Purulent Pericarditis Caused by Nocardia: A Case Report and Literature Review

doi:10.21203/rs.3.rs-4262458/v1

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Systematic Review

Purulent Pericarditis Caused by Nocardia: A Case Report and Literature Review

https://doi.org/10.21203/rs.3.rs-4262458/v1

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Background

Pericarditis caused by Nocardia, a rare opportunistic disease marked by high mortality rates, is frequently misdiagnosed as Mycobacterium tuberculosis (MTB) and bacterial infections.

Case Presentation:

We present a case of pericarditis caused by Nocardia in a patient with acquired immune deficiency syndrome(AIDS). The patient was misdiagnosed on several occasions and received inappropriate anti-tuberculosis treatment for MTB. When timely pericardial puncture and collection of pericardial effusions culture revealed the presence of Nocardia, the patient was started on appropriate antibiotic therapy, which resulted in a cure.

Conclusions

By reporting this case, we aim to enhance clinicians' awareness of the differential diagnosis of purulent pericarditis and the importance of sensitive antibiotic therapy to aid in the timely diagnosis and treatment of nocardial pericarditis. The previously reported cases of laboratory-confirmed nocardial pericarditis are also reviewed and summarized.

Nocardia

pericarditis

antibiotic

pericardiocentesis

Nocardia species is a fibrous, weak acid-fast, aerobic, gram-positive bacteria that is ubiquitous in soil and water[1]. The skin, lungs, and brain are the most frequently affected sites of infection; nevertheless, the disease has the potential to spread and impact every organ in the body[2–5]. A small minority of immunocompetent patients may be infected by Nocardia[6].It was usually regarded as an opportunistic pathogen, with numerous cases documented in individuals with AIDS and those with compromised cell-mediated immunity, such as patients with leukemia or lymphoma, transplant recipients, and individuals undergoing prolonged glucocorticoid therapy[4, 7, 8]. Therefore, the determinants of mortality were influenced by these associated risk factors[9].

Pericarditis caused by Nocardia is a rare opportunistic disease with a high mortality rate and presents with nonspecific clinical symptoms. Given that Nocardia shares similar staining and morphological characteristics with Mycobacterium, nocardiosis is often misdiagnosed as MTB infection[10].This case report describes a patient with AIDS experiencing pericarditis caused by Nocardia infection, who underwent multiple misdiagnoses and received incorrect anti-tuberculosis therapy intended for MTB. When timely pericardial puncture and culture of pericardial effusions revealed the presence of Nocardia, the patient was initiated on appropriate antibiotic therapy, leading to a successful cure. The aim is to highlight the awareness of awareness of the differential diagnosis of purulent pericarditis and the importance of sensitive antibiotic therapy to aid in the timely diagnosis and treatment of nocardial pericarditis Furthermore, we also discuss previously reported cases of AIDS patients with concomitant Nocardia infection causing pericarditis.

A 52-year-old Chinese male patient presented with a chief complaint of “fever, fatigue and dyspnea for half a month”. Given the patient’s immunodeficiency status, exudative pericardial effusions, the adenosine deaminase of pericardial effusions greater than 45U/L, and elevated erythrocyte sedimentation rate(ESR), he was initially diagnosed with pericarditis caused by MTB. The patient underwent pericardial puncture with catheter placement for continuous drainage and received one week of anti-tuberculosis therapy at a local hospital. However, his symptoms did not improve, leading to his transfer to our hospital for further treatment. His medical history reveals that he was recently diagnosed with AIDS, with no monitoring of CD4 count and no initiation of antiretroviral therapy. Vital signs and physical examination were as follows: temperature of 36.7°C; blood pressure of 109/84 mmHg; pulse of 107/min; respiratory rate of 22/min༈under oxygen therapy༉; semi-upright position; decreased bilateral breath sounds; bilateral cardiac enlargement; continuous drainage of purulent viscous pericardial effusions from pericardial puncture; and pitting edema of both lower extremities. Laboratory results demonstrated a reduced lymphocyte ratio of 3.3% (standard range: 20–40%), and a negative result for the gamma interferon release assay. Chest CT scans indicated bilateral symmetrical pleural effusions with localized atelectasis in the lower lobes of both lungs, alongside massive pericardial effusions (Fig. 1A). Echocardiogram reveals a large of pericardial effusions. Due to the absence of neurological symptoms in the patient, we did not perform cranial imaging.

Based on assessments performed at the local hospital and subsequent auxiliary examinations upon admission, the patient continued to receive anti-tuberculosis therapy. However, the patient’s symptoms were progressively worsening, with a blood pressure decrease to 92/63mmHg and shortness of breath. Additionally, there was persistent drainage of a large amount of viscous and purulent pericardial effusions. Given the absence of fibrotic alterations in chest imaging, the scope was narrowed to inflammatory pericardium diseases capable of inducing pericardial effusions. The conditions necessitating exclusion included: 1) Non-tuberculous mycobacterium infection, which was inconsistent with the patient's presentation and generally not considered in the absence of pulmonary lesions. 2) Tuberculous pericarditis(TBP), which seemed unlikely as the patient's symptoms remained unabated despite the administration of highly effective antituberculosis therapy. 3) The serum 1,3-β-d-glucan (BDG) test was negative, which cannot entirely rule out fungal infection.

As a result, the patient received empirical treatment with piperacillin/sulbactam (2.25 g, intravenous, every 12 hours). However, as the condition progressed, laboratory results revealed severe acid-base disturbances (arterial blood pH of 7.631), potassium deficiency, and hypochloremia. Subsequently, the piperacillin/sulbactam was discontinued. The acid-base disturbance was rectified through interventions aimed at improving ventilation and correcting the metabolic alkalosis.

However, cultures for fungi, MTB, viruses, and other bacteria from blood and body effusions were all negative. The possibility of rare opportunistic infections could not be discounted, as the presence of weakly acid-fast and gram-positive bacteria. Subsequently, the culture of pericardial effusions revealed the presence of Nocardia. Unfortunately, due to limited resources, identification of Nocardia species was not possible. The laboratory and pharmacy experts have confirmed the sensitivity of these medications: amikacin, amoxicillin/clavulanic acid, ceftriaxone, imipenem, ciprofloxacin, minocycline, and trimethoprim-sulfamethoxazole(SMZ/TMP). Thereafter, the patient discontinued the anti-tuberculosis treatment and administered combination therapy consisting of ceftriaxone (4 g, intravenous, every day) and amikacin (0.4 g, intravenous, every day) and exhibited a gradual alleviation of symptoms. Concurrently, the volume of pericardial effusions drainage reduced gradually.

However, during the anti-infective treatment, the patient experienced significant decreases in white blood cell count (to a minimum of 1.27×1000/µL) and hemoglobin levels (to a minimum of 61 g/L), in addition to increased serum levels of alanine (ALT) and aspartate (AST) aminotransferases. With the administration of promoting leucopoiesis and intensive hepatoprotective treatment, the patient demonstrated a rapid recovery in white blood cell count, hemoglobin levels and liver function.

Based on the side effects of antibiotics and the patient's status, the SMZ/TMP (0.96 g orally twice daily) was administered, which resulted in a gradual alleviation of symptoms. A chest CT scan performed prior to discharge revealed bilateral pleural and pericardial effusions that had evidently absorbed (Fig. 1B), while an echocardiogram indicated a small amount of residual pericardial effusions. In an outpatient clinic, the patient was prescribed SMZ/TMP (0.96 g orally twice daily) in conjunction with amoxicillin/clavulanic acid (0.686 g orally twice daily) for an additional 6 months. Follow-up demonstrated no worsening infectious symptoms or severe adverse reactions to the treatment regimen. Re-examination via chest CT scan and echocardiogram showed complete absorption of the pericardial effusions with no evidence of residual fibrous calcification (Fig. 1C and D).

Nocardiosis is an opportunistic infection[11]. The clinical presentation and outcome of nocardiosis depend on the patient's initial immune status [12]. Among those diagnosed with AIDS, the incidence of Nocardiosis ranges from 0.2–1.8%[13], while the incidence of pericarditis is even lower. To our understanding, a total of 11 cases of AIDS patients complicated with Nocardia pericarditis have been reported since 1985 (Table 1). The patients' ages ranged from 24 to 52 years, with males accounting for 81.8% (9/11). Cardiac tamponade was a life-threatening complication that ultimately arose in 54.5% (6/11) of the cases. Nocardia species were isolated from the pericardial effusion cultures in all cases. Tragically, 28.3% (3/11) of the cases resulted in fatalities. A case of pericarditis co-infected with both Nocardia and MTB underscores the critical importance of differential diagnosis for these diseases.

Table 1

Summary of all published cases of nocardial pericarditis in AIDS.
Age	Sex	cardiac tamponade	CD4 cell count(cells/mm3)	Misdiagnose tuberculous pericarditis	Drainage /surgery/ drainage flow	Drug Treatment	Antiretroviral therapy	Outcome	References
32	Male	No	48	No	Subxiphoid pericardiostomy (1100 mL fluid)	SMX/TMP, IV	Not reported	Recovered	Holtzet al.[39]
34	Male	No	66	No	Pericardiostomy (400 mL fluid)	SMX/TMP, IV, 3 weeks	Not reported	Died	Holtzet al. [39]
34	Male	Yes	239	No	Pericardiostomy (400 mL fluid)	SMX/TMP, IV, 5 days →Sulfadiazine, PO, 3 months	Yes	Recovered	Rivero et al. [13]
42	Male	No	91	Yes	Pericardial window	SMX/TMP but allergy →Ceftriaxone+ Minocycline, 6 weeks	Not reported	Recovered	Ramanathan and Rahimi[40]
24	Female	Yes	Not reported	No	Pericardial aspirations with indwelling catheter (900 mL fluid)	SMX/TMP, PO	Not reported	Recovered	Leang et al. [41]
44	Male	No	42	Yes	Pericardiocentesis followed by surgical drainage with pericardial window	SMX/TMP, IV →PO	No	Recovered	Jinno et al. [42]
35	Female	Yes	32	Yes	Pericardiocentesis (500 mL fluid)	SMX/TMP + ceftriaxone + doxycycline, IV → SMX/TMP + doxycycline, PO	Yes	Recovered	Chandrashekar et al. [43]
37	Male	Yes	50	No	Subxiphoid pericardial drain (800 mL fluid)	Imipenem/ cilastatin + SMX/ TMP, IV →SMX/TMP, PO	No	Recovered	Aisenberg and Martin[44]
32	Male	Yes	17	Yes	Emergency pericardiocentesis	Imipenem/ cilastatin + SMX/TMP, IV	Yes	Died	Laksananun et al. [45]
32	Male	Yes	4	No	Pericardiocentesis	→SMX/ TMP + Imipenem/ cilastatin, IV, Continue anti-TB therapy(HREZ)	Not reported	Died	Griessel et al. [46]
52	Male	No	Not reported	No	pericardiocentesis with indwelling catheter (4280mL of pus)	SMZ/TMP, PO + ceftriaxone + Amikacin, IV →SMZ/TMP and amoxicillin/ clavulanic acid, PO	No	Recovered	Xinxin Z et al. (current study)
AIDS: Acquired Immune Deficiency Syndrome; SMX/TMP: sulfamethoxazole/trimethoprim; IV: intravenous; PO: per oral; TB: tuberculosis; H: isoniazid; R: rifampin, Z: pyrazinamide; E: ethambutol.

The clinical presentation of pericarditis caused by Nocardia lacks specificity. Apart from non-specific constitutional symptoms, reported cases reveal that patients commonly present with fever, night sweats, dyspnea, loss of appetite and weight, chest pain, chills, cough, and fatigue. Before obtaining the results of etiology detection, clinical diagnosis of pericarditis caused by Nocardia remains a challenge and should be differentiated from other types of purulent pericarditis as follows.

In developing countries, tuberculous pericarditis remains the predominant cause of purulent pericarditis[14].The MTB can disseminate via retrograde lymphatic spread, hematogenous dissemination, or by infiltrating the pericardium through neighboring lung, pleura, and spine[15]. In patients coinfected with HIV, only 35% of individuals with TBP exhibit positive findings in pericardial effusions cultures[16]. Xpert MTB/RIF and Xpert MTB/RIF Ultra are cartridge-based nucleic acid amplification tests that can detect MTB and simultaneously assess rifampicin resistance in less than 2 hours. In a study evaluating the accuracy of Xpert MTB/RIF in TBP and other forms of extrapulmonary tuberculosis, the sensitivity was 63.8%, while demonstrating high specificity (100%)[17]. Besides, in high tuberculosis prevalence areas, the utility of interferon-gamma release assays (IGRAs) is limited, as positive results simply indicate exposure to MTB antigens and do not reliably identify active tuberculosis disease[18]. In our study, the patient was initially misdiagnosed with TBP before obtaining etiological evidence. When patients experience ineffective anti-tuberculosis treatment, they should be alert to the possibility of Nocardia infection and obtain pathogen and drug sensitivity test results as soon as possible. In the case, patient’s pericardial effusions tested negative for Xpert MTB/RIF, cultures, and IGRA, and the ineffectiveness of anti-tuberculosis treatment, a definitive exclusion of the diagnosis of TBP was made.

Methicillin-resistant Staphylococcus aureus (MRSA) pericarditis and pericardial abscesses are rare and typically associated with chronic medical conditions that require prolonged stays in healthcare settings [19, 20]. 94.9% of cases show pericardial effusion, and 83.8% exhibit tamponade[21]. In reported cases of MRSA pericarditis, MRSA has been isolated from pericardial effusions without exception, and 64.1% of MRSA blood cultures test positive [21]. The adult mortality rate is 20.5%, with an average survival of 21.8 days, primarily attributed to multi-organ dysfunction associated with septic shock[21]. In this study, the patient did not have prolonged exposure to healthcare settings, and neither the blood cultures nor the pericardial fluid cultures showed the presence of MRSA. Consequently, the etiology of purulent pericarditis attributed to MRSA can be definitively excluded.

In most reported cases of severe pericarditis or cardiac tamponade secondary to influenza, Influenza A is the implicated virus[22–24]. Isolated pericarditis is more often associated with pericardial effusions [25]. Male and older patients are more likely to have isolated pericarditis, while female and younger patients are more likely to have myopericarditis[25]. Patients of any age presenting with chest pain, tachycardia, and hemodynamic instability within 2–4 weeks of symptom onset should be considered to have cardiac involvement [25]. In our study, the patient presents with pericardial effusion without other typical clinical symptoms such as influenza-like respiratory symptoms or chest pain, exhibiting a low clinical index of suspicion.

Pericarditis caused by fungal infections is rare. β-D-glucan (BDG), found in various fungal cell walls, serves as a surrogate marker for diagnosing invasive fungal infections (IFIs)[26–28]. BDG has been utilized for diagnosing IFIs, including Pneumocystis jirovecii pneumonia (PJP), cryptococcosis, and others in people living with HIV (PLHIV). Several studies of serum BDG, utilizing the Fungitell assay with varying cutoff values for diagnosing PJP, demonstrated a sensitivity ranging from 90–100% and specificity ranging from 61.3–96.4%[29–31]. However, in the diagnosis of cryptococcosis, the sensitivity of BDG in cerebrospinal effusions is 89%, with a specificity of 85%, while in serum, the sensitivity is 79%, with a specificity of 61%[32]. Currently, there is a lack of reports on the sensitivity and specificity of serum BDG in diagnosing pericarditis caused by fungal infections. In our study, the patient’s serum BDG was negative, although fungal etiology causing pericarditis was not promptly ruled out at that time. Subsequent culture of the pericardial effusions, however, revealed the presence of Nocardia species, with negative fungal cultures. Effective antibiotic therapy subsequently excluded fungal etiology as the cause of pericarditis.

Microbiological examination is the gold standard for diagnosing pericarditis caused by Nocardia. However, in AIDS patients with negative pericardial effusion cultures and ineffective antibiotic treatment, extending the culture period to at least 10 days becomes necessary to overcome false-negative results[33]. As we have previously summarized, the presence of fever, dyspnea, chest pain, and pericardial effusion, along with the isolation of slow-growing Gram-positive bacteria in pericardial fluid cultures, should raise suspicion of Nocardia infection.

The clinical features of Nocardia infection include rapid disease progression and a propensity for infection recurrence or exacerbation [33]. In this case, despite the presence of massive purulent pericardial effusions and rapid disease progression, accurate etiological identification, sensitive antibiotics, and timely pericardiocentesis drainage were key factors for successful treatment.

When considering Nocardia infection, empirical antibiotic therapy should be promptly initiated. Early diagnosis, early treatment, adequate dosage, and prolonged treatment duration are recommended. he selection of antimicrobial therapy should take into account factors such as epidemiology, clinical presentation (e.g., severity, organs involved), patient-specific factors, antibiotic minimal inhibitory concentration (MIC), and side effects [2, 34–36]. SMZ/TMP is regarded as the preferred antimicrobial agent for the treatment of nocardiosis [37]. For patients resistant to sulfonamide drugs, high-dose sulfonamide therapy or combination therapy can still be used, among which carbapenems and linezolid exhibit higher sensitivity [12, 38]. Immunocompromised patients typically require prolonged antimicrobial therapy for a duration of at least 6–12 months. [37]. In this case, the pericardial effusion culture of the patient indicated positivity for Nocardia. Following treatment with a combination of ceftriaxone and amikacin, along with SMZ/TMP, a significant reduction in pericardial effusion was observed on chest CT and echocardiography, suggesting favorable therapeutic efficacy of SMZ/TMP combination therapy. This case highlights the necessity to include Nocardia pericarditis in the differential diagnosis of immunosuppressed patients presenting with purulent pericarditis. Early identification, accurate diagnosis, prompt initiation of treatment, and efficacious management can significantly influence patient outcomes. It is crucial to maintain vigilance for timely pericardial puncture, ensure extended antimicrobial therapy, and closely monitor potential side effects associated with antimicrobial drugs.

Pericarditis caused by Nocardia is a rare but potentially fatal opportunistic infection that should be considered in the differential diagnosis of other purulent pericarditis. Bacterial culture is the gold standard for diagnosis. Optimal outcomes can be achieved through timely diagnosis, drainage treatment, and prolonged antimicrobial therapy.

Ethics statement

This study has received ethical approval from the institutional review board of Red Cross Hospital of Yulin City (No.2023-4).

Declaration of competing interest

The author reports no conflicts of interest in this work.

Funding

This research was funded by Bureau of Science and Technology of Yulin (No. 202235090 and No.202235038).

Author contributions

Xinxin Zhong, Ao Lin collected data, review, editing and wrote the original draft. Jian Luo, Shihao Jiang, Yuying Ruan, Shuting Li, Li Zhong re-collected the data and review. Zhiyi He, Fu Cao conceived the manuscript, review and made a revision of it. Xinxin Zhong, Ao Lin contributed equally to this work and should be considered co-first authors. Zhiyi He, Fu Cao contributed equally to this work and should be considered co-corresponding author. All authors read and approved the final manuscript.

Brown-Elliott BA, Brown JM, Conville PS, Wallace RJ: Clinical and laboratory features of the Nocardia spp. based on current molecular taxonomy. Clinical Microbiology Reviews 2006, 19(2):259-282.
Traxler RM, Bell ME, Lasker B, Headd B, Shieh W-J, McQuiston JR: Updated Review on Nocardia Species: 2006-2021. Clinical Microbiology Reviews 2022, 35(4):e0002721.
Saubolle MA, Sussland D: Nocardiosis: review of clinical and laboratory experience. Journal of Clinical Microbiology 2003, 41(10):4497-4501.
McNeil MM, Brown JM: The medically important aerobic actinomycetes: epidemiology and microbiology. Clinical Microbiology Reviews 1994, 7(3):357-417.
Coussement J, Lebeaux D, van Delden C, Guillot H, Freund R, Marbus S, Melica G, Van Wijngaerden E, Douvry B, Van Laecke S et al: Nocardia Infection in Solid Organ Transplant Recipients: A Multicenter European Case-control Study. Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America 2016, 63(3):338-345.
Dumic I, Brown A, Magee K, Elwasila S, Kaljevic M, Antic M, Igandan O, Cardozo M, Rueda Prada L, Paulson M: Primary Lymphocutaneous Nocardia brasiliensis in an Immunocompetent Host: Case Report and Literature Review. Medicina (Kaunas) 2022, 58(4).
Lerner PI: Nocardiosis. Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America 1996, 22(6).
Martínez Tomás R, Menéndez Villanueva R, Reyes Calzada S, Santos Durantez M, Vallés Tarazona JM, Modesto Alapont M, Gobernado Serrano M: Pulmonary nocardiosis: risk factors and outcomes. Respirology (Carlton, Vic) 2007, 12(3):394-400.
Garcia-Bellmunt L, Sibila O, Solanes I, Sanchez-Reus F, Plaza V: Pulmonary nocardiosis in patients with COPD: characteristics and prognostic factors. Arch Bronconeumol (Engl Ed) 2012, 48(8):280-285.
Chang P-L, Hsieh W-S, Chiang C-L, Tuohy MJ, Hall GS, Procop GW, Chang H-T, Ho H-T: The hsp65 gene patterns of less common Mycobacterium and Nocardia spp. by polymerase chain reaction-restriction fragment length polymorphism analysis with capillary electrophoresis. Diagnostic Microbiology and Infectious Disease 2007, 58(3):315-323.
Couture-Cossette A, Morand M, Vinh DC, Gratton M, Martin P: Severe disseminated Nocardia infection associated with ustekinumab treatment for psoriasis. Br J Dermatol 2019, 181(1):194-195.
Haussaire D, Fournier P-E, Djiguiba K, Moal V, Legris T, Purgus R, Bismuth J, Elharrar X, Reynaud-Gaubert M, Vacher-Coponat H: Nocardiosis in the south of France over a 10-years period, 2004-2014. International Journal of Infectious Diseases : IJID : Official Publication of the International Society For Infectious Diseases 2017, 57:13-20.
Rivero A, Esteve A, Santos J, Maŕquez M: Cardiac tamponade caused by Nocardia asteroides in an HIV-infected patient. The Journal of Infection 2000, 40(2):206-207.
Imazio M, Gaita F, LeWinter M: Evaluation and Treatment of Pericarditis: A Systematic Review. JAMA 2015, 314(14):1498-1506.
Spodick DH: Tuberculous pericarditis. AMA Arch Intern Med 1956, 98(6):737-749.
Theron G, Peter J, Calligaro G, Meldau R, Hanrahan C, Khalfey H, Matinyenya B, Muchinga T, Smith L, Pandie S et al: Determinants of PCR performance (Xpert MTB/RIF), including bacterial load and inhibition, for TB diagnosis using specimens from different body compartments. Scientific reports 2014, 4:5658.
Pandie S, Peter JG, Kerbelker ZS, Meldau R, Theron G, Govender U, Ntsekhe M, Dheda K, Mayosi BM: Diagnostic accuracy of quantitative PCR (Xpert MTB/RIF) for tuberculous pericarditis compared to adenosine deaminase and unstimulated interferon-γ in a high burden setting: a prospective study. BMC Med 2014, 12:101.
Cattamanchi A, Smith R, Steingart KR, Metcalfe JZ, Date A, Coleman C, Marston BJ, Huang L, Hopewell PC, Pai M: Interferon-gamma release assays for the diagnosis of latent tuberculosis infection in HIV-infected individuals: a systematic review and meta-analysis. J Acquir Immune Defic Syndr 2011, 56(3):230-238.
Lakhundi S, Zhang K: Methicillin-Resistant Staphylococcus aureus: Molecular Characterization, Evolution, and Epidemiology. Clinical Microbiology Reviews 2018, 31(4).
Rodvold KA, McConeghy KW: Methicillin-resistant Staphylococcus aureus therapy: past, present, and future. Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America 2014, 58 Suppl 1:S20-S27.
Radovanovic M, Petrovic M, Hanna RD, Nordstrom CW, Calvin AD, Barsoum MK, Milosavljevic N, Jevtic D, Sokanovic M, Dumic I: Clinical Presentation and Management of Methicillin-Resistant Staphylococcus aureus Pericarditis-Systematic Review. J Cardiovasc Dev Dis 2022, 9(4).
Pandey Y, Hasan R, Joshi KP, Habash FJ, Jagana R: Acute Influenza Infection Presenting with Cardiac Tamponade: A Case Report and Review of Literature. Perm J 2019, 23.
Sidhu RS, Sharma A, Paterson ID, Bainey KR: Influenza H1N1 Infection Leading To Cardiac Tamponade in a Previously Healthy Patient: A Case Report. Res Cardiovasc Med 2016, 5(3):e31546.
Martín-Lázaro JF, Homs C, Benito R, Pedro AS, Suárez MA: Chronic pericardial effusion secondary to a influenza virus A (H1N1)/2009 infection. Turk Kardiyol Dern Ars 2013, 41(2):157-160.
Radovanovic M, Petrovic M, Barsoum MK, Nordstrom CW, Calvin AD, Dumic I, Jevtic D, Hanna RD: Influenza Myopericarditis and Pericarditis: A Literature Review. Journal of Clinical Medicine 2022, 11(14).
Ambasta A, Carson J, Church DL: The use of biomarkers and molecular methods for the earlier diagnosis of invasive aspergillosis in immunocompromised patients. Med Mycol 2015, 53(6):531-557.
Hammarström H, Stjärne Aspelund A, Christensson B, Heußel CP, Isaksson J, Kondori N, Larsson L, Markowicz P, Richter J, Wennerås C et al: Prospective evaluation of a combination of fungal biomarkers for the diagnosis of invasive fungal disease in high-risk haematology patients. Mycoses 2018, 61(9):623-632.
Hopke A, Brown AJP, Hall RA, Wheeler RT: Dynamic Fungal Cell Wall Architecture in Stress Adaptation and Immune Evasion. Trends Microbiol 2018, 26(4):284-295.
Esteves F, Lee CH, de Sousa B, Badura R, Seringa M, Fernandes C, Gaspar JF, Antunes F, Matos O: (1-3)-beta-D-glucan in association with lactate dehydrogenase as biomarkers of Pneumocystis pneumonia (PcP) in HIV-infected patients. European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology 2014, 33(7):1173-1180.
Desmet S, Van Wijngaerden E, Maertens J, Verhaegen J, Verbeken E, De Munter P, Meersseman W, Van Meensel B, Van Eldere J, Lagrou K: Serum (1-3)-beta-D-glucan as a tool for diagnosis of Pneumocystis jirovecii pneumonia in patients with human immunodeficiency virus infection or hematological malignancy. Journal of Clinical Microbiology 2009, 47(12):3871-3874.
Passos AIM, Dertkigil RP, Ramos MdC, Busso-Lopes AF, Tararan C, Ribeiro EO, Schreiber AZ, Trabasso P, Resende MR, Moretti ML: Serum markers as an aid in the diagnosis of pulmonary fungal infections in AIDS patients. The Brazilian Journal of Infectious Diseases : an Official Publication of the Brazilian Society of Infectious Diseases 2017, 21(6):606-612.
Rhein J, Bahr NC, Morawski BM, Schutz C, Zhang Y, Finkelman M, Meya DB, Meintjes G, Boulware DR: Detection of High Cerebrospinal Fluid Levels of (1→3)-β-d-Glucan in Cryptococcal Meningitis. Open Forum Infectious Diseases 2014, 1(3):ofu105.
Kendrick-Jones J, Ratanjee SK, Taylor SL, Marshall MR: Nocardia asteroides peritoneal dialysis-related peritonitis: a case of successful treatment and return to peritoneal dialysis. Nephrol Dial Transplant 2008, 23(8):2693-2694.
Wang H, Zhu Y, Cui Q, Wu W, Li G, Chen D, Xiang L, Qu J, Shi D, Lu B: Epidemiology and Antimicrobial Resistance Profiles of the Nocardia Species in China, 2009 to 2021. Microbiology spectrum 2022, 10(2):e0156021.
Glutsch V, Gesierich A, Goebeler M, Forster J, Schilling B: Nocardiosis in a patient with anti-PD-1-associated colitis treated with infliximab. European journal of cancer (Oxford, England : 1990) 2018, 101:284-286.
Margalit I, Lebeaux D, Tishler O, Goldberg E, Bishara J, Yahav D, Coussement J: How do I manage nocardiosis? Clinical Microbiology and Infection : the Official Publication of the European Society of Clinical Microbiology and Infectious Diseases 2021, 27(4):550-558.
Mehta HH, Shamoo Y: Pathogenic Nocardia: A diverse genus of emerging pathogens or just poorly recognized? PLoS Pathogens 2020, 16(3):e1008280.
Wang H-K, Sheng W-H, Hung C-C, Chen Y-C, Lee M-H, Lin WS, Hsueh P-R, Chang S-C: Clinical characteristics, microbiology, and outcomes for patients with lung and disseminated nocardiosis in a tertiary hospital. Journal of the Formosan Medical Association = Taiwan Yi Zhi 2015, 114(8):742-749.
Holtz HA, Lavery DP and Kapila R.Actinomycetales infection in the acquired immunodeficiency syndrome.Ann Intern Med 1985; 102: 203–205.
Ramanathan P and Rahimi AR. Nocardia asteroides pericarditis in association with HIV. AIDS Patient Care STDS 2000; 14: 621–625. 2000.
Leang B LL, Lim K, et al: Disseminated nocardiosis presenting with cardiac tamponade in an HIV patient. International Journal of STD & AIDS 2004, 15(12):839-840.
Jinno S, Jirakulaporn T, Bankowski MJ, Kim W, Wong R: Rare case of Nocardia asteroides pericarditis in a human immunodeficiency virus-infected patient. Journal of Clinical Microbiology 2007, 45(7):2330-2333.
Chandrashekar UK AV, Gnanadev NC, et al: Pulmonary nocardiosis presenting with cardiac tamponade and bilateral pleural effusion in a HIV patient. Tropical Doctor 2009, 39(3):184-186.
RME AGaM: Pericardial tamponade caused by Nocardia asteroides in a patient with acquired immunodeficiency syndrome: would sulfa prophylaxis have spared this infection? Infect Dis Clin Pract 2014;22: e34–e36. 2014.
Laksananun N SP, Kaewpoowat Q: Nocardia beijingensis pericarditis presenting with cardiac tamponade: A case report. Int J STD AIDS 2018, 29(5):515-519.
Griessel R, Mitton B, Rule R, Said M: A case report of Nocardia asiatica constrictive pericarditis in a patient with Human Immunodeficiency Virus. Cardiovascular Pathology : the Official Journal of the Society For Cardiovascular Pathology 2022, 58:107403.

No competing interests reported.

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