LAUSR

Cytomegalovirus (CMV) reactivation is well described in patients with inflammatory bowel disease (IBD), particularly in those with acute severe colitis on immunosuppressive therapy. CMV is a herpesvirus that infects 57% of adult Australians, usually resulting in asymptomatic or mild infections; however, it can replicate and cause significant morbidity in immunocompromised patients. A 30-year-old male patient presented to our hospital with a 7-day history of frequent bloody diarrhoea, high-grade fevers, myalgias and headache. This was on a background of ulcerative colitis (UC) diagnosed a year prior and being nonresponsive to 5-ASA and 6-MP consecutively. A year earlier, due to clinically active disease, 40 mg prednisolone and standard dose infliximab were added to his current therapy. His infliximab was subsequently escalated to 4-weekly infusion due to clinically active disease. Prednisolone was continued >20 mg/day throughout the treatment course. Flexible sigmoidoscopy performed 3 months prior showed Mayo 2 colitis. Immunohistochemistry for CMV was negative. On presentation, he was cachectic with 20 kg of weight loss the previous year. There was no abdominal tenderness or distension. His abdominal x-ray showed no evidence of toxic megacolon. His haemoglobin was 156 g/L (138–172 g/L), and CRP was 20 mg/L (<5 mg/L). His ALT and AST were mildly elevated. Stool microbiological testing identified no pathogens. A diagnosis of acute severe UC with primary non-response to infliximab was made, and the patient commenced on intravenous (i.v.) methylprednisolone 20 mg TDS. He underwent a flexible sigmoidoscopy, which demonstrated Mayo 3 proctitis. Despite 72 h of i.v. steroids, he failed to improve. The histology from his colonic biopsies returned, showing numerous intranuclear inclusion bodies, in keeping with CMV colitis (Fig. 1A,B). This was associated with worsening transaminitis, his ALT peaking at 818 U/L (4–36 U/L). His CMV immunoglobulin G (IgG) was noted to be non-reactive in early 2021 but positive on presentation (avidity not available) with high immunoglobulin M and a DNAaemia of 6.92 10 copies/mL. A diagnosis of primary intestinal CMV infection with likely liver involvement was established. He commenced on i.v. ganciclovir for 2 weeks then transitioned to oral valganciclovir. His 6-MP was ceased, and his oral prednisolone decreased to 20 mg. This resulted in a marked clinical improvement and suppression of his CMV viral load. He was started on vedolizumab, his viral load remained undetectable and he had evidence of clinical and endoscopic response. It has been proposed by Beswick et al. that a diagnosis of concurrent CMV colitis can be excluded in patients presenting with steroid-refractory disease who are CMV IgG negative; our case describes likely primary intestinal CMV rather than reactivation of the latent virus. The main risk factors for CMV infection affecting the bowel in IBD include severe UC, steroid refractoriness and azathioprine therapy. It is also proposed that high-grade CMV (high viral tissue density) disease indicates that the virus is acting as the main driver of mucosal disease, whereas in those with low-grade CMV disease (low viral tissue density), the severity of IBD itself is more likely to influence outcome. We present a rare case of primary CMV in an immunocompromised patient manifesting with a constellation of clinical (fever, myalgias and headache), biochemical