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new article for duke university

Chlamydia Escapes Defenses By Cloaking Itself with Lipids
Duke University Medical Center (Press Release) - December 11, 2005<
media contact: Richard Merritt 919-684-4148 merri006@...<
contact sources: Raphael Valdivia 919-668-3831 valdi001@...<

how high is a hígh bacterial load?

hello everybody,


i am new to this forum and already very thankful it exists. i was diagnosed with Cpni on thursday, but i have had the suspicion for some weeks. Symptoms so far: gallbladder inflammation
sore neck and shoulder


my blood tests says:
(chlam. trach.: negative)


chlam pneum:
IgA-EIA: neg.
IgG-EIA: 70
IgM-EIA: 1,3


is that a high load?


does anybody have experience with gallbladder inflammation?


 Could it be a consequence of oral sex? swallowing infected body-fluid?


my doc has started 3 weeks ago with giving me clont and ciprobay.just against the inflammation. it seemes to have helped some. now as we have the diagnose, I am (only)on doxyi 200/d. we have studied the recommended regimens yesterday.


The load of Chlamydia pneumoniae in the Alzheimer's brain varies with APOE genotype

Microb Pathog. 2005 Jul-Aug;39(1-2):19-26.
The load of Chlamydia pneumoniae in the Alzheimer's brain varies with APOE genotype.

Gerard HC, Wildt KL, Whittum-Hudson JA, Lai Z, Ager J, Hudson AP.

Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI 48201, USA.

Studies from this laboratory have indicated that the intracellulari eubacterial respiratory pathogen Chlamydophila (Chlamydia) pneumoniae is commonly found in brain regions displaying characteristic neuropathology in patients with late-onset Alzheimer's diseasei (AD) but not in congruent samples from non-AD control individuals. In later work, we provided evidence suggesting that some relationship exists between the APOE epsilon4 gene product and the pathobiology of this organism. In the present report, in situ hybridization analyses indicated that the number of C. pneumoniae-infected cells in affected brain regions of epsilon4-bearing AD patients was higher overall than that in congruent brain regions from AD patients lacking that allele. Quantitative real-time PCRi analyses of AD brain tissue samples demonstrated that actual bacterial burden in those samples varied over several orders of magnitude, but that samples from epsilon4-bearing patients did have significantly higher bacterial loads than did congruent samples from patients without the allele (ANOVA, p<0.05). These results may explain in part the observations that epsilon4-bearing individuals have a higher risk of developing AD, and that such patients progress more rapidly to cognitive dysfunction than do individuals lacking this allele.

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