Analysis of commercial Entamoeba histolytica ELISA kits for the detection of Entamoeba invadens in reptiles.

Entamoeba invadens is pathogenic in multiple reptile species and has caused severe outbreaks in zoos and other facilities worldwide. Infections can be difficult to diagnose and to differentiate from other reptilian Entamoeba species. The goal of this study was to determine if kits developed to identify the human pathogen Entamoeba histolytica could be used to detect E.

Prevalent human coxsackie B-5 virus infects porcine islet cells primarily using the coxsackie-adenovirus receptor.

Background: We have previously demonstrated that transplanting porcine encephalomyocarditis virus (EMCV)-infected porcine islet cells (PICs) results in transmission of the virus to recipient mice, which is manifested by acute fatal infection within 5 to 8 days. Here, we determined PIC susceptibility to a related and highly prevalent human picornavirus, coxsackie B-5 virus (CVB-5).

Methods: PICs were inoculated with CVB-5 in vitro for up to 96 hours and infectivity, level of virus replication, and cellular function determined.

Transplanting encephalomyocarditis virus-infected porcine islet cells reverses diabetes in recipient mice but also transmits the virus.

Previous studies demonstrated that porcine encephalomyocarditis virus (EMCV) caused acute and persistent infection in the myocardium, central nervous system, and spleen of non-human primates (cynomolgus macaques); and it productively infected primary human cardiomyocytes, suggesting that the virus may pose a risk in pig-to-human transplantation. Recently, transplantation of myocardial and pancreatic tissues from acutely infected pigs transmitted the virus to recipient mice, resulting in acute fatal EMCV disease. Here, we examined whether porcine islet cells (PICs), which are under clinical trial for treatment of type I diabetes in humans, are susceptible to porcine EMCV, and whether EMCV-infected PICs could function in vivo to reverse diabetes.

Transmission of porcine encephalomyocarditis virus (EMCV) to mice by transplanting EMCV-infected pig tissues.

We recently demonstrated that pigs infected with porcine encephalomyocarditis virus (EMCV) develop a persistent infection (up to 90 days post-infection (PI)) in the heart and brain that is accompanied by virus-induced pathologic changes, and that EMCV productively infects human cardiomyocytes in vitro, suggesting that EMCV may pose a risk to humans following transplantation of pig tissues to humans (Brewer et al. J Virol 2001; 75: 11621-11629). In this report, we demonstrate that intra-abdominal of myocardial or pancreatic sections from acutely-EMCV infected pigs (2 days PI) in either non-mutant C57BL/6 or C57BL/6-RAG-1-/- mice that lack B or T lymphocytes, resulted in transmission of the virus and acute fatal disease in all mice.

A wild-type porcine encephalomyocarditis virus containing a short poly(C) tract is pathogenic to mice, pigs, and cynomolgus macaques.

Previous studies using wild-type Encephalomyocarditis virus (EMCV) and Mengo virus, which have long poly(C) tracts (61 to 146 C's) at the 5' nontranslated region of the genome, and variants of these viruses genetically engineered to truncate or substitute the poly(C) tracts have produced conflicting data on the role of the poly(C) tract in the virulence of these viruses. Analysis of the nucleotide sequence of an EMCV strain isolated from an aborted swine fetus (EMCV 30/87) revealed that the virus had a poly(C) tract that was 7- to 10-fold shorter than the poly(C) tracts of other EMCV strains and 4-fold shorter than that of Mengo virus. Subsequently, we investigated the virulence and pathogenesis of this naturally occurring short-poly(C)-tract-containing virus in rodents, pigs, and nonhuman primates.