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This metaphor suggests that slower growing pathogens should be more easily controlled.
Compared with the response to fast growing pathogens, the T-cell response to slow pathogens is delayed in its initiation, lymphocyte expansion is slow and the response often fails to clear the pathogen, leading to chronic infection.
In Dr. Weller's 2004 autobiography, "Growing Pathogens in Tissue Cultures: Fifty Years in Academic Tropical Medicine, Pediatrics, and Virology" (Watson Publishing) he revealed the source of the viral sample for congenital rubella (German measles) nearly a quarter century before: It was the urine of his son Robert, who was 10 when he developed signs of a particularly severe case of measles.
The ability to obtain results quickly has particular value for very slow growing pathogens such as mycobacteria [6].
However, as both Brucella spp and Mycobacterium tuberculosis are slowly growing pathogens, cultures are labor intensive, which can at times lead to unacceptable delays in diagnosis.
This two signal requirement limits the risk of undesired immunopathology but imposes a 5 7 day delay in the induction of an effective antibody response, a delay that might be far too long to fight fast growing pathogens.
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It is a very slow growing pathogen, presumably with limited needs for TMP.
The genomic organization and gene functionality of M. tuberculosis are invaluable for understanding the slowly growing pathogen.
We then show how the immune system uses this information to decide whether or not an antigen is part of a growing pathogen population.
Once released into the cytoplasm, the actively growing pathogen can spread from cell to cell via ActA polymerization of the host cell actin, which supports movement within the cytoplasm to the membrane-membrane interface with adjacent cells.
Not all positive cultures grew pathogens, and the organisms grown were not necessarily consistent with the suspected infection site.
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