Technical Data
C4250-07
Chlamydia trachomatis (FITC)
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Technical Data |
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C4250-07 |
Chlamydia trachomatis (FITC) |
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Description: Applications: Direct FA staining of target antigens in a permissive tissue culture system. Working strength must be determined by the user for each specific application but a starting range of 1:15–1:50 is suggested. Acetone fixation of the antigen source is recommended prior to staining. The titer is 1:1,000 by indirect IF vs. purified EB’s (all serovars, A-K, L1-L3). Chlamydia is caused by the bacterium Chlamydia trachomatis. The intracytoplasmic inclusions caused by the bacterium are draped around the infected cell’s nucleus. Chlamydia has a genome size of approximately 500-1000 kilobases and contains both RNA and DNA. The organism is also extremely temperature sensitive and must be refrigerated at 4°C as soon as a sample is obtained. Colonization of Chlamydia begins with attachment to sialic acid receptors on the eye, throat or genitalia. It persists at body sites that are inaccessible to phagocytes, T-cells, and B-cells. It also exists as 15 different serotypes. These serotypes cause four major diseases in humans: endemic trachoma (caused by serotypes A and C), sexually transmitted disease and inclusion conjunctivitis (caused by serotypes D and K), and lymphogranuloma venereum (caused by serotypes L1, L2, and L3). Studies reveal that Chlamydia, because of its cell wall, is able to inhibit phagolysosome fusion in phagocytes. The cell wall is proposed to be gram-negative in that it contains an outer lipopolysaccharide membrane, but it lacks peptidoglycan in its cell wall. This lack of peptidoglycan is shown by the inability to detect muramic acid and antibodies directed against it. It may, however, contain a carboxylated sugar other than muramic acid. The proposed structure consists of a major outer membrane protein cross-linked with disulfide bonds. It also contain cysteine-rich proteins (CRP) that may be the functional equivalent to peptidoglycan. This unique structure allows for intracellular division and extracellular survival (Hatch 1996). -Kenneth Todar, University of Wisconsin-Madison |
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