Abstract
Bartonella spp. are facultative intracellular bacteria that cause characteristic hostrestricted hemotropic infections in mammals and are typically transmitted by blood-sucking arthropods. In the mammalian reservoir, these bacteria initially infect a yet unrecognized primary niche, which seeds organisms into the blood stream leading to the establishment of a long-lasting intra-erythrocytic bacteremia as the hall-mark of infection. Bacterial type IV secretion systems, which are supra-molecular transporters ancestrally related to bacterial conjugation systems, represent crucial pathogenicity factors that have contributed to a radial expansion of the Bartonella lineage in nature by facilitating adaptation to unique mammalian hosts. On the molecular level, the type IV secretion system VirB/VirD4 is known to translocate a cocktail of different effector proteins into host cells, which subvert multiple cellular functions to the benefit of the infecting pathogen. Furthermore, bacterial adhesins mediate a critical, early step in the pathogenesis of the bartonellae by binding to extracellular matrix components of host cells, which leads to firm bacterial adhesion to the cell surface as a prerequisite for the efficient translocation of type IV secretion effector proteins. The beststudied adhesins in bartonellae are the orthologous trimeric autotransporter adhesins, BadA in Bartonella henselae and the Vomp family in Bartonella quintana. Genetic diversity and strain variability also appear to enhance the ability of bartonellae to invade not only specific reservoir hosts, but also accidental hosts, as shown for B. henselae. Bartonellae have been identified in many different blood-sucking arthropods, in which they are typically found to cause extracellular infections of the mid-gut epithelium. Adaptation to specific vectors and reservoirs seems to be a common strategy of bartonellae for transmission and host diversity. However, knowledge regarding arthropod specificity/restriction, the mode of transmission, and the bacterial factors involved in arthropod infection and transmission is still limited.
| Original language | English (US) |
|---|---|
| Article number | 29 |
| Journal | Veterinary Research |
| Volume | 40 |
| Issue number | 2 |
| DOIs | |
| State | Published - Mar 2009 |
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Keywords
- Bartonella
- Ecological fitness
- Host adaptation
- Pathogenesis
- Vector
ASJC Scopus subject areas
- veterinary(all)
Cite this
Ecological fitness and strategies of adaptation of Bartonella species to their hosts and vectors. / Chomel, Bruno B; Boulouis, Henri Jean; Breitschwerdt, Edward B.; Kasten, Rickie W.; Vayssier-Taussat, Muriel; Birtles, Richard J.; Koehler, Jane E.; Dehio, Christoph.
In: Veterinary Research, Vol. 40, No. 2, 29, 03.2009.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Ecological fitness and strategies of adaptation of Bartonella species to their hosts and vectors
AU - Chomel, Bruno B
AU - Boulouis, Henri Jean
AU - Breitschwerdt, Edward B.
AU - Kasten, Rickie W.
AU - Vayssier-Taussat, Muriel
AU - Birtles, Richard J.
AU - Koehler, Jane E.
AU - Dehio, Christoph
PY - 2009/3
Y1 - 2009/3
N2 - Bartonella spp. are facultative intracellular bacteria that cause characteristic hostrestricted hemotropic infections in mammals and are typically transmitted by blood-sucking arthropods. In the mammalian reservoir, these bacteria initially infect a yet unrecognized primary niche, which seeds organisms into the blood stream leading to the establishment of a long-lasting intra-erythrocytic bacteremia as the hall-mark of infection. Bacterial type IV secretion systems, which are supra-molecular transporters ancestrally related to bacterial conjugation systems, represent crucial pathogenicity factors that have contributed to a radial expansion of the Bartonella lineage in nature by facilitating adaptation to unique mammalian hosts. On the molecular level, the type IV secretion system VirB/VirD4 is known to translocate a cocktail of different effector proteins into host cells, which subvert multiple cellular functions to the benefit of the infecting pathogen. Furthermore, bacterial adhesins mediate a critical, early step in the pathogenesis of the bartonellae by binding to extracellular matrix components of host cells, which leads to firm bacterial adhesion to the cell surface as a prerequisite for the efficient translocation of type IV secretion effector proteins. The beststudied adhesins in bartonellae are the orthologous trimeric autotransporter adhesins, BadA in Bartonella henselae and the Vomp family in Bartonella quintana. Genetic diversity and strain variability also appear to enhance the ability of bartonellae to invade not only specific reservoir hosts, but also accidental hosts, as shown for B. henselae. Bartonellae have been identified in many different blood-sucking arthropods, in which they are typically found to cause extracellular infections of the mid-gut epithelium. Adaptation to specific vectors and reservoirs seems to be a common strategy of bartonellae for transmission and host diversity. However, knowledge regarding arthropod specificity/restriction, the mode of transmission, and the bacterial factors involved in arthropod infection and transmission is still limited.
AB - Bartonella spp. are facultative intracellular bacteria that cause characteristic hostrestricted hemotropic infections in mammals and are typically transmitted by blood-sucking arthropods. In the mammalian reservoir, these bacteria initially infect a yet unrecognized primary niche, which seeds organisms into the blood stream leading to the establishment of a long-lasting intra-erythrocytic bacteremia as the hall-mark of infection. Bacterial type IV secretion systems, which are supra-molecular transporters ancestrally related to bacterial conjugation systems, represent crucial pathogenicity factors that have contributed to a radial expansion of the Bartonella lineage in nature by facilitating adaptation to unique mammalian hosts. On the molecular level, the type IV secretion system VirB/VirD4 is known to translocate a cocktail of different effector proteins into host cells, which subvert multiple cellular functions to the benefit of the infecting pathogen. Furthermore, bacterial adhesins mediate a critical, early step in the pathogenesis of the bartonellae by binding to extracellular matrix components of host cells, which leads to firm bacterial adhesion to the cell surface as a prerequisite for the efficient translocation of type IV secretion effector proteins. The beststudied adhesins in bartonellae are the orthologous trimeric autotransporter adhesins, BadA in Bartonella henselae and the Vomp family in Bartonella quintana. Genetic diversity and strain variability also appear to enhance the ability of bartonellae to invade not only specific reservoir hosts, but also accidental hosts, as shown for B. henselae. Bartonellae have been identified in many different blood-sucking arthropods, in which they are typically found to cause extracellular infections of the mid-gut epithelium. Adaptation to specific vectors and reservoirs seems to be a common strategy of bartonellae for transmission and host diversity. However, knowledge regarding arthropod specificity/restriction, the mode of transmission, and the bacterial factors involved in arthropod infection and transmission is still limited.
KW - Bartonella
KW - Ecological fitness
KW - Host adaptation
KW - Pathogenesis
KW - Vector
UR - http://www.scopus.com/inward/record.url?scp=67949107950&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=67949107950&partnerID=8YFLogxK
U2 - 10.1051/vetres/2009011
DO - 10.1051/vetres/2009011
M3 - Article
C2 - 19284965
AN - SCOPUS:67949107950
VL - 40
JO - Annales de Recherches Veterinaires
JF - Annales de Recherches Veterinaires
SN - 0928-4249
IS - 2
M1 - 29
ER -