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Salmonella causes an estimated 1.3 million human foodborne illnesses and more than 500 deaths each year in the United States, representing an annual estimated cost to the economy of approximately $2.4 billion. Salmonella enterica comprises more than 2,500 serotypes. With this genetic and environmental diversity, serotypes are adapted to live in a variety of hosts, which may or may not manifest with clinical illness. Thus, Salmonella presents a multifaceted threat to food production and safety. Salmonella have been isolated from all food animals and can cause morbidity and mortality in swine, cattle, sheep, and poultry. The link between human salmonellosis and host animals is most clear in poultry. During the early part of the 20th century, a successful campaign was waged to eliminate fowl typhoid caused by Salmonella Gallinarum/Pullorum. Microbial ecology is much like macroecology; environmental niches are filled by adapted and specialized species. Elimination of S. Gallinarum cleared a niche in the on-farm and intestinal microbial ecology that was quickly exploited by Salmonella Enteritidis and other serotypes that live in other hosts, such as rodents. In the years since, human salmonellosis cases linked to poultry have increased to the point that uncooked chicken and eggs are regarded as toxic in the zeitgeist. Salmonellosis caused by poultry products have increased significantly in the past 5 yr, leading to a USDA Food Safety and Inspection Service "Salmonella Attack Plan" that aims to reduce the incidence of Salmonella in chickens below the current 19%. The prevalence of Salmonella in swine and cattle is lower, but still poses a threat to food safety and production efficiency. Thus, approaches to reducing Salmonella in animals must take into consideration that the microbial ecology of the animal is a critical factor that should be accounted for when designing intervention strategies. Use of competitive exclusion, sodium chlorate, vaccination, and bacteriophage are all strategies that can reduce Salmonella in the live animal, but it is vital to understand how they function so that we do not invoke the law of unintended consequences. [ABSTRACT FROM AUTHOR]

Salmonella causes an estimated 1.3 million human foodborne illnesses and more than 500 deaths each year in the United States, representing an annual estimated cost to the economy of approximately $2.4 billion. Salmonella enterica comprises more than 2,500 serotypes. With this genetic and environmental diversity, serotypes are adapted to live in a variety of hosts, which may or may not manifest with clinical illness. Thus, Salmonella presents a multifaceted threat to food production and safety. Salmonella have been isolated from all food animals and can cause morbidity and mortality in swine, cattle, sheep, and poultry. The link between human salmonellosis and host animals is most clear in poultry. During the early part of the 20th century, a successful campaign was waged to eliminate fowl typhoid caused by Salmonella Gallinarum/Pullorum. Microbial ecology is much like macroecology; environmental niches are filled by adapted and specialized species. Elimination of S. Gallinarum cleared a niche in the on-farm and intestinal microbial ecology that was quickly exploited by Salmonella Enteritidis and other serotypes that live in other hosts, such as rodents. In the years since, human salmonellosis cases linked to poultry have increased to the point that uncooked chicken and eggs are regarded as toxic in the zeitgeist. Salmonellosis caused by poultry products have increased significantly in the past 5 yr, leading to a USDA Food Safety and Inspection Service "Salmonella Attack Plan" that aims to reduce the incidence of Salmonella in chickens below the current 19%. The prevalence of Salmonella in swine and cattle is lower, but still poses a threat to food safety and production efficiency. Thus, approaches to reducing Salmonella in animals must take into consideration that the microbial ecology of the animal is a critical factor that should be accounted for when designing intervention strategies. Use of competitive exclusion, sodium chlorate, vaccination, and bacteriophage are all strategies that can reduce Salmonella in the live animal, but it is vital to understand how they function so that we do not invoke the law of unintended consequences. [ABSTRACT FROM AUTHOR]

Gastrointestinal complications of multiple myeloma (MM) treatment are common and include nausea, constipation, and diarrhea. However, acute gastrointestinal events like perforations are rare. We aimed to describe the characteristics and outcomes of patients with MM that had colonic perforations during their treatment. This is a retrospective study that included patients from all three Mayo Clinic sites who had MM and developed a colonic perforation. All patients were diagnosed with colonic perforations based on CT scans and were surgically treated. Patients diagnosed with AL amyloidosis, a perforated colon complicating neutropenic colitis during ASCT and those with perforation due to colonic cancer were excluded. A high dose of dexamethasone was defined as ≥40 mg dexamethasone once a week. Thirty patients met inclusion criteria. All patients received steroids at doses ≥10 mg once weekly prior to the perforation, while four (11%) were on high-dose dexamethasone without chemotherapy. Fourteen patients were given high doses of dexamethasone. Twenty-five patients required ostomies with all surviving surgery. Twenty-four perforations (80%) were associated with diverticulitis. Treatment with steroids was resumed in 23 patients with no further gastrointestinal complications. The median OS was 20 months following perforation (IQR 8-59). Within the same timeframe 5854 patients were treated at Mayo Clinic for MM, making the risk of bowel perforation 0.5%. Intestinal perforations in MM are rare and, in our series, always occurred with dexamethasone ≥10 mg per week. Urgent surgery is lifesaving and resumption of anti-myeloma treatment appears to be safe., (© 2020 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.)