ABSTRACT
Routine examinations of conventional outbred Wistar rats in our laboratory showed increased serum levels of alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, and urea. Electron microscopy and specific reactions showed C. pneumoniae and M. pulmonis in lung, liver, spleen, heart, and kidney sections. We could not exclude the fact that other infectious microorganisms detected through routine health surveillance affected the Wistar rat colony; however, we have not identified any of those microorganisms by electron microscopy of the organs listed. Natural coinfection of C. pneumoniae and M. pulmonis can occur in laboratory rats and is associated with histopathological and functional compromise of many organs. Further studies comparing different conventional animals and specific pathogen-free animals are necessary to better understand the present findings and to define whether coinfection influences the results of experimental studies with rats.
Subject(s)
Animals, Laboratory , Chlamydophila Infections/veterinary , Chlamydophila pneumoniae , Mycoplasma Infections/veterinary , Rats, Wistar , Rodent Diseases/microbiology , Alanine Transaminase/blood , Alkaline Phosphatase/blood , Animals , Animals, Laboratory/microbiology , Aspartate Aminotransferases/blood , Chlamydophila Infections/complications , Chlamydophila pneumoniae/isolation & purification , Heart/microbiology , Kidney/microbiology , Liver/microbiology , Lung/microbiology , Male , Microscopy, Electron , Mycoplasma/isolation & purification , Mycoplasma Infections/complications , Rats , Rats, Wistar/microbiology , Rodent Diseases/blood , Rodent Diseases/pathology , Spleen/microbiology , Urea/bloodABSTRACT
A possible relationship between C.pneumoniae (CP) infection, atherosclerosis and acute myocardial infarction is a debated matter. Now we performed the search of CP in histological segments of fatal ruptured plaques and of stable plaques by histochemistry (Macchiavello stain), immunohistochemistry and in situ hybridization techniques. Electron microscopy and confocal laser microscopy techniques were used in two additional cases. The semi-quantitification of CP + cells (0-4+) and quantification of lymphocytes demonstrated greater amount of CP + cells and more inflammation in the adventitia of vulnerable plaque vessel segments than of stable ones, larger amount of CP + cells in adventitia than in the plaque and high frequency of CP + cells in all groups studied. This preliminary study strongly suggests a direct pathogenetic involvement of adventitial CP in the rupture of the atheromatous plaque, development of acute myocardial infarction and also in the development of atherosclerosis.
