PubMed · 3798553
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M Borda. 1986. Borrelia duttoni infection without tick-bite.. https://doi.org/10.1016/0035-9203(86)90364-0
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Two patients who had undergone nonmyeloablative allogeneic stem cell transplantation 53 and 112 days earlier and were being monitored at the same transplant center developed severe Bordetella bronchiseptica infections within 3 days of each other. Pulsed-field gel electrophoresis analysis indicated that the isolates from the two cases were identical. Neither patient had had direct contact with animals since transplantation. These findings strongly support nosocomial transmission of B. bronchiseptica.
AIM: In pertussis-like respiratory infections, once pertussis has been laboratory confirmed, other potential causative pathogens will seldom be looked for. Probably most mixed infections are found accidentally and since these mixed infections might cause a more severe disease we performed a retrospective study of their incidence. METHODS: We selected from 2 groups of patients with serologically confirmed Bordetella (B.) pertussis infection those in whom serology for other respiratory pathogens had also been performed. Group 1 consisted of 50 pertussis patients with 51 episodes of B. pertussis infection selected from 100 patients with serologically confirmed pertussis. They participated in a long-term follow-up after a B. pertussis infection. In group 2, 31 pertussis patients were selected from 98 consecutive patients with positive pertussis serology from one routine practice. RESULTS: In 23 of 82 pertussis infections (28%) serological evidence of 1 (n = 21) or 2 (n = 2) additional infections were demonstrated. These involved para-influenza virus (n = 6), respiratory syncytial virus (RSV) (n = 6), Mycoplasma pneumoniae (n = 5), adenovirus (n = 4), influenza A virus (n = 3) and influenza B virus (n = 1). CONCLUSIONS: We conclude that in patients with B. pertussis infection, coinfection with another respiratory pathogen is often present.
Two highly infectious bordetellae, Bordetella pertussis and B. parapertussis, have emerged in historical times as co-dominant in human populations. Both of these cause acute disease (whooping cough), whereas their progenitor, B. bronchiseptica, is of variable virulence in a wide variety of animals. The remarkably close phylogenetic relatedness of these three bordetellae and the two independent jumps to humans provide a unique opportunity to examine the evolution and genetics involved in the emergence of acute human pathogens. We hypothesize that the more virulent strains in humans reflects how acutely infectious pathogens might be favored in communities with large contact networks. Furthermore, we suggest that the differential expression of the various virulence factors by the two human pathogens can be explained by immune-mediated competition between the strains. The evolutionarily favored strategies of both of the human bordetellae result in immunizing infections and acute epidemics.