To the Editor: The appearance of cytomegalovirus (CMV) immunoglobulin (Ig)M antibodies in asymptomatic patients, also known as CMV infection, is prevalent in young immunocompetent hosts but symptomatic CMV disease is uncommon in older adults and in immunocompetent patients.1 An elderly immunocompetent man with two rare clinical presentations of CMV disease is presented: colitis and arterial embolism.
An 83-year-old man underwent right inguinal hernia repair. His medical history included ischemic heart disease, systolic heart failure, diabetes mellitus, hypertension, hypothyroidism, and Parkinson's disease. Despite a history of paroxysmal atrial fibrillation, he took no anticoagulants, and electrocardiogram demonstrated sinus rhythm upon admission. Abdominal pain and diarrhea appeared a few days after the operation. Physical examination revealed a tender right inguinal incision. At that time, blood samples showed 21,400/mL leukocytes (86.8% neutrophils) and normal levels of liver enzymes. Abdominal computed tomography demonstrated a collection of fluid beneath the inguinal incision, thickening of the cecal wall, and a thrombus in the superior mesenteric artery. An acute mesenteric event was excluded using an urgent laparoscopy. The collection of fluid was drained, and methicillin-resistant Staphylococcus aureus grew in cultures taken from the fluid. Accordingly, intravenous vancomycin was started. In the following days, the patient was also treated with subcutaneous enoxaparin (40 mg twice daily), oral metronidazole (1,500 mg/d), and oral ciprofloxacin (1,000 mg/d). Despite this treatment, diarrhea continued. Stool cultures were negative. Stool samples for Clostridium difficile toxin were also negative. A second abdominal computed tomography scan showed significant thickening of the cecal wall and a large, new splenic infarct (Figure 1), probably resulting from an embolism of the earlier-mentioned thrombus. Transesophageal echocardiography was performed, but left atrial thrombus, left ventricle thrombus, and definite vegetation were not seen. Physical examination was not consistent with vascular or immunological phenomena of endocarditis. Several blood cultures were taken while antibiotics were stopped and were negative, making the diagnosis of endocarditis unlikely. Negative serology for Q fever, Bartonella henselae, Brucella, Rickettsia, and Toxoplasma made the diagnosis of culture-negative endocarditis also unlikely. Because diarrhea continued, colonoscopy was performed, and demonstrated an inflamed and ulcerated cecal mucosa with granulation tissue. Large endothelial cells inside this tissue were stained immunohistochemically for CMV. With these findings, blood samples for CMV serology were taken and showed IgM antibodies three times in 3 weeks. CMV IgG antibodies were also demonstrated at the same time in increasing titers (7, 14, and 45 AU/mL, respectively), consistent with acute CMV infection rather than reactivation. CMV antigenemia assays were negative twice, probably because these were taken more than 1 week after presentation. No cause for immunosuppression and no source of CMV were apparent. Blood transfusions had not been administrated during the previous months. Antiviral treatment was considered, but the diarrhea eventually resolved. Blood samples were also taken for antiphospholipid antibodies and showed borderline levels of lupus anticoagulant. After discharge, the patient was taking warfarin and was asked to repeat lupus anticoagulant levels in 3 months to determine whether to continue lifelong anticoagulation therapy.
CMV colitis is typically seen in immunocompromised patients and usually represents viral reactivation.1 CMV colitis is a rare cause of diarrhea in immunocompetent patients, even more so in an elderly immunocompetent man with a new viral infection rather than CMV reactivation and associated arterial embolism. This case bears a resemblance to a previous interesting case of CMV colitis and pulmonary embolism in an elderly immunocompetent woman,2 although this time the thrombus was arterial. CMV was the trigger for thrombosis, because a cardiac source for embolism was excluded and because immobility does not increase the risk for arterial embolism, unlike venous embolism.3 To the best of the authors' knowledge, this is the first case of its kind.
The precise mechanism by which CMV triggers thrombosis is not fully understood. Certain theories suggest that CMV enhances platelet adhesion to infected endothelial cells or increases circulatory levels of factor VIII.4 In this case, it was probably CMV-induced antiphospholipid antibody production that triggered thrombus formation. This phenomenon has been reported in the past in association with CMV.5 Although transient most of the time, it might be associated with permanent antiphospholipid antibody production. Hence, anticoagulation cessation depends on repeating lupus anticoagulant levels a few months later, as recommended.