Spontaneous Pneumothorax After Rupture of the Cavity as the Initial Presentation of Tuberculosis in the Emergency Department.

BACKGROUND Spontaneous pneumothorax can be secondary to a wide variety of lung diseases. Spontaneous pneumothorax secondary to pulmonary tuberculosis occurs in rare cases of residual fibrosis with retractions and bullae. CASE REPORT We present the case of a 65-year-old male patient from a rural area in the province of Los Ríos in Babahoyo, Ecuador, with no history of contact with tuberculosis. The patient arrived at the Emergency Department of the Regional Hospital of the Instituto Ecuatoriano de Seguridad Social (IESS), Babahoyo, due to acute respiratory failure, preceded by 10 days of evolution due to cough accompanied by greenish expectoration, chest pain, asthenia, and weight loss. On chest radiography, a left pneumothorax and interstitial pulmonary infiltrate were reported. A chest tube was placed, and the patient was intubated and was placed on invasive mechanical ventilation due to severe respiratory failure. Use of the GeneXpert MTB/RIF System detected Mycobacterium tuberculosis without resistance to rifampicin. Ziehl-Neelsen (ZN) staining for the identification of bacillus acid-resistant alcohol was positive in alveolar bronchial lavage. MALDI-TOF mass spectrometry and phenotypic analysis showed the presence of Pseudomonas aeruginosa and Klebsiella pneumonia with carbapenemases resistance mechanism, and the KPC type enzyme was identified. The culture for Mycobacterium tuberculosis was positive from the fourth week. CONCLUSIONS Secondary pneumothorax due to rupture of the polymicrobial cavity and especially of tuberculous origin is a very special form of acute respiratory failure in patients with previous structural pulmonary lesions in the Emergency Department.

Infectious agents in coronary atheromas: a possible role in the pathogenesis of plaque rupture and acute myocardial infarction.

In this review we report our recent findings of histopathological features of plaque instability and the association with Mycoplasma pneumoniae (MP) and Chlamydia pneumoniae (CP) infection, studying thrombosed coronary artery segments (CAS) of patients who died due to acute myocardial infarction. Vulnerable plaques are known to be associated with fat atheromas and inflammation of the plaque. Here we demonstrated that vulnerability is also related with focal positive vessel remodeling that maintains relatively well preserved lumen even in the presence of large atheromatous plaques. This phenomena may explain why the cinecoronariography may not detect large and dangerous vulnerable plaques. Greater amount of these bacteria in vulnerable plaques is associated with adventitial inflammation and positive vessel remodeling: the mean numbers of lymphocytes were significantly higher in adventitia than in the plaque, good direct correlation was obtained between numbers of CD20 B cells and numbers of CP infected cells in adventitia, and between % area of MP-DNA in the plaque and cross sectional area of the vessel, suggesting a cause-effect relationship. Mycoplasma is a bacterium that needs cholesterol for proliferation and may increase virulence of other infectious agents. In conclusion, co-infection by Mycoplasma pneumoniae and Chlamydia pneumoniae may represent an important co-factor for plaque instability, leading to coronary plaque thrombosis and acute myocardial infarction, since larger amount of these bacteria strongly correlated with histological signs of more vulnerability of the plaque. The search of CMV and Helicobacter pilori in these tissues resulted negative.