<unk>  is a transmissible spongiform<unk>  of cattle associated with abnormal prion proteins in the brain. Affected animals develop excitability and salivation followed by ataxia. This disorder has been associated with consumption of scrapie infected ruminant derived protein. This condition may be transmitted to humans, where it is referred to as variant or new variant CREUTZFELDT-JAKOB SYNDROME. Publius Flavius Vegetius Renatus records cases of a disease with similar characteristics in the 4th and 5th Century AD. The origin of the disease itself remains unknown. The current scientific view is that infectious proteins called prions developed through spontaneous mutation, probably in the 1970s, and there is a possibility that the use of organophosphorus pesticides increased the susceptibility of cattle to the disease. Between 460,000 and 482,000<unk> -infected animals had entered the human food chain before controls on high-risk offal were introduced in 1989. It is believed that the disease may be transmitted to human beings who eat infected carcasses. In humans, it is known as new variant Creutzfeldt-Jakob disease (vCJD or nvCJD), and by June 2007, it had killed 165 people in Britain, and six elsewhere with the number expected to rise because of the disease's long incubation period. Based on the biochemical signatures of the disease-associated prion protein,<unk>  spongiform encephalopahty <unk>  may be classified as either classic or atypical. Atypical<unk>  may further be classified into H- and L-types. Due to the accumulation of amyloid protein in the brain in cattles with L-type<unk> , its also known as<unk>  amyloidotic spongiform<unk>  (BASE). It is understood that<unk>  <unk>  is caused by a misfolded prion protein. Misfolded prion proteins carry the disease between individuals and cause deterioration of the brain.<unk>  is a type of transmissible spongiform<unk>  (TSE).<unk>  <unk>  may be caused by different strains including the classic<unk>  strain (which is responsible for the outbreak in the United Kingdom) and two atypical strains (H and L strains).<unk>  must be differentiated from other diseases that cause hyperesthesia, nervousness, reluctance to be milked, aggression, low head carriage, tremors, ataxia, disrupted milk production, and weight loss in animals, such as scrapes, rabies, encephalitic listeriosis, hypomagnesemia, lead poisoning, downer cow syndrome, nervous ketosis, polioencephalomalacia, ingestion of plant or fungal tremoragens, intracranial abscess or tumors, trauma to the spinal column, and other viral and bacterial neuroinfectious diseases. Following an epizootic of<unk>  in Britain, 165 people (up until 2007) acquired and died of a disease with similar neurological symptoms subsequently called vCJD, or (new) variant Creutzfeldt-Jakob disease. It is estimated that 400,000 cattle infected with<unk>  entered the human food chain in the 1980s. Although the<unk>  epizootic was eventually brought under control by culling all suspect cattle populations, people are still being diagnosed with vCJD each year. It is notable that there are no cases reported in Australia and New Zealand where cattle are mainly fed outside on grass pasture and, mainly in Australia, non-grass feeding is done only as a final finishing process before the animals are processed for meat. The most potent risk factor in the development of<unk>  is the consumption of meat-and-bone meal (MBM) by cattle. There is insufficient evidence to recommend routine screening for<unk>  <unk> . The symptoms of<unk>  typically develop 2-8 years after exposure to prions. Prognosis is generally poor, and death occurs approximately 3 months after the appearance of the first clinical signs.<unk>  is primarily diagnosed based on the clinical presentation. However, postmortem examination should be performed for the definitive diagnosis. The postmortem investigation might be done with either western blot, ELISA, rapid test for<unk>  (ID-Lelystad), or histopathology. The confirmation of the diagnosis is possible either with the detection of PrPBSE in the brain tissue (either by western blot, ELISA, or ID-Lelystad), or vacuolation of neurons and neuropil in the histopathologic examination of medulla oblongata specimen. The most common symptoms of<unk>  include hyperesthesia, nervousness, reluctance to be milked, aggression, low head carriage, tremors, ataxia, disrupted milk production, and weight loss in animals. Common physical examination findings of<unk>  include ataxia, tremor, abnormal head carriage, hyperesthesia, excessive licking, loss of weight, recumbency, and abnormal ear position. Laboratory findings consistent with the diagnosis of<unk>  include the detection of PrPBSE in the brain tissue (either by western blot, ELISA, or ID-Leystad), the detection of Scrapie-Associated Fibrils in the brain tissue (by electron microscopy), and specific histopathologic findings such as vacuolation of neurons and neuropil. There are no ECG findings associated with<unk> . There are no x-ray findings associated with<unk> . There are no echocardiography/ultrasound findings associated with<unk> . There are no CT scan findings associated with<unk> . T2-weighted (T2W) MRI may be helpful in the diagnosis of<unk> . Findings on T2W-MRI suggestive of<unk>  include T2W-MRI hyperintensity in the thalamic nuclei. There are no other imaging findings associated with<unk> . There are no other diagnostic studies associated with<unk> . There is no treatment for<unk> . There are no recommended therapeutic interventions for the management of<unk> . Surgical intervention is not recommended for the management of<unk> . Effective measures for the primary prevention of<unk>  include control measures such as surveillance, banning specified risk materials, culling sick animals, and excluding all animals more than 30 months of age from the human food and animal feed supplies. There are no established measures for the secondary prevention of<unk> .
Bovine spongiform encephalopathy
Feline spongiform encephalopathy
St. Louis encephalitis
Creutzfeldt-Jakob disease
Nipah virus encephalitis
Eastern equine encephalitis
Japanese encephalitis
La Crosse encephalitis