Effect of the caprine variant of Mycoplasma mycoides subsp mycoides on endothelium, monocytes, and complement of guinea pig, calf, sheep, and goat serum
Rosendal, S.
American Journal of Veterinary Research 45(11): 2396-2402
1984
ISSN/ISBN: 0002-9645 PMID: 6395728 Document Number: 226767
The caprine variant of Mycoplasma mycoides subsp mycoides causes septicaemia with coagulopathy in goats. Pathogenetic mechanisms that might explain the coagulopathy, the ability of the Mycoplasma to persist in the blood, and its specificity for goats were studied. Severe endothelial damage was seen by electron microscopy of goat aorta tissue exposed in vitro to 107 colony-forming units of mycoplasmas. The Mycoplasma did not damage 51Cr-labelled adherent cells from peripheral blood of goats. The haemolytic complement titre was reduced by 94%, 50%, 50%, and 25% in guinea pig, calf, sheep, and goat serum, respectively, 30 minutes after treatment with 8 x 109 colony-forming units of the Mycoplasma. Freshly prepared serum from these species killed the Mycoplasma. Heat-inactivated serum was not mycoplasmacidal. Complement from these 4 animal species was activated by the Mycoplasma through the classical pathway, because ethyleneglycoltetraacetic acid precipitation of serum Ca2+ inhibited activation. Proof that the classical pathway was functional in goats was not conclusive because Ca2+ supplementation of ethyleneglycoltetraacetic acid-treated serum did not restore complement activity. Endothelial damage and complement activation may explain the coagulopathy. The function that complement activation may have in the inflammatory response of this disease is not known. Difference in susceptibility of calves, sheep, and goats to M. mycoides septicaemia cannot be explained by species variation in complement mycoplasmacidal activity.