Isolated Pulmonic Valve Infective Endocarditis: A Persistent Challenge

Hamza, Nadir; Ortiz, Jose; Bonomo, Robert A.

doi:10.1007/s15010-004-3022-3

Cited by 50 publications

(41 citation statements)

References 32 publications

(27 reference statements)

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“…Only one of seven isolates was resistant to ampicillin, which is consistent with the rates of ampicillin resistance (between 0.9 and 2.7%) observed in E. faecalis isolates in the United States (5,8). The mechanism of resistance to ampicillin in the isolate from patient 5 ( Table 2) was not mentioned in the case report (7). Most patients were treated with either ampicillin or penicillin, and synergistic bactericidal combination therapy with an aminoglycoside was given to four patients.…”

supporting

confidence: 80%

“…In the six previously reported cases of VR E. faecalis in our review, only two of the patients were treated with linezolid ( Table 2, patients 5 and 6). Patient 5 was treated with linezolid for 6 weeks because he had an ampicillin-resistant strain of VR E. faecalis (7). He had multiple negative surveillance blood cultures during antibiotic therapy, although he died from an unknown cause 1 week after completion of linezolid therapy.…”

mentioning

confidence: 99%

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Vancomycin-Resistant Enterococcus faecalis Endocarditis: Linezolid Failure and Strain Characterization of Virulence Factors

et al. 2007

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supporting

confidence: 80%

mentioning

confidence: 99%

Vancomycin-Resistant Enterococcus faecalis Endocarditis: Linezolid Failure and Strain Characterization of Virulence Factors

et al. 2007

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“…5,6 An even smaller proportion of all cases of IE, ≈1.5 to 2.0%, are isolated to the pulmonic valve. 3,7,8 The highest-risk group for right-sided endocarditis has long been recognized as intravenous drug users; however, patients with pre-existing valvular disease, patients with congenital heart disease, and those with intracardiac devices are also at increased risk. 9 The clinical manifestations of right-sided IE are similar to those of left-sided IE, including fever, malaise, and immune complications.…”

Section: Discussionmentioning

confidence: 99%

No Right Answer

et al. 2015

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2259 ForewordInformation about a real patient is presented in stages (boldface type) to an expert clinician (Dr Adler), who responds to the information, sharing his reasoning with the reader (regular type). A discussion by the authors follows. P atient presentation: Mr H is a 61-year-old man with a medical history significant for hypertension, hyperlipidemia, and benign prostatic hyperplasia who was admitted to the medical service with a chief complaint of fevers. Eleven years before presentation, the patient underwent a prostate biopsy for a rapidly rising prostate-specific antigen, and there was no evidence for malignancy. The biopsy was complicated by septicemia, which was treated with antibiotics. Four months before admission, the patient presented to the urology clinic with worsening urinary retention, and the decision was made to proceed to transurethral resection of the prostate. A preoperative workup was significant only for a urine culture growing 1000 colonies of enterococcus, and no antimicrobial treatment was given. He underwent a technically successful transurethral resection of the prostate and was discharged home the next day after passing a voiding trial.Two days after being discharged, the patient had fevers to 102°F and was readmitted to the hospital. He was found to have an Enterococcus faecalis urinary tract infection and was treated with 1 day of intravenous cefepime before being discharged the next day on a 7-day course of amoxicillin-clavulanic acid. On the day after discharge, blood cultures that were drawn on admission grew E faecalis with the same susceptibility pattern cultured from the urine, but there was no alteration in the treatment plan. The patient's fevers resolved.One month before admission, the patient presented to an outside emergency department with decreased exercise capacity, pleuritic back pain, and malaise. Computed tomography of the chest with contrast identified a right upper-lobe consolidation (Figure 1), and a 10-day course of levofloxacin was prescribed for presumed communityacquired pneumonia. His fever improved, but his shortness of breath progressed, and he became symptomatic with even minimal exertion. On the day of admission, he developed a fever of 101°F and went to the emergency department for further care.On presentation to our hospital, the patient's physical examination revealed a temperature of 101.1°F, heart rate of 140 bpm and regular, blood pressure of 141/74 mm Hg, respiratory rate of 18 breaths per minute, and oxygen saturation of 93% on room air. The neck veins were elevated to 10 cm H 2 O with prominent a and v waves. The carotid upstrokes and volumes were normal. The lungs were clear to auscultation. The point of maximal impulse was displaced laterally. There was a normal-sounding S1 and a physiologically split S2. A grade II/IV decrescendo diastolic murmur was loudest at the left upper sternal border and could be heard equally well supine and upright. There was no S3. Peripheral pulses were normal. There was trace ankle edema. He denied any his...

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“…For the competitive athlete, the Special Task Force report 34 recommends that PS patients with gradients Ͻ50 mm Hg may participate in all competitive sports; those with severe PS should only participate in low-intensity sports. Pulmonary endocarditis is rare, 35 and some recommend prophylaxis only with a Ͼ25 mm Hg gradient. 36 The guidelines continue to endorse endocarditis prophylaxis, however, 37 although it is anticipated that newer revisions of the guidelines will not recommend it.…”

Section: Following Up the Unoperated Patient With Pv Stenosismentioning

confidence: 99%

Adult Congenital Heart Disease

Bashore

2007

Circulation

127

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It has variably been estimated that between 800 000 and 1 million patients with congenital heart disease are now adults and that by 2010 more patients older than 16 years will undergo surgery for congenital heart disease than those younger than 16 years. 1 This review will focus on the clinical aspects of identifying and caring for the portion of the unique population that have right ventricular (RV) outflow tract lesions. Clinical Morphology of the RV Outflow TractThe left ventricle (LV) and RV both have inlet, apical, and outlet portions, although they differ considerably. 2 The inlet of the RV includes the tricuspid valve, and it is separated from the pulmonary valve (PV) by the crista supraventricularis. This structure results in the PV being raised upward. The apical portion of the RV has coarse trabeculations. As shown in Figure 1, the septum is home to a large septomarginal (septal) trabeculation that divides into the anterior and posterior limbs in the outflow tract. A series of septoparietal trabeculations arise along the free wall. The crista supraventricularis inserts between these limbs and is made up of 3 components: the muscular outlet septum, the ventriculoinfundibular fold, and the inner curvature of the RV. 3 The small part that separates the RV and LV cavities is the outlet or conal septum. A loop including the septal trabeculation, the moderator band, septoparietal trabeculations, and the outlet septum can be conceptualized as circling the RV outflow tract. The PV is supported by the circular muscular infundibulum rising outside the RV proper. Abnormalities involving the RV outflow tract involve malpositioning of 1 or more of these structures.

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Isolated Pulmonic Valve Infective Endocarditis: A Persistent Challenge

Cited by 50 publications

References 32 publications

Vancomycin-Resistant Enterococcus faecalis Endocarditis: Linezolid Failure and Strain Characterization of Virulence Factors

Vancomycin-Resistant Enterococcus faecalis Endocarditis: Linezolid Failure and Strain Characterization of Virulence Factors

No Right Answer

Adult Congenital Heart Disease

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