Development of a rat model for respiratory infection with Bordetella pertussis

Woods, Donald E.; Franklin, Rudolph M.; Cryz, S J; Ganss, M.; Peppler, M S; Ewanowich, Carol A.

doi:10.1128/iai.57.4.1018-1024.1989

Cited by 38 publications

(35 citation statements)

References 8 publications

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“…The model has for example been used to investigate the effect of chronic P aeruginosa lung infection on the pulmonary circulation (1 6) and the effect of ibuprofen therapy on chronic P aeruginosa lung infection (36). Others have used Bordetella pertussis (58) and Haemophilus infruenzae (39,50) in similar studies of chronic pneumonia.…”

Section: Johansen Ct Almentioning

confidence: 99%

Chronic Pseudomonas aeruginosa lung infection in normal and athymic rats

Johansen

Espersen

Pedersen

et al. 1993

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We have compared a chronic lung infection with Pseudomonas aeruginosa embedded in alginate beads in normal and athymic rats with an acute infection with free live P. aeruginosa bacteria. The following parameters were observed and described: mortality, macroscopic and microscopic pathologic changes, and antibody responses. The rats challenged with P. aeruginosa alginate beads experienced a generally more severe lung pathology and the antibody responses were more homogeneous with less dispersion as compared to the rats having free live P. aeruginosa bacteria. In general, manifestations were more severe in the athymic rats compared to the normal rats. It is, however, notable that the athymic rats developed similar microscopic lung manifestations as the normal rats when given a large number of P. aeruginosa in the beads, with dense accumulation of neutrophil granulocytes and microcolonies comparable to the lesions seen in cystic fibrosis (CF) patients. Early transitory IgM titers were demonstrated in both normal and athymic rats. Whilst athymic rats produced much lower IgG titers than the normal rats, presumably due to the absence of CD4+ cells, higher primary IgA titers were achieved. These two models in normal and athymic rats of the chronic lung infection resembling that seen in CF lungs make it possible to study the influence of the various components of the specific and nonspecific defence systems on the course of the chronic P. aeruginosa lung infection and to evaluate the effect of various immunization schedules and immunomodulatory drugs.

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Section: Johansen Ct Almentioning

confidence: 99%

Chronic Pseudomonas aeruginosa lung infection in normal and athymic rats

Johansen

Espersen

Pedersen

et al. 1993

APMIS

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“…Woods et al investigated the ability of virulent and avirulent strains to survive and persist in a rat model for respiratory infection with B. pertussis (64). Avirulent B. pertussis was not recovered after 3 days from lungs of infected rats, while virulent B. pertussis was recovered on days 3 and 7 after inoculation but not on days 10 and 14. Recovery of viable B. pertussis from lungs of infected rats was again possible on day 21.…”

mentioning

confidence: 99%

“…Electron micrographs of lungs of infected animals revealed that the lung cells contained B. pertussis which appeared viable at 14 days. The authors propose that B. pertussis was not recoverable on days 10 and 14 because the microbe was residing intracellularly inside lung cells, perhaps alveolar macrophage (64).…”

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confidence: 99%

Uptake and intracellular survival of Bordetella pertussis in human macrophages

et al. 1992

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Recent reports have demonstrated that Bordetella pertussis has invasive behavior in vivo and in vitro. In this study, we investigated the ability of a virulent strain, avirulent mutants, and mutants deficient in specific virulence factors to enter and survive intracellularly in human macrophages in vitro. Uptake of virulent B. pertussis was dose dependent and occurred in the absence of serum or specific antibody, with entry occurring via a microfilament-dependent phagocytic process. The virulent wild-type parental strain was internalized and persisted intracelularly over the 3 days of experiments, as determined by transmission electron microscopy and by recovery of viable plate counts. This is the first report of long-term survival of B. pertussis in human macrophages. Avirulent mutants entered macrophages, but at only an average of 1.5% of virulent parental levels, and did not survive intracellularly. Mutants which did not express adenylate cyclase toxin, filamentous hemagglutinin, or pertussis toxin had decreased abilities to enter and to survive inside macrophages. The results suggest that the internalization process, as well as intracellular survival, is virulence dependent and that mutations which inactivate expression of virulence factors may affect both. The ability of B. pertussis to enter and persist inside macrophages may be important not only for survival of the bacteria but also in the pathogenesis of whooping cough.

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“…Great apes hold the best promise for a realistic model of disease but are prohibitively expensive for all but the most focused of studies. Rabbits become infected but do not become ill. New studies using rats appear to be promising (40), but much investigation remains to be done toward characterization of this disease model.…”

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confidence: 99%

Lethal infection by Bordetella pertussis mutants in the infant mouse model

1989

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Different aspects of lethal infection of infant mice with Bordetella pertussis were examined. Mutants deficient in vir-regulated genes were tested for the ability to cause a lethal infection in the infant mouse model. Adenylate cyclase toxin-hemolysin and pertussis toxin were required to cause a lethal infection at low doses. Mixed infection caused by challenging the mice with an equal number of pertussis toxin and adenylate cyclase toxin-hemolysin mutants at a dose at which neither alone was lethal was also unable to cause a lethal infection. Production of the filamentous hemagglutinin and the dermonecrotic toxin was not required to cause a lethal infection. Nine other mutants in vir-regulated genes whose phenotypes have yet to be determined were also tested. Only two of these mutants were impaired in the ability to cause a lethal infection. Expression of fimbriae does not appear to affect the dose required to cause a lethal infection; however, fimbrial expression was correlated with the later stages of a nonlethal, persistent infection. Growth of the bacteria in MgSO4, a condition which reversibly suppresses expression of the genes required for virulence, did not alter the ability of the bacteria to cause a lethal infection. Auxotrophic mutants deficient in leucine biosynthesis were as virulent as the parental strain; however, mutants deficient in methionine biosynthesis were less virulent. A B. parapertussis strain was much less effective in promoting a lethal infection than any of the wild-type B. pertussis strains examined. A persistent infection in the lungs was observed for weeks after challenge for mice given a sublethal dose of B. pertussis, and transmission from infected infants to the mother was never observed.

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Development of a rat model for respiratory infection with Bordetella pertussis

Cited by 38 publications

References 8 publications

Chronic Pseudomonas aeruginosa lung infection in normal and athymic rats

Chronic Pseudomonas aeruginosa lung infection in normal and athymic rats

Uptake and intracellular survival of Bordetella pertussis in human macrophages

Lethal infection by Bordetella pertussis mutants in the infant mouse model

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