Blocking Campy’s ability to latch on

A team at Griffith University in Queensland, Australia, has found a way to disable one sensor of Campylobacter jejuni, that stops it from being able to attach to its host and therefore cause gastroenteritis.

chickenThe findings were published in Nature Communications and show a wide range of possibilities for tackling various strands of gastro, lead researcher Professor Victoria Korolik said.

“We conducted the study in chickens by disabling this particular sensor (CcrG) and we found that it does reduce the level of colonisation,” she said.

“We found this sensor (CcrG) does not occur in all strains of this bacteria, only in about 10 or 11 per cent, but those strains tend to be those isolated from really sick people such as those that have meningitis as a consequence of gastro.”

Professor Korolik described the sensor as a type of “hand” that grabbed onto a specific molecule within the stomach of its host that could lead the bacteria to cells from which to colonise and cause gastroenteritis.

“This sensor grabs a molecule, it grabs it and holds it like you would a ball in your hand and that molecule tells the bacteria they are on the right track and moving towards the right cell,” she said.

“They also have a part that goes inside the cell and sends a signal – to go forward or turn around depending on what is happening.

“Because it can find the human cells efficiently and quickly, it can attack and cause disease.”

Professor Korolik said an antimicrobial drug that acted as a synthetic “ball” could block the sensor and prevent it from finding the cell.

“If you block the hand part of the receptor, the signal is stuck and the bacteria goes around in circle and can’t find its target,” she said.

“If we can design a ‘ball’ that is a better fit than the natural one then we can block the receptor – if the bacteria can’t find its direction because it doesn’t know what else is on the environment because it is blocked and it goes around and around and is eventually passed out.”

Professor Korolik said every bacteria has a variety of sensory structures that are separate from each other which allows one sensor of one bacteria to be targetted without impacting on existing gut flora.

Campylobacter jejuni bacteria is the most common cause of food poisoning in Australia and hospitalised more than 3200 people in 2014, according to Queensland Health.

More than 500 cases have been reported in Queensland in the past month, with the gastrointestinal disease impacting 16,436 across Australia this year so far, according to the national department of health.

Campy in organic and conventional layer chickens

Poultry is a major source of Campylobacter, which can cause foodborne bacterial gastroenteritis in humans. Additionally, poultry-associated Campylobacter can develop resistance to important antimicrobials, which increases the risk to public health. While broiler chickens have been the focus of many studies, the emergence of antimicrobial-resistant Campylobacter on layer farms has not received equal attention. However, the growing popularity of cage-free and organic layer farming necessitates a closer assessment of (1) the impact of these farming practices on the emergence of antimicrobial-resistant Campylobacter and (2) layers as a potential source for the transmission of these pathogens.

chicken-thermHere, we showed that the prevalence of Campylobacter on organic and conventional layer farms was statistically similar (p > 0.05). However, the average number of Campylobacter jejuni-positive organically grown hens was lower (p < 0.05) in comparison to conventionally grown hens. Campylobacter isolated from both production systems carried antimicrobial resistance genes. The tet(O) and cmeB were the most frequently detected genes, while the occurrence of aph-3-1 and blaOXA-61 was significantly lower (p < 0.05). Farming practices appeared to have an effect on the antimicrobial resistance phenotype, because the isolates from organically grown hens on two farms (OF-2 and OF-3) exhibited significantly lower resistance (p < 0.05) to ciprofloxacin, erythromycin, and tylosin. However, on one of the sampled organic farms (OF-1), a relatively high number of antimicrobial-resistant Campylobacter were isolated.

We conclude that organic farming can potentially impact the emergence of antimicrobial-resistant Campylobacter. Nevertheless, this impact should be regularly monitored to avoid potential relapses.

Antimicrobial-resistant Campylobacter in organically and conventionally raised layer chickens

Foodborne Pathogens and Disease. September 2016, ahead of print. doi:10.1089/fpd.2016.2161.

Kassem Issmat I., Kehinde Olugbenga, Kumar Anand, and Rajashekara Gireesh

Crypto: My big barfing Greek wedding

Amanda Devlin of The Sun reports a  bride and groom who thought they were suffering from wedding day jitters had actually been struck down by a gastric illness – as well as half of their guests.

big-fat-greek-weddingGemma Tepper, 32, her partner, Lee, 36, say their big day was ruined by the outbreak of Cryptosporidium – a respiratory and gastic illness – at their hotel on the Greek island of Zante.

Now 60 holidaymakers have hired international personal injury lawyers, Irwin Mitchell, to investigate the outbreak.

Gemma, a transport administration clerk, who was staying at the Marelen Hotel with her husband-to-be and their daughter Sylvie said: “When we both started suffering illness on our wedding day we just put it down to being nervous, but we quickly realised it was a lot more than that when the symptoms continued for the next few days.”

The symptoms persisted and both Gemma and Lee, from Pontefract, West Yorks., were forced to time off work when they returned home.

Tests confirmed Gemma was suffering from Cryptosporidium.

To serve humans: It’s a cookbook! Soylent brand Food Bar recalled due to illnesses

Following on from reports that Soylent food bars were making people barf – most unfortunate food product name in history? – the Canadian Food Inspection Agency reports that Rosa Foods Inc. is recalling Soylent brand Food Bar from the marketplace due to reported illnesses. Consumers should not consume the recalled products described below.

soylentThe following products have been sold through the Internet at

Brand name//Common name//size//Code(s) on Product//UPC

Soylent//Food bar//60g//14JUL17, 15JUL17, 18JUL18, 02AUG17, 04AUG17, 08AUG17, 10AUG//None

Soylent//Food bar//12x60g//14JUL17, 15JUL17, 18JUL17, 02AUG17, 04AUG17, 08AUG17, 10AUG//858369006023

There have been reported illnesses associated with the consumption of these products.

Saskatchewan crypto outbreak folks settle additional cases 15 years later

Make people sick, expect to pay; even after over a decade.

According to CBC, the city of North Battleford, the Saskatchewan government and the water folks have $3.3 million for minors who were ill in 2001.

A settlement agreement for minors who had water contaminated with cryptosporidium in North Battleford, Sask., 15 years ago has been given preliminary

Thousands of people got sick in March and April 2001 when the parasite, which can cause diarrhea and vomiting, was found in the city’s drinking water.

In 2003, 700 people were paid compensation from a pool of $3.2 million depending how sick they had been.

The newest settlement applies to those in an “infant class”, people who were under 18 when they got sick. The agreement still needs final approval from the courts on Dec. 1.

How bacteria build biofilms

Princeton researchers have for the first time revealed the mechanics of how bacteria build up slimy masses, called biofilms, cell by cell. When encased in biofilms in the human body, bacteria are a thousand times less susceptible to antibiotics, making certain infections, such as pneumonia, difficult to treat and potentially lethal. 

biofilm-illustration_1150In a study published Sept. 6 in the Proceedings of the National Academy of Sciences, a team at Princeton tracked a single bacterial cell as it grew into a mature biofilm of 10,000 cells with an ordered architecture. The findings should help scientists learn more about bacterial behavior and open up new ways of attacking biofilms with drugs.

“No one’s ever peered inside a living biofilm and watched it develop cell by cell,” said Bonnie Bassler, a senior author of the paper and the Squibb Professor in Molecular Biology at Princeton, as well as a Howard Hughes Medical Institute Investigator. “With this paper, we can now understand for the first time how communities of bacteria form a biofilm.”

The discovery became possible thanks to a special microscopy method pioneered at Princeton by a former postdoctoral research associate, Knut Drescher, which allowed the imaging of single cells, letting researchers follow a budding biofilm in real time.

“We have used a state-of-the-art technique to see into the core of a living, growing biofilm,” said postdoctoral research associate Jing Yan, lead author of the new study. Along with membership in Bassler’s lab, Yan belongs to the Complex Fluids Group led by paper senior co-author Howard Stone, the Donald R. Dixon ’69 and Elizabeth W. Dixon Professor of Mechanical and Aerospace Engineering at Princeton. Yan is further advised by paper senior author Ned Wingreen, the Howard A. Prior Professor of the Life Sciences and acting director of the Lewis-Sigler Institute for Integrative Genomics at Princeton.

“The research that produced this paper sits at the frontier between materials science, engineering, physics and biology and represents a fantastic collaboration across Princeton University,” said Bassler.

Along with Yan, Bassler, Stone and Wingreen, a fifth co-author of the paper is Andrew Sharo, a former undergraduate in Princeton’s Department of Physics and now at the University of California-Berkeley.

The researchers chose Vibrio cholerae for their model biofilm organism because of its long history of study and threat to human health, causing the diarrheal disease cholera. A curved, rod-shaped bacterium, V. cholerae lives as a free-swimming cell in brackish water or saltwater. When V. cholerae makes contact with a food particle, perhaps on the shell of a crab or a shrimp, or a human intestinal cell during disease, the bacterium attaches itself and begins to reproduce. The expanding colony’s members secrete a glue-like substance to keep from getting washed away and to protect themselves from competing bacteria.

Previous efforts to delve into how the cells in a burgeoning biofilm interact had failed because of insufficient optical resolution; basically, what one cell was doing in the opaque mass could not be distinguished from its neighbors. 

The Princeton researchers overcame this problem in several ways. First, they genetically modified the bacterial strain so the cells produced proteins that glow brightly when illuminated by specific colors of light. The proteins selected offer the brightest available fluorescence, making each cell easier to pick out, while reducing the intensity of potentially cell-damaging light required for the experiment.

The team then used a confocal microscope, a device that focuses on a single portion of a specimen from a certain distance. By making hundreds of such observations, images can be stacked together to create a three-dimensional image of the entire specimen. “It’s like looking deep into the interior of a biofilm without having to slice it open,” said Yan.

Another boost for the research team came from computer algorithms originally developed for fields like materials science. The algorithms differentiated closely clustered sources of light, in this case the many bunched-up V. cholerae cells in a thickening biofilm. 

What the Princeton team saw was remarkable. At first, the bacterial colony expanded horizontally on the given surface in the experiment. As each cell split, the resulting daughter cells firmly attached to the surface alongside their parent cells. Squeezed by increasing numbers of offspring bacteria, however, the cells at the heart of expanding colony were forced to detach from the surface and point vertically. The bacterial colony thus went from a flat, two-dimensional mass to an expanding, three-dimensional blob, all held together by gunk in the developing biofilm.

The Princeton team dug a bit deeper into the genetics behind this cellular behavior. A single gene, dubbed RbmA, is key to behavior in which new cells connect in such a way to develop a three-dimensional biofilm. When the researchers deactivated the gene, a big, diffuse and floppy biofilm formed. When RbmA performed as normal, though, a denser, stronger biofilm resulted as the cells stayed linked to each other. Thus, RbmA provides the biofilm its resilience, providing insight into a potential Achilles heel that could be targeted for therapeutic intervention.

Ongoing work is now measuring the physical forces experienced by cells uplifting at the biofilm’s center so the overall mechanics can be precisely worked out. “We are currently trying to develop a mathematical model for how the bacterial colony grows in time and how the spatial features are linked to typical mechanical features of the biofilm,” said Stone. 

Toxo in cat poop threatens Hawaiian monk seals

Two wildlife issues have collided in Hawaii, pitting one group of animal defenders against another in an impassioned debate. The point of contention? Deadly cat poop and the feral felines that produce it.

hawaiian-monk-sealsFederal researchers believe feces from the legions of stray cats roaming Hawaii is spreading a disease that is killing Hawaiian monk seals, some of the world’s most endangered marine mammals. Some conservationists advocate euthanizing those cats that no one wants, and that has cat lovers up in arms.

“It’s a very difficult, emotional issue,” said state Sen. Mike Gabbard, chairman of a committee that earlier this year heard a proposal to ban the feeding of feral cats on state land. The panel abandoned the bill after an outcry.

“It struck a nerve in our community,” he said.

The problem stems from a parasite common in cats that can cause toxoplasmosis, a disease that has killed at least five female Hawaiian monk seals and three males since 2001, according to the National Oceanic and Atmospheric Administration.

“While eight seals may not sound like a lot of animals, it actually has pretty large ramifications for an endangered population where there’s only about 1,300 seals in existence at this point in time,” said Michelle Barbieri, veterinary medical officer for NOAA’s Hawaiian monk seal research program. Scientists believe monk seals become exposed by ingesting contaminated water or prey.

Stray cats, meanwhile, have no predators in Hawaii and have ballooned in numbers across the state. Some 300,000 feral cats roam Oahu alone, according to marketing research commissioned by the Hawaiian Humane Society in 2015.

Mighty Taco outbreak pathogen revealed; John McEnroe was wrong

Almost every time someone mentions B. cereus to me I respond with ‘you cannot B. cereus’ as an homage to tennis legend and tantrum thrower John McEnroe’s excellent autobiography. I don’t know if anyone gets the joke.

WGRZ news reports that over 160 Mighty Taco patrons were ill because of B. cereus in refried beans.mte4mdazndewnja3nzy5mtay

The bacteria Bacillus cereus was found in patient clinical specimens and in samples of refried beans from Mighty Taco restaurants, according to a statement from the DOH released Monday.

Bacillus cereus usually causes vomiting within 30 minutes to 6 hours after eating contaminated food, the department says, which is consistent with symptoms described by those who ate at Mighty Taco.

The FDA is looking into the refried beans supplier, Pellegrino Food Products in Warren, Pennsylvania.


‘It depends and it’s complicated’ Schaffner on the 5-second rule

Friend of the shares his thoughts about the five-second rule, peer-reviewed research, and media attention. Thanks for doing this, Don.


In March 2014 I got angry. I saw an article in the popular press indicating that researchers from Aston University in the United Kingdom had “proved the five second rule was real”  It was not the finding that made me angry as much as the science behind it. Or more properly the lack of science behind it.

don-schaffner-214x300We’ve been studying microbial cross-contamination in my lab for more than 15 years, and I have considered myself a quantitative food microbiologist for my entire career. Given those two observations, it’s only natural that I be interested in an article like this. But when I reached out to the University for more information I learned the research had not been peer-reviewed, and the best that they could offer was a PowerPoint presentation. A PowerPoint presentation is not science. Science proceeds through peer review. Like democracy it’s a terrible system, just the best one we have found so far.

After I got angry, I got busy.  And like any good professor by “got busy”, I mean that a graduate student got busy doing the actual  work of science.  I had a brand-new MS student starting in my lab, and she had funding from another source, but needed a research project. We worked together to design an appropriate series of studies that would advance our understanding of microbial cross-contamination while at the same time could generate a press release that might get a little bit of attention. Like any good scientists we built on the work of others. We acknowledged non-peer-reviewed work from other institutions that paved the way like high school student Jillian Clarke in Hans Blaschek’s lab at the University of Illinois. We also acknowledged the first peer-reviewed research from Paul Dawson’s lab at Clemson University.

Flash forward a couple of years, we submitted our article to one of the best journals out there that publishes food microbiology research, Applied and Environmental Microbiology and after peer review and appropriate revisions our article was accepted for publication.  I reached out to a colleague in the media relations department at Rutgers University, and we worked together to write a press release.

As you may have noticed, we have garnered extensive media attention with thousands of articles published around the world. The New York Times did a particularly nice piece interviewing me as well as my colleague Bill Hallman, and barfblog’s Doug Powell.  It has been a fun ride, but I’m looking forward to getting back to other things.  Just keeping up with the requests for interviews has been almost a full-time job, I have generally resisted the temptation to respond to commenters on the Internet, who complain about everything from the waste of grant funds (not the case, we used discretionary funds I raised myself), to suggestions that I studied the wrong thing.

But before we close the books on this one, I do want to respond to Aaron Carroll, a medical doctor who became interested in the topic when he co-authored a book on medical myths. Carroll insists that it’s not any of the factors we studied that are important, but rather how dirty the surface might be.  He is certainly correct in that the level of contamination, as well as the type of contamination are important (pro tip: coliforms don’t make us sick), but the degree to which those microbes transfer is also essential in determining risk. As I’ve said in many interviews, if there are no pathogens present on the surface, the risk is zero. The immune state of the person doing the eating also makes a difference. The risk for someone who is immunocompromised is higher than the risk someone who has a healthy immune system.

schaffner-facebook-apr_-14So as any listener to our food safety podcast will know, it turns out “it depends” and “it’s complicated.” The level of contamination, the type of contamination, the nature of the surface, the nature of the food, as well as the immune state of the person all matter in determining risk of eating food off the floor.

Longer contact times increase cross-contamination of Enterobacter aerogenes from surfaces to food

Applied and Environmental Microbiology; Appl. Environ. Microbiol. November 2016 vol. 82 no. 21 6490-6496

Robyn C. Miranda and Donald W. Schaffner


Bacterial cross-contamination from surfaces to food can contribute to foodborne disease. The cross-contamination rate of Enterobacter aerogenes on household surfaces was evaluated by using scenarios that differed by surface type, food type, contact time (<1, 5, 30, and 300 s), and inoculum matrix (tryptic soy broth or peptone buffer). The surfaces used were stainless steel, tile, wood, and carpet. The food types were watermelon, bread, bread with butter, and gummy candy. Surfaces (25 cm2) were spot inoculated with 1 ml of inoculum and allowed to dry for 5 h, yielding an approximate concentration of 107 CFU/surface. Foods (with a 16-cm2contact area) were dropped onto the surfaces from a height of 12.5 cm and left to rest as appropriate. Posttransfer, surfaces and foods were placed in sterile filter bags and homogenized or massaged, diluted, and plated on tryptic soy agar. The transfer rate was quantified as the log percent transfer from the surface to the food. Contact time, food, and surface type all had highly significant effects (P < 0.000001) on the log percent transfer of bacteria. The inoculum matrix (tryptic soy broth or peptone buffer) also had a significant effect on transfer (P = 0.013), and most interaction terms were significant. More bacteria transferred to watermelon (∼0.2 to 97%) than to any other food, while the least bacteria transferred to gummy candy (∼0.1 to 62%). Transfer of bacteria to bread (∼0.02 to 94%) was similar to transfer of bacteria to bread with butter (∼0.02 to 82%), and these transfer rates under a given set of conditions were more variable than with watermelon and gummy candy.

IMPORTANCE The popular notion of the “five-second rule” is that food dropped on the floor and left there for <5 s is “safe” because bacteria need time to transfer. The rule has been explored by a single study in the published literature and on at least two television shows. Results from two academic laboratories have been shared through press releases but remain unpublished. We explored this topic by using four different surfaces (stainless steel, ceramic tile, wood, and carpet), four different foods (watermelon, bread, bread with butter, and gummy candy), four different contact times (<1, 5, 30, and 300 s), and two bacterial preparation methods. Although we found that longer contact times result in more transfer, we also found that other factors, including the nature of the food and the surface, are of equal or greater importance. Some transfer takes place “instantaneously,” at times of <1 s, disproving the five-second rule.

Disinfection tolerance of C. perfringens on farms and in processing

Clostridium perfringens is a Gram-positive, aerotolerant anaerobic spore-forming bacterium that causes a wide variety of diseases in humans and animals, primarily as a result of its ability to produce many different toxins (Markey et al., 2013). In humans, C. perfringens is responsible for gas gangrene, enteritis necroticans, food poisoning, and antibiotic-associated diarrheas ( Myers et al., 2006). Currently, C. perfringens type A food poisoning ranks as the second most commonly reported foodborne illness in Canada (Thomas et al., 2013).

c-perfringens-farmIn poultry, avian-specific C. perfringens strains cause necrotic enteritis, an economically significant poultry disease that costs the global industry over $2 billion annually in losses and control measures (Stanley et al., 2014). In some countries, this disease appears to be on the rise because of removal of antibiotic growth promoters (Stanley et al., 2014). C. perfringens is also a cause of various enterotoxemia in other animal species. Isolates of animal origin constitute a risk for transmission to humans through the food chain.

In order to persist in the environment, many bacteria have evolved the ability to form biofilms (Davey and O’Toole, 2000 and Jefferson, 2004). In fact, the predominant organizational state of bacteria in nature is biofilms (Costerton, 1999). Important features of cells in biofilms include: aggregation in suspension or on solid surfaces, increased antibiotic tolerance, and resistance to physical and environmental stresses (Davey and O’Toole, 2000, Davies, 2003 and Hall-Stoodley and Stoodley, 2009). It is now generally accepted that the biofilm growth mode induces bacterial tolerance to disinfection that can lead to substantial economic and health concerns (Bridier et al., 2011). Although the precise mechanism of such tolerance remains unclear, a review has recently discussed the subject as a multifactorial process involving the spatial organization of the biofilm (Bridier et al., 2011). More recently, we, and others, have described the formation of biofilms in C. perfringens (Charlebois et al., 2014 and Varga et al., 2006). We demonstrated that the biofilm formed by C. perfringens could protect the cells from an exposure to atmospheric oxygen and to high concentrations of antibiotics and anticoccidial agents ( Charlebois et al., 2014). It has also been observed that the biofilm formed by C. perfringens could protect the cells from an exposure to 10 mM of hydrogen peroxide even though this bacterium is catalase-negative (Varga et al., 2006). The capacity of C. perfringens to be part of dual- or multi-species biofilm has recently been reviewed ( Pantaleon et al., 2014) and C. perfringens biofilm was detected in many types of multi-species biofilm including biliary stents (Leung et al., 2000 and Pantaleon et al., 2014).

However, susceptibilities of C. perfringens mono- and dual-species biofilms exposed to most disinfectants are currently unknown. This study was undertaken to investigate the tolerance of C. perfringens mono- and dual-species biofilms to disinfectants used in farms and food processing environments.

Tolerance of Clostridium perfringens biofilms to disinfectants commonly used in the food industry

Journal of Food Microbiology

Volume 62, April 2017, p. 32-38

Charlebois, Audrey. Et al.