Prevalence of Neospora caninum Exposure in Wild Pigs (Sus scrofa) from Oklahoma with Implications of Testing Method on Detection.

Neospora caninum is a protozoan parasite, reported as a leading cause of cattle abortions and reproductive failure worldwide, costing the cattle industry approximately $1.3 billion annually. With wild pig (Sus scrofa) populations estimated at over six million in the United States, contact between wild pigs and livestock is inevitable, mainly because of the widespread geographic co-occurrence of the two species. As a known reservoir for numerous fungal, bacterial, viral and parasitic diseases, wild pigs are of particular importance for human and veterinary health relative to the prevention of infectious diseases. The seroprevalence of N. caninum in wild pig populations was previously documented in the United States, raising the question as to their exposure point of prevalence. This research screened 116 individual wild pigs for N. caninum using a variety of available assays. Using two different commercially available ELISA test kits, seroprevalence ranged from 12.5% to 67.8%. The Indirect Fluorescent Antibody Test resulted in our highest percent seroprevalence for these samples, at 84.1%. However, none of our samples showed any presence of N. caninum or associated pathologies via histological evaluation of representative tissues. Importantly, the assays used in this study were not congruent with all duplicate samples or between the test types used. The implications of these non-congruent results demonstrates that currently available testing assays produce variable results, underscoring the need for more reliable testing kits and a standardized methodology when assessing disease prevalence in wildlife, particularly for N. caninum in wild pigs, which impacts prevalence and comparability across studies.

Differential Susceptibility to T Cell-Induced Colitis in Mice: Role of the Intestinal Microbiota.

One of the best characterized mouse models of the inflammatory bowel diseases (IBD; Crohn's disease, ulcerative colitis) is the CD4+CD45RBhigh T cell transfer model of chronic colitis. Following our relocation to Texas Tech University Health Sciences Center (TTUHSC), we observed a dramatic reduction in the incidence of moderate-to-severe colitis from a 16-year historical average of 90% at Louisiana State University Health Sciences Center (LSUHSC) to <30% at TTUHSC. We hypothesized that differences in the commensal microbiota at the 2 institutions may account for the differences in susceptibility to T cell-induced colitis. Using bioinformatic analyses of 16S rRNA amplicon sequence data, we quantified and compared the major microbial populations in feces from healthy and colitic mice housed at the 2 institutions. We found that the bacterial composition differed greatly between mice housed at LSUHSC vs TTUHSC. We identified several genera strongly associated with, and signficantly overrepresented in high responding RAG-/- mice housed at LSUHSC. In addition, we found that colonization of healthy TTUHSC RAG-/- mice with feces obtained from healthy or colitic RAG-/- mice housed at LSUHSC transferred susceptibility to T cell-induced colitis such that the recipients developed chronic colitis with incidence and severity similar to mice generated at LSUHSC. Finally, we found that the treatment of mice with preexisting colitis with antibiotics remarkably attenuated disease. Taken together, our data demonstrate that specific microbial communities determine disease susceptibility and that manipulation of the intestinal microbiota alters the induction and/or perpetuation of chronic colitis.

Protective and pro-inflammatory roles of intestinal bacteria.

The intestinal mucosal surface in all vertebrates is exposed to enormous numbers of microorganisms that include bacteria, archaea, fungi and viruses. Coexistence of the host with the gut microbiota represents an active and mutually beneficial relationship that helps to shape the mucosal and systemic immune systems of both mammals and teleosts (ray-finned fish). Due to the potential for enteric microorganisms to invade intestinal tissue and induce local and/or systemic inflammation, the mucosal immune system has developed a number of protective mechanisms that allow the host to mount an appropriate immune response to invading bacteria, while limiting bystander tissue injury associated with these immune responses. Failure to properly regulate mucosal immunity is thought to be responsible for the development of chronic intestinal inflammation. The objective of this review is to present our current understanding of the role that intestinal bacteria play in vertebrate health and disease. While our primary focus will be humans and mice, we also present the new and exciting comparative studies being performed in zebrafish to model host-microbe interactions.

Role of the enteric microbiota in intestinal homeostasis and inflammation.

The mammalian intestine encounters many more microorganisms than any other tissue in the body thus making it the largest and most complex component of the immune system. Indeed, there are greater than 100 trillion (10(14)) microbes within the healthy human intestine, and the total number of genes derived from this diverse microbiome exceeds that of the entire human genome by at least 100-fold. Our coexistence with the gut microbiota represents a dynamic and mutually beneficial relationship that is thought to be a major determinant of health and disease. Because of the potential for intestinal microorganisms to induce local and/or systemic inflammation, the intestinal immune system has developed a number of immune mechanisms to protect the host from pathogenic infections while limiting the inflammatory tissue injury that accompanies these immune responses. Failure to properly regulate intestinal mucosal immunity is thought to be responsible for the inflammatory tissue injury observed in the inflammatory bowel diseases (IBD; Crohn disease, ulcerative colitis). An accumulating body of experimental and clinical evidence strongly suggests that IBD results from a dysregulated immune response to components of the normal gut flora in genetically susceptible individuals. The objective of this review is to present our current understanding of the role that enteric microbiota play in intestinal homeostasis and pathogenesis of chronic intestinal inflammation.