title: Morphometrical quantification of Chlamydia pneumoniae and Mycoplasma pneumoniae in human atherosclerotic abdominal aortic aneurysms.
abstract: OBJECTIVE
  Atherosclerotic inflammation with a possible role of infectious agents can contribute to the pathogenesis of abdominal aortic aneurysms (AAA). The finding of Chlamydia pneumoniae (CP) in these lesions in previous non-quantifying studies ranged from 0-100%. The objective is to quantify the presence of CP and Mycoplasma pneumoniae (MP) in AAA.
  
  
  METHODS
  The thickness, and the number of cells positive for CP detected by the immunohistochemistry (immunoperoxidase, which is a type of immunohistochemical stain used in molecular biology, medical research, and clinical diagnostics), and the percentage of the area occupied by the Mycoplasma pneumoniae detected by in situ hybridization in three layers of the aorta were measured using an image-analysis system in 10 necropsies of abdominal aneurysmatic aortas. Three groups were used as controls: 1) samples of the same aortas, outside the aneurysms, except if the dilatation took the whole sub-renal portion of the artery (n=7); 2) aortas with severe atherosclerosis but without aneurysms (n=10); 3) aortas without or with mild atherosclerosis (n=10). All specimens were obtained at necropsies. Wald's test was used to compare groups; significance level was established at 5%.
  
  
  RESULTS
  The tunica intima was thinner and the tunica media was thicker in the normal cases than in the other groups (p<0.01). Positive cells for CP were found in all groups, more frequently at the adventitia; no significant difference was detected between the groups (p>0.05). MP was also detected in all groups. This agent predominated in the group of patients with atherosclerosis, but without aneurysms at both tunica intima and adventitia; nevertheless, there were no significant differences between the groups (p>0.05).
  
  
  CONCLUSIONS
  Our data suggested that the bacteria we focused to, does not play an important role in the pathogenesis of AAA.
authors.affiliation: Instituto do Coração (InCor) do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, SP, Brasil.
authors.forename: Lucas José Tachotti
authors.initials: LJ
authors.lastname: Pires
authors.forename: Paulo Sampaio
authors.initials: PS
authors.lastname: Gutierrez
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001012:Aorta, Abdominal / Q000382:microbiology / Q000473:pathology; D017544:Aortic Aneurysm, Abdominal / Q000382:microbiology* / Q000473:pathology; D001161:Arteriosclerosis / Q000382:microbiology* / Q000473:pathology; D016022:Case-Control Studies; D016993:Chlamydophila pneumoniae / Q000302:isolation & purification*; D003238:Connective Tissue / Q000382:microbiology / Q000473:pathology; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D008297:Male; D008875:Middle Aged; D009177:Mycoplasma pneumoniae / Q000302:isolation & purification*; D012720:Severity of Illness Index; D017539:Tunica Intima / Q000382:microbiology / Q000473:pathology; D017540:Tunica Media / Q000382:microbiology / Q000473:pathology