Human listeriosis results from the ingestion of foods contaminated with Listeria monocytogenes (Lm). About 1600 listeriosis cases are reported every year in the USA with >95% hospitalization and 15–20% death. The proportions of persons with listeriosis hospitalized and who die are very similar in Europe with slightly higher rates in Scandinavian countries. The occurrence of disease requires adaptation, survival, and usually growth of Lm in foods before consumption by members of the susceptible population. Despite concerted efforts by the food safety community, the disease incidence has not changed significantly since 2001 and remains higher than the Healthy People 2020 target of 0.2 cases per 100,000 individuals.
In recent years, human listeriosis cases have been reported to involve non-typical foods, e.g. celery, cantaloupe, caramel apple, frozen vegetables and ice cream. In some outbreaks, a few infected individuals were considered outside the realm of the standard vulnerable population group. Our recent work with the outbreak associated with ice cream samples, indicated that a low-level contamination in a food that does not support growth can cause listeriosis in highly susceptible populations. Separately, using a combination of polymerase chain reaction (PCR)-based serotyping and whole genome sequencing (WGS)-based analyses; we have discovered that a genetic variant of the serotype 4b strain, called 4bV, was responsible for 3–4 recent outbreaks in the USA. Three of the four products associated with these outbreaks were grown in a small geographical region of the USA while the fourth was never linked to a specific grower, but rather a processing facility. These 4bV strains contain a 6.3kb DNA fragment normally associated with lineage II Lm strains. The significance of this DNA fragment in the serotype 4b background is currently being investigated. This article reviews current listeriosis outbreaks with an emphasis on the expansions in food niche, case demography and genotypes of Lm. The discussion raises important questions about Lm adaptation in different foods and environments and the role of certain genotypes in such adaptation and disease outcome.
Aspergillus flavus is best known for producing the family of potent carcinogenic secondary metabolites known as aflatoxins. However, this opportunistic plant and animal pathogen also produces numerous other secondary metabolites, many of which have also been shown to be toxic. While about forty of these secondary metabolites have been identified from A. flavus cultures, analysis of the genome has predicted the existence of at least 56 secondary metabolite gene clusters. Many of these gene clusters are not expressed during growth of the fungus on standard laboratory media. This presents researchers with a major challenge of devising novel strategies to manipulate the fungus and its genome so as to activate secondary metabolite gene expression and allow identification of associated cluster metabolites. In this review, we discuss the genetic, biochemical and bioinformatic methods that are being used to identify previously uncharacterized secondary metabolite gene clusters and their associated metabolites. It is important to identify as many of these compounds as possible to determine their bioactivity with respect to fungal development, survival, virulence and especially with respect to any potential synergistic toxic effects with aflatoxin.
Monitoring and management programs for marine toxins in seafood depend on efficient detection tools for their success in protecting public health. Here we review current methods of detection for neurotoxic shellfish poisoning (NSP) toxins, and current knowledge in brevetoxin metabolism in shellfish. In addition, we discuss a novel approach to developing monitoring tools for NSP toxins in molluscan shellfish. NSP is a seafood-borne disease caused by the consumption of brevetoxin-contaminated shellfish. Brevetoxins are a suite of cyclic polyether compounds found in blooms of the marine dinoflagellate Karenia brevis (K. brevis) and are potent neurotoxins. Preventive controls for NSP in the U.S. currently rely upon environmental monitoring of K. brevis blooms and assessment of their shellfish toxicity by mouse bioassay. The mouse bioassay for NSP approved by National Shellfish Sanitation Program was developed in the 1960s when very little information on the structural and toxicological properties of brevetoxins in algae and shellfish was available. Alternative methods to mouse bioassay based on current scientific knowledge in the area are needed for monitoring NSP toxins. It is now established that brevetoxins are metabolized extensively in shellfish. Algal brevetoxins undergo oxidation and reduction, as well as conjugation with fatty acids and amino acids in shellfish. Recently, three metabolites have been identified as biomarkers of brevetoxin exposure and toxicity in Eastern oyster (Crassostrea virginica) and hard clam (Mercenaria sp.). The role of these biomarkers in monitoring NSP toxins in K. brevis exposed molluscan shellfish is reviewed. Comparisons of biomarker levels by liquid chromatography-mass spectrometry (LC-MS) with composite toxin as measured by enzyme linked immunosorbent assay (ELISA), and shellfish toxicity by mouse bioassay, support the application of these biomarkers as a dynamic and powerful approach for monitoring brevetoxins in shellfish and prevention of NSP.
In this study, a collection of Salmonella enterica subspecies obtained from live mice caught on 32 poultry farms in the Northeast US between 1995 to 1998 was evaluated to provide a historical reference for serotype distribution during a time when egg contamination by serotype Enteritidis was at its peak. Of 821 mice cultured, 157 were positive (19.1%). Seven mice harbored two serotypes of Salmonella. Nine serotypes were detected, eight of which are often associated with foodborne illness. The three most prevalent serotypes were Enteritidis, Heidelberg, and Typhimurium. Enteritidis and Typhimurium were obtained from both spleens and intestines without preference according to type of sample. In contrast, Heidelberg was isolated most often from intestines and Schwarzengrund was most often obtained from spleens. These results support that the house mouse Mus musculus was a risk factor for introduction of multiple pathogenic Salmonella serotypes in poultry raised in the Northeast US during the mid-1990s. Isolates were submitted to the Food and Drug Administration and draft genomes for 64 isolates of Salmonella enterica serovar Enteritidis data have been released through the National Center for Biotechnology Information via the GenomeTrakr network.