Eyes of cattle may become new windows to detect mad cow disease

The eyes may or may not be windows to the soul, as the old adage goes, but scientists are reporting evidence that a peek into the eyes of cattle may become the basis for a long-sought test to detect infection with the agent that causes Mad Cow Disease. That test could help prevent the disease from spreading in the food supply. A study on using the tell-tale glow given off by eyes infected with the Mad Cow agent appears in ACS’ semi-monthly journal Analytical Chemistry.

Jacob Petrich and colleagues note that the human form of Mad Cow Disease is linked to eating beef from animals infected with abnormal proteins called prions implicated in a range of brain diseases. Scientists are trying to develop tests to detect infected cattle before they enter the food supply. Past studies suggest that chemical changes in an animal’s retina, the light sensitive nerve tissue in the back of the eye, may provide a basis for detecting prion diseases.

The scientists showed that retinas of sheep infected with scrapie, a disease similar to Mad Cow Disease, emit a characteristic glow when examined with a beam of light from a special instrument. They suggest that eye tests based on the finding could become important in the future for fast, inexpensive diagnosis of prion diseases and other neurological diseases.


“Fluorescence Spectroscopy of the Retina for Diagnosis of Transmissible Spongiform Encephalopathies”




Jacob Petrich, Ph.D.

Department of Chemistry

Iowa State University

Ames, Iowa 50011

Phone: 515-294-9422

Fax: 515-294-0105

Email: [email protected]

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3 thoughts on “Eyes of cattle may become new windows to detect mad cow disease”

  1. would not matter one bit if this eye test was validated 100%, bottom line, the USDA refuses to test to find any strain of BSE. the enhanced 2004 BSE testing and surveilance program consisted of testing _HEALTHY USDA CATTLE BRAINS_, brains they knew did not have mad cow disease. so there ya go…….this test would not matter in the USA. just ask CREEKSTONE. …TSS

    Evidence uncovered during the government’s investigation established that Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted Cattle Population. Specifically, Farm Fresh Meats and Farabee submitted, or caused to be submitted, obex samples from healthy, USDA inspected cattle, in order to steal government moneys.



    the usda et al would not use a BSE test of any kind, even if it was validated 1,000 percent. they know what they would find…



    Monday, September 13, 2010

    atypical BSE strains and sporadic CJD strains, is there a connection and why shouldn’t there be $


    • this link still works ;


      Date: June 21, 2007 at 2:49 pm PST

      Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program

      An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduledfor May 2007.


      Topics that will be covered in ongoing or planned reviews under Goal 1 include:

      soundness of BSE maintenance sampling (APHIS), implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),


      The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.



  2. Spongiform encephalopathies- as a loss of parasympathetic
    function ?

    The loss of parasympathetic function unmasks the baseline syphathetic bias inherent
    in the end-organs, resulting in the familiar signs of aging including tachycardia,
    constipation, insomnia, erectile dysfunction, fluid retention, and systemic inflamantion. These consequences in turn may contribute to many of the common diseases associated with aging including type-2 diabetes, Alzheimer´s, atherosclerosis, and cancer. Maintenance and
    resoration of the parasympathetic function may enable upstream control over the
    deleterious aspects of inherent end-organ adrenergic bias (LEE et al., 2004).
    Most cases of BSE in Great Britain have occurred in dairy cows between 3 and 6 years of
    age… There were variations in the frequency with which some signs were recorded in
    animals observed at different times during the epidemic (WILESMITH et al., 1992). These
    „different variations“ in older animals; it seems are in connection with the neurovegetative
    disorders… Cows affected by BSE show a reduced time spent ruminating, although eating time is maintained at normal levels. This reduction can be marked and rumination can
    cease (AUSTIN and SIMMONSON, 1993).
    In the eye, the thin layer of tissue that lies between the sclera and the retina is the choroid. This is rich in blood vessels that nourish the retina, and the dark pigments of the choroid absorb light rays so that they are not reflected back out of the eye. STEINLE et al. (2000) concluded that sympathetic -noradrenergic vasoconstriction occurs throughout the choroid, whereas parasympathetic nitrergic vasodilation plays a selective role in modulating blood flow in anterior tissues of the eye. Choroidal blood flow in eyes is light driven and controlled by a parasympathetic input from ciliary ganglion (KIMBLE et al., 2006). In addition, CUTHBERTSON et al. (2003) about the retina parasympathetic control found that with the FG (fluorochrome) labeling is evident a strong white glow in the choroid and sclera. Now researchers found that the retinas of infected sheep emitted a distinct “glow”; the scrapie-positive retinas fluoresce a lot – they gave a lot of light back, and this light was very structured….
    . Transmissible spongiform encephalopathies are commonly propagated by extracerebral
    inoculation of the infectious agent. Indirect evidence suggests that entry into the central
    nervous system occurs via the peripheral nervous system. GLATZEL et al. (2001) concluded
    that sympathetic innervation of lymphoid organs is rate limiting for prion neuroinvasion
    and that splenic sympathetic nerves may act as extracerebral prion reservoirs.
    The autonomic nervous system (ANS) regulates bodily functions and the activity of
    specific organs. As example, the ANS plays a role in the diameter of the pupils. The
    mechanism of mydriasis usually involve either a disruption of the parasympathetic nerve
    which causes contraction of the pupil, or over- activity of the sympathetic nervous system
    (SNS). LEGGETT et al (1990) reported that a cat which developed a change of temperament,
    with muscle tremors, ataxia and pupillary dilatation was suspected and later confirmed
    histopathologically to have a spongiform encephalopathy.
    So we can conclude that the loss of parasympatetic function can be found when the SNS
    prevails and sympathetic vasoconstriction occurs throughout the choroid- in spongiform encephalopathies.
    In addition, calcium and magnesium regulate the sympathetic nervous system (SNS) which controls our “fight or flight” reaction. SNS is stimulated by calcium, and inhibited by magnesium.
    Some of the theories established by ongoing research. According to my “BSE ammonia- magnesium ”theory, the origins of the diseases may lie in chronic magnesium deficiency coupled with a high protein intake. According to this alternative theory , the origins of the neurodegenerative diseases may lie in chronic magnesium deficiency (coupled with a high protein intake in ruminants).
    So defective prions are markers of the diseases rather than the cause and BSE can be a naturally occurring disease, not an infectious disease. WHY? Because the connection about BSE/ vCJD diseases; this was never justified scientifically! It was pure, math-model-driven science fiction. But it was pushed very vigorously by the British science establishment, which has never confessed to its errors… See more about the; BSE/ vCJD mathematical- models, see my large comments in Telegraph.co.uk (www.telegraph.co.uk/health/healthnews/7168326/D oes-vCJD-still-pose-a-major-public-health-threat .html).
    See also other relationships (WHY great progress about BSE eradicating within the EU…?) , according to my web http://www.bse-expert.cz and recent presentation at 29th World Veterinary Congress in Vancouver; Neurodegenerative Diseases and Schizophrenia as a Hyper or Hypofunction of the NMDA Receptors (www.bse-expert.cz/pdf/Veter_kongres.pdf). So according to this theory the story of BSE in Britain is a consequence of “intensive farming” (metabolic disease disease and “neurotoxicity”) and belongs in the “agricultural ecology”

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