Probably: Should the toilet seat be closed before flushing?

About 30 years ago, I learned to consistently put the toilet seat down after spraying most of my urine into the bowl.

A wife, four daughters, another wife, another daughter, put the damn seat down. I get it.

With the tradies doing renos and using the loo, I had to remind the boys, house full of females, close the lid.

But should people, regardless of gender, close the seat before flushing?

I have anecdotally noticed more media references of a recommendation to close the lid before flushing, so I asked Dr. Don.

That’s Don Schaffner of Rutgers University, podcaster with Chapman, and friend of the barfblog.

(He gets paid to look up this stuff, I don’t, I’m just curious.)

Don replied within hours to say that it looks like there is some pretty good science to show this is more than a theoretical risk.

The potential spread of infection caused by aerosol contamination of surfaces after flushing a domestic toilet.

Microbial biogeography of public restroom surfaces

“On toilet surfaces, gut-associated taxa were more prevalent, suggesting fecal contamination of these surfaces.”

Potential for aerosolization of Clostridium difficile after flushing toilets: the role of toilet lids in reducing environmental contamination risk.

Chapman even chipped with a couple of papers from Chuck Gerba.

My risk-based recommendation?

Maybe.

And be careful (At home, I pee sitting down to minimize the mess, and complaints. That’s minimize, not eliminate).

Foodborne pathogen typing: Getting it right, it’s sorta important

In 2012, the European Centre for Disease Prevention and Control (ECDC) initiated external quality assessment (EQA) schemes for molecular typing including the National Public Health Reference Laboratories in Europe.

get-it-rightThe overall aim for these EQA schemes was to enhance the European surveillance of food-borne pathogens by evaluating and improving the quality and comparability of molecular typing. The EQAs were organised by Statens Serum Institut (SSI) and included Salmonella enterica subsp. enterica, verocytotoxin-producing Escherichia coli (VTEC) and Listeria monocytogenes. Inter-laboratory comparable pulsed-field gel electrophoresis (PFGE) images were obtained from 10 of 17 of the participating laboratories for Listeria, 15 of 25 for Salmonella, but only nine of 20 for VTEC. Most problems were related to PFGE running conditions and/or incorrect use of image acquisition. Analysis of the gels was done in good accordance with the provided guidelines. Furthermore, we assessed the multilocus variable-number tandem repeat analysis (MLVA) scheme for S. Typhimurium. Of 15 laboratories, nine submitted correct results for all analysed strains, and four had difficulties with one strain only. In conclusion, both PFGE and MLVA are prone to variation in quality, and there is therefore a continuous need for standardisation and validation of laboratory performance for molecular typing methods of food-borne pathogens in the human public health sector.

Evaluation of molecular typing of foodborne pathogens in European reference laboratories from 2012 To 2013

Eurosurveillance, Volume 21, Issue 50, 15 December 2016

S Schjørring, T Niskanen, M Torpdahl, JT Björkman, EM Nielsen

http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=22673

Salmonella on tomato leaves

Thirty years ago, I was a graduate student inoculating different lines of tomatoes with Verticillium wilt.

I hated it.

tomato.verticilliumSo I became editor of the student newspaper.

But those plant pathogens and tomatoes are still embedded in my DNA, so when I see an abstract like this, I gotta send it out.

Plant pathogen infection is a critical factor for the persistence of Salmonella enterica on plants. We investigated the mechanisms responsible for the persistence of S. enterica on diseased tomato plants by using four diverse bacterial spot Xanthomonas species that differ in disease severities. Xanthomonas euvesicatoria and X. gardneri infection fostered S. enterica growth, while X. perforans infection did not induce growth but supported the persistence of S. enterica. X. vesicatoria-infected leaves harbored S. enterica populations similar to those on healthy leaves. Growth of S. enterica was associated with extensive water-soaking and necrosis in X. euvesicatoria- and X. gardneri-infected plants. The contribution of water-soaking to the growth of S. enterica was corroborated by an increased growth of populations on water-saturated leaves in the absence of a plant pathogen. S. enterica aggregates were observed with bacterial spot lesions caused by either X. euvesicatoria or X. vesicatoria; however, more S. entericaaggregates formed on X. euvesicatoria-infected leaves as a result of larger lesion sizes per leaf area and extensive water-soaking. Sparsely distributed lesions caused by X. vesicatoria infection do not support the overall growth of S. entericaor aggregates in areas without lesions or water-soaking; S. enterica was observed as single cells and not aggregates.

Thus, pathogen-induced water-soaking and necrosis allow S. enterica to replicate and proliferate on tomato leaves. The finding that the pathogen-induced virulence phenotype affects the fate of S. entericapopulations in diseased plants suggests that targeting of plant pathogen disease is important in controlling S. enterica populations on plants.

 Plant Pathogen-Induced Water-Soaking Promotes Salmonella enterica Growth on Tomato Leaves

Applied and Environmental Microbiology, Volume 81, Number 23, December 2015

N Potnis, J Colee, J Jones, J Barak

Device speeds concentration step in food-pathogen detection

Researchers have developed a system that concentrates foodborne salmonella and other pathogens faster than conventional methods by using hollow thread-like fibers that filter out the cells, representing a potential new tool for speedier detection.

The machine, called a continuous cell concentration device, could make it possible to routinely analyze food or water samples to screen for devicespeedspathogens within a single work shift at food processing plants.

“This approach begins to address the critical need for the food industry for detecting food pathogens within six hours or less,” said Michael Ladisch, a distinguished professor of agricultural and biological engineering at Purdue University. “Ideally, you want to detect foodborne pathogens in one work shift, from start to finish, which means extracting the sample, concentrating the cells and detection.”

Findings are detailed in a research paper to appear in November in the journal Applied and Environmental Microbiology. The paper was authored by doctoral student Xuan Li; LORRE research scientist Eduardo Ximenes; postdoctoral research associate Mary Anne Roshni Amalaradjou; undergraduate student Hunter B. Vibbert; senior research engineer Kirk Foster; engineering resources manager Jim Jones; microbiologist Xingya Liu; Arun K. Bhunia, a professor of food microbiology; and Ladisch.  Findings showed the system was able to concentrate inoculated salmonella by 500 to 1,000 times the original concentration in test samples.

Nestle to boost foodborne pathogen research

Nestle SA, the world’s biggest food and drink company, is, according to Associated Press, boosting research to tackle the threat of ever-stronger strains of bacteria and germs in food manufacturing.

The Vevey, Switzerland-based company said Thursday it will initially focus on several types of foodborne bacteria — particularly a dangerous strain nestle-of bacterium E. coli that infects people and pumps out a poison called Shiga toxin — and Norovirus and Hepatitis A.

Company officials and industry experts looked over more than 20 new microbiology labs that Nestle opened Thursday within its research center outside Lausanne, the last time they will be shown publicly before sealing them off and restricting access to scientists in protective clothing.

They described the spotless new labs as among the world’s most advanced microbiology research facilities, and the most sophisticated in the food industry, some at biosafety containment level three, on a scale of one to four.

John O’Brien, a former chief executive of the Food Safety Authority of Ireland who is now head of food safety at Nestle’s research center, said the company “cannot afford errors” as it aims for better ways of processing food that kills germs but keeps as much of the nutrients and taste as possible. That requires a lot of genetic and enzymatic testing.

“With the increasing problem of emerging food-borne pathogens, such as the Shiga toxin-producing strains of E. coli, a risk assessment is only possible once we know what genes are carried by that organism,” O’Brien told officials. “So we need to get down to the genome level increasingly. Now, that requires a lot of molecular detective work, which is why we are investing so much in molecular tools.”

Canadian MDs want junk food in same category as E. coli

From the I’m-not-sure-they’ve-thought-this-through category, a cardiologist and two public-health professors from Alberta argue in the Canadian Journal of Cardiology that junk food and its ingredients are such major health hazards that products with excessive amounts of sugar, salt and saturated fats should be labelled as “pathogens” — a word normally applied to viruses and other disease-causing bugs.

The National Post reports that authorities and the media grab public attention now when they report the spread of traditional pathogens — like listeria or E. coli — in contaminated food or water, and should similarly highlight food ingredients that are responsible for killing vastly more Canadians, says the article.

“It’s really just a nomenclature to attract attention to the fact we have a problem here and something needs to be done about it,” said Dr. Norm Campbell, a University of Calgary cardiologist and co-author of the paper. “It will hopefully … result in an evolution of our food so it’s again a source of health, not a source of disease.”

A combination of two Greek words, pathogen literally means producer of illness, though most often refers specifically to a bacteria, virus or other infectious agent.

Dr. Campbell, a specialist in hypertension and the effects of sodium on it, denied that his idea amounts to nanny-state interference in the marketplace, arguing there is as much or more reason to regulate food as to control highway speed limits or air traffic, government interventions that Canadians tolerate. Some evidence suggests that salt in food alone contributes to 14,000 deaths and 40,000 hospitalizations yearly, he said.’

“Why regulate crime? ‘Oh, it’s a murder, they shouldn’t be allowed a second chance.’ Well, the food industry kills many thousands more than that murderer ever had a hope of doing.”

Can E. coli get inside plant vascular system? 2009 research says unlikely

The paper was published in July 2009 but the U.S. Department of Agriculture put out a press release today saying that Escherichia coli is not likely to contaminate the internal vascular structure of field-grown leafy greens and thus increase the incidence of foodborne illness.

The timing was probably coupled with pretty pictures of the research, appearing in the April 2011 issue of USDA’s Agricultural Research magazine.

Agricultural Research Service (ARS) microbiologist Manan Sharma wanted to find out if plant roots could draw in E. coli pathogens from the soil when taking in nutrients and water. He and colleagues modified several types of E. coli—including some highly pathogenic strains that cause foodborne illness—by adding a gene for fluorescence. This allowed them to track the pathogen’s journey from the field to the produce.

The team, which is located at the ARS Environmental Microbial and Food Safety Laboratory in Beltsville, Md., confirmed that the pathogenic E. coli could survive in the soil for up to 28 days. They also observed that the fluorescent E. coli cells were capable of migrating into the roots of spinach plants.

The researchers also examined baby spinach plants over the course of 28 days after germination to see if any of the E. coli strains were taken up past the roots and into the plant’s interior structures. For this part of the study, they grew baby spinach in pasteurized soil and hydroponic media.

At day 28, there was no evidence that the E. coli had become "internalized" in leaves or shoots of baby spinach plants grown in the pasteurized soil. E. coli could be detected in hydroponically-grown spinach samples, but its survival in shoot tissue was sporadic 28 days after the plants had germinated.

These findings strongly suggest that although E. coli can survive in soils, it’s highly unlikely that foodborne illness would result from the bacterium becoming "internalized" through roots in leafy produce.

Chapman reviewed the idea of internalization of human pathogens by plants for barfblog in 2008 and it’s available at
http://barfblog.foodsafety.ksu.edu/blog/139669/08/05/28/pathogens-produce-brief-review

The original abstract is below:
A novel approach to investigate the uptake and internalization of Escherichia coli O157:H7 in spinach cultivated in soil and hydroponic medium.
Sharma M, Ingram DT, Patel JR, Millner PD, Wang X, Hull AE, Donnenberg MS.
J Food Prot. 2009 Jul;72(7):1513-20.

Internalization of Escherichia coli O157:H7 into spinach plants through root uptake is a potential route of contamination. A Tn7-based plasmid vector was used to insert a green fluorescent protein gene into the attTn7 site in the E. coli chromosome. Three green fluorescent protein-labeled E. coli inocula were used: produce outbreak O157:H7 strains RM4407 and RM5279 (inoculum 1), ground beef outbreak O157:H7 strain 86-24h11 (inoculum 2), and commensal strain HS (inoculum 3). These strains were cultivated in fecal slurries and applied at ca. 10(3) or 10(7) CFU/g to pasteurized soils in which baby spinach seedlings were planted. No E. coli was recovered by spiral plating from surface-sanitized internal tissues of spinach plants on days 0, 7, 14, 21, and 28. Inoculum 1 survived at significantly higher populations (P < 0.05) in the soil than did inoculum 3 after 14, 21, and 28 days, indicating that produce outbreak strains of E. coli O157:H7 may be less physiologically stressed in soils than are nonpathogenic E. coli isolates. Inoculum 2 applied at ca. 10(7) CFU/ml to hydroponic medium was consistently recovered by spiral plating from the shoot tissues of spinach plants after 14 days (3.73 log CFU per shoot) and 21 days (4.35 log CFU per shoot). Fluorescent E. coli cells were microscopically observed in root tissues in 23 (21%) of 108 spinach plants grown in inoculated soils. No internalized E. coli was microscopically observed in shoot tissue of plants grown in inoculated soil. These studies do not provide evidence for efficient uptake of E. coli O157:H7 from soil to internal plant tissue.
 

Acuff speaks, over and over and over (because it’s on video at bites.ksu.edu)***

Dr. Gary Acuff game a seminar at Kansas State University on Nov. 9, 2010, entitled, The End Game: What is Really Achievable in Pathogen Reduction.

The slides for Acuff’s talk are available at: http://bites.ksu.edu/ksu-seminar

The video is available at: http://bites.ksu.edu/sites/default/files/Gary-Acuff-Guest-Lecture-Nov-2010_0.mp4

Or under the video section on the front page of bites.ksu.edu.

Texas A&M University announced last month that Acuff was going to become director for the Center for Food Safety, and will lead expanded food safety efforts.

Prior to his appointment as Director of the Center for Food Safety, Acuff served as interim head and then head of the department of animal science from 2004 to 2010. And before that he taught undergraduate and graduate level courses and laboratories in food microbiology for 20 years and conducted research on the microbiological quality and safety of foods through his appointment with Texas AgriLife Research.

A past-president of the International Association of Food Protection, Acuff currently is chairman of a 10-member committee for the National Research Council, which evaluates food safety requirements for the Federal Purchase Ground Beef Program.