MedStar Washington Hospital Center Washington, DC, United States
Award: Presidential Poster Award
Danial Nadeem, MD1, Tenzin Choden, MD2, Yiannis Dimopoulos, MD3, Mark C. Mattar, MD2 1MedStar Washington Hospital Center, Washington, DC; 2MedStar Georgetown University Hospital, Washington, DC; 3Georgetown University Hospital, Washington, DC
Introduction: Histoplasmosis is a fungal infection caused by Histoplasma capsulatum, a dimorphic fungus found in the central and eastern United States. In immunocompetent individuals, this infection rarely causes symptoms but immunosuppressed patients may suffer from a wide range of pulmonary, cardiac, rheumatologic, and dermatologic manifestations. Here, we present a patient on chronic immunosuppressive therapy for Crohn’s Disease, found to have disseminated histoplasmosis.
Case Description/Methods: A 34 year old female with a medical history of established inflammatory ileocolonic Crohn's disease on adalimumab presented to the hospital with acute onset fevers. Prior to this, she had reported worsening abdominal pain for two months, and had been treated with two courses of steroids outpatient with plans for medication change to vedolizumab.
A computed tomography scan of the abdomen showed long segment jejunal enteritis with loculated free air in the mesentery as well as free air within the peritoneal cavity, concerning for perforation (Figure 1). After starting broad spectrum antibiotics an emergent exploratory laparotomy was performed. She was found to have two areas of small bowel perforation amidst inflammation, which were resected with primary anastomosis. Due to persistent septic shock from recurrent perforations, she ultimately required ileocecetomy and end ileostomy. Pathology of the surgical specimens revealed focal ulceration, granuloma formation, both acute and chronic serositis, but also revealed ovoid, small, and relatively uniform intracellular organisms, found to be histoplasmosis (Figure 2). Her course was further complicated by pericarditis and recurrent peritonitis, but ultimately responded to antibiotic treatment.
One year later, she underwent an ileoscopy and colonoscopy which showed no active inflammation in the ileum and histologically mild colitis in the rectum. She subsequently underwent ostomy reversal with plans to start vedolizumab post-operatively. She remains in clinical remission and continues on posiconazole for ongoing prophylaxis against Histoplasmosis.
Discussion: This patient was treated with intravenous steroids multiple times for recurrent Crohn’s disease flares with no improvement, ultimately leading to worsening inflammation and bowel perforation from Histoplasmosis. Clinicians should strongly consider opportunistic infections such as Histoplasmosis when treating immunocompromised patients with inflammatory bowel disease presenting with steroid-refractory symptoms.
Figure: Figure 1A - Axial view of the Abdomen and Pelvis showing free air in the abdominal cavity (top arrow). Also visible is engorgement of the vasa recta adjacent to an inflamed loop of bowel, as well as mesenteric fat stranding (lower arrow).
Figure 1B - Jejunal wall thickening with evidence of distension, inflammation and edema (arrow).
Figure 2 2A - H&E stain. Low power view, showing diffuse and vaguely nodular full thickness involvement of the small intestinal wall. (Mucosa on the left and muscularis propria/serosa on the right).
2B - High power view showing sheets of histiocytes without distinct granuloma formation. Multiple intracellular Histoplasma organisms are seen in the cytoplasm of these cells (arrow). These organisms are ovoid, small, and relatively uniform in size.
2C - The intracellular organisms are highlighted the PAS special stain (arrow),