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Virulence of strains of C. trachomatis.

Virulence means the capacity to survive in the host and to cause disease. The most obvious virulence difference occurs among C. trachomatis strains. C. trachomatis serotypes L1, L2 and L3 cause invasive genital tract infection (lymphogranuloma venereum, LGV) with marked lymph node pathology. These strains are clearly different from other C. trachomatis strains, being characterised, for example, by their ability to infect susceptible cells in the laboratory without the need for centrifugation and by faster growth. Collectively these three serotypes of C. trachomatis belong to the so-called LGV biovar. The remaining strains of C. trachomatis belong to the so called trachoma-inclusion conjunctivitis or TRIC biovar. They tend to cause superficial infections of the surface of the eye or the genital tract, without only limited tissue invasion. In the laboratory centrifuge assisted infection of susceptible cell lines is usually necessary. Theoretically it is considered that the evolution of virulence among microbial pathogens is dependent on two epidemiological factors; the dominant mode of transmission, i.e. vertical [to one’s children] or horizontal [to others] [Herre, 1995] and the likelihood of multiple infection of a particular host [Nowak & May, 1994]. Horizontally transmitted pathogens which spread sideways from host to host with a high probability of causing multiple infection in a particular host tend to evolve towards virulence [Ebert, 1998]. A possible illustration of this concept occurs among commercial sex workers in Nairobi, among whom LGV strains of C. trachomatis are common, and often related to HIV infection, although such strains are rare in general populations in Winnipeg [Brunham, 1999] or the developed world generally. Here, it is suggested [Brunham, 1999] repeated exposure to infection in these prostitutes is likely to lead to immunity to the usual TRIC strains of C. trachomatis genital tract infection, selecting out the more virulent LGV strains capable of causing more invasive disease. Within the TRIC biovar, serotypes A, B and C tend to be associated with endemic trachoma, whereas the remaining non LGV serotypes cause oculo-genital infection. Whether this reflects genuine biological differences between these groups [as seems likely] or simply geographical / epidemiological factors is unknown. 

For the TRIC biovar, although it has been reported that serovar F may be more associated with abdomenal pain in women, there is really no strong evidence that any particular serotype is associated with more severe or invasive disease [Geisler et al., 2003]. However serovar-associated differences in chlamydial tryptophan synthase may account for some of the differential sensitivity to interferon gamma that has been observed among C. trachomatis isolates [Shaw et al., 2000].  For an account of the Millman et al., 2001 study on the possible role of recombination events in the gene encoding MOMP in determining serovar specific differences in the tissue tropism and virulence of C. trachomatis, click here

[MEW] April 2003

Update: See: Role of C. trachomatis serovars in urogenital infection

NEXT: Chlamydia and apoptosis.

References

Brunham, R. C. (1999). Human immunity to Chlamydiae. Pages 211-238. In: Chlamydia. Intracellular biology, pathogenesis and immunity. (Stephens, R. S. ed.). ASM Press, Washington D.C. USA. ISBN 1-55581-155-8. [Thoughtful review].

Ebert, D. (1998). Experimental evolution of parasites. Science 282, 1432 - 1435. [Interesting concept]

Geisler, W. M., Suchland, R. J., Whittington, W. L. & Stamm, W. E. (2003). The relationship of serovar to clinical manifestations of urogenital Chlamydia trachomatis infection. Sexually Transmissible Diseases 30, 160 - 165.

Herre, E. A. (1995). Factors affecting the evolution of virulence: nematode parasites of fig wasps as a case study. Parasitology 111, S179 - S191.

Millman, K. L., Tavare, S. & Dean, D. (2001). Recombination in the ompA gene but not the omcB gene of Chlamydia contributes to serovar-specific differences in tissue tropism, immune surveillance, and persistence of the organism. Journal of Bacteriology 183, 5997 - 6008. Full article [Acrobat] [Excellent and thoughtful study. Good literature review].

Nowak, M. A. & May, R. M. (1994). Superinfection and the evolution of parasite virulence. Proceedings of the Royal Society of London Series B 255, 81 - 89. [Hypothesis driven review].

Shaw, A. C., Christiansen, G., Roepstorff, P. & Birkelund, S. (2000). Genetic differences in the Chlamydia trachomatis tryptophan synthase alpha-subunit can explain variations in serovar pathogenesis. Microbes and Infection 2, 581 - 592.

NEXT: Chlamydia and apoptosis.

 


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