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ask yourselves!

exactly what is this "mad cow" disease which comes about shortly after the 'swine flu and bird flu' which brings about the wanton slaughter of american "food supply resources" during our nations "financial squabbles with other nations" which further brings about the sharp rise in food prices here in this country?
Posted on June 7, 2014 by V.K. Durham

Texas man fourth in U.S. to die from rare brain disease: CDC

Reuters 1 day ago By Reuters

AUSTIN Texas (Reuters) - A Texas man has died of the fatal brain illness variant Creutzfeldt-Jakob Disease, the fourth person to die of the disease in the United States, according to the Centers for Disease Control.

CJD is a rare, degenerative, fatal brain disorder in humans, believed to be caused by consumption of products from cows with bovine spongiform encephalopathy (BSE), or "mad cow" disease.

"The history of this fourth patient, including extensive travel to Europe and the Middle East, supports the likelihood that infection occurred outside the United States," the CDC said in a statement this week.

In each of the three previous cases, infection likely occurred outside the United States, it said. The Texas patient was not identified.

(Reporting by Jon Herskovitz, editing by G Crosse)




I would rather call it the SPEciaL FLU.. as that is what I truly feel that it is.. but the following is the explanation put out by the CDC.. [remember these infra-structures of FDA-CDC etc were sold off and/or privatized under G.H.W. Bush's Executive Order 12803 in 1992.. this leaves the theory of the FDA and CDC being one of those SPEciaL Groups running the US CORPORATE FEDERAL GOVT..
Lets take a look at all this stuff.. [I keep thinking about what grand-father said about politicians when he would pull a funny.. he would say "How do you know a politician is lying? We would always say "I don't know!" Grand-father would say "you can always tell because his lips are moving".. We just might be looking at a similar situation in the "MAD COW" disease hype. Read the following.. [VKD]

vCJD (Variant Creutzfeldt-Jakob Disease)

Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas

Posted: June 2, 2014

Laboratory tests have confirmed a diagnosis of variant CJD (a fatal brain disorder) in a patient who recently died in Texas. The confirmation was made when laboratory results from an autopsy of the patient's brain tested positive for variant CJD.

First described in 1996 in the United Kingdom, variant CJD is a rare, degenerative, fatal brain disorder in humans. It is believed to be caused by consumption of products from cows with the disease bovine spongiform encephalopathy (BSE, or "mad cow" disease).

Worldwide, more than 220 variant CJD patients have been reported, with a majority of them in the United Kingdom (177 cases) and France (27 cases). This case is the fourth to be reported in the United States. In each of the three previous cases, infection likely occurred outside the United States, including the United Kingdom (2 cases) and Saudi Arabia (1 case). The history of this fourth patient, including extensive travel to Europe and the Middle East, supports the likelihood that infection occurred outside the United States.

CDC assisted the Texas Department of State Health Services (DSHS)'s investigation of this case and will continue to help confirm further details of the patient's history, including the potential source of infection.

A classic form of CJD, which is not caused by the BSE agent, occurs worldwide, including in the United States. Annually, for every 1 million people in the United States, 1 to 2 develops classic CJD. More information about variant CJD, including how it differs from classic CJD, is available in the Variant Creutzfeldt-Jakob Disease Fact Sheet.

Date: June 2, 2014
Content source: Centers for Disease Control and Prevention
National Center for Emerging and Zoonotic Infectious Diseases (NCEZID)
Division of High-Consequence Pathogens and Pathology (DHCPP)


V.K.D. ARE YOU PAYING ATTENTION!? DID YOU NOTICE THE TWO WORDS? i.e., Encephalitis and Encephalopathy? Are they related, or one and the same thing?

Found this..

Encephalitis and Encephalopathy Associated with an Influenza Epidemic in Japan

Tsuneo Morishima1,
Takehiro Togashi2,
Shyumpei Yokota3,
Yoshinobu Okuno4,
Chiaki Miyazaki5,
Masato Tashiro6, and
Nobuhiko Okabe6
+ Author Affiliations

1 Department of Health Science, Nagoya University, Nagoya
2 Department of Pediatrics, Sapporo City Hospital, Sapporo
3 Department of Pediatrics, Yokohama City University, Yokohama
4 Osaka Institute of Public Hygiene, Osaka
5 Fukuoka Center for Handicapped Children, Fukuoka
6 National Institute for Infectious Diseases, Tokyo, Japan
Reprints or correspondence: Dr. Tsuneo Morishima, Dept. of Health Science, Nagoya University, 1-1-20, Daiko-minami, Higashi-ku, Nagoya 461-0047, Japan ( morishim@met.nagoya-u.ac.jp).

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During the winter of 1998-1999, there was an outbreak of encephalitis/encephalopathy in Japan that appeared to be associated with influenza. We conducted a national survey of the prevalence and clinical features of disease and the associated outcomes and prognostic factors related to this outbreak. A total of 202 cases were analyzed, of which 148 were diagnosed as influenza-associated encephalitis/encephalopathy on the basis of virologic analysis. Of the 148 cases studied, 130 (87.8%) were type A influenza and 17 were type B. Encephalitis/encephalopathy developed mainly in children age <5 years, either on the day that influenza signs appeared or on the next day. The major signs included altered consciousness or loss of consciousness, convulsions, cough, and vomiting. In many patients, multiple-organ failure developed, and rates of mortality (31.8%) and disability (27.7%) were high. Thrombocytopenia and severely elevated transaminase levels were factors associated with a poor prognosis. Thus, influenza-associated encephalitis/encephalopathy progressed rapidly and was associated with poor outcomes.

Encephalitis lethargica is a lethal, epidemic brain infection that was first described by Flexner [1]. An epidemic of CNS infections raged between 1918 and 1930, coinciding with the influenza pandemic, the so-called "Spanish flu" [2, 3]. Despite intensive investigation, the relationship between influenza and epidemic encephalitis remains unclear [1-5]. Some CNS diseases have been reported to accompany influenza infection, including Reye syndrome, influenza-associated encephalitis/encephalopathy, myelitis, and acute necrotizing encephalitis. Reye syndrome, which involves acute encephalopathy and fatty degeneration in the liver, often follows viral infection and salicylate therapy [6-8]. In addition to cases of Reye syndrome, many investigators have described cases of influenza-associated encephalitis/encephalopathy [9-12]. However, the clinical features of this disease have not yet been clarified.

Recently, the number of reports of encephalitis/encephalopathy associated with influenza has increased in Japan, especially reports of cases in children aged <5 years. During the winters of 1997-1998 and 1998-1999, when an epidemic of type A influenza (H3N2) occurred, many pediatricians reported cases of influenza-associated encephalitis/encephalopathy [13-17]. The abrupt onset of seizure and coma a few days after development of high-grade fever is a prominent indicator of CNS involvement during influenza infection. Therefore, we conducted a national survey to investigate the various parameters of the disease outbreak (prevalence and clinical features of disease and associated outcomes and prognostic factors) that occurred in Japan during the winter of 1998-1999.

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Materials and Methods
Data collection

Questionnaires were developed by the Collaborative Study Group on Influenza-Associated Encephalopathy, which was organized by the Japanese Ministry of Health, Labor, and Welfare. The study was done as a cross-sectional survey of cases of influenza treated at all medical facilities. In July 1999, every local health care center in Japan received a questionnaire that asked for the number of cases of influenza-associated encephalitis/encephalopathy in all hospitals, clinics, and local pediatric practices within their jurisdiction. In addition to virus isolation, the sudden onset of high fever with respiratory signs, myalgia, and headache were used as diagnostic markers. A total of 217 cases were reported in returns of the primary questionnaires [16]. Subsequently, a second questionnaire that sought data on matched cases and detailed clinical and laboratory data was sent to each hospital. A total of 202 cases (corresponding to an effective answer rate of 93%) were reported and deemed appropriate for further study.

Case definition

The diagnosis of encephalitis/encephalopathy was made on the basis of all clinical signs. All patients had altered consciousness or loss of consciousness. Patients with meningitis, myelitis, and febrile convulsions without prolonged unconsciousness were excluded. Postictal unconsciousness with prompt recovery was classified as febrile convulsion.

Influenza infection was defined on the basis of either (1) a positive result of a viral culture, a viral antigen test, or viral RNA PCR or (2) by significant increases in hemagglutination inhibition-test titers (table 1). Specimens from throat swabs were used for viral culture, viral antigen testing, and viral RNA PCR. Viral antigens were detected by ELISA (Directigen fluA; Becton Dickinson). Viral RNA was detected by reverse-transcriptase (RT) PCR [18]. When virus was isolated, the subtype was determined by means of a hemagglutination inhibition test that used antisera to current antigens. For other patients, the virus subtype was determined by the detection of subtype-specific antibodies.

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Table 1

Methods used to confirm influenza infection and infecting influenza virus types in 148 patients with influenza-associated encephalitis/encephalopathy.

Patients with doubtful cases were excluded from further analysis (54 patients). Overall, 148 patients with cases defined as influenza-associated encephalitis/encephalopathy were enrolled in this study. The outcomes of influenza-associated encephalitis/encephalopathy were defined as the following: (1) normal resolution, (2) mild sequelae, (3) severe sequelae that require personal help for daily life activities, and (4) death.

Statistical analysis
Statistical analysis was done by use of Dr. SPSS, version 8.0J, for Windows (SPSS Japan).

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During the winter of 1998-1999, a large influenza epidemic occurred in Japan that was associated with many reports of acute encephalitis and encephalopathy. During this epidemic, millions of patients had "the flu," and the number of associated deaths was estimated to be 22.65 deaths per 100,000 persons [19]. The unforeseen CNS disease that occurred during the influenza epidemic attracted a great deal of attention.

Influenza-associated encephalitis/encephalopathy was diagnosed in 148 patients (78 male and 70 female patients). Of these 148 patients, 121 (81.8%) were aged 10 years. Of the 148 patients, 125 (84.5%) had no underlying disease, which indicates that most of the patients were otherwise healthy.

Figure 1
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Figure 1
Age distribution of patients with influenza-associated encephalitis/encephalopathy associated with an influenza epidemic in Japan during the winter of 1998-1999.

The influenza virus type was determined in 147 cases: 130 patients were infected with influenza A, and 17 patients were infected with influenza B (table 1). All cases of influenza A infection in which the subtype could be determined were due to type H3N2. The genetic analysis showed that most type A isolates were A/Sydney/5/97-like. The incidence of encephalitis/encephalopathy increased to a peak of type A (H3N2) infection approximately during the third week of 1999 and gradually decreased thereafter. Subsequently, another peak of type B infection occurred during the eighth week of 1999. According to the information from the National Institute of Infectious Diseases, Japan, the influenza subtypes recovered from patients aged <15 years during this second season were 2626 type A (H3N2) (from 42.8% of patients) and 3506 type B isolates (from 57.2% of patients). On the other hand, the influenza virus type recovered from most patients with encephalitis/encephalopathy was type A (87.8% of patients). Our data indicate that type A influenza (H3N2) was significantly associated with encephalitis/encephalopathy (P < .0001; &#967;2 test). There were no regional differences in the incidence of disease. The main routes of virus transmission were between family members (43.9% of cases) and within elementary schools and nursery schools (20.9% of cases).

Clinical features

The major clinical signs reported were loss of consciousness, convulsions, cough, and vomiting (table 2). Approximately one-third of the patients had convulsions or coma on

the day of the onset of fever. Overall, 79.8% of patients developed CNS diseases either on the day that influenza signs appeared or on the next day. Of the 147 patients for whom outcomes were noted, 31.8% died and 27.7% experienced disability (8.8% had severe sequelae and 18.9% had mild sequelae). Approximately 40% of the fatalities were due to rapidly progressing multiple-organ failure that occurred &#10877;2 days after the development of neurological signs. None of the patients showed any signs that suggested other microbial infections, such as measles, rubella, mumps, exanthem subitum, infectious mononucleosis, or enterovirus infection. Aspirin was administered to only 2 patients,

1 of whom had a history of Kawasaki disease. Ibuprofen was administered to 2 patients, diclofenac sodium to 18, mephenamate to 6, and acetaminophen to 58. None of the patients had received influenza vaccinations before the season.

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Table 2
Major clinical signs of influenza-associated encephalitis/encephalopathy in 148 patients.

Laboratory findings

We frequently observed decreased platelet counts, liver dysfunction with elevation of serum levels of transaminases and lactate dehydrogenase (LDH), and prolonged coagulation time. On the other hand, hypoglycemia (blood glucose level, 100 µg/dL) was observed in 15 patients (10.1%). CSF analyses showed that 134 of the patients had normal cell counts. We categorized influenza-associated CNS diseases into 3 types on the basis of laboratory findings (table 3): (1) encephalitis with increased CSF WBC counts (>8 cells/µL); (2) Reye syndrome-like condition, with normal cell counts, hypoglycemia (glucose level, <60 mg/dl), and increased serum transaminase levels; and (3) all other conditions. Patients with encephalitis were older, and had later onset of neurological signs than did the other patients, although these differences were not statistically significant (P = .16 and P = .74, respectively; Kruskal-Wallis test). Patients with a Reye syndrome-like condition showed a trend toward worse prognosis than patients in the other 2 categories (P = .08; Pearson's &#967;2 test). The patients in the category "other" made up 86% of all patients and seemed to comprise those who had influenza-associated CNS diseases during the 1998-1999 season.

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Table 3

Comparison of the characteristics of 148 patients with influenza-associated encephalitis/encephalopathy, according to 3 clinical categories of disease.

It is noteworthy that blood abnormalities correlated with disease outcome. The platelet count correlated with the outcome of influenza-associated encephalitis/encephalopathy. Of the patients with thrombocytopenia (1000 IU/L) was associated with poor outcome (mortality rate, 74.2%; table 5). Elevated serum levels of alanine aminotransferase, LDH, and creatine phosphokinase, as well as prolonged coagulation test times, were also linked to unfavorable outcomes (data not shown). These trends were also observed when the patients with encephalitis and Reye syndrome-like condition were excluded.

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Table 5

Association between serum aspartate aminotransferase (AST) level and prognosis for 148 patients with influenza-associated encephalitis/encephalopathy.

For 86% of patients, electroencephalogram findings were abnormal. Brain CT revealed abnormalities in 66% of patients. The most frequent findings, seen in 20% of patients, were brain edema and low densities in localized areas, such as in the thalamus, brain stem, and parenchyma. Acute necrotizing encephalopathy, which is characterized by multifocal, symmetric brain lesions that affect the thalami bilaterally, was recently proposed to be one of the features of influenza-associated encephalitis/encephalopathy [20, 21]. The characteristic radiological finding of acute necrotizing encephalopathy was noted for &#8764;10% of the patients we studied.

Autopsies were performed in some cases, and 4 autopsy reports are currently available. Brain, lung, bronchus, spleen, liver, kidney, heart, bone marrow, and lymph nodes were examined. In these 4 patients, the main finding was massive brain edema without inflammatory cell infiltration. Immunostaining with use of a monoclonal antibody against the influenza nucleoprotein was performed, but influenza antigens were not detected in the brain, including areas such as the cerebrum, hippocampus, cerebellum, brain stem, basal ganglia, and thalamus. In blood vessels, including those outside the brain, microemboli and hyalinization of the small vessels were observed. Plasma influxes from vessels to the visceral parenchyma were found in 3 patients. In 2 patients, hemophagocytosis was observed, which suggests the activation of macrophages by hypercytokinemia.

In 18 patients, we attempted to detect influenza RNA in CSF specimens by use of RT-PCR, but specimens from only 3 patients yielded positive results. Detection of the herpes simplex virus by PCR was attempted for 20 patients, but no virus DNA was detected. Virus isolation from CSF specimens was attempted for 21 patients, but all samples were negative for other viruses. In the present study, patients were not assessed for the infection with human herpesvirus 6 and human herpesvirus 7, which were recently shown to be detectable in CSF from patients with influenza encephalopathy [22].

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During the winter of 1998-1999, when Sydney-type H3N2 influenza was pandemic, there was an outbreak of encephalitis/encephalopathy in Japan. During the same period, cases of meningitis associated with influenza were reported in the United Kingdom [23]. We conducted a national survey that included all hospitals and pediatric clinics and analyzed 148 cases of influenza-associated encephalitis/encephalopathy. To the best of our knowledge, this is the first nationwide clinical survey of influenza-associated encephalitis/encephalopathy. We found that the disease developed mainly in children aged <5 years, with onset either on the day that influenza signs appeared or on the next day. Patients often developed multiple-organ failure and either died or suffered severe disability. Thrombocytopenia and severely elevated levels of transaminases were factors associated with a poor prognosis.

Reye syndrome, which is closely associated with the administration of aspirin, is one of the best-known encephalopathies associated with epidemics of influenza [6-8]. There are several differences between Reye syndrome and the cases of influenza-associated encephalitis/encephalopathy seen in the present study. First, classical Reye syndrome is usually associated with type B influenza [24]. Second, only a small percentage of our patients had hypoglycemia and/or hyperammonemia, which are characteristic of classical Reye syndrome. Third, aspirin was administered to only 2 of our patients. However, it should be noted that some nonsalicylate antipyretic drugs—for example, diclofenac sodium and mephenamate—might be associated with the development of influenza-associated encephalitis/encephalopathy or affect the severity of the disease. Case-control studies are currently under way to clarify the relationship between these drugs and influenza-associated CNS diseases.

The pathogenesis of influenza-associated encephalitis/encephalopathy is unclear. Whether the influenza virus invades the brain parenchyma is still a controversial issue. Fujimoto et al. [13] reported that viral RNA was frequently detected in the CSF by RT-PCR. However, recent reports have indicated that viral RNA is not detected in the CSF of most patients with influenza-associated encephalitis/encephalopathy [18, 25]. In the present study, only a small number of patients had CSF samples that tested positive for viral RNA. Findings of pathologic examination, including the lack of detectable viral antigen in brain tissues, also have suggested that direct viral invasion and inflammation are unlikely to be the causes of this disease. Disease progression appears to be too rapid for the virus to invade the CNS directly and to replicate in CNS tissue, causing brain damage. The observed absence of viral antigen in affected tissues and the rapid progression of disease differentiate this disease from herpes simplex encephalitis, which is caused by direct invasion by and cytopathic effects of herpes simplex virus [26, 27].

In influenza-associated encephalitis/encephalopathy, elevated concentrations of several cytokines, such as soluble TNF receptor-1, IL-1&#946;, and IL-6, have been observed in serum and CSF [18, 28]. Elevated levels of serum transaminases and LDH, vascular damage throughout the body, and the rapid progression to multiple-organ failure suggest that hypercytokinemia and injury to blood vessels or vascular endothelia may play important roles in the pathogenesis of influenza-associated encephalitis/encephalopathy [29]. These characteristics are often seen in virus-associated hemophagocytic syndrome or systemic inflammatory response syndrome. Kawasaki disease, which is characterized by systemic inflammatory responses or vascular injury, is often seen in Japan. Japanese people might have genetic backgrounds that facilitate the development of systemic inflammatory responses or hypercytokinemia; they might, therefore, have a tendency to develop influenza-associated encephalitis/encephalopathy. These speculations may explain why epidemic encephalitis was not seen throughout the world during the pandemic of influenza A (H3N2). Another possibility is that the virus strain that spread in Japan might have been more virulent with respect to the CNS or might have been prone to induce systemic inflammation. Further investigation into the molecular pathogenesis and epidemiology of this disease is necessary to better our understanding and to enable the development of effective strategies to manage outbreaks.

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We thank all of the physicians and pediatricians who participated in the present study.

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Financial support: Ministry of Health, Labor, and Welfare of Japan (grant H12-S-11).

Received November 6, 2001.
Revision received March 5, 2002.
Accepted August 7, 2002.
© 2002 by the Infectious Diseases Society of America
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References  http://cid.oxfordjournals.org/content/35/5/512.full

My son died of human form of mad cow disease aged just 24 years old 11.Jun.2014 01:53

Christine Lord award winning documentary journalist mschristinelord@aol.com

My name is Christine Lord and since the unlawful death of my son Andrew Black aged 24 in 2007 I have investigated the Mad Cow scandal, Human BSE. This has resulted in three documentaries one for BBC1 if you click on to the documentary page of www.justice4andy.com you can view this programme in which I filmed the last days of my only sons life. It also contains factual and thorough research of the mad cow disease epidemic and those responsible and how many millions of us globally were exposed to infected UK beef, animal feed, food and medicines. I have also written a best seller Amazon Who killed my son? which explains how vcjd Human BSE became transmitted to humans even though my son Andrew and our family had not eaten beef or beef products since 1988. BSE has long incubation periods in animals and in humans upwards of 40 years. Currently one in a thousand of the UK population carry vcjd HUman BSE according to latest research by the UK health protection agency. I would like anyone reading this comment to check out the website, documentary and either/or my book and then make their own minds up about the disease. My son Andrew when he was dying pleaded with me ' find out who did this to me mum' and always worried about others ' this must never happen to anyone else again'. I continue to honour the promises I gave my dying son, I have no political agenda, no financial gain ( profits from the book go back to the campaign supporting thousands of families worldwide affected by cjd) all I want is to make sure other mums and dads do not suffer the heartbreak I do every day, missing my Andrew, wishing he was still here living his life. He went from a healthy young man working for sky/BBC as a producer/researcher to being blind quadriplegic within 6 months, because his vaccines, school meals, baby food was laced with BSE infected material which flooded the human food and medicine chain for over a decade. Cow still die of BSE, still carry BSE help me to raise awareness,this ticking health time-bomb.

4 St Peters Lodge Southsea UK