Gastrointestinal symptoms after infectious diarrhea: a five-year follow-up in a Swedish cohort of adults.

BACKGROUND & AIMS: Gastrointestinal infection is a well-recognized trigger for functional bowel disorder. This study evaluated gastrointestinal symptoms and risk factors for their development after diarrheal disease of proven or strongly suspected infectious etiology in adults. METHODS: The cohort of patients was derived from a previous study that determined the rate at which enteropathogens could be isolated at the time of diarrheal disease in adults. After 5 years, 717 of 851 patients were accessible for a questionnaire asking for persistence of gastrointestinal symptoms. RESULTS: Of 508 returned questionnaires, 333 were from patients with no previous gastrointestinal complaints. Forty-one (12%) of them had gastrointestinal symptoms for 3 months or more after the infectious diarrhea, and 31 (9%) still had symptoms at the end of the follow-up period. Irritable bowel syndrome was most common (68%), but other functional bowel disorder diagnoses were found in all but one of the others. Female gender (odds ratio, 2.65, 95% confidence interval, 1.28-5.50) and use of antibiotic treatment (odds ratio, 2.37; 95% confidence interval, 1.07-5.25) were risk factors for development of postinfectious functional bowel disorder. No increase in risk was associated with the type of enteropathogen causing diarrhea. CONCLUSIONS: Infectious diarrhea in previously healthy adults carried a substantial risk of triggering postinfectious functional bowel disorder. Irritable bowel syndrome was the most common, but other functional bowel disorders were also found. We did not find any new clinical tools that would facilitate the prediction of long-standing symptoms.

Human herpesvirus-8-encoded LNA-1 accumulates in heterochromatin- associated nuclear bodies.

Subnuclear distribution of the human herpesvirus-8 (HHV-8)- encoded nuclear protein LNA-1 was analysed at high resolution in body cavity (BC) lymphoma-derived cell lines, in cell hybrids between BC cells and various human and mouse cells and in freshly infected K562 and ECV cell lines. Three-dimensional reconstruction of nuclei from optical sections and quantitative analysis of the distribution of LNA-1 fluorescence in relation to chromatin showed that LNA-1 associates preferentially with the border of heterochromatin in the interphase nuclei. This was further confirmed in the following systems: in endo- and exonuclease-digested nuclei, in human-mouse (BC-1-Sp2- 0) hybrids and on chromatin spreads. LNA-1 was found to bind to mitotic chromosomes at random. Epstein-Barr virus (EBV), but not HHV-8, was rapidly lost from mouse-human hybrid cells in parallel with the loss of human chromosomes. HHV-8 could persist on the residual mouse background for more than 8 months. In early human-mouse hybrids that contain a single fused nucleus, LNA-1 preferentially associates with human chromatin. After the gradual loss of the human chromosomes, LNA-1 becomes associated with the murine pericentromeric heterochromatin. In human-human hybrids derived from the fusion of the HHV-8-carrying BCBL-1 cells and the EBV-immortalized lymphoblastoid cell line IB4, LNA-1 did not co-localize with EBNA-1, EBNA-2, EBNA-5 or EBNA-6. LNA-1 was not associated with PML containing ND10 bodies either. DNase but not RNase or detergent treatment of isolated nuclei destroys LNA-1 bodies. In advanced apoptotic cells LNA- 1 bodies remain intact but are not included in the apoptotic bodies themselves.