Author: Mangesh Mange, et al.
Cureus, April 2026
Infective endocarditis usually presents with fever, a new or changing heart murmur, positive blood cultures, and embolic or immunologic findings. This case demonstrates that infective endocarditis can instead present primarily as severe acute respiratory failure, closely resembling acute respiratory distress syndrome, even when the initial cardiovascular examination is normal.
Case presentation
A previously healthy 24-year-old man presented with three days of progressive shortness of breath, productive cough, and fever.
During the preceding weeks, he had experienced:
• Unintentional weight loss
• Drenching night sweats
• Generalized malaise
• Left cervical lymphadenopathy
A lymph node biopsy and PET-CT performed approximately two weeks earlier were interpreted as reactive viral lymphadenitis. Testing also showed active Epstein-Barr virus infection.
On admission, the patient was severely hypoxemic, tachypneic, and febrile. His oxygen saturation was 84% while receiving 60% oxygen.
Pulmonary examination revealed widespread bilateral crackles. However, the cardiovascular examination was initially unremarkable:
• No audible heart murmur
• No elevated jugular venous pressure
• No peripheral edema
• No Janeway lesions
• No Osler nodes
• No splinter hemorrhages
• No other peripheral signs of infective endocarditis
Initial evaluation
The patient had severe hypoxemic respiratory failure, with a PaO₂/FiO₂ ratio of approximately 90 mmHg.
Laboratory findings included:
• White blood cell count of 18.6 × 10⁹/L
• Neutrophilia of 88%
• C-reactive protein of 180 mg/L
• Erythrocyte sedimentation rate of 65 mm/hour
• Procalcitonin of 4.2 ng/mL
• Normal troponin
Chest radiography demonstrated diffuse bilateral pulmonary infiltrates consistent with severe pulmonary edema or ARDS.
The initial diagnosis was presumed ARDS caused by viral infection with superimposed bacterial pneumonia. The patient received intravenous piperacillin-tazobactam but deteriorated and required endotracheal intubation.
Mechanical ventilation was managed with a lung-protective strategy, including tidal volumes of no more than 6 mL/kg predicted body weight and plateau pressures below 30 cm H₂O.
Blood cultures
Blood cultures obtained on admission became positive for Staphylococcus aureus on hospital day two.
Sensitivity testing confirmed methicillin-sensitive Staphylococcus aureus, and antibiotic therapy was changed to intravenous flucloxacillin.
The patient initially improved and was extubated on hospital day four.
Rapid deterioration after extubation
Within 12 hours of extubation, the patient experienced abrupt respiratory deterioration.
His oxygen requirements increased rapidly, requiring high-flow nasal oxygen, continuous positive airway pressure, and ultimately reintubation.
A repeat chest radiograph showed worsening bilateral pulmonary edema.
During repeat cardiovascular examination, clinicians detected new murmurs that had not been audible on admission:
• An early diastolic murmur along the left sternal border
• A pansystolic murmur at the cardiac apex
The combination of new murmurs and Staphylococcus aureus bacteremia immediately prompted echocardiographic evaluation.
Echocardiographic findings
Urgent transthoracic echocardiography revealed:
• Large mobile vegetations on the aortic valve
• Large mobile vegetations on the mitral valve
• Severe aortic regurgitation
• Severe mitral regurgitation
• Preserved left ventricular ejection fraction of 55%
• Elevated pulmonary artery systolic pressure of 55 mmHg
• Left atrial enlargement
Transesophageal echocardiography confirmed the findings and excluded a perivalvular abscess or fistula.
The severe aortic regurgitation had an effective regurgitant orifice area of 0.35 cm² and a regurgitant fraction of 55%.
The severe mitral regurgitation had an effective regurgitant orifice area of 0.45 cm² and a regurgitant fraction of 60%.
Diagnosis
The patient met two major modified Duke criteria:
• Staphylococcus aureus identified in two separate blood culture sets
• Echocardiographic evidence of endocardial infection with large vegetations and severe valvular regurgitation
These findings established a definite diagnosis of infective endocarditis.
The respiratory failure was primarily attributed to cardiogenic pulmonary edema resulting from acute destruction of both the aortic and mitral valves.
Emergency surgery
Because the patient had refractory heart failure caused by severe valvular regurgitation, he met a Class I indication for urgent surgery.
A multidisciplinary team involving critical care, cardiology, microbiology, and cardiothoracic surgery arranged emergency transfer to a tertiary cardiac center.
On hospital day six, the patient underwent emergency replacement of both the aortic and mitral valves.
Intraoperative examination confirmed:
• Large friable vegetations
• Extensive destruction of the aortic valve
• Extensive destruction of the mitral valve
• Active infective endocarditis
Because of the patient’s young age, mechanical prosthetic valves were implanted to provide greater long-term durability.
Outcome
The patient recovered without major postoperative complications.
His respiratory symptoms resolved, and he was discharged on hospital day 14.
Discharge treatment included:
• Six weeks of intravenous flucloxacillin
• Lifelong warfarin therapy
• Target international normalized ratio of 2.5 to 3.5
• Ongoing cardiology follow-up
• Anticoagulation clinic follow-up
Why the initial murmur may have been absent
The absence of a murmur on admission did not exclude acute severe valvular regurgitation.
In acute aortic regurgitation, rapid equalization of aortic and left ventricular diastolic pressures can shorten and soften the diastolic murmur.
In acute mitral regurgitation, a rapid rise in left atrial pressure can reduce the pressure gradient between the left ventricle and left atrium, resulting in a softer or abbreviated systolic murmur.
Tachycardia, tachypnea, respiratory distress, and mechanical ventilation can make these subtle murmurs even more difficult to hear.
The case therefore emphasizes the importance of repeated cardiovascular examinations in critically ill patients rather than relying on a single normal examination.
ARDS versus cardiogenic pulmonary edema
The patient’s initial presentation met clinical criteria for severe ARDS, but the bilateral pulmonary infiltrates were ultimately caused primarily by acute cardiogenic pulmonary edema.
Several findings favored a cardiac cause:
• Staphylococcus aureus bacteremia was present on admission
• Sputum cultures were negative
• Large vegetations were present on two valves
• Severe aortic and mitral regurgitation developed
• Respiratory failure rapidly recurred after extubation
• Pulmonary edema worsened despite treatment for pneumonia and ARDS
The authors acknowledged that bacterial pneumonia, ARDS, and cardiogenic pulmonary edema may have contributed simultaneously.
An admission NT-proBNP level and early bedside echocardiography might have helped distinguish these possibilities sooner.
Potential effect of fluid resuscitation
Standard sepsis treatment frequently includes aggressive intravenous fluid administration.
However, large fluid volumes may precipitate or worsen pulmonary edema in patients with unrecognized severe aortic or mitral regurgitation.
This case demonstrates the importance of assessing cardiac function before continuing aggressive fluid resuscitation in septic patients with unexplained respiratory failure.
Possible source of infection
The patient denied intravenous drug use and had no known preexisting cardiac disease.
The cervical lymph node biopsy performed approximately two weeks before admission was considered a possible source of transient Staphylococcus aureus bacteremia, although a causal relationship could not be proven.
The concurrent active Epstein-Barr virus infection may also have produced immune dysfunction or created a misleading alternative explanation for the patient’s constitutional symptoms and pulmonary findings.
Dual-valve involvement
Simultaneous aortic and mitral valve infection is uncommon but can occur through contiguous spread along the aortomitral curtain.
The aortomitral curtain is the fibrous continuity between the posterior aortic root and the anterior mitral valve leaflet.
Infection can spread directly from one valve to the other through this anatomical connection.
Recognition of dual-valve involvement is important because it increases disease severity and significantly affects surgical planning.
Clinical implications
Clinicians should consider infective endocarditis in patients with unexplained respiratory failure, particularly when blood cultures identify Staphylococcus aureus.
Important lessons include:
• A normal initial cardiovascular examination does not exclude infective endocarditis.
• Acute severe valvular regurgitation may produce soft or absent murmurs.
• Cardiogenic pulmonary edema can closely resemble ARDS.
• Staphylococcus aureus bacteremia should prompt early echocardiography.
• Serial cardiovascular examinations are essential in deteriorating patients.
• Early transthoracic and transesophageal echocardiography can identify valvular destruction before irreversible deterioration occurs.
• Aggressive fluid administration may worsen respiratory failure when severe valvular regurgitation is present.
• Rapid multidisciplinary evaluation and urgent surgery can be lifesaving.
Important limitations
This report describes a single patient, so its findings cannot determine how frequently infective endocarditis presents primarily as respiratory failure.
The precise cause of the initial pulmonary infiltrates could not be established with certainty. The presentation may have represented cardiogenic pulmonary edema, ARDS, bacterial pneumonia, or a combination of these processes.
NT-proBNP was not measured, and echocardiography was not performed during the initial admission assessment. Both might have allowed earlier differentiation between pulmonary and cardiac causes of respiratory failure.
Bottom line
Infective endocarditis can cause acute severe aortic and mitral regurgitation that presents primarily as respiratory failure and bilateral pulmonary infiltrates.
The absence of a murmur or peripheral signs of endocarditis at presentation does not rule out the diagnosis.
In patients with unexplained acute respiratory failure and Staphylococcus aureus bacteremia, early bedside echocardiography and repeated cardiovascular examinations are essential.
Prompt recognition of severe valvular destruction, immediate multidisciplinary consultation, and emergency valve surgery were lifesaving in this young patient.
Thank you to Cureus for allowing us to summarize this article.