Isolation of Helicobacter pylori from femoral or iliac atherosclerotic plaques

Abstract

Background. Studies on the aetiology of atherosclerosis suggest the existence of a relationship between inflammatory reaction and the evolution of plaques. These have focused on, among others, viral and bacterial infections, including Helicobacter pylori. The presence of these rod-like bacteria was discovered with the aid of DNA investigation, using PCR. However, few authors could prove presence of viable Helicobacter pylori in plaques with the aid of bacterial cultures. The aim of this study was to isolate Helicobacter pylori rods from atherosclerotic plaques harvested from femoral or iliac arteries, and an evaluation of the susceptibility of the cultured strains to antibiotics.
Materials and methods. Atherosclerotic plaques were harvested intraoperatively from 51 patients (from the femoral artery in 31 cases and from the iliac artery in 20 cases). The samples were cultured in the relevant media and incubated under microaerophilic conditions for 4–7 days at 37°C. Bacterial strains were then identified based on their morphological and biochemical features. The susceptibility of the cultured strains to antibiotics (doxycycline, clarithromycin, amoxicillin, and metronidazole) was also evaluated.
Results. Helicobacter pylori rods were successfully isolated from 6.4% of atherosclerotic plaques from femoral arteries and from 5.0% of samples from iliac arteries. All strains were susceptible to doxycycline and clarithromycin but were resistant to metronidazole.
Conclusions. 1. Helicobacter pylori rods remain viable in atherosclerotic plaques, which enables successful culturing on special media under microaerophilic conditions. 2. The incidence of Helicobacter pylori strains in atherosclerotic plaques from patients operated on because of lower limb ischaemia was as follows: 6.4% of patients had bacteria in plaques from femoral arteries, and 5% tested positive in plaques from iliac arteries. 3. The cultured Helicobacter pylori strains were resistant to metronidazole but were susceptible to doxycycline, clarithromycin, and amoxicillin.
Acta Angiol 2010; 16, 3: 129–134