Case Presentation: A 56-year-old man with a history of ulcerative colitis (UC), treated with Adalimumab, returned from a 10-day cruise to Puerto Rico. He presented with 5-days of fever, chills, fatigue, anorexia and multiple loose stools daily. On presentation, he was ill-appearing, febrile (T = 102.8oF) and tachycardic (HR = 124 bpm). RR = 16 bpm; BP = 122/89 mm Hg. His abdomen was specifically non-tender. Laboratory results included: WBC = 4.7 109/L (19% bandemia), hemoglobin = 16 g/dL, platelets = 117 109/L, AST = 227 IU/L, and ALT = 137 IU/L. CT abdomen/pelvis revealed wall thickening of the transverse colon, descending colon, and rectum consistent with UC. GI multiplex was negative. He was admitted to the hospital with intravenous broad-spectrum antibiotics for acute colitis. Blood cultures and stool tests for ova/parasites were negative. On day 5, antibiotics were discontinued; budesonide was started. He continued to have fevers (up to 103oF), nausea, hematochezia, anorexia, poor oral intake, and worsening hepatic transaminitis. Malaria, EBV, HIV, Dengue, Q fever, Bartonella, Ehrlichia, Chikungunya, Syphilis, RMSF, and Lyme studies were negative. MRCP showed hepatosplenomegaly. Sigmoidoscopy (day 6) showed acute rectal inflammation with ulcers, erosions, and bowel edema. Biopsies of the rectal/sigmoid walls revealed active colitis with crypts. CMV immunochemical testing was positive; CMV IgM was elevated at 161 AU/ml (> 35 AU/ml is considered abnormal); valganciclovir 900 mg orally twice daily was begun on (day 9) after discontinuation of budesonide. CMV IgG (0.62 IU/ml) and plasma CMV DNA (2.79 IU/ML) were elevated. He continued having fevers, anorexia, and worsening diarrhea. By day 12, he had lost 15 pounds. Repeat CT abdomen/pelvis showed worsening pancolitis and proctitis. Due to concerns with poor absorption, intravenous ganciclovir was started. On day 13 a repeat sigmoidoscopy showed severe colitis, proctosigmoiditis. Pathology revealed CMV colitis with ulceration, viral inclusions and positive immunohistochemical staining. Due to persistent fevers, solumedrol was started intravenously (day 18). By day 20, his appetite improved and he was afebrile. On day 21 he was discharged with a 3-week course of intravenous ganciclovir and 40 mg steroid daily. After his treatment, at the infectious disease clinic the patient reported clinical improvement.
Discussion: Acute CMV infections are due to primary infection or reactivation of a dormant virus. CMV-aggravated UC has a high mortality rate. Our case illustrates the severity of the disease, non-specific presentation of symptoms, diagnostic complexity, lack of response to oral antivirals, and eventual response to intravenous ganciclovir and steroids. Endoscopic findings, distinguishing CMV colitis from UC, is difficult; if immunohistochemical staining is not ordered, the diagnosis can be delayed, especially if the initial sigmoidoscopic findings do not show viral inclusions. Diagnostic tools for a CMV infection are high plasma CMV IgM Ab, Antigenemia assay, DNA PCR, biopsies with “owl eye appearance” inclusion bodies, and positive immunohistochemistry.
Conclusions: Acute CMV infection is a severe illiness with poor prognosis if not treated quickly. Diagnosis of CMV colitis in UC patients is difficult; a high index of suspicion is needed, particularly when patients have severe illness resistant to steroids and antibiotics. Treatment with the antiviral ganciclovir is suggested for people with severe disease.