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Background Infection is one of the most common complications of Left Ventricular Assist Devices (LVADs). Pseudomonas aeruginosa (PsA) LVAD infections in particular are challenging due to limited antibiotic options and tendency to form biofilm making eradication difficult. In this study we examined the implications of bacteremia in patients with PsA LVAD infections. Methods This was a retrospective study of patients treated at our institution between July 1, 2007 and February 1, 2021 who had proven or probable driveline infection (DLI), pump pocket, or pump/cannula infection due to PsA according to International Society for Heart & Lung Transplantation criteria. Results Of 717 patients with an LVAD, 51 patients had had proven or probable VAD-specific infections due to PsA.16/51 (31%) had Pseudomonas bloodstream infection associated with the VAD infection, with a median 400 days from initial diagnosis. Only 29% of those with DLI were bacteremic, vs. 66% of those with pump pocket infection, and 50% of those with mediastinitis (Fig 1). Patients who developed bacteremia had a median of 3 episodes (range, 1-5). All but 1 patient with bacteremia received surgery. Of the 16 patients who developed bacteremia, 11 (69%) died vs 9/35 (26%) in patients who were not bacteremic (Fig 2). 10/11 patients who were bacteremic and died had infections limited to driveline. In 21/41 (51%) of episodes of bacteremia identified, patients were already on antibiotics for PsA with a median duration of 49 days (7-198) prior to onset of bacteremia. Conclusion A significant number of patients with PsA LVAD infections develop bacteremia, especially in those with involvement of central LVAD components. The presence of bacteremia should prompt evaluation for ascending infection. Most of the patients who developed bacteremia died, even when infection appeared limited to driveline, and it is possible that endoluminal infections were present in these cases. A substantial proportion of patients with bacteremia were on antibiotics at the time of bacteremia, which suggests that suppressive antibiotics alone may not be effective in controlling PsA LVAD infections. Disclosures All Authors: No reported disclosures.

Background Ventricular assist device (VAD) infections caused Pseudomonas aeruginosa (PA) are difficult to treat given limited antibiotic options, development of resistance and biofilm formation in the presence of retained hardware. We looked at outcomes of patients who developed Pseudomonas aeruginosa LVAD infection (PA-LVADI) Methods Single center retrospective study of patients older than 18 years who received LVAD from 7/1/2007 to 2/1/2021 and subsequently developed PA-LVADI. Patients with proven or probable VAD-specific infections: driveline infection (DLI), pump pocket, and pump/cannula infections were included. The cumulative incidences of death, transplant, and LVAD explant, following Pseudomonas aeruginosa infection, were evaluated as competing outcomes. Fig 1:Classification of Pseudomonas aeruginosa LVAD Infections at diagnosisFigure 3:Cumulative incidence of death, transplant, or explant following Pseudomonas aeruginosa LVAD infection Results 51 patients with VAD-specific PA-LVADI were identified (Fig 1). Median age at the time of first LVAD placement was 55 years (23 – 74). Of the 28 patients ever listed for transplant, 13 (46%) received heart transplant, 8 (29%) were delisted, 7 (25%) were alive on transplant list (Fig 2). The median number of days from LVAD placement to first PA infection was 587 (54 – 3389). 30 (59%) had PA as the first causative organism. The extent of first PA-LVADI was superficial DLI in 43(84%), deep DLI in 5 (10%), pump pocket in 2(4%) and pump/cannula in 1(2%). 46 (90%) of patients received intravenous (IV) therapy with median duration of 84 (2 – 525) total IV antibiotic days. Antibiotic resistance emerged in 25/51 (49%) patients, with 32% being multi-drug resistant (MDR). Surgery was performed in 30 (58%). 12/13 who received heart transplants were followed for at least 1 year post-transplant and all were alive. 5 of the remaining 38 patients underwent pump exchange or explant. 20/38 (53%) of patients who were not transplanted died (Fig 3). Conclusion This is the largest study on PA-LVADI to date. We noted significant morbidity and mortality, with 90% of patients requiring prolonged IV antibiotics and over half requiring surgical treatment. Drug resistance emerged in a significant proportion of patients. Survival after transplant was excellent, but by 2 years of infection over half of the patients have been transplanted, explanted, or died. Disclosures All Authors: No reported disclosures.

A patient in Pennsylvania, USA, with common variable immunodeficiency sought care for fever, cough, and abdominal pain. Imaging revealed lesions involving multiple organs. Liver resection demonstrated necrotizing granulomas, recognizable tegument, and calcareous corpuscles indicative of an invasive cestode infection. Sequencing revealed 98% identity to a Versteria species of cestode found in mink.

Background Herpes simplex virus (HSV) is the most common cause of infectious encephalitis in the United States. While early treatment with acyclovir has improved acute management, long-term morbidity and mortality remain high and warrant further characterization. Methods We retrospectively identified adult patients (≥18 years) with HSE admitted to the Cleveland Clinic Main Campus and affiliated regional hospitals from April 2006 to June 2016. HSE diagnosis was concordant with Infectious Disease Society of America Encephalitis Guidelines. HSE diagnosis was confirmed in that HSV-1 DNA was detected in cerebrospinal fluid (CSF) by polymerase chain reaction (PCR) assay for all patients included in this study. Patients for which HSV-2 was detected in the CSF were excluded to avoid inclusion of HSV meningitis. Clinical information was collected in a REDCap database and analyzed by descriptive statistics. Patients were indexed at the date of admission, and Kaplan–Meier analysis was used to estimate overall survival. Results We identified 32 patients with confirmed HSE. The median patient age was 62 years (interquartile range [IQR] 45–72). All patients received treatment with intravenous (IV) acyclovir, with a median treatment duration of 24 days (IQR 19–30). The median time from initial symptom onset to IV acyclovir treatment was 5 days (IQR 3–8). Three patients (9%) died during the hospitalization course, 16 (50%) were discharged to a nursing facility, 11 (35%) returned home, and two (6%) transitioned to an acute care facility (Figure 1). Within three months of discharge, 15 (47%) patients were readmitted, six (19%) of which readmitted for HSE relapse. The overall survival rate at one month was 84% and 74% at 12 months (Figure 2). At outpatient follow-up, cognitive deficits were self-reported by 19 (66%) patients, followed in frequency by motor (31%) and sensory deficits (7%). Conclusion Despite appropriate treatment with IV acyclovir, HSE survivors frequently experienced severe morbidities after initial hospitalization, including HSE relapse, discharge to long-term care facilities, and neurocognitive impairment. Risk of death was highest within one month of admission. Further investigation is needed to optimize treatment of HSE to improve mortality and to reduce permanent neurologic deficits. Disclosures All Authors: No reported Disclosures.

Background A 68-year-old woman with hypogammaglobulinemia and prior treated lymphoma presented with fever and abdominal pain. Evaluation revealed numerous nodules in the lung, eye, brain, and liver (Figure 1). Initial lung and liver biopsies showed necrotizing granulomas with no organisms and negative serology and cultures. After progression while on broad-spectrum antibiotics for 4 months, an open liver biopsy revealed numerous nodular lesions and a mass made up of multifocal coalescing cystic lesions. The mass consisted of a degenerating 3-layered membrane without scoleces characterized by a wavy protuberant ciliated eosinophilic outer layer, subjacent degenerating cells with pyknotic nuclei, and loose connective tissue suggestive of a bladder wall and calcareous corpuscles in a matrix of granulomatous inflammation with areas of necrosis (Figure 2). This was diagnostic of disseminated metacestodes (larval stage) of a cestode (tapeworm). Treatment with praziquantel and albendazole led to improvement of symptoms and lesions. Disseminated cestode infections other than due to Echinococcus species are rare in humans. Sequencing was pursued due to the unusual findings. Methods DNA was extracted from liver tissue followed by targeted amplification of the cestode COX1 gene. PCR products confirmed to be 134 bp, as expected for a cestode COX1 gene, then inserted into a 2.1 Topo vector and cloned. Five separate isolates were sequenced, and 4 were interpretable. The 129-bp consensus sequence is shown in Figure 3. Basic Local Alignment Search Tool (NCBI BLAST) was used to find highly similar sequences. Results The sequence matched to Versteria sp. (T. mustelae) COX1 gene from a mink in Oregon (accession KT223034) with 98% identity. Conclusion Metacestodes have the propensity to proliferate and rarely disseminate. There is one reported case of Versteria sp. causing a lethal disseminated infection of an orangutan. This is the first report of a Versteria sp. disseminated infection in a human and is singular because the patient survived. The patient likely accidentally ingested ova shed from a tapeworm in a mink or similar mammalian host. Histopathologic assessment is crucial in diagnosing cestode infection. COX1 gene sequencing is useful for cestode identification. Disclosures All authors: No reported disclosures.

Objectives Propionibacterium acnes remains a rare cause of infective endocarditis (IE). It is challenging to diagnose due to the organism's fastidious nature and the indolent presentation of the disease. The purpose of this study was to describe the clinical presentation and management of P. acnes IE with an emphasis on the methods of diagnosis. Methods We identified patients from the Cleveland Clinic Infective Endocarditis Registry who were admitted from 2007 to 2015 with definite IE by Duke Criteria. Propionibacterium acnes was defined as the causative pathogen if it was identified in at least two culture specimens, or identified with at least two different modalities: blood culture, valve culture, valve sequencing or histopathological demonstration of microorganisms. Results We identified 24 cases of P. acnes IE, 23 (96%) of which were either prosthetic valve endocarditis or IE on an annuloplasty ring. Invasive disease (71%) and embolic complications (29%) were common. All but one patient underwent surgery. Propionibacterium acnes was identified in 12.5% of routine blood cultures, 75% of blood cultures with extended incubation, 55% of valve cultures, and 95% of valve sequencing specimens. In 11 of 24 patients (46%), no causative pathogen would have been identified without valve sequencing. Conclusions Propionibacterium acnes almost exclusively causes prosthetic valve endocarditis and patients often present with advanced disease. The organism may not be readily cultured, and extended cultures appear to be necessary. In patients who have undergone surgery, valve sequencing is most reliable in establishing the diagnosis.

Aminoglycosides are a mainstay of treatment for enterococcal infective endocarditis. However, the benefit of adding aminoglycosides to cell wall-active agents after surgery is unclear. The aim of this study was to determine if adjunctive aminoglycoside treatment after surgery for enterococcal endocarditis leads to better outcomes. We included patients who underwent surgery for enterococcal endocarditis at our institution between July 2007 and July 2014. Treatment was defined as at least 1 dose of an aminoglycoside after surgery. Propensity to receive aminoglycosides was calculated in a model that included age, native vs prosthetic valve endocarditis, chronic kidney disease, high-level aminoglycoside resistance, metastatic infection, invasive disease, positive valve culture, and creatinine on the day of surgery. A multivariable Cox proportional hazards model was used to compare the primary outcome of death, adjusted for propensity to receive aminoglycosides, among patients who did and did not receive aminoglycosides. A total of 108 patients were identified of whom 37 (34%) received at least 1 dose of an aminoglycoside after surgery, with a median duration of 5 days (interquartile range: 2.5-10). In the multivariable model, patients treated with adjunctive aminoglycoside therapy had better survival than those treated with a cell wall-active agent alone, although the difference did not reach statistical significance (hazard ratio = 0.65, 95% CI: 0.32-1.33). The survival difference was consistently present in subgroups stratified by all-purpose refined diagnosis-related group mortality risk, and with varying definitions of aminoglycoside therapy. In conclusion, antibiotic monotherapy with a cell wall-active agent after surgery for enterococcal endocarditis may be inferior to combination therapy including an aminoglycoside.