Dermonecrotic toxin and tracheal cytotoxin, putative virulence factors of Bordetella avium

Abstract

We examined Bordetella avium for virulence factors common to Bordetella pertussis, including pertussis toxin, filamentous hemagglutinin, adenylate cyclase, dermonecrotic toxin, and tracheal cytotoxin. B. avium produced a dermonecrotic toxin and a tracheal cytotoxin. The dermonecrotic toxin of B. avium is a 155,000-molecular-weight, heat-labile protein which was lethal for mice, guinea pigs, young chickens, and turkey poults and produced dermonecrosis when injected intradermally into guinea pigs, chickens, and turkey poults. High-pressure liquid chromatography of B. avium culture supernatant fluid revealed the presence of a tracheal cytotoxin chemically identical to that produced by B. pertussis. B. avium isolates were negative for B. pertussis-like filamentous hemagglutinin and pertussis toxin when assayed with antibody against B. pertussis filamentous hemagglutinin and pertussis toxin. Furthermore, B. avium failed to induce the clustered CHO cell morphology characteristic of pertussis toxin. Adenylate cyclase assays indicated that B. avium does not produce an extracytoplasmic adenylate cyclase, even after passage through embryonated turkey eggs. Since production of virulence proteins by B. pertussis is regulated by growth in media containing nicotinamide or MgSO4 or by growth at reduced temperatures, we determined the eifect of these supplements and growth conditions on production of dermonecrotic toxin by B. avium. Production of dermonecrotic toxin in B. avium was not altered by growth in media containing 100 ,uM FeSO4 or 500 ,ig of nicotinamide per ml or by growth at 25 or 42°C, but production was significantly decreased by growth in media containing 20 mM MgSO4 and slightly reduced by growth in media containing 500 ,Ig of nicotinic acid per ml. These studies revealed that B. avium is similar to B. pertussis in that both species produce a dermonecrotic toxin and a tracheal cytotoxin and production of dermonecrotic toxin is regulated by nicotinamide and MgSO4. The presence of dermonecrotic toxin and tracheal cytotoxin in all Bordetella species indicates that these products may be important virulence factors in bordetellosis.

Chromosomal DNA from both flagellate and non-flagellate Bordetella species contains sequences homologous to the Salmonella H1 flagellin gene

“…and by DNA-rRNA hybridisation studies, although B. avium has a lower G + C content (61.6-62.6 mol%) than that (67.7-69.5 mol%) of other bordetellae [3]. All the Bordetella species share certain virulence factors which include a heat-labile dermonecrotizing toxin and a tracheal cytotoxin [4], but B. avium lacks the genes for agglutinogens, adenylate cyclase toxinand pertussis toxin present in the other three species [5,6,7]. Although B. pertussis is the only Bordetella to produce pertussis toxin (PT), B. parapertussis and B. bronchiseptica have been shown to contain mutated, transcriptionally-silent PT genes [8].…”

Characterization of the outer membrane proteins of Bordetella avium

“…Spontaneous phase variants of B. avium which did not express the dermonecrotic toxin and the 27K, 38K, 48K, and 93K OMPs were isolated (16). The same proteins, which were detected by using Western blot analysis, were not expressed in bacteria grown in the presence of MgSO4 or nicotinic acid, two nutrients that induce phenotypic modulation in B. pertussis (15,16). In this study, production of the 22K, 26K, 56K, and 73K OMPs was reduced or eliminated when strain 75 was grown in medium containing MgSO4 but not nicotinic acid.…”

Electron Microscopic Observations on Ciliated Epithelium of Tracheal Organ Cultures Infected with Bordetella bronchiseptica

“…The former seems to result in an aggregation of cilia as observed previously by SEM (16), and in the extrusion of both ciliated and nonciliated cells. The purified TCT, a soluble peptidoglycan fragment common to all Bordetella species (4,5,14), induces selectively ciliated-cell damages but it does not act on nonciliated cells (6)(7)(8). However, in the previous in vivo study (16), we noticed that the destruction occurred not only in ciliated cells but also in nonciliated cells, suggesting the possibility of the participation of different toxins from TCT, capable of acting on both ciliated and nonciliated cells.…”