A Rare Case of Pyopericardium After Blunt Thoracic Trauma.

The bacterial purulent pericarditis is rapidly progressive and represents a highly fatal infection, with mortality rates reaching up to 100% if untreated. Approximately 40% to 50% of all cases are caused by Gram-positive bacteria, especially Streptococcus pneumoniae. We describe an extremely rare case of S. pneumoniae purulent pericarditis as a delayed complication of a blunt thoracic trauma. The patient was successfully treated with urgent pericardiocentesis, thoracoscopic pericardial fenestration, and broad-spectrum antibiotics. Owing to the high mortality rate of a purulent pericarditis, a high index of suspicion is needed in order to instaurate an appropriate therapy with drainage and antibiotics.

Aspergillus mediastinitis in a post-operative immunocompetent child.

Post-operative Aspergillus mediastinitis is regarded to be a devastating infection, usually affecting patients undergoing cardiothoracic surgery with specific predisposing factors characterised by a high mortality and chronic morbidity. Patient outcome after such a complication is extremely poor despite antifungal therapy and surgery. We describe the case of an immunocompetent 2-month-old child with obstructed supracardiac total anomalous pulmonary venous circulation (TAPVC) and severe pulmonary artery hypertension, who underwent TAPVC repair through median sternotomy and developed post-operative mediastinitis due to Aspergillus flavus.

Insights into leghorn male hepatocellular cells response to fowl adenovirus serotype 4 infection by transcriptome analysis.

Fowl adenovirus serotype 4 (FAdV-4), a member of the Aviadenovirus genus of the Adenoviridae family, causes hepatitis-hydropericardium syndrome (HHS) in chickens. It causes mortality of up to 80% in 3-6-week-old broilers, posing a substantial threat to the poultry industry. However, the specific host responses to the virus are not well understood. To better understand the interactions between the host and FAdV-4 and to explore the pathogenesis of this virus, a high-throughput RNA-seq technology was utilized with leghorn male hepatocellular (LMH) cells at 12, 24, and 48 h after FAdV-4 infection. We identified a total of 7000 differentially expressed genes (DEGs), which were enriched in a variety of biological processes and pathways using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Several immune related pathways, including Toll-like receptor (TLR) signaling pathway and cytokine-cytokine receptor interaction pathway, were activated after the FAdV-4 infection. The transcriptional data were validated by quantitative real-time PCR. The expression profiles of 10 genes involved in FAdV-4-infected chicken livers, including TLR2A, TLR3, TLR5, MyD88, IL12B, IL15, IL18, CCL20, TNFRSF21, and CD30, were consistent with RNA-seq profiles. By transfecting small interfering RNA into LMH cells, our results confirmed that MyD88 mediated FAdV-4-induced inflammation. To our knowledge, this was the first study to use transcriptome analysis to investigate host responses to FAdV-4 infection. These findings provide insights into the mechanisms of FAdV-4 pathogenesis and host-FAdV-4 interaction.

The relationship between causative microorganisms and cardiac lesions caused by infective endocarditis: New perspectives from the contemporary cohort of patients.

BACKGROUND: The etiology of infective endocarditis (IE) is changing. More aggressive forms with multiple IE cardiac lesions have become more frequent. This study sought to explore the relationship between contemporary causative microorganisms and IE cardiac lesions and to analyze the impact of multiple lesions on treatment choice. METHODS: In 246 patients hospitalized for IE between 2008 and 2015, cardiac lesions caused by IE were analyzed by echocardiography, classified according to the 2015 European Society of Cardiology guidelines and correlated with microbiological data. We defined a new parameter, the Echo IE Sum, to summarize all IE cardiac lesions in a single patient, enabling comprehensive comparisons between different etiologies and treatment strategies. RESULTS: Staphylococcus aureus was associated with the development of large vegetation (OR 2.442; 95% CI 1.220-4.889; p=0.012), non-HACEK bacteria with large vegetation (OR 13.662; 95% CI 2.801-66.639; p=0.001), perivalvular abscess or perivalvular pseudoaneurysm (OR 5.283; 95% CI 1.069-26.096; p=0.041), and coagulase-negative staphylococci (CoNS) with leaflet abscess or aneurysm (OR 3.451; 95% CI 1.285-9.266, p=0.014), and perivalvular abscess or perivalvular pseudoaneurysm (OR 4.290; 95% CI 1.583-11.627; p=0.004). The Echo IE Sum significantly differed between different etiologies (p<0.001), with the highest value in non-HACEK and the lowest in streptococcal endocarditis. Patients operated for IE had a significantly higher Echo IE Sum vs those who were medically treated (p<0.001). CONCLUSION: None of the IE cardiac lesions is microorganism-specific. However, more severe lesions were caused by S. aureus, CoNS, and non-HACEK bacteria. The highest propensity to develop multiple lesions was shown by the non-HACEK group. Higher Echo IE Sum in patients sent to surgery emphasized the importance of multiple IE cardiac lesions on treatment choice and potential usage of Echo IE Sum in patient management.

Pericarditis caused by Campylobacter fetus subspecies fetus associated with ingestion of raw beef liver.

Campylobacter fetus is an organism residing primarily in the gastrointestinal tracts of cattle and sheep and transmitting to humans through ingestion of contaminated food products or surface water. The organism has caused various extraintestinal infections but, to date, purulent pericarditis due to the organism has rarely been described. We report a case of purulent pericarditis due to C. fetus subsp. fetus, occurring in a patient having several predisposing conditions, including receiving hemodialysis therapy, recent surgery for cecal cancer, and administration of esomeprazole. The patient mentioned having eaten homemade raw beef liver two weeks before the onset, suggesting that the ingested food product was contaminated with C. fetus and the organism transmitted to the pericardium through the bloodstream although blood culture was negative. The causative organism, recovered from the pericardial effusion, was unidentifiable with commercial systems but determinable with molecular methods at the subspecies level. The patient fully improved with pericardiocentesis and subsequent administration of ciprofloxacin, to which the organism was considered susceptible, for a total of four weeks. This is the first case of C. fetus pericarditis in which a history of ingesting a raw food product was clearly mentioned.

Epicardial adipose tissue microbial colonization and inflammasome activation in acute coronary syndrome.

BACKGROUND: Epicardial adipose tissue (EAT) has a close functional and anatomic relationship with epicardial coronary arteries. Accumulating evidence suggests that host microbiome alterations may play a role in several inflammatory/immune disorders, triggering a robust proinflammatory response also involving interleukin-1ß (IL-1ß) and the NALP3 inflammasome. In the current study, we explore the hypothesis that in patients with non-ST elevation acute coronary syndrome (ACS), EAT contains potentially pro-atherosclerotic bacteria that might elicit inflammasome activation. METHODS: EAT samples were obtained during coronary artery bypass grafting from ACS (n=18) and effort stable angina (SA; n=16) patients, and as controls, from patients with angiographically normal coronary arteries undergoing surgery for mitral insufficiency (MVD; n=13). In all patients, NALP3 and proIL-1ß mRNA expressions were evaluated with qRT-PCR. In 3 patients from each group, EAT microbiota composition was determined using next-generation sequencing technologies. RESULTS: In EAT, mRNA expression of both NALP3 and pro-IL1ß was significantly higher in ACS than in SA and MVD (P=0.028 and P=0.005, respectively). A broad range of bacterial species (n=76) was identified in both ACS and SA, with different predominant species. In contrast, microbial DNA was barely observed in MVD. CONCLUSIONS: Our study demonstrated the presence of bacterial DNA directly into EAT, surrounding diseased coronary arteries, of patients with ACS. Furthermore, ACS is associated with NALP3/inflammasome pathway activation in EAT. Our data suggest that the EAT environment is susceptible to microbial colonization that might stimulate a proinflammatory response. These findings add new elements to the pathogenesis of ACS and suggest novel therapeutic targets.

[An uncommon detection of Mycobacterium tuberculosis in pericardial effusion]. / Ojedinelý prípad izolovaného výskytu Mycobacterium tuberculosis v perikardiálním výpotku.

Pericardial tuberculosis is a specific pericarditis which is rarely reported in the absence of pulmonary tuberculosis. A case history is presented of a 74-year-old patient, immunocompromised as a result of kidney and liver cancer therapy. Mycobacterium tuberculosis was repeatedly recovered from pericardial effusion but not from other clinical specimens. Despite the early treatment of specific pericarditis, the patient died.

Esophageal cancer with an esophagopericardial fistula and purulent pericarditis.

We herein present the case of a 56-year-old Japanese woman who developed purulent pericarditis after undergoing chemoradiotherapy for esophageal cancer. She developed epigastralgia and a fever and was admitted to our hospital. A physical examination revealed hypotension, tachycardia and pericardial friction rub. Echocardiography revealed moderate pericardial effusion. Based on these observations, the patient was diagnosed with cardiac tamponade. Computed tomography confirmed the presence of an esophagopericardial fistula. Treatment with pericardiocentesis, drainage and short-term intrapericardial administration of antibiotics relieved the patient's symptoms. Daily rinsing through a catheter with normal saline prevented relapse of the purulent pericarditis. Esophagopericardial fistulas are so rare that their treatment is not well-established. We herein report successful palliative care of a malignant esophagopericardial fistula associated with purulent pericarditis.

Cutaneo-pericardial fistula after transapical aortic valve implantation.

Transcatheter aortic valve implantation (TAVI) represents a therapeutic option of increasing impact for the treatment of high-risk patients with symptomatic, severe aortic valve stenosis. We report here the case of an 86-year old patient with a cutaneo-pericardial fistula after a transapical TAVI procedure.

Tuberculous pericarditis with and without HIV.

The human immunodeficiency virus (HIV) has altered the epidemiology, clinical manifestations, treatment considerations and natural history of tuberculous (TB) pericarditis with significant implications for clinicians. The caseload of TB pericarditis has risen sharply in TB endemic areas of the world where co-infection with HIV is common. Furthermore, TB is the cause in greater than 85 % of cases of pericardial effusion in HIV-infected cohorts. In the absence of HIV, the morbidity of TB pericarditis is primarily related to the ferocity of the immune response to TB antigens within the pericardium. In patients with HIV, because TB pericarditis more often occurs as part of a disseminated process, the infection itself has a greater impact on the morbidity and mortality. HIV-associated TB pericarditis is a more aggressive disease with a greater degree of myocardial involvement. Patients have larger pericardial effusions with more frequent hemodynamic compromise and more significant ST segment changes in the electrocardiogram. HIV alters the natural history and outcomes of TB pericarditis. Immunocompromised participants appear less likely to develop constrictive pericarditis and have a significantly higher mortality compared with their immunocompetent counterparts. Finally co-infection with HIV has resulted in a number of areas of uncertainty. The mechanisms of myocardial dysfunction are unclear, new methods of improving the yield of TB culture and establishing a rapid bacterial diagnosis remain a major challenge, the optimal duration of anti-TB therapy has yet to be established, and the role of corticosteroids has yet to be resolved.

Pyopericardium followed by constrictive pericarditis due to Corynebacterium diphtheriae.

Pyopericardium is a rare entity associated with a high mortality. We report a case of a 44-year old man presenting with simultaneous constrictive pericarditis and pyopericardium due to Corynebacterium diphtheriae. Pericardiectomy and epicardiectomy were performed without cardiopulmonary bypass, with an excellent result.

Constrictive pericarditis presenting as chylothorax.

Chylothorax is a rare clinical condition that can be attributed to a damaged thoracic duct. The condition is suggested by aspiration of milky white fluid from the pleural cavity and is commonly associated with either malignant diseases or trauma (e.g. cardiothoracic surgery). We present the case of a 15-year-old boy with chylothorax, whose effusion was due to constrictive pericarditis. The definitive treatment of chylothorax involves identification and management of the underlying pathology. We suggest that when dealing with cases of chylothorax, constrictive pericarditis should be considered among the causes.

Purulent pericarditis.

BACKGROUND: Bacterial pericarditis has become a clinical rarity since the onset of antimicrobial therapy, yet remains fatal in a large majority of cases. AIM: We present the case of a 57-year-old male, admitted with a short history of pleuritic chest pain and dyspnoea. Investigations led to diagnosis of pyopericardium, most likely secondary to fistulating thoracic malignancy. Despite maximum medical treatment this condition proved fatal. CONCLUSION: This case highlights the still unfortunately poor prognosis of purulent pericarditis in the antibiotic era. Underlying aetiological factors should be searched for and eliminated where possible when a diagnosis of purulent pericarditis is made.