Parvovirus B19 Infection Localized in the Intestinal Mucosa and Associated with Severe Inflammatory Bowel Disease

Abstract

Infection by human parvovirus B19 is widespread and can be associated with a wide range of different pathologies and clinical manifestations. We provide the first evidence of localization of an active parvovirus B19 infection in the intestinal mucosa and its association with a severe inflammatory bowel disease, characterized by duodenal villous atrophy with increased intraepithelial lymphocytes and inflammatory infiltrates in the colonic mucosa. Virus in the intestinal mucosa was detected in cells of the inflammatory infiltrate, identified as T lymphocytes and selectively localized in sites of active tissue degeneration. CASE REPORTIn February 2004, a diagnosis of extensive ulcerative colitis in a 52-year-old Caucasian man was made. Treatment with oral methylprednisolone (20 to 60 mg/day) resulted in improvement of the condition.In June 2004, he presented with a subacute bulbar syndrome. Spinal fluid analysis showed increased white blood cells. No specific infection was detected, and, as neoplastic and autoimmune diseases were excluded, an unrecognized infective etiology was hypothesized. Treatment with acyclovir was begun, along with corticosteroid maintenance (methylprednisolone, 20 to 60 mg/ day). Encephalitis healed within 2 months.In August 2004, ulcerative colitis was not responsive to medical treatment (methylprednisolone, 40 to 60 mg/day). A total colectomy with temporary ileostomy was performed, and corticosteroid treatment was stopped.In January 2005, bloody diarrhea with an ileostomy output of 5,000 to 6,000 ml/day, severe malabsorption, and systemic inflammatory reaction appeared. Ileoscopy revealed a diffuse superficial ulceration of the ileum. Histology showed a reactive inflammatory infiltrate with eosinophils as well as an increased number of intraepithelial lymphocytes associated with degenerative changes of the epithelial lining. A diagnosis of aspecific enteritis was made. Treatment with intravenous methylprednisolone (60 mg/day), oral fasting, and total parenteral nutrition were started.In March 2005, histology of the ileum showed ulcerative enteritis with focal pseudomembranes. Treatment with oral azathioprine, 50 to 100 mg/day, was started.In May 2005, ileostomy output was 3,000 to 4,000 ml/day and histology of the ileum was unchanged. Upper endoscopy showed a granular duodenal mucosa with severe villous atrophy, crypt hyperplasia, and inflammatory infiltrate with plasma cells, and more than 25 intraepithelial lymphocytes per 100 enterocytes were observed. Autoimmune enteropathy was excluded by a search for serum enterocyte autoantibodies, and intestinal lymphoma was excluded by immunohistochemistry. Serum chromogranin A concentration was normal. Tests for antitransglutaminase and antigliadin antibodies were negative. Serum immunoglobulin A (IgA) concentration was normal. HLA typing for celiac disease indicated that DQA1*0501 was absent, DQB1*0201 was present, and DQB1*0302 was absent; that for chronic inflammatory bowel disease indicated that DRB1*07 was present.Infections by Salmonella, B...

Parvovirus B19 Achievements and Challenges

“…A possible similar mechanism, involving macrophages, dendritic follicular cells, and lymphocytes rather than synovial cells, has been reported in tissues from rheumatoid arthritis patients [153] but awaits confirmation and further investigation. The involvement of lymphocytes, possibly productively infected by B19V, has also been reported in a case series of chronic inflammatory joint diseases [215] and can be a rare and unexpected finding in atypical clinical situations characterized by chronic inflammation [216].…”

Galacto-oligosaccharides Protect the Intestinal Barrier by Maintaining the Tight Junction Network and Modulating the Inflammatory Responses after a Challenge with the Mycotoxin Deoxynivalenol in Human Caco-2 Cell Monolayers and B6C3F1 Mice

“…Moreover, a reduction of the inflammatory response (CXCL8 and Cxcl1) after a deoxynivalenol challenge could be observed in line with a prevention of deoxynivalenol-induced alterations in villus architecture in the mouse intestine. Considering that the deoxynivalenol-induced alterations in the intestinal tract resemble those of human chronic inflammatory diseases (64)(65)(66) and the regular exposure of humans to deoxynivalenol because of its presence in wheat and wheat-derived products, further studies are warranted to assess in more detail the potential beneficial effects of GOS as supportive therapy in the prevention of toxin-induced inflammatory bowel diseases and related syndromes.…”

The role of infection in the aetiology of inflammatory bowel disease

“…Several viruses have also been implicated as exacerbating agents in IBD. These include chiefly cytomegalovirus (CMV), but recently parvovirus B19, norovirus and Epstein-Barr virus have all been suggested as exacerbating agents [96][97][98]. CMV appears to act through latent reactivation (reviewed succinctly by Hommes et al [99]).…”