Summary 1.Pathogen spillover occurs when disease levels for a given population are driven by transmission from a reservoir species that carries a high pathogen load. Pathogen spillover is widely documented in crop systems, but has been little studied in natural plant communities. 2. The abundant seed production of weedy species may create a scenario where spillover of a generalist seed pathogen onto less abundant seeds of native hosts is possible. The invasive annual weed cheatgrass (Bromus tectorum) is a potential reservoir species for Pyrenophora semeniperda, a multiple-host fungal seed pathogen that naturally occurs in the semi-arid western United States. 3. To investigate potential community-level consequences of spillover by this pathogen in plant communities invaded by cheatgrass, we first used artificial inoculation studies to determine the relative susceptibility of seeds of cheatgrass and five co-occurring native grasses to P. semeniperda. Secondly, we quantified the pathogen reservoir (density of pathogen-killed seeds) in the spring seed bank for cheatgrass monoculture, cheatgrass-invaded native grass, and uninvaded native grass patches. Thirdly, potential pathogen spillover onto co-occurring native grasses was quantified by planting native grass seeds into field-collected seed-zone samples from each vegetation patch type and scoring subsequent seed mortality. 4. All species tested were susceptible to infection by P. semeniperda, but their vulnerability to seed death varied as a function of germination time and degree of susceptibility. 5. Seed bank samples from cheatgrass-dominated patches contained seed densities over four times higher than samples from uninvaded native grass patches, and P. semeniperda-killed seeds were also present at much higher densities, indicating that cheatgrass can function as a reservoir for P. semeniperda. Native seeds planted into seed-zone samples from cheatgrass-dominated patches were more likely to be killed by P. semeniperda than those planted into samples from uninvaded native patches. Seed mortality also varied across years, sites and host species. 6. Synthesis. Pathogen spillover onto native seeds is likely to operate within seed banks of semi-arid communities invaded by cheatgrass, and perhaps other weeds, and may have broad consequences for community structure. Our findings also demonstrate the ecological significance of multiple-host pathosystems that operate at the seed stage.

Colorectal cancer begins as a polyp that is a benign growth on the mucosal surface of the colon or rectum. Over a period of 5 to 15 years, polyps can degenerate into a cancer, thus invading the colonic wall. Colorectal screening methods are designed to diagnose and remove polyps before they acquire invasive potential and develop into cancer. Screening for colorectal cancer can prevent and reduce mortality. Given the benefits and effectiveness of screening, guidelines exist from multiple organizations. These guidelines risk-stratify patients to determine the age of screening initiation and the interval for repeat screening. Categories of colorectal cancer risk include average risk, increased risk, and high risk based on individual and family medical history. Screening methods vary widely in the ability to diagnose and treat polyps and in the degree of invasiveness or risk of complication to the patient. Colonoscopy is held as the “gold standard” by which all other methods are compared; however, less-invasive modalities including computed tomographic colonography are increasing in popularity.

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BackgroundTrisomy 13 is one of the most common autosomal trisomies, and although increasing in number, patients surviving past the neonatal period remain rare. The natural history and expected complications in these patients as they age remains unknown. Despite the rarity of this condition, unusual malignancies have been reported in the medical literature for decades. It is clear that providers should suspect unusual malignancies in these patients, particularly as they age.Case presentationWe report a 20-year-old Caucasian woman with Trisomy 13 who presented with colonic volvulus, found to have colonic polyposis and adenocarcinoma of the colon. Genetics of pathology specimens revealed 47(XX) + 13 without other mutations. She underwent prophylactic completion colectomy due to presumed risk of colorectal cancers given underlying adenomatous polyposis. She has recovered well without evidence of recurrence.ConclusionsThe presence of colonic polyposis and colorectal cancer without family history or known mutations for polyposis syndrome suggests an intrinsic predisposition toward colorectal cancer in this patient with Trisomy 13. Recent research into colorectal cancer oncogenes supports that aneuploidy or increased copy number of certain genes on chromosome 13 may increase the risk of malignant transformation. This is an important correlation for researchers studying these topics and clinicians caring for patients with Trisomy 13 as they age.