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Published on: April 7, 2015
Chlamydia pneumoniae and stroke: is there a direct relationship?
Rubens J Gagliardi1, Helio H Caiaffa-Filho
1Faculty of Medical Sciences, Santa Casa de São Paulo, São Paulo, SP, Brazil. rubensjg@apm.org.br
Insights
This study found no evidence that Chlamydia pneumoniae infection is linked to atherothrombotic stroke or carotid plaque instability. Researchers did not detect a significant association between the bacteria and ischemic stroke or transient ischemic attack.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Neurology
Background:
- Atherothrombotic stroke is a significant cause of morbidity and mortality.
- The role of infectious agents, such as Chlamydia pneumoniae, in atherogenesis and stroke is under investigation.
Purpose of the Study:
- To determine if Chlamydia pneumoniae is associated with atherothrombotic stroke.
- To investigate the potential role of Chlamydia pneumoniae in carotid plaque destabilization.
Main Methods:
- 150 patients with carotid atherothrombosis were categorized into ischemic stroke (IS), transient ischemic attack (TIA), and control groups.
- Carotid atheromatosis was diagnosed via Doppler-ultrasonography; patients with cardioembolic or non-atherothrombotic causes were excluded.
- Polymerase chain reaction (PCR) was used to detect Chlamydia pneumoniae.
Main Results:
- Only one patient in the control group tested positive for Chlamydia pneumoniae.
- No significant correlation was observed between Chlamydia pneumoniae presence and atherothrombotic stroke or TIA.
- The bacterium was not detected in patients with carotid plaque destabilization.
Conclusions:
- The findings do not support a role for Chlamydia pneumoniae in the onset of ischemic stroke or transient ischemic attack.
- Chlamydia pneumoniae does not appear to be implicated in the destabilization of carotid plaques based on this study.
Objective:
To investigate the possible relationship between atherothrombotic stroke and Chlamydia pneumoniae.
Method:
150 patients with carotid atherothrombosis were enrolled. The casuistic was divided in three groups: ischemic stroke (IS): 65 patients; transient ischemic attack (TIA): 26 patients; and control: 59. The IS or TIA onset was up to 30 days from the beginning of the study. Carotid atheromatoses was diagnosed by Doppler-ultrasonography. Patients with cardioembolic risk or non-atherothrombotic origin were excluded. Comparisons were done between the three groups, and within each group according to the different age sub-groups, to the main arteries affected, and to the atherogenic risk factors. Bacteria detection was done using polimerase chain reaction.
Results:
Only one patient tested positive for C. pneumoniae belonging to the control group.
Conclusion:
These results do not suggest that C. pneumoniae participated in the onset of IS or TIA or that it has a role in carotid plaque destabilization.
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