Playing “Patty Cake” with E. Coli Amid Hygienic Anarchy in US Slaughterhouses

E. coli contamination in meat is the ultimate example of “crap in; crap out.” Not only can Escherichia coli 0157:H7 make you violently sick or kill you, it is a grim reminder of where the beef you ate came from and the fact that the cow didn’t die voluntarily.

That’s why big meat and the government agencies that protect it want to keep the focus on beef packagers like Topps Foods and Cargill Inc. If the E. coli problem can be blamed on packaging workers who didn’t wash their hand or held over day-old meat or didn’t wear a hairnet, then no one’s going to ask about the other s-word: slaughterhouse.

Lucky for big meat, state and federal lawmakers have long anticipated the need to protect businesses–if not people–when outbreaks of potentially lethal pathogens occur in meat and enacted shield laws. That’s why the identities of restaurants and grocery stores in California who served beef from a mad cow in 2003 were kept secret as well as the identities of Texas and Alabama ranches which gave rise to mad cows soon after.

So even as 67-year-old Elizabeth, NJ-based Topps Meat Company shuts down after having to recall 21.7 million pounds of ground beef products it won’t snitch on its slaughterhouse like the beaten woman who won’t answer “who did this to you?”

Neither has Wayzata, MN-based Cargill Inc., which had to recall 840,000 pounds of Cargill Meat Solutions ground beef products from Wal-Mart Stores Inc owned Sam’s Club, named its slaughterhouse supplier or suppliers.

Of course, federal inspectors like Dr. Lester Friedlander who trained vets for the USDA until 1995 have long warned about hygienic anarchy in the slaughterhouses.

“My plant in Pennsylvania processed 1,800 cows a day, 220 per hour,” says Friedlander. The meat regularly contained, “[h]ormones, antibiotics, hair, feces, cancers, tumors.”

Stopping the slaughterhouse assembly line costs about $5,000 a minute says Friedlander, so pressure is intense on veterinarians “to look the other way” and it is “tacitly demanded” by their employer, the federal government.

Profit watching causes other health risks in the slaughterhouse too, Friedlander says; it costs more money to make “two incisions in the cow” so inspectors just make one, which cuts the spinal cord, spreading disease.

But rather than fix the inspection system, after four people died from Jack in the Box beef in 1993 and 25 million pounds of contaminated ground beef from Hudson Foods were recalled in 1997, the government gave more, not less control to the slaughterhouses under the Hazard Analysis and Critical Control Point (HACCP) system.

Dubbed “Have a Cup of Coffee and Pray” by critics who say it lets the fox guard the chicken coop, HACCP is an honor system in which slaughterhouses police themselves, federal inspectors simply auditing compliance with their self created inspection systems. (“And how did you do in September?” they’re probably asking now.)

In 2000, 62 percent of slaughterhouse workers interviewed for a study by the Government Accountability Project and Public Citizen said they had allowed feces, vomit and other contamination through the line that they would have stopped before HACCP; 20 percent said they had been told not to document violations.

It’s obvious that Topps and Cargill didn’t grow their own E. coli. It’s a “systemic problem” says Fast Food Nation author Eric Schlosser, “starting in the feedlots, spreading in the slaughterhouses, and winding up in the ground beef at plants that make frozen patties. Putting Topps out of business isn’t going to solve that fundamental problem.” But who did it?

* The Grand Island, NE Swift plant that recently departing (timing!) Agriculture Secretary Mike Johanns stripped of its right to ship to Japan in February 2006?

* The Florida cattle plant where a USDA inspector told Slaughterhouse author Gail Eisnitz cattle were skinned while fully alive and his superiors did nothing when alerted?

* Or the notorious Iowa Beef Packers (IBP) plant in Wallula, WA where second legger Ramon Moreno whose job was to cut hocks off carcasses at a rate of 309 an hour told the Washington Post the fully alive animals, “blink. They make noises. The head moves, the eyes are wide and looking around” even as he cuts.

IBF, which was recently bought by Tyson Foods, was charged with smuggling 2,000 illegal Guatemalan workers across the Mexico border to work in its slaughterhouses in 2001?

(Slaughterhouse work is so aversive, inmates released from prisons to work in the Smithfield Foods’ Tar Heel plants preferred prison and quit, wrote the New York Times.)

Big meat doesn’t want you to know which slaughterhouses are the culprits. Having you know what is in the meat is bad enough–but showing kicking cows hanging upside down on the kill floor, cows which clearly don’t want to die, can really kill your appetite.

Martha Rosenberg is a columnist/cartoonist who writes about public health. Her latest book is Big Food, Big Pharma, Big Lies (2023). Her first book was Born with a Junk Food Deficiency: How Flaks, Quacks and Hacks Pimp the Public Health. She can be reached at: Read other articles by Martha.

One comment on this article so far ...

Comments RSS feed

  1. Terry S. Singeltary Sr. said on October 8th, 2007 at 10:24am #

    > That’s why the identities of restaurants and grocery stores in California who served beef from a mad cow in 2003

    > were kept secret as well as the identities of Texas and Alabama ranches which gave rise to mad cows soon after.

    martha, the texas mad cow and the alabama mad cow were both h-base type, both more virulent to humans and animals that the UK BSE strain. also, there have recently been 3 documented cases of the NOR-98 atypical scrapie in the USA that no one is speaking much about. BOTH the h-BASE mad cow and the NOR-98 atypical scrapie, both are pathologically more similar to the sporadic CJD than the UK nvCJD. lot of folks scrambling behind closed doors now due to these findings, but still, not to many speaking of this. ………terry

    October 2007 Update on Feed Enforcement Activities to Limit the Spread of BSE

    Transmissible Spongiform Encephalopathy UPDATE USA OCTOBER 2007


    Subject: Aspects of the Cerebellar Neuropathology in Nor98 Date: September 26, 2007 at 4:06 pm PST

    Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. *** The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

    From: “Terry S. Singeltary Sr.”

    Sent: Tuesday, August 21, 2007 9:50 AM

    Subject: TWO MORE Nor98 atypical Scrapie cases detected in USA bringing total to 3 cases to date

    Infected and Source Flocks As of June 30, 2007, there were …..

    One field case and one validation case were consistent with Nor-98 scrapie.

    IN the February 2007 Scrapie report it only mentions: ”One case was consistent with Nor98 scrapie.”

    also here

    An evaluation of scrapie surveillance in the United States


    MR. Jolley, you see why this cannot be done in a 10 minute interview, or a one page story,

    SO, lets move on from typical and atypical scrapie, to CWD in deer and elk, and why are

    either important to the cattle producer and humans? Because they all transmit to each other

    in the lab, and there are potential ramifications from the environmental transmission of these

    TSE, and as they have mutated, they become more virulent, so the potential for some TSE

    to transmit via the environment is very real i.e. casual contact between sheep, goat, deer, elk,

    with cattle in the field. This has never been documented in cattle, yet,

    to date. lets look at some of the data there to date ;

    Survival of PrPSc during Simulated Wastewater Treatment Processes
    Pedersen et al

    Concern has been expressed that prions could enter wastewater treatment systems through sewer and/or septic systems (e.g., necropsy laboratories, rural meat processors, private game dressing) or through leachate from landfills that have received TSE-contaminated material. Prions are highly resistant to degradation and many disinfection procedures raising concern that they could survive conventional wastewater treatment. Here, we report the results of experiments examining the partitioning and survival of PrPSc during simulated wastewater treatment processes including activated and mesophilic anaerobic sludge digestion. We establish that PrPSc can be efficiently extracted from activated and anaerobic digester sludges with 1% sodium dodecyl sulfate, 10% sodium undecyl sulfate, and 1% sodium N-lauryl sarcosinate. Activated sludge digestion does not result in significant degradation of PrPSc. The protein partitions strongly to the activated sludge solids and is expected to enter biosolids treatment processes. A large fraction of PrPSc survived simulated mesophilic anaerobic sludge digestion. Our results suggest that if prions were to enter municipal waste water treatment systems, most of the agent would partition to activated sludge solids, survive mesophilic anaerobic digestion, and be present in treated biosolids. Land application of biosolids containing prions could represent a route for their unintentional introduction into the environment. Our results argue for excluding inputs of prions to municipal wastewater treatment facilities that would result in unacceptable risk of prion disease transmission via contaminated biosolids.

    Chronic Wasting Disease in a Captive White-Tailed Deer Farm
    Keane et al

    A white-tailed deer farm in Portage, Wisconsin, was depopulated in January 2006, after chronic wasting disease (CWD) had been initially discovered on the property in September 2002. …

    Quantifying the Species Barrier in Chronic Wasting Disease by a Novel in vitro Conversion Assay
    Li et al

    Background: Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy that can affect North American cervids (deer, elk, and moose). Although the risk of CWD crossing the species barrier and causing human disease is still unknown, however, definite bovine spongiform encephalopathy (BSE) transmission to humans as variant CJD (vCJD), it would seem prudent to limit the exposure of humans to CWD.

    Conclusions: Our work correctly predicted the transmission of CWD to a wild moose.

    Clinical Observations of BSE Infection in Red Deer
    Steele et al

    Observation of clinical signs is often the first step in the diagnosis of TSE diseases in experimental, farmed and wild animals. Clinical presentation of chronic wasting disease (CWD) infected deer varies widely as disease progresses and many clinical signs observed can be non-specific to TSE infection, however by terminal stage the majority of cases involve behavioural changes and loss of body condition. We present here the first description of clinical disease in deer experimentally infected with BSE. These data are part of the results of an ongoing project to investigate the susceptibility of UK red deer (Cervus elaphus elaphus) to BSE infection either by alimentary or intra-cerebral infection. Eighteen European red deer calves (mean 64 days old) were challenged intragastrically with 25g of BSE-infected bovine brain. … Our results prove for the first time that UK red deer are susceptible to intra-cerebral BSE infection and shows that the clinical presentation of disease shares many similarities to that recorded for CWD.

    Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles
    Christopher J. Johnson1,2, Joel A. Pedersen3, Rick J. Chappell4, Debbie McKenzie2, Judd M. Aiken1,2*

    Soil may serve as an environmental reservoir for prion infectivity and contribute to the horizontal transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) of sheep, deer, and elk. TSE infectivity can persist in soil for years, and we previously demonstrated that the disease-associated form of the prion protein binds to soil particles and prions adsorbed to the common soil mineral montmorillonite (Mte) retain infectivity following intracerebral inoculation. …

    In conclusion, our results provide compelling support for the hypothesis that soil serves as a biologically relevant reservoir of TSE infectivity. Our data are intriguing in light of reports that naïve animals can contract TSEs following exposure to presumably low doses of agent in the environment [5,7­9]. We find that Mte enhances the likelihood of TSE manifestation in cases that would otherwise remain subclinical (Figure 3B and 3C), and that prions bound to soil are orally infectious (Figure 5). Our results demonstrate that adsorption of TSE agent to inorganic microparticles and certain soils alter transmission efficiency via the oral route of exposure.

    full text is here:


    From: “Terry S. Singeltary Sr.” Subject: CWD UPDATE 88 AUGUST 31, 2007

    Date: Wed, 29 Aug 2007 21:13:08 -0500
    From: “Terry S. Singeltary Sr.”
    Subject: CWD NEW MEXICO RECORDS IT’S 19 CASE (near Texas border again)

    Monitoring the Potential Transmission of Chronic Wasting Disease to Humans Using a Hunter Registry Database in Wyoming
    From: Terry S. Singeltary Sr. Date: Thu, 30 Aug 2007 21:23:42 -0500

    J Biol Chem. 2007 Aug 20; : 17709374
    Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain.


    our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions.




    BASE Transmitted to Primates and MV2 sCJD Subtype Share PrP27-30 and PrPSc C-terminal Truncated Fragments
    Zanusso et al

    The etiology of sporadic Creutzfeldt-Jakob disease (sCJD), the most frequent human
    prion disease, remains still unknown.

    Transmission of Italian BSE and BASE Isolates in Cattle Results into a Typical
    BSE Phenotype and a Muscle Wasting Disease
    Zanusso et al

    The clinical phenotype of bovine spongiform encephalopathy has been extensively reported in early accounts of the disorder. Following the introduction of statutory active surveillance, almost all BSE cases have been diagnosed on a pathological/molecular basis, in a pre-symptomatic clinical stage. … Clinically, BSE-infected cattle developed a disease phenotype highly comparable with that described in field BSE cases and in experimentally challenged cattle. On the contrary, BASE-inoculated cattle developed an amyotrophic disorder accompanied by mental dullness.
    … This study further confirms that BASE is caused by a distinct prion isolate and discloses a novel disease phenotype in cattle,
    closely resembling the phenotype previous reported in scrapie-inoculated cattle and in
    some subtypes of inherited and sporadic Creutzfeldt-Jakob disease.

    Pathological Interaction Between Protein Misfolding Disorders: Prions and Alzheimer’s Disease
    Morales, R; Estrada, L; Castilla, J; Soto, C

    Protein Misfolding Disorders (PMD) include several diverse diseases, such Alzheimer’s,
    Parkinson’s, Transmissible Spongiform Encephalopathies, Diabetes Type II and various
    systemic amyloidosis. The central event in these diseases is the accumulation of a
    misfolded, ß-sheet rich aggregated form of a naturally expressed protein. In vitro
    studies have shown that protein misfolding and aggregation follows a seedingnucleation
    mechanism similar to the process of crystallization. … Our findings
    suggest an interaction between Alzheimer’s and prion pathologies, indicating that one
    protein misfolding process may be an important risk factor for the development of a
    second perhaps more prevalent disease.

    Subject: Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
    Date: September 29, 2007 at 12:50 pm PST

    Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
    Holznagel et al


    In 2001, a study was initiated in primates to assess the risk for humans
    to contract BSE through contaminated food. For this purpose, BSE brain was
    titrated in cynomolgus monkeys.


    In an ongoing study, a considerable number of high-dosed macaques already
    developed simian vCJD upon oral or intracerebral exposure or are at the onset of the
    clinical phase. However, there are differences in the clinical course between orally and
    intracerebrally infected animals that may influence the detection of biomarkers.


    Simian vCJD can be easily triggered in cynomolgus monkeys on the oral
    route using less than 5 g BSE brain homogenate. The difference in the incubation
    period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However,
    there are rapid progressors among orally dosed monkeys that develop simian vCJD as
    fast as intracerebrally inoculated animals.

    Case Report of Variant Creutzfeldt-Jakob Disease in a Macaque after Blood Transfusion
    Lescoutra-Etchegaray et al

    A fourth human case of probable transmission of vCJD through transfusion has
    now been reported but a number of features affecting transfusion-related
    infection remain imprecise, including infectious dose, length of incubation period and
    critical infectious window of blood donors.

    Atypical Presentation of Variant Creutzfeldt-Jakob Disease in a 73 Year Old
    Blood Transfusion Recipient
    Wroe et al

    We report atypical presentation of variant Creutzfeldt-Jakob Disease (vCJD) identified
    ante-mortem in a 73 year-old recipient of blood products. This patient was transfused
    following orthopaedic surgery in December 1997. Tracing of blood products identified
    a single unit of non-leucodepleted red cells from an individual who developed
    neuropathologically confirmed vCJD eleven months after donation. Nine years post
    transfusion, this individual was referred to the National Prion Clinic for specialist
    investigation. Six years post transfusion the recipient complained of fluctuating fatigue
    and impaired concentration. At this time neurological examination and MRI brain
    (T1/T2 weighted/DWI) were normal. Progressive symptoms emerged six months later
    with imbalance and deteriorating cognition. … This case highlights
    the significant risk encountered by recipients of contaminated blood products and the
    necessity for their specialist monitoring.

    Prions in Plasma of Patients with Sporadic Creutzfeldt-Jakob Disease
    Safar et al

    Date: Mon, 24 Sep 2007 21:31:55 -0500

    I suggest that you all read the data out about h-BASE and sporadic CJD, GSS, blood, and some of the other abstracts from the PRION2007. …


    USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were ”H-TYPE”, personal communication Detwiler et al Wednesday, August 22, 2007 11:52 PM. …TSS

    ALL IN ALL, it’s a terribly failed system of TSE surveillance and attempted erradication of this agent in the USA,
    a failed policy driven by industry greed and ignorance. …

    Terry S. Singeltary Sr.
    P.O. Box 42
    Bacliff, Texas USA 77518