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Cytomegalovirus colitis in a critically ill patient following elective repair of an abdominal aortic aneurysm.


We describe a case of cytomegalovirus colitis in a critically ill but otherwise immunocompetent 61-year-old male. Infection was demonstrated by histology and confirmed by plasma polymerase chain reaction and detection of cytomegalovirus IgM antibody. The patient was treated with ganciclovir with resolution of the cytomegalovirus viraemia. Cytomegalovirus colitis may be an under-recognised problem in immunocompetent patients who are critically ill. Quantification of plasma cytomegalovirus DNA by polymerase chain reaction is a non-invasive method of supporting the diagnosis and can be used to monitor the treatment of cytomegalovirus infection in the immunocompetent.

Key Words: cytomegalovirus, colitis, immunocompetent, ganciclovir, polymerase chain reaction, aortic aneurysm



A 61-year-old HIV negative male with hypertension and ischaemic heart disease underwent elective repair of an abdominal aortic aneurysm. The patient was managed in a high dependency unit, having suffered peripheral ischaemic damage to the lower limbs during surgery. He required five units of red cell concentrate and three units of fresh frozen plasma intraoperatively, followed by six further units of red cell concentrate over the next two weeks. On day four post-surgery he was transferred to intensive care with evidence of perioperative myocardial infarction and subsequently developed respiratory failure. He was intubated, ventilated and treated for a presumed bacterial pneumonia with meropenem and vancomycin. The following day he developed diarrhoea, which tested positive for Clostridium difficile toxin. He received 14 days of oral metronidazole and his diarrhoea settled, but then subsequently worsened again while he was still receiving metronidazole. Stool samples repeatedly tested negative for C. difficile toxins A/B. On day 30 post-surgery, a flexible sigmoidoscopy revealed extensive colitis with a diffusely inflamed and exudative mucosa. In view of the negative C. difficile toxin results, ischaemic colitis was suspected. However, when the biopsies were examined, inclusion bodies typical of cytomegalovirus (CMV) infection were seen (Figure 1) and immunohistochemistry staining was positive for CMV (Figure 2). Quantitative realtime polymerase chain reaction (PCR) of his EDTA plasma revealed a high CMV viraemia with 96,600 copies/ml and CMV IgM antibody was detected. At this point, he was producing up to two litres of diarrhoea over a 24-hour period and intravenous ganciclovir 5 mg/kg 12 hourly was commenced. After the first week of ganciclovir the CMV viraemia remained high (123,000 copies/ml) but was undetectable by the end of the second week of treatment. His diarrhoea, although not fully resolved, was considerably better and continued to test negative for C. difficile toxin. After 58 days in the intensive care unit, he was discharged to a general ward and thereafter to a rehabilitation unit. He had ongoing problems with diarrhoea thought to be secondary to ischaemic colitis and was treated for a recurrence of C. difficile toxin positive diarrhoea. Plasma CMV PCR was checked again on two occasions and remained undetectable. His general condition remained poor and he died from a cerebral infarct 109 days after discharge from the intensive care unit. Autopsy confirmed widespread atheromatous vascular disease with evidence of bowel ischaemia and no evidence of recurrence of his CMV disease.




Human CMV is a human herpesvirus that has a seroprevalence of 30 to 70% in developed countries (1). Primary infection in the immunocompetent host rarely causes serious disease and often passes unnoticed, sometimes causing a mononucleosis syndrome similar to primary Epstein-Barr virus infection (2). After initial infection the virus remains in a persistent state with the host, but can reactivate and has the potential to affect most organs. It is well recognised that CMV reactivation causes disease in severely immunosuppressed patients, most notably in HIV infection, solid organ transplantation and bone marrow transplantation (3). Our patient was immunocompetent to the extent that he had none of the immunosuppressive conditions that are traditionally associated with CMV reactivation causing infection, although occult CMV reactivation is recognised in critically ill patients (4-6). However, it is unclear how often reactivation of CMV in this subset of relatively immunocompromised patients causes disease and contributes to morbidity. CMV colitis has primarily been described in HIV infection and its diagnosis has relied on demonstrating typical CMV intranuclear inclusions in biopsy specimens (7,8). There are a number of reports implicating CMV as a primary cause of colitis in otherwise healthy immunocompetent individuals (9-12), but its role in immunocompetent critically ill patients is less well defined (13). Disruption of enteric mucosa might predispose immunocompetent individuals to CMV colitis (14). Our patient had underlying ischaemic colitis and C. difficile toxin associated diarrhoea preceded the CMV colitis. The demonstration of CMV replication in colonic mucosa, the high level of CMV viraemia with a positive CMV IgM serology and the patient's response to ganciclovir is strong evidence for clinically significant CMV colitis. This was most likely due to reactivation, as he was found to be CMV Igg seropositive on a stored sample from two years prior to the operation. Alternatively, he may have been reinfected with a different serotype of CMV (15) through the blood products he received perioperatively (16,17). However, the blood products were leukocyte-depleted which is thought to significantly lessen transfusion-related transmission of CMV.

In conclusion, CMV colitis may be an underrecognised problem in critically ill patients. It can mimic ischaemic colitis (18), inflammatory bowel disease, sepsis or antibiotic-associated colitis (10), all of which are common in the critically ill and it may coexist with other bowel pathology (10,14). CMV colitis can be difficult to diagnose, requiring a colonic biopsy demonstrating typical inclusion bodies and specific immunohistochemistry staining. Even with a biopsy, the viral inclusion bodies can be missed10 and specific staining for CMV may not be carried out when an alternative pathology has been identified. Previously, colitis cases in the immunocompetent have in the main been described on histological diagnosis. Diagnosis of CMV infection is also possible by quantification of plasma CMV DNA, as illustrated in this case, although the role of quantitative PCR is better defined in the immunocompromised (19,20). We suggest that, regardless of the underlying immune status, critically ill patients with unexplained symptoms of colitis should, where the test is available, have plasma CMV PCR as part of the investigation process. Use of plasma CMV quantification does not require a biopsy, which may not always be practical and CMV quantification can be used to monitor the disease course during treatment. The role of treatment with ganciclovir is well defined in CMV disease where there is severe immunosuppression (21,22), but there are no randomised trials to support its use in the immunocompetent, although evidence from case series suggests that it may be effective (10,11).

Accepted for publication on August 30, 2007.


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K.O. HELGASON *, S.J.M. RABY ([dagger]), H.M.H. KAMEL ([double dagger]), I.E. LAURENSON ([section]), K. TEMPLETON **, T S. WALSH ([dagger dagger])

Critical Care Unit, Edinburgh Royal Infirmary, Edinburgh, United Kingdom

* Cand. Med. et. Chir., M.R.C.P, Specialist Registrar, Microbiology and Infectious Diseases.

([dagger]) M.B., Ch.B., B.Sc. (Hons.), M.R.C.P, Senior House Officer, Critical Care Unit.

([double dagger]) Ph.D., ER.C.Path., Consultant, Pathology Department.

([section]) F.R.C.P, ER.C.Path., Consultant, Microbiology Department.

** Ph.D., M.R.C.Path., Consultant, Specialist Virology Centre.

([dagger dagger]) M.D., ER.C.P, ER.CA, Consultant, Critical Care Unit.

Address for reprints: Dr K O. Helgason, Department of Microbiology, Edinburgh Royal Infirmary, 51 Little France Crescent, EH16 4SA, Edinburgh, U.K
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Article Details
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Title Annotation:Case Reports
Author:Helgason, K.O.; Raby, S.J.M.; Kamel, H.M.H.; Laurenson, I.E; Templeton, K.; Walsh, T.S.
Publication:Anaesthesia and Intensive Care
Article Type:Clinical report
Geographic Code:4EUUK
Date:Jan 1, 2008
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