Introduction
Background
Cytomegalovirus (CMV) is a member of the Herpesviridae family, along with herpes simplex viruses 1 and 2, Epstein-Barr virus, and varicella-zoster virus. It is a double-stranded DNA virus with a protein coat and lipoprotein envelope. Similar to other herpesviruses, CMV is icosahedral and replicates in the host's nucleus. Like the other members of this family, CMV has the ability to produce a latent infection. Replication in the host cell is typically represented by large intranuclear inclusion bodies and smaller cytoplasmic inclusions. The virus preferentially grows in fibroblast cells in tissue culture and has been replicated in numerous other cell types.
Studies have shown that 50-80% of the world's population is seropositive for CMV. With the advent of immunosuppressive medications and the rise of HIV infection and AIDS in the early 1980s, a new class of CMV infection has been described. CMV retinitis, adrenalitis, pneumonitis, colitis, and esophagitis are some of the infections observed in immunocompromised hosts. CMV is the third most common pathogen in patients with AIDS, superseded by Pneumocystis carinii and Candida.
CMV GI disease in adults was described in the 1960s. CMV colitis is the second most common CMV infection in patients with AIDS (after retinitis) and was first described in 1983. Of patients with AIDS who have GI infection caused by CMV, 67% had involvement of the colon. CMV colitis is uncommon in patients who are not severely immunocompromised with only 44 cases described in the literature. GI tract involvement may occur either alone or in the setting of disseminated disease.
CMV may complicate steroid-dependent ulcerative colitis (UC), further complicating both disease processes. Patients with steroid-dependent UC who present with refractory disease should be evaluated for CMV infection. Up to 59% of patients with steroid-refractory UC have been shown to also have CMV colitis. The prognosis for patients with UC complicated by CMV infection is worse than that for patients with UC alone.
Pathophysiology
CMV has 3 major patterns of infection.
The first is primary infection, in which the patient has never been exposed to the pathogen but becomes infected by a patient who is seropositive for the virus (60%). Primary infection in immunocompetent hosts causes few or no symptoms. After the initial infection, the genome of the virus persists in the host.
The second, reactivation, occurs in a patient who is seropositive with a latent virus that becomes reactivated if the host's immune system becomes compromised (10-20%).
The third, superinfection, occurs when a patient who is CMV-seropositive receives latently infected cells from another patient who is seropositive. The resulting CMV infection is from the latent donor cells, not from the recipient cells (20-40%).
Once a patient becomes infected, CMV can persist indefinitely in the host tissues. If the host's T-cell response becomes compromised by disease or iatrogenic processes, latent virus can reactivate and cause a variety of syndromes. When the colon becomes affected, ulcerative changes can be seen. As the body mounts an inflammatory response, watery diarrhea may begin to develop. As ulcers increase in depth, erosion into blood vessels can cause profuse bloody diarrhea. Over time, inflammatory polyps may develop, which, rarely, may obstruct the colon. Severe inflammation and vasculitis may lead to ischemia and transmural necrosis of the bowel, resulting in perforation and peritonitis.
Frequency
United States
CMV colitis is rare in immunocompetent patients. It occurs in 2-16% of patients who have received solid organ transplants and in 3-5% of patients with HIV infection or AIDS. A recent study documented CMV infection in 27.3% of patients with steroid-refractory UC and 9.1% of patients with nonrefractory colitis.
Mortality/Morbidity
- Since the introduction of effective antiviral agents, morbidity and mortality have been reduced.
Race
- No racial predilection has been documented.
Sex
- No sexual predilection is recognized.
Age
- Reports of patients who are not immunocompromised contracting CMV colitis indicate that the illness tends to occur in patients older than 70 years. Otherwise, no age predilection is documented for CMV colitis in immunocompromised patients.
- Newborns infected with HIV have contracted CMV colitis.
Clinical
History
Patients may present with the following symptoms:
- Fever
- Anorexia
- Malaise
- Weight loss
- Dehydration
- Abdominal pain
- Abdominal distention
- Nausea
- Vomiting
- Chronic watery diarrhea
- Bloody diarrhea
- Constipation
- Worsening symptoms of inflammatory bowel disease
Physical
Patients with CMV colitis may exhibit a wide range of abdominal findings depending on the stage of their disease.
- Abdominal signs are not present early in the disease.
- Tenderness may develop in the descending and sigmoid colon as the bowel becomes more involved.
- Peritoneal signs and fever may be present. If the bowel becomes ischemic or perforates, stigmata of an acute abdomen may develop.
Causes
Any factor that causes a decrease in a patient's immunity increases the risk for CMV colitis.
- Adults older than 70 years, especially if nutritionally depleted
- HIV infection and AIDS
- High- and low-dose steroid therapy and therapy with other immunosuppressive medications
- Transplantation patients (especially patients receiving CMV-positive organs)
- Hemodialysis
- Neoplasia
- Inflammatory bowel disease
- Alcoholism
- Collagen-vascular disease (seems to be related to immunosuppressive therapy)
- Blood transfusions
- Malnutrition
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Further Reading
Keywords
CMV, CMV infection, Herpesviridae, herpesvirus, herpes simplex virus, HSV, Epstein-Barr virus, varicella-zoster virus, HIV, AIDS, CMV colitis, CMV gastrointestinal disease, CMV GI disease, HIV disease complications, bloody diarrhea, watery diarrhea, AIDS complications, CMV ulcerative colitis, cytomegalovirus ulcerative colitis, cytomegalovirus UC, steroid-dependent ulcerative colitis, cytomegalovirus infection, cytomegalovirus
