- 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)
- 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. firstname.lastname@example.org
- 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
- PMID: 10824036, UI: 20285511
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