Journal of Postgraduate Medicine
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Year : 2023  |  Volume : 69  |  Issue : 2  |  Page : 105-107  

Native tricuspid valve endocarditis presenting as pyrexia of unknown origin

S Singh, A Goel 
 Department of Medicine, Lady Hardinge Medical College and Dr. Ram Manohar Lohia Hospital, Delhi, India

Correspondence Address:
Dr. S Singh
Department of Medicine, Lady Hardinge Medical College and Dr. Ram Manohar Lohia Hospital, Delhi


Native tricuspid valve endocarditis is quite rare without any predisposing factors and poses a diagnostic challenge because of fewer cardiac symptoms and lesser peripheral manifestations. This is a case report of a 25-year-old female who presented with high-grade fever, dry cough, decreased appetite, and weight loss for 1 month with no history of intravenous drug use or evidence of underlying cardiac abnormality and was diagnosed with native tricuspid valve endocarditis.

How to cite this article:
Singh S, Goel A. Native tricuspid valve endocarditis presenting as pyrexia of unknown origin.J Postgrad Med 2023;69:105-107

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Singh S, Goel A. Native tricuspid valve endocarditis presenting as pyrexia of unknown origin. J Postgrad Med [serial online] 2023 [cited 2023 Sep 23 ];69:105-107
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Pyrexia of unknown origin (PUO) refers to prolonged febrile illness without an established etiology despite intensive evaluation and diagnostic testing. The diagnosis of PUO is always challenging and despite best efforts remains undiagnosed in 30%–50% of cases.[1] Infective endocarditis (IE) constitutes less than 5% of all cases of PUO.[2] Isolated native tricuspid valve endocarditis (TVE) is quite uncommon in an immunocompetent adult in the absence of risk factors.[3] We present an interesting case of PUO secondary to native TVE in a young female without any predisposing factors.

 Case Report

A 25-year-old female with no prior comorbidities presented to our hospital with high-grade intermittent fever, dry cough, decreased appetite, and weight loss for 1 month. There was a history of spontaneous abortion 6 months back, for which dilatation and curettage were done at a private hospital, and the patient was discharged within 2 days. There was no history of any high-risk behavior, intravenous drug use, or history suggestive of rheumatic fever or congenital heart disease. The patient had been extensively investigated in a private hospital for fever, but no conclusive diagnosis was established.

At admission, she had a fever of 100.1 F and pallor. Her spleen was palpable two finger breadths below the costal margin and was nontender and firm in consistency. Chest auscultation revealed normal vesicular breath sounds, and cardiac auscultation revealed normal S1 and S2 without any significant murmur. The rest of the physical examination was unremarkable.

Initial laboratory investigations [Table 1] showed normocytic normochromic anemia, neutrophilic leucocytosis, elevated inflammatory markers, and raised procalcitonin. Routine biochemical tests including liver and kidney function tests and urine microscopic examination were normal. Initial chest X-ray showed no abnormalities, and electrocardiogram showed sinus tachycardia. Serology for enteric fever, viral infections, human immunodeficiency virus (HIV), and autoimmune diseases were negative. Tuberculosis workup of induced sputum and Mantoux were negative. Urine and blood cultures were noncontributory, and ultrasonography of the abdomen revealed splenomegaly.{Table 1}

The patient was started empirically on injection ceftriaxone but showed no improvement. Chest X-ray [Figure 1] was repeated after 1 week, which showed opacities in the right middle and lower zone with right costophrenic (CP) angle blunting. Computed tomography (CT) chest [Figure 2] was done which revealed bilateral posterior-basal lung cavitation and consolidation with bilateral pleural effusion. Diagnostic thoracentesis was done showing exudative pleural fluid with negative culture for tuberculosis{Figure 1}{Figure 2}

In view of persistent pyrexia and leucocytosis, a possibility of septic pulmonary emboli was kept, and 2D echocardiography was performed to look for evidence of infective endocarditis. Echocardiography [Figure 3] revealed a vegetation of 1.5 × 1.8 cm on the anterior tricuspid valve leaflet with severe tricuspid regurgitation with right ventricular systolic pressure (RVSP) of 30 mm Hg and ejection fraction (EF) of 55%–60%. Fundus examination was normal. Repeated blood cultures showed growth of Staphylococcus aureus sensitive to oxacillin and vancomycin. With fulfillment of one major criteria along with three minor criteria including high-grade pyrexia, pulmonary infarcts, and positive blood culture, a definite diagnosis of native TVE was made using modified Dukes criteria.{Figure 3}

The patient was started on treatment for IE but continued to remain febrile even after 7 days. A workup for fungal IE was carried out, but serum galactomannan and two fungal cultures were negative. The patient was started on injection amphotericin empirically but continued to remain febrile even after 3 weeks of antifungal therapy. The patient was transferred to the department of cardiothoracic surgery where she underwent computed tomography (CT) cardiac angiography showing intracardiac mass enhancing lesion of size 2.3 × 2.3 × 1.5 cm, arising from tricuspid valve causing partially valve stenosis.

The patient underwent surgery with partial valve repair and became afebrile after 2 days of the surgery. Histopathological examination of the tissue [Figure 4] showed fibrinosuppurative exudate, with numerous bacterial colonies and interspersed with acute inflammatory cells infiltrate. No granuloma or fungal profile was seen in any section. The culture of the specimen showed growth of Staphylococcus aureus.{Figure 4}


Infective endocarditis constitutes less than 5% of the cases of PUO.[2] Left-sided IE is more common than right-sided IE. Right-sided IE accounts for approximately 5 to 10 percent of all IE cases.[4] Among patients with right-sided IE, the tricuspid valve is involved in approximately 90 percent of cases, and the remaining is due to pulmonic valve involvement.[5] Risk factors for right-sided IE include injection drug use (IDU), the presence of a cardiac implantable electronic device (CIED) or other intravascular devices, and the presence of an underlying right-sided cardiac anomaly. Case reports describing native TVE in an immunocompetent young adult without any predisposing factors or apparent symptoms and signs of endocarditis are extremely rare.

Patients with isolated right-sided IE often have faint or no cardiac murmur, and signs of systemic embolization as seen in left-sided IE are notably absent making the task of diagnosis even more challenging.[6] Fever is the most common symptom seen in up to 90% of patients. Other symptoms include malaise, headache, myalgias, arthralgias, night sweats, anorexia, and weight loss. Septic pulmonary emboli are common in up to 75 percent of patients with tricuspid involvement. These emboli manifest as nodular pulmonary infiltrates, cavitation, and occasionally empyema mimicking a respiratory tract infection, thus making the diagnosis difficult. Persistent fever associated with pulmonary events, anemia, and microscopic hematuria is known as “tricuspid syndrome,” and should alert physicians for right-sided endocarditis.[7]


The majority of patients with TVE have a history of drug use, pre-existing congenital heart disease, or an acquired valvular lesion. TVE without any predisposing factors is relatively rare. Our patient represents the subset of individuals without a history of intravenous drug use or any evidence of underlying cardiac abnormality. Hence, there should be a high index of suspicion of TVE in cases of PUO who have pulmonary infiltrates and anemia even without any risk factors, and echocardiography should be done at the earliest to confirm the diagnosis.

Declaration of patient consent

The authors certify that appropriate patient consent was obtained.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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