Chlamydia Pneumoniae (Pneumonic disease – pp 367)

More than 50% of population has serological evidence of past infection. Widespread. Causes 25-45% of atypical pneumonias in USA. Can cause atherosclerosis, although pathogenesis is not fully understood. It is know, however, that this can grow inside smooth muscle cells.

Diagnosis (Murray 3^rd Ed pp 366)

Laboratory diagnosis can be made by cytology, serology and culture. For UG disease: you take scrapings and prepare a Giemsa-stain. You are looking for the presence of inclusions (cytology). This method is not sensitive as culture or immunofluorescence. You can do a serological test (used for Psittacosis) and look for a 4 fold increase in titre – CF (complement fixing antibodies). For LGV, you can do a skin test (Frei test) but is basically useless because it is insensitive, and non-specific. You can also do PCR or LCR (Ligase chain reaction), where amplification of nucleic acid and you look for specific acid sequences. This is extremely sensitive – 90-98%. You can also culture the bacteria because they only infect a restricted type of cells in vitro (e.g.: HeLa-229, McCoy, BHK-21, Buffalo green monkey kidney cells), which is also true for cells in vivo.

You can also do an antigen detection test – direct immunofluorescence staining (DFA) or enzyme-linked immunoassays. Here, antibodies are prepared against the LPS or chlamydial MOMP.

Treatment (Murray 3^rd pp 367)

Tetracyclines, sulphonamides, erythromycin, azithromycin, chloramphenicol.

Category: Microbiology Notes