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Bordetella pertussis isolates in Finland: serotype and fimbrial expression
Eriikka Heikkinen1, Dorothy K Xing, Rose-Marie Olander
1Pertussis Reference Laboratory, National Public Health Institute, Kiinamyllynkatu 13, 20520 Turku, Finland. Eriikka.Heikkinen@ktl.fi
Background:
Bordetella pertussis causes whooping cough or pertussis in humans. It produces several virulence factors, of which the fimbriae are considered adhesins and elicit immune responses in the host. B. pertussis has three distinct serotypes Fim2, Fim3 or Fim2,3. Generally, B. pertussis Fim2 strains predominate in unvaccinated populations, whereas Fim3 strains are often isolated in vaccinated populations. In Finland, pertussis vaccination was introduced in 1952. The whole-cell vaccine contained two strains, 18530 (Fim3) since 1962 and strain 1772 (Fim2,3) added in 1976. After that the vaccine has remained the same until 2005 when the whole-cell vaccine was replaced by the acellular vaccine containing pertussis toxin and filamentous hemagglutinin. Our aims were to study serotypes of Finnish B. pertussis isolates from 1974 to 2006 in a population with > 90% vaccination coverage and fimbrial expression of the isolates during infection. Serotyping was done by agglutination and serotype-specific antibody responses were determined by blocking ELISA.
Results:
Altogether, 1,109 isolates were serotyped. Before 1976, serotype distributions of Fim2, Fim3 and Fim2,3 were 67%, 19% and 10%, respectively. From 1976 to 1998, 94% of the isolates were Fim2 serotype. Since 1999, the frequency of Fim3 strains started to increase and reached 83% during a nationwide epidemic in 2003. A significant increase in level of serum IgG antibodies against purified fimbriae was observed between paired sera of 37 patients. The patients infected by Fim3 strains had antibodies which blocked the binding of monoclonal antibodies to Fim3 but not to Fim2. Moreover, about one third of the Fim2 strain infected patients developed antibodies capable of blocking of binding of both anti-Fim2 and Fim3 monoclonal antibodies.
Conclusion:
Despite extensive vaccinations in Finland, B. pertussis Fim2 strains were the most common serotype. Emergence of Fim3 strains started in 1999 and coincided with nationwide epidemics. Results of serotype-specific antibody responses suggest that Fim2 strains could express Fim3 during infection, showing a difference in fimbrial expression between in vivo and in vitro.
Insights
Bordetella pertussis Fim2 strains predominated in Finland despite high vaccination rates. However, Fim3 strains emerged in 1999, coinciding with epidemics, suggesting altered fimbrial expression during infection.
Area of Science:
- Microbiology
- Immunology
- Epidemiology
Background:
- Bordetella pertussis causes whooping cough and possesses fimbriae as key adhesins.
- B. pertussis exhibits distinct serotypes: Fim2, Fim3, and Fim2,3.
- Vaccination history in Finland includes whole-cell vaccines with Fim3 and Fim2,3 strains, later replaced by acellular vaccines.
Purpose of the Study:
- To investigate the serotypes of B. pertussis isolates in Finland from 1974 to 2006.
- To analyze fimbrial expression of B. pertussis during human infection.
- To correlate serotype distribution with vaccination status and disease outbreaks.
Main Methods:
- Serotyping of 1,109 B. pertussis isolates using agglutination.
- Determination of serotype-specific antibody responses via blocking ELISA.
- Analysis of paired sera from patients to assess immune responses to fimbriae.
Main Results:
- Fim2 strains were dominant (94%) from 1976 to 1998.
- Fim3 strains increased significantly from 1999, reaching 83% during a 2003 epidemic.
- Antibody responses indicated Fim3-infected patients produced Fim3-specific antibodies, while some Fim2-infected patients showed cross-reactivity.
Conclusions:
- B. pertussis Fim2 strains remained prevalent despite extensive vaccination in Finland.
- The emergence of Fim3 strains since 1999 correlated with nationwide pertussis epidemics.
- Findings suggest Fim2 strains may express Fim3 in vivo, indicating differential fimbrial expression during infection.
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