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New, 'Simple Blood Test'
For BSE/Mad Cow Said
To Be A Fraud
9-28-00
 
Hi,
 
A false story is about to be ciculated that Acinetobacter calcoaceticus bacteria causes Mad Cow and variant CJD. The story is fake. The following journal extract proves Acinetobacter calcoaceticus is easily killed by boiling, yet autoclaving at 160C for 40 minutes does not kill CJD. So CJD could not possibly be caused by Acinetobacter calcoaceticus. Also, gemifloxacin can easily kill Acinetobacter calcoaceticus bacteria, so anyone who took gemifloxacin would immeadiately recover from CJD if that bacteria actually did cause CJD. (see reference at bottom)
 
moonbeam
 
Microbiol Immunol 1982;26(1):15-24 The effects of temperature and pH on the growth of eight enteric and nine glucose non-fermenting species of gram-negative rods.
 
Tsuji A, Kaneko Y, Takahashi K, Ogawa M, Goto S
 
We studied the heat resistance and the range of growth temperature on ............. Acinetobacter calcoaceticus. All the bacterial species tested were killed within 30 min at 60 or 70 C. Among the sugar non-fermenting rods, A. calcoaceticus had the widest range of growth temperature (20-45 C) and also multiplied rapidly. The above results are correlated fairly well with the incidence of clinical cases of infection.
 
PMID: 7087800, UI: 82219247
 
 
NOW THE FAKE STORY.............
 
A New, Simple Test Could Detect CJD - The Human Form Of BSE/Mad Cow
 
By David Brown - Agriculture Editor, The Telegraph 9-26-00
 
A simple blood test which could enable doctors to diagnose victims of the human form of mad cow disease at an early stage has been developed by a team of scientists at King's College, London.
 
The test, which identifies antibodies to bacteria, has already been used accurately to identify BSE in cattle. Previously, the only sure way of confirming whether or not cattle had BSE was by post mortem examination of the brain. So far 74 people have died from new variant Creutzfeldt-Jakob disease (vCJD), which has been linked to BSE. Another eight are believed to be dying from the disease.
 
Details of the new test will be described in America next week by Alan Ebringer, Professor of Immunology at King's College, who says it supports his theory that BSE was caused by Acinetobacter calcoaceticus, a bacterium common in the environment.
 
All of the diseased cattle tested had high levels of antibodies to Acinetobacter calcoaceticus in their blood. This bacterium is commonly found in animal faeces, sewage, contaminated water and the soil. Prof Ebringer argues that the BSE epidemic started when large amounts of this bacterium damaged the auto-immune system of cattle after they were fed rations containing the processed remains of the intestines of sheep and other animals.
 
According to his theory, a general lowering of temperatures in the animal rendering process in Britain allowed the bacteria to survive.
 
Suspected cases of BSE in Britain have fallen to about 30 a week, compared with more than 1,000 cases a week at the peak of the epidemic in 1993, the Ministry of Agriculture reported yesterday.
 
 
J Antimicrob Chemother 2000 Apr;45 Suppl 1:71-7
 
 
Bactericidal and bacteriostatic activity of gemifloxacin against Acinetobacter spp. in vitro.
 
Higgins PG, Coleman K, Amyes SG
 
Department of Medical Microbiology, The Medical School, University of Edinburgh, Teviot Place, Edinburgh EH8 9AG, UK. paul.hoggins@ed.ac.uk
 
This study compared the in vitro bacteriostatic activity of gemifloxacin (SB-265805) and a panel of test antimicrobial agents against 100 clinical isolates of Acinetobacter spp. (47 Acinetobacter baumannii, 18 Acinetobacter anitratus, 18 Acinetobacter lwoffii, 13 Acinetobacter calcoaceticus and four other Acinetobacter spp.). Gemifloxacin (MIC(50/90) 0.06/16 mg/L) was more than eight-fold more potent than ciprofloxacin (0.5/128 mg/L), two- to eight-fold more potent than grepafloxacin, moxifloxacin, levofloxacin, ofloxacin and gatifloxacin, and of similar potency to trovafloxacin and sparfloxacin. Cross-resistance was seen only within the quinolone group and did not extend to non-quinolone antimicrobials. The bactericidal activities of gemifloxacin and the six comparator quinolones were investigated by dose-response and time-kill studies against A. baumannii ATCC 19606 at their optimum bactericidal concentration (OBC) and at 4 x MIC. At the OBC there was no significant difference between the quinolones, but at 4 x MIC gemifloxacin showed superior activity, reducing the viable count by almost 2 log(10) in 30 min compared with a 1 log(10) reduction seen with the other drugs. This enhanced killing extended over 24 h, reducing cell numbers by 4 log(10). These data suggest that gemifloxacin has the potential to be of therapeutic value in the treatment of infection by Acinetobacter spp.
 
PMID: 10824036, UI: 20285511

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