Two Listeria monocytogenes outbreaks in a cancer centre: onsite food premises and their potential health risk to patients.

BACKGROUND: This report describes two L. monocytogenes outbreak investigations that occurred in March and September of 2018 and that linked illness to a food premises located in an Ontario cancer centre. The cancer centre serves patients from across the province. METHODS: In Ontario, local public health agencies follow up with all reported laboratory-confirmed cases of listeriosis to identify possible sources of disease acquisition and to carry out investigations, including at suspected food premises. The Canadian Food Inspection Agency (CFIA) is notified of any Listeria-positive food product collected in relation to a case. The CFIA traces Listeria-positive product through the food distribution system to identify the contamination source and ensure the implicated manufacturing facility implements corrective measures. RESULTS: Outbreaks one and two each involved three outbreak-confirmed listeriosis cases. All six cases were considered genetically related by whole genome sequencing (WGS). In both outbreaks, outbreak-confirmed cases reported consuming meals at a food premises located in a cancer centre (food premises A) before illness onset. Various open deli meat samples and, in outbreak two, environmental swabs (primarily from the meat slicer) collected from food premises A were genetically related to the outbreak-confirmed cases. Food premises A closed as a result of the investigations. CONCLUSIONS: When procuring on-site food premises, healthcare facilities and institutions serving individuals with immuno-compromising conditions should consider the potential health risk of foods available to their patient population.

Getting a grippe on severity: a retrospective comparison of influenza-related hospitalizations and deaths captured in reportable disease and administrative data sources in Ontario, Canada.

BACKGROUND: Since 2009, in Ontario, reportable disease surveillance data has been used for timely in-season estimates of influenza severity (i.e., hospitalizations and deaths). Due to changes in reporting requirements influenza reporting no longer captures these indicators of severity, necessitating exploration of other potential sources of data. The purpose of this study was to complete a retrospective analysis to assess the comparability of influenza-related hospitalizations and deaths captured in the Ontario reportable disease information system to those captured in Ontario's hospital-based discharge database. METHODS: Hospitalizations and deaths of laboratory-confirmed influenza cases reported during the 2010-11 to 2013-14 influenza seasons were analyzed. Information on hospitalizations and deaths for laboratory-confirmed influenza cases were obtained from two databases; the integrated Public Health Information System, which is the provincial reportable disease database, and the Discharge Abstract Database, which contains information on all in-patient hospital visits using the International Classification of Diseases, 10th Revision, Canada (ICD-10-CA) coding standards. Analyses were completed using the ICD-10 J09 and J10 diagnosis codes as an indicator for laboratory-confirmed influenza, and a secondary analysis included the physician-diagnosed influenza J11 diagnosis code. RESULTS: For each season, reported hospitalizations for laboratory-confirmed influenza cases in the reportable disease data were higher compared to hospitalizations with J09 and J10 diagnoses codes, but lower when J11 codes were included. The number of deaths was higher in the reportable disease data, whether or not J11 codes were included. For all four seasons, the weekly trends in the number of hospitalizations and deaths were similar for the reportable disease and hospital data (with and without J11), with seasonal peaks occurring during the same week or within 1 week of each other. CONCLUSION: In our retrospective analyses we found that hospital data provided a reliable estimate of the trends of influenza-related hospitalizations and deaths compared to the reportable disease data for the 2010-11 to 2013-14 influenza seasons in Ontario, but may under-estimate the total seasonal number of deaths. Hospital data could be used for retrospective end-of-season assessments of severity, but due to delays in data availability are unlikely to be timely estimates of severity during in-season surveillance.

Nuggets of Wisdom: Salmonella Enteritidis Outbreaks and the Case for New Rules on Uncooked Frozen Processed Chicken.

In 2014 and 2015, three Canadian Salmonella serotype Enteritidis outbreak investigations implicated uncooked, frozen, processed chicken products produced at the same establishment, namely establishment A. In November 2014, a sustained increase in the number of reported domestically acquired Salmonella Enteritidis cases in Ontario led to the first outbreak investigation, which implicated uncooked, frozen, processed chicken products produced at establishment A. In June 2015, the identification of pulsed-field gel electrophoresis patterns that had not been previously reported in Canada led to a national Salmonella Enteritidis investigation. Of 51 cases reported nationally, 35 were from Ontario. Uncooked, frozen, processed chicken products produced at establishment A were identified as the source of the outbreak, and public health action was taken as a result of this second investigation. In September 2015, a sustained increase in the number of domestically acquired Salmonella Enteritidis PT13a cases in Ontario led to a third outbreak investigation, which identified a total of 36 PT13a cases. Uncooked, frozen, processed chicken products produced at establishment A were again identified as the source of the outbreak. Outbreaks have been linked to uncooked, frozen, processed chicken products since the late 1990s. Information collected during the three outbreak investigations, and from other jurisdictions, suggests that the breaded and prebrowned appearance of the product, as well as factors related to product packaging and marketing, result in consumer misperception that this raw product is cooked. This misperception may result in mishandling and improper cooking. The three outbreaks described in this article highlight the potential ongoing risks to consumers from these products and support interventions to prevent contamination at the source level and infection at the consumer level.

Neisseria gonorrhoeae-derived heptose elicits an innate immune response and drives HIV-1 expression.

Clinical and epidemiological synergy exists between the globally important sexually transmitted infections, gonorrhea and HIV. Neisseria gonorrhoeae, which causes gonorrhea, is particularly adept at driving HIV-1 expression, but the molecular determinants of this relationship remain undefined. N. gonorrhoeae liberates a soluble factor that potently induces expression from the HIV-1 LTR in coinfected cluster of differentiation 4-positive (CD4(+)) T lymphocytes, but this factor is not a previously described innate effector. A genome-wide mutagenesis approach was undertaken to reveal which component(s) of N. gonorrhoeae induce HIV-1 expression in CD4(+) T lymphocytes. A mutation in the ADP-heptose biosynthesis gene, hldA, rendered the bacteria unable to induce HIV-1 expression. The hldA mutant has a truncated lipooligosaccharide structure, contains lipid A in its outer membrane, and remains bioactive in a TLR4 reporter-based assay but did not induce HIV-1 expression. Mass spectrometry analysis of extensively fractionated N. gonorrhoeae-derived supernatants revealed that the LTR-inducing fraction contained a compound having a mass consistent with heptose-monophosphate (HMP). Heptose is a carbohydrate common in microbes but is absent from the mammalian glycome. Although ADP-heptose biosynthesis is common among Gram-negative bacteria, and heptose is a core component of most lipopolysaccharides, N. gonorrhoeae is peculiar in that it effectively liberates HMP during growth. This N. gonorrhoeae-derived HMP activates CD4(+) T cells to invoke an NF-κB-dependent transcriptional response that drives HIV-1 expression and viral production. Our study thereby shows that heptose is a microbial-specific product that is sensed as an innate immune agonist and unveils the molecular link between N. gonorrhoeae and HIV-1.