grounds such as presentation and time from transplant. A review of transplant records may yield clues, such as the recipient's and donor's CMV status prior to transplantation. The disposition of the patient depends on the clinical setting, not on the diagnosis of CMV, and should be discussed with the patient's primary care provider.

CMV is treated with either ganciclovir or foscarnet. Ganciclovir is approved for therapy of CMV retinitis in AIDS patients and for prevention of CMV in transplant patients. It is also used for treating CMV infections in other organ systems. In AIDS-associated CMV retinitis, ganciclovir is given initially at higher doses for 2 to 3 weeks, followed by lifetime suppressive therapy. For other CMV infections, ganciclovir is given for a period of 2 to 3 weeks and then stopped. Foscarnet is used for resistant CMV infections or for patients unable to take ganciclovir. Neither medication cures patients of CMV, but instead they suppress the acute disease process.

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