A Rare Case of Effusive-Constrictive Pericarditis Caused by Streptococcus agalactiae: Emergency Surgical Treatment.

A 70-year-old male patient was admitted to the emergency room in cardiac arrest. The patient was resuscitated and then referred to our cardiac surgery department, where he was diagnosed with suspected effusive constrictive pericarditis. A failed trial of TEE-guided pericardiocentesis led to the decision of surgical intervention. Sternotomy was performed and revealed pericardial thickening and very dense adhesions involving the pericardium and both pleurae, suggesting a neoplastic disease. An extensive pericardiectomy and bilateral pleural decortication were performed. After surgery, the patient improved significantly and was discharged from the intensive care unit 24 h later. Pericardial thickening, dense adhesions, the amount and color of pericardial fluid and the aspect of epicardial tissue increased our suspicion of neoplastic disease. Histological samples were sent to be analyzed immediately; a few days later, they were unexpectedly negative for any neoplastic disease but showed a group-B-hemolytic Streptococcus agalactiae infection, which causes pericarditis in extremely rare cases. Postoperatively, the patient, under intravenous antibiotic and anti-inflammatory therapy, remained asymptomatic and was discharged ten days after the surgery. At the three-month follow-up, transthoracic echocardiography showed a normal right and left ventricular function with no pericardial effusion.

Gastropericardial fistula induced acute purulent pericarditis.

Gastropericardial fistula is a rare but lethal condition. Several etiologies have been reported, including previous gastric or esophageal surgery, malignancy, trauma, infection, and ulcer perforation. Typical symptoms included chest pain, epigastric pain, fever and dyspnea. Gastropericardial fistula can lead to serious complications, including cardiac tamponade, sepsis, hemodynamic compromise and death. Therefore, early diagnosis and timely management are important for physicians to prevent from catastrophic complications. Here, we present a case of a man who presented with acute purulent pericarditis secondary to a gastropericardial fistula to highlight the pathogenesis and suggest therapeutic strategies.

Actinomyces in Forensic Practice.

ABSTRACT: A 19-year-old woman in septic shock with recent computed tomography findings of a loculated hepatic abscess was transferred to an intensive care unit where she went into asystolic cardiac arrest. After resuscitation, surgical exploration revealed a purulent pericardial effusion with tamponade and a liver abscess. Microbiological analyses from both sites were negative. Shortly after surgical exploration, she developed multiorgan failure and died. At autopsy, pus was observed both within the pericardial cavity and around the left lobe of the liver. Green "sulfur granules" suggestive of infection with Actinomyces spp. were able to be extruded from the liver during the postmortem examination and cultures returned positive for Actinomyces israelii. This case is a rare example of primary hepatic actinomycosis infection that resulted in the death of a young woman. Nonspecific clinical manifestations may delay diagnosis; however, the finding of "sulfur granules" in areas of abscess formation at autopsy should be taken as an indication of possible underlying Actinomyces infection.

Perivalvular Mitral Abscess Fistulised to the Pericardial Cavity Revealing Staphylococcal Endocarditis.

BACKGROUND: Fistula to the pericardial cavity is a very rare complication of perivalvular abscess during infective endocarditis, with Staphylococcus aureus being the most commonly associated microorganism. METHODS: We report a fatal septic shock due to a mitral endocarditis revealed by a myocardial abscess fistulised toward the pericardial cavity. RESULTS: A 66-year-old female without previous valvular disease was admitted to intensive care for severe sepsis. A few hours after admission, an unexpected cardiac arrest occurred. Chest computed tomographic-scan and transoesophageal echocardiography revealed a pericardial effusion due to a perivalvular mitral abscess fistulised toward the pericardial cavity. Despite prompt management including surgical debridement and appropriate antibiotics, death occurred 36hours after intensive care admission. All blood cultures as well as native mitral valve and pericardial fluid grew methicillin-sensitive Staphylococcus aureus. CONCLUSIONS: Intensivists should consider this rare complication in patients with staphylococcal infective endocarditis and perivalvular abscess.

A Rare Case of Rush Progression of Purulent Pericarditis by Escherichia coli in a Patient with Malignant Lymphoma.

Purulent pericarditis is a rare disease in the antibiotic era. The common pathogens of purulent pericarditis are gram-positive species such as Staphylococcus aureus. Streptococcus pneumoniae, Salmonella, Haemophilus, fungal pathogens/tuberculosis can also result in purulent pericarditis. We report an old male case of purulent pericarditis by Escherichia coli. He came to our hospital suffering from leg edema for 3 months. Echocardiography revealed the large amount of pericardial effusion, and he was admitted to test the cause of pericardial effusion without high fever, tachycardia, and shock vital signs. On the third day, he suddenly presented vital shock. We performed emergency cardiopulmonary resuscitation and pericardiocentesis. Appearance of pericardial effusion was hemorrhagic and purulent. The gram stain revealed remarkable E. coli invasion to pericardial space. Antibiotic therapy was immediately started; however, he died on sixth day with septic shock. The cytological examination of pericardial effusion suggested the invasion of malignant lymphoma to pericardium. This case showed subacute or chronic process of pericarditis without severe clinical and laboratory sings before admission. Nevertheless, bacterial purulent pericarditis usually shows acute clinical manifestation; the first process of this case was very silent. Immunosuppression of malignant lymphoma might make E. coli translocation from gastrointestinal tract to pericardial space, and bacterial pericarditis was progressed to purulent pericarditis. In the latter process, this case showed unexpected rush progression to death by sepsis from purulent pericarditis. Immediate pericardiocentesis should be performed for a prompt diagnosis of purulent pericarditis, and it might have improved the outcome of this case.

[Infected Thoracic Aortic Aneurysm Secondary to the Purulent Pericarditis;Report of a Case].

A 69-year-old man was hospitalized urgently to the department of cardiology, with the progressive general malaise. On admission, his blood pressure was 80/42 mmHg, his white cell count 13,700/µl, and C-reactive protein 25.55 mg/dl suggesting existence of aggressive infection with impaired circulation. Massive pericardial effusion was detected in echocardiography. Pericardial drainage was undergone promptly. There was drainage of 700 ml and the property was purulent. Pneumococcus was detected by the culture test of the pericardial fluid. Antibiotic administration was started by a diagnosis of the purulent pericarditis. His general condition was improved. However, a rapidly expanding saccular aneurysm was found in a descending thoracic aorta by computed tomography( CT). As an infected thoracic aortic aneurysm secondary to the purulent pericarditis, we performed thoracic endovascular aneurysm repair (TEVAR). The intravenous administration of antibiotics was continued for 2 weeks after TEVAR, which was followed by oral antibiotic administration for 1 year. The aneurysm completely disappeared by CT, 10 months after TEVAR. In case with an infected thoracic aortic aneurysm, TEVAR can be a 1st choice of treatment, depending on a causative organism and the morphology of the aneurysm.

Cardiac tamponade - unusual clinical manifestation of undiagnosed malignant neoplasm.

Cardiac tamponade may be the first or predominant symptom of some pathologies but its etiology is not uncommonly unknown on admission to hospital. The purpose of this study was to evaluate the predominant causes of cardiac tamponade in previously healthy patients treated emergently in a single cardiac surgical center. The study involved 81 patients with the mean age of 58.1±16.0 years who underwent emergent subxyphoid pericardiotomy due to cardiac tamponade. Pericardial effusion was analyzed macro- and microscopically. Examinations done in the cardiac surgical department revealed pericarditis secondary to infection (n=17) or autoimmunologic processes (n=2) and malignancy in 18 patients (predominantly of the lungs (n=11)). Pericardial effusion obtained from patients with viral and autoimmunologic-induced pericarditis was straw-color and odorless while with bacterial infections dark yellow, iridescent and usually malodorous. Additional workup in the regional hospitals enabled to reveal malignant tumors in 29 patients, leukemia or lymphoma in 5 subjects. In all but one of the neoplastic cases, pericardial fluid was turbid and dark red or plummy. In 10 patients etiology of tamponade remained unknown. In conclusion, cardiac tamponade in previously healthy patients may be occasionally the predominant symptom of cancer, especially of the lungs. Macroscopic intraoperative appearance of pericardial fluid may be helpful in identification of causative condition of cardiac tamponade.

Purulent pericardial effusion and mycotic pseudoaneurysm following insertion of a bare metal stent.

A 65-year-old male was diagnosed with purulent pericarditis, caused by Staphylococcus aureus five weeks after bare metal stenting for a 90% stenosis of the right coronary artery ostium. Subsequently, he developed a pseudoaneurysm in the right coronary sinus of Valsalva (CSV) requiring surgical intervention during the treatment of the pericarditis. Bacteremia after percutaneous coronary intervention (PCI) occurs in < 1% of patients and usually has insignificant clinical sequelae. We present an infected coronary bare metal stent of the proximal right coronary artery after PCI that resulted in a purulent pericardial effusion and mycotic pseudoaneurysm of the right coronary sinus of Valsalva (CSV). The patient successfully underwent surgical treatment.

Spontaneous bacterial coronary sinus septic thrombophlebitis treated successfully medically.

A 38-year-old farmer was hospitalized for fever, chills, cough, and chest pain lasting for 7 days. Due to persistent symptoms, patient was referred to hospital. Blood cultures identified oxacillin-sensitive Staphylococcus aureus (OSSA). Transthoracic echocardiography (TTE) showed large pericardial effusion, a mobile heterogeneous mass originating from the coronary sinus ostium, no sign of valvular endocarditis. Pericardiocentesis was done carrying out purulent fluid, microbiological culture isolating an OSSA. Parenteral penicillin M was administered for 6 weeks. At the end of this antibiotherapy regimen, TTE showed no coronary sinus mass with complete vacuity of the coronary sinus vein and no pericardial effusion.

[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.

Detection of drug-resistant Mycobacterium tuberculosis in pericardial fluid culture and its correlation with cartridge based nucleic acid amplification test and adenosine deaminase activity.

BACKGROUND: Pericardial effusion is the accumulation of fluid in the pericardial cavity. In nations with high tuberculosis (TB) load, TB is the most common cause of pericardial effusion. 1-2% of patients with pulmonary TB develop Pericardial TB worldwide. Multi-drug-resistant (MDR) TB, including extrapulmonary TB (EPTB) cases, are rising in number. Adenosine Deaminase (ADA) is an enzyme in lymphocytes and myeloid cells, which has certain immune functions in the body. ADA levels are increased in inflammatory conditions, like pleural, pericardial, or joint effusions, of bacterial etiology, granulomatous conditions, neoplasms, and autoimmune pathologies. TB is the only lymphocytosis involving disease with increased ADA levels. MDR EPTB is rare, but cases are on the rise, and tuberculous pericardial effusion is one such example. Hence, it is important to know the percentage of cases detected by a culture that can be identified by cartridge-based nucleic acid amplification test (CBNAAT), their resistance patterns, and to identify potential markers like ADA, which can help in early identification of cases. The objectives of this study were to identify the Mycobacterium tuberculosis (MTB) bacilli in culture, and correlate them with cartridge-based nucleic acid amplification test (CBNAAT) results and their drug-resistance, in the Pericardial tubercular effusion, and to find if Adenosine Deaminase (ADA) levels can be used as a predictor of the presence of MTB in pericardial fluid. METHODOLOGY: We enrolled 52 patients with moderate to large tuberculous pericardial effusion, based on pericardial fluid analysis, CBNAAT, and culture methods, between January 2021 and December 2021. RESULTS: The mean age of the patients was 41.85 + 17.88 years, with a median of 38 years. Males made up 57.7% of the total patients. MTB was detected in 16 (30.8%) patients in the CBNAAT evaluations. 14 (87.5%) of the CBNAAT-positive TB patients were sensitive to Rifampicin, whereas the remaining 2 (12.5%) were resistant to Rifampicin on CBNAAT. MTB was found to be growing in 8 (15.38%) drug sensitivity test cultures. Out of these 8, 6 were sensitive to first-line drugs, whereas 2 were resistant to both Isoniazid and Rifampicin. The presence of cough was found to have a significant difference between CBNAAT-detected MTB positive and negative patients (p = 0.020), whereas an insignificant difference was found for the presence of hypertension, diabetes mellitus, obesity, dyspnea, or fever. There was also an insignificant difference between the number of patients positive for the Tuberculin skin test, between the two groups. ADA was significantly higher in the MTB-detected CBNAAT group (85.91 + 37.60U/L vs 39.78 + 24.31U/L, p = 0.005), whereas the total leukocyte count, lymphocytes, neutrophils, random blood sugar levels, and serum protein levels had no significant difference. The area under the Receiver Operator Curve (CBNAAT positive: dependent variable; ADA: test result variable) was 0.854 (null hypothesis rejected), with a standard error of 0.078. CONCLUSIONS: Culture is the gold standard method to diagnose tuberculosis. Detection of MTB on pericardial fluid culture is very uncommon, though in our study, culture came out positive in 16% of patients, and 4% were resistant to rifampicin and isoniazid. Higher ADA levels in pericardial fluid are an indicator of tuberculous pericardial effusion.

Detection of Anaplasma phagocytophilum in an inflammatory pericardial effusion of a dog.

An 11-year-old female spayed German Wirehaired Pointer with a 1-week history of lethargy, hyporexia, diarrhea, and coughing presented with pericardial effusion causing cardiac tamponade. An echocardiogram revealed no structural cause for pericardial effusion. The pericardial effusion was an exudate with mixed macrophagic and neutrophilic inflammation. Morulae occasionally were found within neutrophils. The pericardial fluid and blood were qPCR and cPCR positive for Anaplasma phagocytophilum (NC State University, Vector-borne Disease Diagnostic Laboratory, Raleigh, NC). The dog's blood was negative by ELISA (Vetscan Flex4 Rapid Test, Zoetis, Parsippany, NJ) for A. phagocytophilum antibodies at initial presentation and subsequently positive (SNAP4DxPlus, IDEXX, Westbrook, ME) 7 days later. After pericardiocentesis and administration of doxycycline (5 mg/kg PO q12h for 14 days), a repeat echocardiogram performed 1 month later showed no recurrence of pericardial effusion.

HIV-1 infection alters CD4+ memory T-cell phenotype at the site of disease in extrapulmonary tuberculosis.

HIV-1-infected people have an increased risk of developing extrapulmonary tuberculosis (TB), the immunopathogenesis of which is poorly understood. Here, we conducted a detailed immunological analysis of human pericardial TB, to determine the effect of HIV-1 co-infection on the phenotype of Mycobacterium tuberculosis (MTB)-specific memory T cells and the role of polyfunctional T cells at the disease site, using cells from pericardial fluid and blood of 74 patients with (n = 50) and without (n = 24) HIV-1 co-infection. The MTB antigen-induced IFN-γ response was elevated at the disease site, irrespective of HIV-1 status or antigenic stimulant. However, the IFN-γ ELISpot showed no clear evidence of increased numbers of antigen-specific cells at the disease site except for ESAT-6 in HIV-1 uninfected individuals (p = 0.009). Flow cytometric analysis showed that CD4+ memory T cells in the pericardial fluid of HIV-1-infected patients were of a less differentiated phenotype, with the presence of polyfunctional CD4+ T cells expressing TNF, IL-2 and IFN-γ. These results indicate that HIV-1 infection results in altered phenotype and function of MTB-specific CD4+ T cells at the disease site, which may contribute to the increased risk of developing TB at all stages of HIV-1 infection.

Primary hepatic actinomycosis presenting as purulent pericarditis with cardiac tamponade.

Cardiac tamponade constitutes an exceptional form of actinomycosis. We describe a case of primary hepatic actinomycosis presenting as purulent pericarditis with cardiac tamponade in a 20-year-old patient with previous esophagectomy and colonic interposition, successfully managed by computed tomography-guided percutaneous drainage and a prolonged course of antibiotic treatment. Actinomyces israelii was identified in the pericardial fluid by 16S rRNA gene sequencing. The literature on the simultaneous presentation of cardiac and hepatic actinomycosis is reviewed.

Clostridium sordellii as a cause of constrictive pericarditis with pyopericardium and tamponade.

Systemic infections caused by Clostridium sordellii are rare. They are usually reported in cases of skin and soft tissue infections and sometimes in cases of toxic shock syndrome involving exotoxins. We report here the first case of Clostridium sordellii infection associated with acute constrictive pericarditis and with pyopericardium and tamponade.

[Culture-negative, purulent pericarditis]. / 44-jähriger Patient mit kulturnegativer, purulenter Perikarditis.

We report about a patient with purulent pericarditis due to Neisseria meningitidis pretreated with antibiotics. Clinical signs were suggestive of pericardial tamponade. Cultures from blood and pericardial aspirate remained negative. Broad-range polymerase chain reaction from pericardial fluid detected Neisseria sp.. Latex agglutination assay from pleural fluid showed positive reaction with meningococcal antigen serogroup C. Meningococcal pericarditis without meningitis is a rare manifestation. Non-culture based diagnostic methods in patients with such severe infections and negative cultures play an important role.

Mycoplasma hominis pericarditis in a lung transplant recipient: review of the literature about an uncommon but important cardiothoracic pathogen.

Purulent pericarditis due to Mycoplasma hominis is rare, and is usually associated with mediastinitis or pleuritis following cardiothoracic surgery. We report the first case to our knowledge of isolated purulent pericarditis caused by M. hominis in a lung transplant recipient and review previously reported cases of this disease.