Macromolecular Composition

Chlamydiae have a bilayered cell membrane similar to other Gram-negative bacteria. The cell membrane contains species-specific antigens such as the major outer membrane protein (MOMP), as well as common antigens such as lipopolysaccharide (LPS).[4] Major outer membrane protein is the most prominent membrane protein making up about 60% of the surface proteins. Variable domains of this protein allow the division of C. trachomatis but not C. pneumoniae, into different serovars. In the genome of C. pneumoniae open reading frames of 21 putative polymorphic membrane proteins (Pmp) have been found.[5] For some, presence on the surface of chlamydiae and immunogenicity could be demonstrated.[4,6]

All chlamydiae share the same LPS structure[7] with a comparably low number of acylic groups, which is probably responsible for the low endotoxic activity. Lipopolysaccharide is used as a group complementation fixation antigen and recombinant ELISA-antigen for chlamydial serodiagnosis. Heat shock proteins, such as the genus-specific heat shock protein 60 (HSP60), are additional important immunogenic antigens although they are scarcely expressed on the surface. Also of interest is a Type III secretion apparatus that is expressed on the surface of reticulate bodies as well as EBs.[5]

Table 1 Proposed taxonomy of Chlamydiales

Order

Family I Genus Species

Genus Species

Family II

Species Family III Species

Family IV unnamed Species

Chlamydiales

Chlamydiaceae Chlamydia

Chlamydia muridarum sp. nov. Chlamydia suis sp. nov. Chlamydia trachomatis Biovar trachoma Biovar LGV Chlamydophila

Chlamydiophila abortus sp. nov. Chlamydiophila caviae sp. nov. Chlamydiophila felis sp. nov. Chlamydiophila pecorum comb. nov. Chlamydiophila pneumoniae comb. nov. Biovar TWAR Biovar Koala Biovar Equine Chlamydiophila psittaci comb. nov. Simkaniaceae fam. nov. Simkania negevensis sp. nov. Parachlamydiaceae fam. nov. Parachlamydia acanthamoebae sp. nov. and others

Waddlia

Additional contemporary information about the chlamydial genomes can be accessed on the Internet: http:// www.ncbi.nlm.nih.gov/genomes/MICROBES/Complete. html, http://www.tigr.org/tdb/, http://chlamydia-www. berkeley.edu:4231/.

CLINICAL SIGNIFICANCE Respiratory Tract Infections

C. pneumoniae is endemic worldwide and is responsible for an estimated 10-20% of community acquired pneumoniae. The first contact with C. pneumoniae usually occurs at a young age leading to a seroprevalence of 50% to 60% by the age of 30, which slowly rises with age.

Infection is transmitted via respiratory secretions. After a variable incubation period of up to 4 weeks the disease begins with growing hoarseness and aching throat, mild cough, and fever and does later develop into an atypical pneumonia.[12,13] In rare cases infection may also present as sinusitis or otitis media or lead to the aggravation of asthma.[14] In immunocompetent individuals the infection is usually self-limiting, but may be complicated by superinfections. In immunocompromised persons infection may take a more severe course. Reinfections do occur but are generally milder than primary infections.[13]

C. pneumoniae and Atherosclerosis

Genome

The genomes of four C. pneumoniae strains (CWL029, AR39, J138, TW183) have been sequenced and pub-lished.[5,8-10] Additionally, the genomes of three C. trachomatis strains (trachoma serovar D: D/UW-3Cx; serovar L2 L2/434/Bu; Nigg-MoPn, proposed Chlamydia muridarum), one C. psittaci (GPIC, proposed Chlamydia caviae)[2-4] and one parachlamydial strain[1] are available and more genomes are soon to be published.

With slightly more than 1 million base pairs (1.23 million for C. pneumoniae) chlamydiae possess one of the smallest genomes in the bacterial world.[8,10] The different chlamydial genomes have a homology of about 80% and there are very few genetic differences within the species of C. pneumoniae.

Chlamydiae were previously considered to be ATP-parasites but interestingly possess putative proteins for the synthesis of ATP.[5] The presence of two genes encoding (ADP)ATP-translocases, however, make it likely that chlamydiae additionally import host cell ATP.[11]

In some strains of C. pneumoniae, and also C. psittaci, different bacteriophages have been demonstrated.[8]

Since the first report of a link between C. pneumoniae and coronary heart disease (CHD) in 1988,[15] the chlamydia-arteriosclerosis theory has been challenged by a vast number of epidemiological and experimental studies, resulting, however, in contradictory outcomes. Recent meta-analysis of serological studies did not confirm the early reports of a serologic correlation.[16,17] But direct investigation of arteries by PCR and immunohistochem-istry revealed that 25% to 50% of atherosclerotic vessels contain chlamydiae compared to only 2% of healthy vessels.[17,18] There is, however, considerable variation among different studies and only poor correlation between the different detection methods.[17]

In vitro, chlamydiae were able to infect all cells relevant in the development of arteriosclerosis, including macrophages, endothelial cells, and smooth muscle cells.[19] Chlamydiae further promoted the expression of proatherogenic receptors, second messengers, and enzymes in cell culture experiments.[19]

While early studies addressing antibiotic intervention of arteriosclerosis seemed to show a positive effect, this result has not been confirmed in recent studies.[20]

Animal experiments with mice and rabbits have also produced conflicting results concerning the development

Fig. 1 C. pneumoniae in HeLa cells 72 hr post infection. The transmission electron microscopic image shows an inclusion containing reticulate bodies which are still dividing (long arrows) and already developed elementary bodies (short arrows) as well as intermediate forms (N = nucleus of the cell). The right pictures represent 3-D images of an immunofluorescent staining with a FITC-labeled antibody targeting chlamydial LPS (green) and a fluorescence in situ hybridization with a Cy-3-labeled DNA-probe targeting specific sequences on the chlamydial ribosomal RNA (red), respectively. Some inclusions are already rupturing and their infectious content is spreading ready to infect new host cells. (Photos courtesy of Poppert and Horn.) (View this art in color at www.dekker.com.)

Fig. 1 C. pneumoniae in HeLa cells 72 hr post infection. The transmission electron microscopic image shows an inclusion containing reticulate bodies which are still dividing (long arrows) and already developed elementary bodies (short arrows) as well as intermediate forms (N = nucleus of the cell). The right pictures represent 3-D images of an immunofluorescent staining with a FITC-labeled antibody targeting chlamydial LPS (green) and a fluorescence in situ hybridization with a Cy-3-labeled DNA-probe targeting specific sequences on the chlamydial ribosomal RNA (red), respectively. Some inclusions are already rupturing and their infectious content is spreading ready to infect new host cells. (Photos courtesy of Poppert and Horn.) (View this art in color at www.dekker.com.)

of arteriosclerosis after infection with C. pneumoniae}21'22 Although the enthusiasm regarding the detection of a bacterial cause of atherosclerosis has been dampened by the contradictory results, the debate is still ongoing.

Getting Started With Dumbbells

Getting Started With Dumbbells

The use of dumbbells gives you a much more comprehensive strengthening effect because the workout engages your stabilizer muscles, in addition to the muscle you may be pin-pointing. Without all of the belts and artificial stabilizers of a machine, you also engage your core muscles, which are your body's natural stabilizers.

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