Cytopathic effects of Mycoplasma pulmonis in vivo and in vitro

Abstract

This study was performed to evaluate the cytopathic features resulting from Mycoplasma pulmonis infection of tracheal organ cultures compared to with those seen in in vivo infection and to use this system to determine possible differences in cytopathic effects in two M. pulmonis variants found to cause different diseases in vivo. The attachment of M. pulmonis to respiratory epithelium was similar in vivo and in vitro. Cytopathic effects seen in both systems were also similar in loss of tight junctions between cells and exfoliation of respiratory cells, resulting in exposure of the subepithelial layer. These similarities indicate that the observed tissue damage is initiated by the mycoplasmas rather than by immunologic host responses but does not exclude the possibility that host responses may subsequently contribute to the cytopathological events. Comparison of the effects of the two variants (one known to cause death in vivo) did not reveal differences in vitro. This suggests that host factors (not present in vitro) may account for differences in virulence. Detailed in vitro studies allowed the identification of the time frame corresponding to the in vivo infection and also revealed the limitations of the in vitro system.

Field Isolates of Mycoplasma ovipneumoniae Exhibit Distinct Cytopathic Effects in Ovine Tracheal Organ Cultures

“…More recently, DEBEY and Ross (1994) reported that ciliostasis induced by M. h_opneumoniue in porcine tracheal ring cultures diminished with in vitm passage of the organism. This is consistent with our observations and differs from the results reported by STADTLANDER et al (1991) who did not find any observable differences of cytopathic potential between a high passage M.pulmonis strain and its parent low passage strain. DEBEY and ROSS (1994) also related their results to loss of ability of the organism to colonize host cells.…”

“…These studies have yielded conflicting results, possibly due to variations in pathogenicity of different strains, attenuation during isolation and cloning on U.S Copynght (:leuance Ccntrr Code Staremmt: 0931 -1 84)3/98/4501-0029 $14.00/0 artificial medium, and genetic background or physiological status of the experimental animals (JONIiS et al, 1982;IONAS et al, 1991). Evaluation of the effects of mycoplasma species on tracheal organ cultures is utilized to study their pathogenicity, since interference with the mucociliary clearance mechanism is an important consideration in the induction of respiratory disease (CHERRY and TAYI.OR-ROBINSON, 1970;LEVISOFIN et al, 1986;THOMAS et al, 1987;STADTLANDER et al, 1991;DEBBY and ROSS, 1994). In these instances, subjective measurement of ciliary activity, light .and electron microscopic observations, and measurement of metabolic activities (e.g.…”

A model of the deciliation process caused by Mycoplasma fermentans strain incognitus on respiratory epithelium

“…It appears that this event significantly reduces the ciliary activity and, at the same time, makes the epithelial cell surface accessible for a more massive mycoplasma attack. The third phase includes the formation of abnormally shaped In the same in-vitro system under comparable cultivation conditions, these mycoplasma species cause more severe tissue damage (i.e., extensive exfoliation of epithelial cells) in a significantly shorter time period (within 3 to 6 days) and at lower initial infection doses (approximately 10 3 -10 4 CFU) (Stadtländer 1991;Stadtländer et al 1991aStadtländer et al , 1993. Because the infection with M. fermentans strain incognitus was progressing relatively slowly, resulted in complete deciliation, and more than one factor most likely contributed to the destruction of the cilia, the name "cilia wasting syndrome" was selected for the events which took place on the surface of respiratory epithelium (Stadtländer 2004).…”

T lymphocyte responses are critical determinants in the pathogenesis and resistance to mycoplasma respiratory disease

“…However, MHC I restricted antigen presentation is the major pathway for CD8 + T cell activation, and this pathway is most commonly associated with presentation of antigen derived from intracellular pathogens. Although some mycoplasma have been shown to have intracellular phases (103,104), M. pulmonis has not been found to do this, despite studies which have examine this possibility (105). One possibility is suggested by recent studies demonstrating the ability of dendritic cells to present exogenous antigen in the context of MHC I through a novel pathway (106)(107)(108), but further studies are needed to support the role of dendritic cells in eliciting mycoplasma immune responses.…”