Bordetella avium virulence measured in vivo and in vitro.

Bordetella avium causes an upper-respiratory-tract disease called bordetellosis in birds. Bordetellosis shares many of the clinical and histopathological features of disease caused in mammals by Bordetella pertussis and Bordetella bronchiseptica. In this study we determined several parameters of infection in the domestic turkey, Meleagris galapavo, and compared these in vivo findings with an in vitro measure of adherence using turkey tracheal rings. In the in vivo experiments, we determined the effects of age, group size, infection duration, and interindividual spread of B. avium. Also, the effect of host genetic background on susceptibility was tested in the five major commercial turkey lines by infecting each with the parental B. avium strain and three B. avium insertion mutants. The mutant strains lacked either motility, the ability to agglutinate guinea pig erythrocytes, or the ability to produce dermonecrotic toxin. The susceptibilities of 1-day-old and 1-week-old turkeys to B. avium were the same, and challenge group size (5, 8, or 10 birds) had no effect upon the 50% infectious dose. Two weeks between inoculation and tracheal culture was optimal, since an avirulent mutant (unable to produce dermonecrotic toxin) persisted for a shorter time. Communicability of the B. avium parental strain between confined birds was modest, but a nonmotile mutant was less able to spread between birds. There were no host-associated differences in susceptibility to the parental strain and the three B. avium mutant strains just mentioned: in all turkey lines tested, the dermonecrotic toxin- and hemagglutination-negative mutants were avirulent whereas the nonmotile mutants showed no loss of virulence. Interestingly, the ability of a strain to cause disease in vivo correlated completely with its ability to adhere to ciliated tracheal cells in vitro.

Formation of the notochord in living ascidian embryos.

The dynamic behaviour of cells during formation of the notochord in the ascidian, Ciona intestinalis, was examined by means of Differential Interference Contrast (DIC) microscopy and time-lapse videorecording. The initial rudiment is formed in part as a consequence of the pattern of mitotic divisions as the blastopore shifts posteriorly. Vertical and horizontal rearrangements produce an elongate rod of disc-shaped cells stacked end to end. Further elongation is accompanied by a cell shape change. Some cell growth or swelling is indicated to occur later in development, but this growth appears to contribute mostly to an increase in the diameter, and only insignificantly to the length of the notochord. Intracellular vacuoles that appear around 13 h after fertilization increase in size and fuse at about 16 h form intercellular ones. These in turn merge to form the central matrix core of the notochord at around 18 to 20 h. As the notochord elongates and cells change in shape, the basal surfaces bleb actively. This surface activity may be related to formation of the perinotochordal sheath.