Home-canned carrots linked to North Carolina botulism case

A couple of weeks ago I ran into a barfblog reader who commented to me, ‘You’re really scared of botulism, aren’t you?’ This wasn’t a random question, it was related to a few things I had posted following over 20 illnesses linked to a potluck dinner at Cross Pointe Free Will Baptist Church in Lancaster, Ohio.

Scared isn’t how I would describe it. Rattled and in awe of are probably better terms. The toxin blocks motor nerve terminals at the myoneural junction, causing paralysis. It starts with the mouth, eyes, face and moves down through the body. It often results in paralysis of the chest muscles and diaphragm, making a ventilator necessary. Months of recovery follow an intoxication.Carrots

Maybe I am scared.

There isn’t a whole lot of botulism in the U.S. every year, and not all of it is foodborne – (infant botulism is more common); over the past two decades, improperly home preserved foods are the main source.

Any case is notable.

Earlier this year there was a botulism illness in Ashe County, North Carolina that was

The case was first reported during a panel at the NC Food Safety and Defense Task Force annual meeting. Rose Hoban of North Carolina Health News captured the highlights.
It only took one bite.

Five days later, an Ashe County woman lay in the hospital, on a ventilator, unable to breathe.

Home canning food has a technical aspect to it that’s dangerous to ignore, said Ben Chapman from N.C. State University.

The woman, who’s name has not been released, told health officials she didn’t even swallow the carrot. She opened the home-canned jar of carrots, tasted one, decided it looked and tasted off, and spit it out.

But that was enough to give her botulism, sending her to the hospital for an 11-week stay.

She was lucky there was an off flavor, said Ben Chapman, a food-safety expert from N.C. State University.

“The toxin itself doesn’t have the sensory attributes that we associate with spoilage,” Chapman said this week at a presentation about the case during a meeting of the Governor’s Task Force on Food Safety and Defense that was held at the N.C. Biotechnology Center in Research Triangle Park.

Chapman said the procedure the woman had used to treat the carrots may have left some other bacteria behind that created the off taste. But her canning technique was not correct, which also left behind botulism spores in her carrots.

She was fortunate to have ingested a small enough amount that her hospital stay was relatively short compared to what happens in many botulism cases, Chapman said.

And he offered the story as a cautionary tale as we head into the main growing season when many people pull out pots and jars to preserve the fruits of the season.

It took several days for a possible diagnosis of botulism poisoning to show up in the woman’s medical record, said Nicole Lee, an epidemiologist from the state Department of Health and Human Services. The woman’s daughters and a friend told doctors that she canned her own food. Before she was intubated, the woman said she suspected the carrots.

But doctors also needed to rule out a stroke or other neurological problems. It took more than a week for doctors to tell state health officials that they suspected botulism.

“That immediately got our attention,” said Lee. “We had gotten wind that this person was canning her own food. We weren’t sure if these items were being sold in commerce or across state lines.”

“I was on my way to Morganton and I got a call to divert,” recounted Susan Parrish, a food regulatory supervisor for the state Department of Agriculture and Consumer Services.

Parrish, who monitors food outbreaks around the state, was given the carrots by one of the woman’s friends.

“They were in a quart jar,” said Parrish, who put on a biohazard suit to handle it. “Obviously, she had only tasted a bite, because the jar was full.”

A sample of the carrots was shipped to the Food and Drug Administration.

The results came back from the FDA “barely positive,” said the FDA’s Mancia Walker. “But with [botulism], barely positive is like a little bit pregnant.”

“This was a tragic mistake that can happen to anyone not using proper canning procedures,” he said, explaining that the woman had not pressure canned the carrots, which would have created temperatures high enough to kill botulism spores.

“There are very passionate people who are maybe not doing canning with science-based recommendations,” said Chapman, who has studied how people preserve food.

He said that when he’s asked canners where they learned to can, they tell him the knowledge has been passed down rather than learned in a home economics class or a workshop that’s strong on the science.

“We’ve seen in other cases where [a] family link perpetuates error,” said Chapman, who said there are plenty of books, classes and online instructions from agricultural extension services.

Use a thermometer? NYC chef teaches students to make solar-powered meals

Kale nachos sound gross; wellness sounds like quackery; using kids without a safety is dangerous.

barfblog.Stick It InA city chef is challenging the idea that New Yorkers don’t have the space to employ solar power by using the sun’s rays to quickly whip up meals for local kids.

Anyone planning a day in Central Park, a trip to the beach or with a rooftop or outdoor space can use a solar cooker — which involves a set of mirrored panels that direct the sun’s heat onto a ceramic dish — to make snacks or full meals, said chef Cynthia Tomasini.

On Thursday, Tomasini used that technique to teach students at P.S. 87 about the eco-friendly method, using a solar cooker to whip up a bunch of kale nachos.

Her work at the elementary school comes through the nonprofit Wellness in Schools (WITS), which is focused on improving healthy eating and increasing student movement and exercise.

Tomasini, 43, who is also a personal chef for local families, spends about a third of her time going to elementary schools in Manhattan as a WITS liaison.

Why I now boil all frozen berries: Norovirus source in Sweden

Norovirus struck the care home in Ljungby a week ago, initially causing the deaths of two people, with another guest dying later in the week.

raspberrySweden’s national food agency (Livsmedelsverket) said in a statement on Monday that tests had confirmed that imported frozen fruits were the source of the sickness outbreak.

It is suspected that the raspberries became contaminated during the packing process, when boxes of berries were hand-packed by a worker who was carrying the virus.

“It is not uncommon for imported frozen raspberries to be contaminated with Norovirus,” Livsmedelsverket said in a statement on its website.

Trichinellosis in Corsica: Ton of sausages entered after case

A ton of charcuterie was seized in Aullène, South Corsica, following a complaint from a person who has fallen ill after consuming. Recalled products, with an estimated street value of more than EUR 50 000, must be destroyed.

charcuterieA ton of charcuterie was seized Thursday in Aullene in Corse-du-Sud, after reporting a case of trichinosis, a disease characterized by fever or complications if the patient is not treated , will we learned this Friday from the gendarmerie.

The seizure was conducted Thursday morning by the Departmental Directorate of social cohesion and the protection of populations (DDCSPP), in collaboration with the police. At the root of this, a person fell ill after eating cold cuts a small-scale producer, contacted the DDCSPP, said the gendarmerie, confirming a report by France 3 Corse.

Steak still seems safe

It’s always BBQ season. In Canada I would BBQ in February. In the snow.

ben-newResearchers have quantified inactivation of Shiga toxin–producing Escherichia coli (STEC) cells within knitted/cubed beef steaks following cooking on a nonstick griddle. Both faces of each beef cutlet (ca. 64 g; ca. 8.5 cm length by 10.5 cm width by 0.75 cm height) were surface inoculated (ca. 6.6 log CFU/g) with 250 μl of a rifampin-resistant cocktail composed of single strains from each of eight target serogroups of STEC: O26:H11, O45:H2, O103:H2, O104:H4, O111:H2, O121:H19, O145:NM, and O157:H7.

Next, inoculated steaks were (i) passed once through a mechanical tenderizer and then passed one additional time through the tenderizer perpendicular to the orientation of the first pass (single cubed steak; SCS) or (ii) passed once through a mechanical tenderizer, and then two tenderized cutlets were knitted together by passage concomitantly through the tenderizer two additional times perpendicular to the orientation of the previous pass (double cubed steak; DCS). SCS and DCS were individually cooked for up to 3.5 min per side in 30 ml of extra virgin olive oil heated to 191.5°C (376.7°F) on a hard-anodized aluminum nonstick griddle using a flat-surface electric ceramic hot plate.

Regardless of steak preparation (i.e., single versus double cubed steaks), as expected, the longer the cooking time, the higher the final internal temperature, and the greater the inactivation of STEC cells within cubed steaks. The average final internal temperatures of SCS cooked for up 2.5 min and DCS cooked for up to 3.5 min ranged from 59.8 to 94.7°C and 40.3 to 82.2°C, respectively. Cooking SCS and DCS on an aluminum griddle set at ca. 191.5°C for 0.5 to 2.5 min and 1.0 to 3.5 min per side, respectively, resulted in total reductions in pathogen levels of ca. 1.0 to ≥6.8 log CFU/g.

These data validated that cooking SCS (ca. 0.6 cm thick) or DCS (ca. 1.3 cm thick) on a nonstick aluminum griddle heated at 191.5°C for at least 1.25 and 3.0 min per side, respectively, was sufficient to achieve a 5.0log reduction in the levels of the singlesteak to achieve a 5.0log reduction in the levels of the single strains from each of the eight target STEC serogroups tested.

Thermal inactivation of shiga toxin–producing Escherichia coli cells within cubed beef steaks following cooking on a griddle

Journal of Food Protection

Swartz, Richard S.; Luchansky, John B.; Kulas, Megan; Shoyer, Bradley A.; Shane, Laura E.; Strasser, Hannah; Munson, Madison; Porto-Fett, Anna C. S.

http://www.ingentaconnect.com/content/iafp/jfp/2015/00000078/00000005/art00021

Bugs in sushi in Norway

I don’t like sushi.

sushiI don’t like raw fish.

Researchers in Norway found that retail fresh sushi is gaining popularity in Europe. This study was conducted to investigate the microbiological quality of selected samples of fresh sushi with a shelf life of 2 to 3 days offered as complete meals in Norwegian supermarkets.

Analysis of aerobic plate counts in 58 sushi samples from three producers revealed large variations in microbiological quality, and 48% of the analyzed sushi boxes were rated as unsatisfactory (> 6.0 log CFU/g). Mesophilic Aeromonas spp. was detected in 71% of the samples. In a follow-up study, we collected products and raw materials directly from the production facility of one producer and observed a significant decrease (P < 0.01) in aerobic plate counts compared with the initial sampling. The observed difference between products purchased in stores compared with those collected directly from the factory suggests that poor temperature control during distribution and display in stores leads to reduced microbiological quality. Microbiological analysis of the sushi ingredients revealed that potentially pathogenic bacteria such as mesophilic Aeromonas spp. or bacteria belonging to the Enterobacteriaceae can be introduced into sushi through both raw vegetables and fish. The results highlight the importance of high quality ingredients and proper temperature control to ensure stable quality and safety of these food products.

Assessment of microbiological quality of retail fresh sushi from selected Sources in Norway

Journal of Food Protection

Hoel, Sunniva; Mehli, Lisbeth; Bruheim, Torkjel; Vadstein, Olav; Jakobsen, Anita Nordeng

http://www.ingentaconnect.com/content/iafp/jfp/2015/00000078/00000005/art00015

Action and dysfunction in the U.S. food-safety effort

I’ve played, coached and sometimes participated in administration for almost 50 years of ice hockey.

hockey.praciceThings don’t really change.

The parents aren’t as drunk as they used to be, but they can still be difficult; that’s why coaches have to go through at least two days of training, far more than what’s requested of people who serve food.

And if people expect food safety to change by better regulation, they’re delusional.

The old grey lady – N.Y. Times – has further succumbed to decades-old rhetoric that isn’t going to make fewer people barf (or die).

 

Nosestretcher alert: Invite some germs to dinner

When Michael Pollan endorses an article, I know it’s BS.

sprout.santa_.barf_.xmas_-300x254So it is with Kate Murphy’s piece in the New York Times on Sunday, that says the U.S. food supply is “arguably the safest in the world” and asks “whether our food could perhaps be too clean.”

I’ve been hearing this for 25 years. It’s a tantalizing belief but at this point that’s all it is – a belief.

Cherry-picking data to support a pre-existing theory remains a belief.

I could tell an equal number of stories about my mother who got undulate fever from raw milk as a child, or my aunt who suffered with cyclospora from basil in Florida, or Champan who spent a weekend in our toilet from Campylobacter in Kansas, but it’s not science.

There are research areas worth exploring, but we humans don’t know much about applying this germ theory, especially to the genetically susceptible.

The theory that there might be such a thing as “too clean” food stems from the hygiene hypothesis, which has been gaining traction over the last decade. It holds that our modern germaphobic ways may be making us sick by harming our microbiome, which comprises all the microscopic beasties — bacteria, viruses, fungi, mites, etc. — that live in and on our bodies.

Research so far has focused primarily on the detrimental effects of cesarean births and not breast-feeding, which may inhibit the formation of a robust microbiome, and the use of antibacterial soaps and antibiotics, which diminish the microbiome once it is established.

A result is an immune system that essentially gets bored, spoiling for a fight and apt to react to harmless substances and even attack the body’s own tissues. This could explain the increasing incidence of allergies and autoimmune disorders such as asthma, rheumatoid arthritis and inflammatory bowel syndrome.

It could also explain my latest fart.

There is also the suggestion that a diminished microbiome disrupts hormones that regulate hunger, which can cause obesity and metabolic disorders.

When it comes to foodborne illness, the idea is that fewer good bacteria in your gut means there is less competition to prevent colonization of the bad microbes, leading to more frequent and severe bouts of illness.

Moreover, your underutilized immune system may lose its ability to discriminate between friend and foe, so it may marshal its defenses inappropriately (e.g., against gluten and lactose) or not at all.

All of this is hard to prove.

That should be the headline.

Anyone who has visited a country with less than rigorous sanitation knows the locals don’t get sick from foods that can cause tourists days of toilet-bound torment.

sprouts_sandwich(1)That’s because the susceptible ones have died off.

“We have these tantalizing bits of evidence that to my mind provide pretty good support for the hygiene hypothesis, in terms of foodborne illness,” said Guy Loneragan, an epidemiologist and professor of food safety and public health at Texas Tech.

Yes, it’s tantalizing.

This is not to say we’d be better off if chicken producers eased up on the salmonella inspections, we ate recalled ice cream sandwiches and didn’t rinse our produce.

Rinsing produce ain’t going to do much either way; but may make the consumer feel cleaner.

Murphey says it is worth noting that serious foodborne diseases — the ones that make it into the news, like listeria, salmonella, E. coli, cryptosporidium and campylobacter — are mainly diseases of immuno-compromised populations.

Nonsense.

The E. coli O104 outbreak in sprouts in Germany in 2011 that killed 53 and sickened 4,400 primarily struck middle-aged, health women, because they eat more salads.

That’s science.

Always cameras: South Africa KFC branch shuts after images go viral

Fast food franchise KFC has announced its store in Braamfontein has been closed until further notice after images of staff “washing chickens” on a dirty floor surfaced on social media this week.

kfc.wash.chickenA Facebook user posted images of what appeared to be KFC staff in Braamfontein allegedly taking chicken pieces out of containers, placing them on a concrete floor and hosing them down.

The person who posted the images, Mfumo Bamuza, received them from an anonymous Joburg resident who took them from the balcony of his Clifton Heights flat in Braamfontein.

In the two images, staff can be seen using a hose to spray a large volume of water on to the uncooked chicken pieces.

In one image, blood and water can be seen streaming across the floor.

Bamuza captioned the picture: “KFC Braamfontein comrades!!! This is how they wash your meat. On the ground!!!!! Photocred goes to a south point (Clifton Heights) resident. #knowwhatyoueat.”

Seek and ye shall find: E. coli O26:H11 in cows

Escherichia coli O26 has been identified as the most common non-O157 Shiga toxin-producing E. coli (STEC) serogroup to cause human illnesses in the United States and has been implicated in outbreaks around the world. E. coli has high genomic plasticity, which facilitates the loss or acquisition of virulence genes.

cow.poop2Attaching and effacing E. coli (AEEC) O26 strains have frequently been isolated from bovine feces, and there is a need to better characterize the relatedness of these strains to defined molecular pathotypes and to describe the extent of their genetic diversity.

High-throughput real-time PCR was used to screen 178 E. coli O26 isolates from a single U.S. cattle feedlot, collected from May to July 2011, for the presence or absence of 25 O26 serogroup-specific and virulence-associated markers. The selected markers were capable of distinguishing these strains into molecularly defined groups (yielding 18 unique marker combinations). Analysis of the clustered regularly interspaced short palindromic repeat 1 (CRISPR1) and CRISPR2a loci further discriminated isolates into 24 CRISPR types. The combination of molecular markers and CRISPR typing provided 20.8% diversity. The recent CRISPR PCR target SP_O26-E, which was previously identified only in stx2-positive O26:H11 human clinical strains, was identified in 96.4% (161/167 [95% confidence interval, 99.2 to 93.6%]) of the stx-negative AEEC O26:H11 bovine fecal strains. This supports that these stx-negative strains may have previously contained a prophage carrying stx or could acquire this prophage, thus possibly giving them the potential to become pathogenic to humans.

These results show that investigation of specific genetic markers may further elucidate our understanding of the genetic diversity of AEEC O26 strains in bovine feces.

Genetic diversity and pathogenic potential of attaching and effacing Escherichia coli O26:H11 strains recovered from bovine feces in the United States

Applied and Environmental Microbiology

Sarah A. Ison, Sabine Delannoy, Marie Bugarel, Kendra K. Nightingale, Hattie E. Webb, David G. Renter, Tiruvoor G. Nagarajac, Guy H. Loneragana and Patrick Fachb

http://aem.asm.org/content/81/11/3671.abstract?etoc

 Shiga toxin-producing Escherichia coli (STEC) is a foodborne pathogen that may be responsible for severe human infections. Only a limited number of serotypes, including O26:H11, are involved in the majority of serious cases and outbreaks. The main virulence factors, Shiga toxins (Stx), are encoded by bacteriophages.

cowSeventy-four STEC O26:H11 strains of various origins (including human, dairy, and cattle) were characterized for their stx subtypes and Stx phage chromosomal insertion sites. The majority of food and cattle strains possessed the stx1a subtype, while human strains carried mainly stx1a or stx2a. The wrbA and yehV genes were the main Stx phage insertion sites in STEC O26:H11, followed distantly by yecE and sbcB. Interestingly, the occurrence of Stx phages inserted in the yecE gene was low in dairy strains. In most of the 29 stx-negative E. coli O26:H11 strains also studied here, these bacterial insertion sites were vacant. Multilocus sequence typing of 20 stx-positive or stx-negative E. coli O26:H11 strains showed that they were distributed into two phylogenetic groups defined by sequence type 21 (ST21) and ST29. Finally, an EspK-carrying phage was found inserted in the ssrA gene in the majority of the STEC O26:H11 strains but in only a minority of the stx-negative E. coli O26:H11 strains.

The differences in the stx subtypes and Stx phage insertion sites observed in STEC O26:H11 according to their origin might reflect that strains circulating in cattle and foods are clonally distinct from those isolated from human patients.

 Diversity of shiga toxin-producing Escherichia coli (STEC) O26:H11 strains examined via stx subtypes and insertion sites of stx and espk bacteriophages

Applied and Environmental Microbiology

Ludivine Bonanno, Estelle Loukiadis, Patricia Mariani-Kurkdjian, Eric Oswald, Lucille Garnier, Valérie Michel and Frédéric Auvray

http://aem.asm.org/content/81/11/3712.abstract?etoc