A fatal Candida albicans pericarditis presenting with cardiac tamponade after COVID-19 infection and cardiothoracic surgery.

BACKGROUND: Candida pericardial infection is a rare clinical entity usually related to recent cardiothoracic surgery and chronic debilitating conditions. During the COVID-19 pandemic, invasive fungal infections have been on the rise, likely due to a combination of factors such as immunosuppression, underlying conditions like diabetes, and surgical procedures. CASE PRESENTATION: Herein, we report a 67-year-old diabetic woman with a history of COVID-19 infection who received a high dose of corticosteroids a few months before admission, and previous myocardial infarction for more than 12 years. The patient had a positive cardiac tamponade with signs of dyspnea, chest pain, and low blood pressure. Echocardiographic data were more in favor of constrictive pericarditis. The patient underwent urgent echocardiography-guided pericardiocentesis and then broad-spectrum antibiotic treatment was prescribed. Repeated echocardiography implied a persistent pericardial effusion 10 days later. Subxiphoid aspirates and biopsied tissues showed budding yeast cells and yeast colonies grew on culture media identified as Candida albicans. CONCLUSION: This report should bring to the attention of physicians toward the possibility of Candida pericardial infection presenting with cardiac tamponade after COVID-19 infection and cardiothoracic surgery. Echocardiographic assessment, prompt pericardiotomy, molecular-based identification of causative agent, and early administration of appropriate antifungal treatment should improve the patient's survival.

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.

Chlamydia pneumoniae-associated pleuropericarditis: a case report and systematic review of the literature.

BACKGROUND: Chlamydia pneumoniae is a common cause of atypical community acquired pneumonia (CAP). The diagnostic approach of chlamydial infections remains a challenge. Diagnosis of delayed chlamydial-associated complications, involving complex autoimmune pathophysiological mechanisms, is still more challenging. C. pneumoniae-related cardiac complications have been rarely reported, including cases of endocarditis, myocarditis and pericarditis. CASE PRESENTATION: A 40-year old female was hospitalized for pleuropericarditis following lower respiratory tract infection. The patient had been hospitalized for CAP (fever, dyspnea, chest X-ray positive for consolidation on the left upper lobe) 5 weeks ago and had received ceftriaxone and moxifloxacin. Four weeks after her discharge, the patient presented with fever, shortness of breath and pleuritic chest pain and was readmitted because of pericardial and bilateral pleural effusions (mainly left). The patient did not improve on antibiotics and sequential introduction of colchicine and methylprednisolone was performed. The patient presented impressive clinical and laboratory response. Several laboratory and clinical assessments failed to demonstrate any etiological factor for serositis. Chlamydial IgM and IgG antibodies were positive and serial measurements showed increasing kinetics for IgG. Gold standard polymerase chain reaction of respiratory tract samples was not feasible but possibly would not have provided any additional information since CAP occurred 5 weeks ago. The patient was discharged under colchicine and tapered methylprednisolone course. During regular clinic visits, she remained in good clinical condition without pericardial and pleural effusions relapse. CONCLUSIONS: C. pneumoniae should be considered as possible pathogen in case of pleuritis and/or pericarditis during or after a lower respiratory tract infection. In a systematic review of the literature only five cases of C. pneumoniae associated pericarditis were identified. Exact mechanisms of cardiovascular damage have not yet been defined, yet autoimmune pathways might be implicated.

Bacterial pericarditis and empyema caused by Cutibacterium acnes in a patient with metastatic lung cancer.

Bacterial pericarditis and empyema due to Cutibacterium acnes has rarely been reported. C.acnes, a normal component of human skin flora, is often considered a contaminant when isolated from body fluids and thus cases may be underreported. We report the first case of concurrent purulent pericarditis and empyema caused by C. acnes in a patient with newly diagnosed metastatic lung cancer. Our patient underwent pericardial window creation and placement of pericardial and bilateral chest tubes and was successfully treated with culture directed antibiotic therapy.

Recognizing Cutibacterium acnes as a cause of infectious pericarditis: A case report and review of literature.

Cutibacterium acnes is an anaerobic bacterium commonly thought of as a culture contaminant rather than a pathogen. We present a case of Cutibacterium acnes pericarditis in a 22-year-old immunocompetent woman managed with surgical pericardial window and a 4-week course of penicillin G and review related literature on Cutibacterium acnes pericarditis.

Cryptococcal pericarditis in a heart transplant recipient.

We present a case of Cryptococcus neoformans pericarditis in a cardiac transplant recipient. This article reviews the diagnosis, treatment, and complications of cryptococcosis specifically in transplant patients. While pericarditis is a rare manifestation of Cryptococcus infection, this case highlights that cryptococcosis should be considered in the differential diagnosis for solid organ transplant and immunocompromised patients presenting with pericardial effusions.

Intrapericardial recombinant tissue plasminogen activator in purulent pericarditis- case series.

BACKGROUND: Pericardial constriction is one of the complications of purulent pericarditis (PP). Most difficult to treat, which may develop both in early and in the late period of the disease, resulting in a very poor prognosis. CASE PRESENTATION: We present case series of 4 patients with purulent pericarditis, in whom direct intrapericardial administration of recombinant tissue plasminogen activator (r-tPA) was used. Management of PP requires a combined surgical and medical approach. The most important is complete drainage of the effusion by subxiphoid pericardiotomy connected with complementary use of broad-spectrum antibiotics. Despite the use of broad- spectrum antibiotics, in some patients a large volume of daily drainage is still present. Constrictive pericarditis as a complication of PP is observed in majority of patients. Intrapericardial administration of fibrinolytic agents, although not strongly recommended, can improve efficacy of antibiotic treatment especially in patients with loculation fluid and can prevent the development of constrictive pericarditis. r-tPA was applied at a dose of 20 mg dissolved in 100 ml of normal saline in a 100 ml syringe, administered by a large pericardial drain (Pezzer drain) installed into the pericardial cavity during pericardioscopy. The tube was closed and re-opened after 24 h. No serious complications, such as bleeding, allergy or hypotension, were noted. CONCLUSION: We present case series of 4 patients with purulent pericarditis, in whom direct intrapericardial administration of recombinant tissue plasminogen activator (r-tPA), prevented the development of constrictive pericarditis, and increased efficacy of antibiotic treatment without any significant complications.

Infectious pseudo-aneurysm of the left ventricle: a case report and a review of the literature.

BACKGROUND: In the workup of a pediatric patient with pericarditis we found evidence of a pseudo-aneurysm of the left ventricle, which is a rare complication of purulent pericarditis. CASE PRESENTATION: We present a case of a six-year-old girl who was diagnosed with pericarditis and a fistula between the pericardial and the intra-luminal space of the left ventricle of the heart. She was successfully treated with antibiotics and cardio-thoracic surgery. We found 23 published cases (21 with follow-up) of infectious pseudo-aneurysm of the heart, of which 19 underwent surgery, 5 had fatal outcome, and 2 who refused surgery survived. The majority of cases were associated with Staphylococcus aureus. The exact mechanisms of this rare complication remain unknown. CONCLUSIONS: A pseudo-aneurysm of the left ventricle is a rare and not well understood complication of a purulent pericarditis most commonly caused by Staphylococcus aureus infection. Because of risk of rupture, surgical intervention is advised.

Cryptococcus neoformans pericarditis in a lung transplant recipient: Case report, literature review and pearls.

A 68-year-old man presented for outpatient evaluation of dyspnea and new-onset atrial fibrillation 9 months after undergoing bilateral lung transplantation. Echocardiography prior to cardioversion raised concern for tamponade. Therapeutic pericardiocentesis returned fluid containing 1875 wbc/mcl (68% pmn) and yielded Cryptococcus neoformans in culture. Cryptococcal antigen was detected in serum at a titer of 1:20. Cerebrospinal (CSF) fluid was without evidence of inflammation and without detectable cryptococcal antigen. There was no radiographic evidence of pulmonary cryptococcosis. Cultures of blood and CSF were without growth. Liposomal amphotericin B (3 mg/kg/day) was administered for 15 days. Oral fluconazole was added on day seven of amphotericin, and the patient was discharged to home 3 days later. Daily dosages of prednisone (10 mg), mycophenolate (500 mg), and tacrolimus (3 mg) at discharge were the same as at hospital admission. He was readmitted 12 days later with dyspnea and with re-accumulation and loculation of pericardial fluid. A pericardial window was created. Pericardial fluid contained 722 wbc/mcl (35% pmn); Cryptococcus was not identified on direct examinations or cultures of pericardial fluid or tissue. Cryptococcus antigen was present in serum at 1:160. Liposomal amphotericin B was resumed and continued for 2 weeks followed by resumption of fluconazole. Mycophenolate was stopped. Prednisone and tacrolimus were continued. Restrictive pericarditis was evident 3 weeks after window creation. Colchicine was initiated, prednisone increased to 15 mg daily and pericardiectomy planned. We aim to raise awareness to Cryptococcus as a potential etiology for pericarditis in solid organ transplant recipients.

Early pneumopericardium after heart transplantation.

A 60-year-old woman with a history of dilated cardiomyopathy underwent heart transplantation. One month post discharge, she presented to clinic with low-grade fever and productive cough. Her chest radiograph showed air-fluid levels in the pericardial silhouette. Transthoracic echocardiogram showed a large complex pericardial collection with no evidence of cardiac tamponade. The patient was urgently taken to the operating room for exploration. A large "egg-shaped" mass in the pericardium measuring 10 × 12 cm with gaseous material was aspirated. As the posterior wall of the mass was firmly adhered to the right atrium, the capsule was incompletely excised. We present the case of a potentially life-threatening complication post transplantation that required surgical debridement and life-long antibiotic suppressive therapy. To our knowledge, this is the first report of purulent pericardial collection caused by Enterobacter cancerogenous. Further research is required to better understand the biology of this microorganism and the role it may play as a pathogen in immunocompromised patients following solid organ transplantation.

Pathogenic variability among Pasteurella multocida type A isolates from Brazilian pig farms.

BACKGROUND: Pasteurella multocida type A (PmA) is considered a secondary agent of pneumonia in pigs. The role of PmA as a primary pathogen was investigated by challenging pigs with eight field strains isolated from pneumonia and serositis in six Brazilian states. Eight groups of eight pigs each were intranasally inoculated with different strains of PmA (1.5 mL/nostril of 10e7 CFU/mL). The control group (n = 12) received sterile PBS. The pigs were euthanized by electrocution and necropsied by 5 dpi. Macroscopic lesions were recorded, and swabs and fragments of thoracic and abdominal organs were analyzed by bacteriological and pathological assays. The PmA strains were analyzed for four virulence genes (toxA: toxin; pfhA: adhesion; tbpA and hgbB: iron acquisition) by PCR and sequencing and submitted to multilocus sequence typing (MLST). RESULTS: The eight PmA strains were classified as follows: five as highly pathogenic (HP) for causing necrotic bronchopneumonia and diffuse fibrinous pleuritis and pericarditis; one as low pathogenic for causing only focal bronchopneumonia; and two as nonpathogenic because they did not cause injury to any pig. PCR for the gene pfhA was positive for all five HP isolates. Sequencing demonstrated that the pfhA region of the HP strains comprised four genes: tpsB1, pfhA1, tpsB2 and pfhA2. The low and nonpathogenic strains did not contain the genes tpsB2 and pfhA2. A deletion of four bases was observed in the pfhA gene in the low pathogenic strain, and an insertion of 37 kb of phage DNA was observed in the nonpathogenic strains. MLST clustered the HP isolates in one group and the low and nonpathogenic isolates in another. Only the nonpathogenic isolates matched sequence type 10; the other isolates did not match any type available in the MLST database. CONCLUSIONS: The hypothesis that some PmA strains are primary pathogens and cause disease in pigs without any co-factor was confirmed. The pfhA region, comprising the genes tpsB1, tpsB2, pfhA1 and pfhA2, is related to the pathogenicity of PmA. The HP strains can cause necrotic bronchopneumonia, fibrinous pleuritis and pericarditis in pigs and can be identified by PCR amplification of the gene pfhA2.

Purulent pericarditis secondary to influenza and community-acquired methicillin-resistant Staphylococcus aureus co-infection.

Purulent pericarditis occurs rarely in the current antibiotic era. We describe clinical and echocardiographic features of purulent pericarditis in a previously healthy child with influenza and community-acquired methicillin-resistant Staphylococcus aureus co-infection. The child was already on appropriate antibiotics and had a very subtle clinical presentation, with prominent abdominal symptoms. Timely surgical drainage led to complete recovery.

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.

Acute Myopericarditis Associated with Tickborne Rickettsia sibirica mongolitimonae.

We report an unusual case of myopericarditis caused by Rickettsia sibirica mongolitimonae. Because of increasing reports of Rickettsia spp. as etiologic agents of acute myopericarditis and the ease and success with which it was treated in the patient reported here, rickettsial infection should be included in the differential diagnosis for myopericarditis.

First case report of myopericarditis linked to Campylobacter coli enterocolitis.

BACKGROUND: Campylobacter spp. are a common cause of mostly self-limiting enterocolitis. Although rare, pericarditis and myopericarditis have been increasingly documented as complications following campylobacteriosis. Such cases have occurred predominantly in younger males, and involved a single causative species, namely Campylobacter jejuni. We report the first case of myopericarditis following Campylobacter coli enterocolitis, with illness occurring in an immunocompetent middle-aged female. CASE PRESENTATION: A 51-yo female was admitted to a cardiology unit with a 3-days history of chest pain. The woman had no significant medical history or risk factors for cardiac disease, nor did she report any recent overseas travel. Four days prior to the commencement of chest pain the woman had reported onset of an acute gastrointestinal illness, passing 3-4 loose stools daily, a situation that persisted at the time of presentation. Physical examination showed the woman's vital signs to be essentially stable, although she was noted to be mildly tachycardic. Laboratory testing showed mildly elevated C-reactive protein and a raised troponin I in the absence of elevation of the serum creatinine kinase. Electrocardiography (ECG) demonstrated concave ST segment elevations, and PR elevation in aVR and depression in lead II. Transthoracic echocardiogram (TTE) revealed normal biventricular size and function with no significant valvular abnormalities. There were no left ventricular regional wall motion abnormalities. No pericardial effusion was present but the pericardium appeared echodense. A diagnosis of myopericarditis was made on the basis of chest pain, typical ECG changes and troponin rise. The chest pain resolved and she was discharged from hospital after 2-days of observation, but with ongoing diarrhoea. Following discharge, a faecal sample taken during the admission, cultured Campylobacter spp. Matrix assisted laser desorption ionization time-of-flight (Bruker) confirmed the cultured isolate as C. coli. CONCLUSION: We report the first case of myopericarditis with a suggested link to an antecedent Campylobacter coli enterocolitis. Although rare, myopericarditis is becoming increasingly regarded as a complication following campylobacteriosis. Our report highlights potential for pericardial disease beyond that attributed to Campylobacter jejuni. However uncertainty regarding pathogenesis, coupled with a paucity of population level data continues to restrict conclusions regarding the strength of this apparent association.

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.

Nonrheumatic myopericarditis post acute streptococcal pharyngitis: An uncommon cause of sore throat with ST segment elevation.

Nonrheumatic myopericarditis is an uncommon complication of acute pharyngitis caused by Group A Streptococcal infection (GAS). While the natural history of carditis complicating acute rheumatic fever is well established, the incidence, pathophysiology and clinical course of nonrheumatic myopericarditis are ill defined. Advances in rapid bedside testing for both myocardial injury and GAS pharyngitis have allowed for increasing recognition of this uncommon complication in patients presenting with a sore throat with associated chest discomfort. We describe a case of a 34years old man with GAS pharyngitis complicated by acute myopericarditis who presented with chest pain, ST segment elevation on electrocardiogram, and elevated cardiac biomarkers.

Cardiac tamponade secondary to purulent pericarditis diagnosed with the aid of emergency department ultrasound.

Purulent pericarditis is a rare but devastating disease process and even when treated, carries a poor prognosis. Cardiac tamponade is the most severe complication of purulent pericarditis and without acute surgical intervention, is often fatal. Diagnosis requires pericardiocentesis; however, early consideration of the disease and its complications in the emergency department (ED) can be life-saving. Here, we present a case of an intravenous drug user who presented with altered mental status and a rectal temperature of 105.4°. While in the ED, the patient acutely decompensated. The ED physician performed bedside cardiac ultrasound that a showed pericardial effusion and right ventricle diastolic collapse concerning for cardiac tamponade. The patient underwent urgent pericardiocentesis which revealed 300 ml of purulent fluid. Both blood and pericardial cultures grew methicillin-sensitive Staphylococcus aureus. Despite a complicated hospital course, with appropriate antibiotic coverage and surgical intervention, the patient was discharged in good neurologic condition. This rare case of purulent pericarditis underscores the utility of bedside ultrasound in the ED and the complicated nature of altered mental status in intravenous drug users.

Acute-Onset Chest Pain in a 17-Year-Old Female Adolescent With Systemic Lupus Erythematosus.

We report the case of a 17-year-old adolescent girl with systemic lupus erythematosus with disseminated pneumococcal infection leading to purulent pericarditis with cardiac tamponade. Although pericarditis is not an uncommon entity in autoimmune diseases such as systemic lupus erythematosus, purulent pericarditis is a rare cause (<1%) of this presentation.