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SESSION TITLE: Procedures in Chest Infections Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Pneumocystis jirovecii pneumonia (PJP) is known to cause potentially life-threatening pneumonia in patients on immunosuppressive therapy. Here we describe a case of an elderly man on low dose methotrexate with PJP pneumonia initially mistaken for drug induced pneumonitis. CASE PRESENTATION: A 79 year old man with T-cell large granular lymphocytic leukemia on methotrexate, indeterminate colitis on azathioprine and sulfasalazine and interstitial lung disease was admitted for 3 week history of worsening dyspnea, lethargy and cough. On arrival his oxygen saturation was 87% on room air, requiring 5 liters oxygen via nasal canula. Lung examination was notable for bilateral crackles. Laboratory studies showed white blood cell count 12.4k/μL, lactate 2.7mmol/L, procalcitonin 0.137ng/mL, lactate dehydrogenase(LDH) 925 IU/L, 1,3 β-D glucan elevated at 154pg/mL. Infectious work up including COVID-19 testing was unremarkable. Chest radiograph showed bilateral diffuse interstitial infiltrates (figure 1) and computed tomography (CT) scan showed peripheral reticular changes and patchy ground glass opacities bilaterally (figures 2;3). He was initially treated for possible bacterial pneumonia;then with 125mg of methylprednisolone for presumed methotrexate induced pneumonitis without improvement. He underwent bronchoscopy with bronchoalveolar lavage(BAL) gram stain showing numerous histiocytes and scattered lymphocytes;no infectious organisms were isolated. PJP PCR from BAL came back positive and trimethoprim-sulfamethoxazole (TMP-SMX) was started. Despite maximum therapy he deteriorated clinically, transitioned to comfort care and expired. DISCUSSION: Diagnosis of PJP is made by visualization of cystic or trophic forms in respiratory tissue obtained via biopsy, BAL or sputum. Fungal burden is typically lower in non-HIV patients with PJP, and may result in negative BAL or sputum stain. Thus PCR testing is a useful diagnostic tool. Positive PCR alone cannot distinguish between colonization and active disease, and should be performed when clinical suspicion is high. 1,3 β-D glucan and LDH are nonspecific markers that help in presumptive diagnosis. First line therapy for PJP is TMP-SMX, with atovaquone, dapsone and pentamidine available as alternative therapies. Duration of therapy should be at least 21 days. Adjunctive corticosteroids show survival benefit in HIV-infected individuals. In severely hypoxic patients, corticosteroids are beneficial if started within 72 hours of antibiotic initiation. Their use in non-HIV PJP cases remains controversial. CONCLUSIONS: This case highlights the risk of PJP with long term methotrexate therapy. Cough, hypoxemia and bilateral interstitial infiltrates should prompt work-up for PJP. Timely recognition and early treatment are crucial to prevent mortality. Further studies are needed to assess the efficacy and provide guidelines for primary prophylaxis in this population. Reference #1: Wilson JW, Limper AH, Grys TE, Karre T, Wengenack NL, Binnicker MJ. Pneumocystis jirovecii testing by real-time polymerase chain reaction and direct examination among immunocompetent and immunosuppressed patient groups and correlation to disease specificity. Diagn Microbiol Infect Dis. 2011 Feb;69(2):145-52. doi: 10.1016/j.diagmicrobio.2010.10.021. PMID: 21251557;PMCID: PMC6855182. Reference #2: Salzer HJF, Schäfer G, Hoenigl M, Günther G, Hoffmann C, Kalsdorf B, Alanio A, Lange C. Clinical, Diagnostic, and Treatment Disparities between HIV-Infected and Non-HIV-Infected Immunocompromised Patients with Pneumocystis jirovecii Pneumonia. Respiration. 2018;96(1):52-65. doi: 10.1159/000487713. Epub 2018 Apr 10. PMID: 29635251 DISCLOSURES: No relevant relationships by Rutendo Jokomo-Nyakabau No relevant relationships by Richard Swaney No relevant relationships by Manasa Velagapudi
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Introduction: Blastomyces species are thermally dimorphic fungi endemic to North America, especially areas bordering the Mississippi, Ohio and St. Lawrence rivers, and the Great Lakes. Blastomycosis infections are estimated to occur in 3-13% in the pediatric population. Pediatric literature for blastomycosis has been mostly limited to small studies and case series. Recent literature suggests increasing rates of infections, less morbidity and mortality as compared to adults, with asthma as the most common comorbid condition. Although pulmonary disease is the most common presentation, it rarely progresses to acute respiratory distress syndrome (ARDS). Case Description: A 17- year-old female, living in the Chicago area, and with type 1 diabetes mellitus and childhood asthma, presented to the emergency room with acute hypoxemic respiratory failure after 14 days of cough, dyspnea, chest pain, and fevers as high as 105°F. Her initial radiographic imaging revealed bilateral infiltrates and consolidations in the right middle and lower lobes. She was admitted to the step down unit for further care. A respiratory viral panel, including COVID-19 evaluation, was negative. She was started on low-flow nasal cannula, ceftriaxone, azithromycin, albuterol, and maintenance IV fluids. On hospital day 2, she was transferred to the pediatric intensive care unit for worsening respiratory distress and escalated to high-flow nasal cannula. She was treated empirically for presumed bacterial pneumonia with ceftriaxone (7-day course), azithromycin (5-day course), cefepime (5-day course), clindamycin (2-day course), and vancomycin (14-day course). Despite this treatment, repeat chest imaging showed worsening disease and she required escalation to BiPAP for progression of her ARDS and impending respiratory failure. Karius testing results indicated Blastomyces dermatitidis at low levels typically not clinically relevant. Sputum and bronchoalveolar lavage cultures demonstrated no significant pathogenic bacteria. Pathology exam of the biopsy obtained from bronchoscopy was consistent with Blastomyces. Urine antigen test was positive for both Blastomyces and Histoplasma. She clinically improved after initiating Amphotericin B lipid complex (6-day course), with transition to oral itraconazole and adjunctive therapy with IV methylprednisolone. She was discharged home after a 30-day hospital stay. Discussion: Pulmonary blastomycosis presents with a broad variety of signs and symptoms. Timely diagnosis is challenging. Pulmonary blastomycosis has no pathognomonic radiographic patterns. Severe acute pulmonary infection that fails to respond to antibacterial treatment should prompt investigation for fungal infection, including urine antigen tests for Histoplasma and Blastomyces, serum galactomannan, beta-1,3-D-glucan, and next-generation sequencing of microbial cell-free DNA (eg, Karius test). Close respiratory monitoring should occur in a pediatric intensive care unit. Conclusion: Blastomycosis is not typically in the initial differential diagnosis unless the patient has other clinical findings, fails to improve on antibacterial therapy, or has identified risk factors for exposure. Failure of prompt recognition is associated with poor outcomes, increased morbidity and mortality, increased length of hospital stay, and cost.
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CASE: A 75-year-old male with history of sarcoidosis, heart failure, atrial fibrillation, hypertension, and mitral valve replacement presented to the emergency department with dyspnea and dry cough for one week. He endorsed fatigue and chills, but denied subjective fever, weight loss, edema, or congestion. Vitals were notable for a temperature of 100.3 F, respiratory rate of 25, and SpO2 of 82% on room air, which increased to 95% on 10 L of oxygen. Physical exam revealed clear lung sounds bilaterally without accessory muscle use. Labs showed a leukocytosis of 15.6, hemoglobin of 11.6, and pro-BNP of 631.2. ABG revealed compensated respiratory alkalosis. BMP, troponin, EKG, and COVID-19 PCR tests were all unremarkable. Of note, the patient had been on prednisone 10 mg daily for the past four years for sarcoidosis which was increased to 20 mg daily one month prior. After admission, further work-up revealed elevations in pro-calcitonin of 0.61, LDH of 396, and 1,3-beta-D-glucan of >500. Chest CT revealed bilateral scattered ground-glass opacities and underlying evidence of chronic interstitial disease. The patient was continued on a higher dose of prednisone 40 mg twice daily and started on atovaquone 750 mg twice daily for empiric Pneumocystis jiroveci pneumonia (PJP) therapy. Unfortunately, he continued to deteriorate and required intubation. His bronchoalveolar lavage fluid returned positive for Pneumocystis jiroveci by DFA. The patient was started on high- dose TMP-SMX. However, he developed DIC, bilateral upper extremity DVTs, and hyperkalemia thought to be secondary to TMP-SMX. The family decided to withdraw care and the patient passed. IMPACT/DISCUSSION: The role of Pneumocystis jiroveci pneumonia (PJP) prophylaxis in non-HIV patients on chronic steroids remains poorly elucidated and lacks evidence in literature. While some experts support prophylaxis for those on daily prednisone equivalents of greater than 20 mg for over 4 weeks, others suggest that daily prednisone equivalents of greater than 30 mg for over 12 weeks should warrant prophylaxis. We describe a patient with sarcoidosis who was on 20 mg of daily prednisone for over 4 weeks without PJP prophylaxis and subsequently died while battling PJP. Nearly 53% of PJP infections occur in nonHIV patients. Studies in patients with leukemia or organ transplant have shown that PJP prophylaxis with TMP-SMX decreases PJP occurrence by 85% and PJP-related mortality by 83%. The scarcity of literature on the use of PJP prophylaxis, particularly in those with chronic lung diseases such as sarcoidosis that require prolonged steroids, impedes timely consideration of PJP prophylaxis and poses a significant risk to these patients. CONCLUSION: We describe a patient with sarcoidosis on chronic steroids who subsequently developed a fatal case of PJP. Our case highlights the need to consider PJP as a differential diagnosis in non-HIV patients on steroids, and more importantly, to consider PJP prophylaxis in these individuals.
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Background. Candidemia is a rare but serious complication of SARS-CoV-2 hospitalization. Combining non-culture and culture-based diagnostics allows earlier identification of candidemia. Given higher reported incidence during COVID-19 surges, we investigated the use of (1-3)-β-D-glucan (BDG) assay at our institution in those who did and did not develop candidemia. Methods. Retrospective study of adults admitted to The Mount Sinai Hospital between March 15-June 30 2020 for SARS-CoV-2 infection, with either ≥1 BDG assay or positive fungal blood culture. Data was collected with the electronic medical record and Vigilanz. A BDG value ≥ 80 was used as a positivity cutoff. Differences in mortality were assessed by univariate logistic regression using R (version 4.0.0). Statistical significance was measured by P value < .05. Results. There were 75 patients with ≥1 BDG assay resulted and 28 patients with candidemia, with an overlap of 9 between the cohorts. Among the 75 who had BDG assay, 23 resulted positive and 52 negative. Nine of 75 patients developed candidemia. Of the 23 with a positive assay, 5 developed candidemia and 18 did not. Seventeen of the 18 had blood cultures drawn within 7 days +/- of BDG assay. Four patients with candidemia had persistently negative BDG;2 had cultures collected within 7 days +/- of BDG assay. With a cut-off of >80, the negative predictive value (NPV) was 0.92. When the cut-off increased to >200, NPV was 0.97 and positive predictive value (PPV) was 0.42. Average antifungal days in patients with negative BDG was 2.6 vs. 4.2 in those with a positive. Mortality was 74% in those with ≥1 positive BDG vs. 50% in those with persistently negative BDGs. There was a trend towards higher odds of death in those with positive BDG (OR = 2.83, 95% CI: 1.00-8.90, p < 0.06). Conclusion. There was substantial use of BDG to diagnose candidemia at the peak of the COVID-19 pandemic. Blood cultures were often drawn at time of suspected candidemia but not routinely. When cultures and BDG were drawn together, BDG had a high NPV but low PPV. High NPV of BDG likely contributed to discontinuation of empiric antifungals. The candidemic COVID-19 patients had high mortality, so further investigation of algorithms for the timely diagnosis of candidemia are needed to optimize use of antifungals while improving mortality rates.
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TYPE: Case Report TOPIC: Critical Care INTRODUCTION: COVID-19 infection may moderately or severely compromise the patient´s immunity. CASE PRESENTATION: A case of CAPA in a 38 years female whose COVID PCR was positive. She did not have host factors and clinically responded to 6 weeks voriconazole. She was presented with fever, tachypnea, tachycardia, pleuritic Chest pain and High oxygen requirement.she developed ARDS and mechanically ventilated. CRP, procalcitonin. Blood culture, sputum bacterial, fungal cultures, and autoimmune markers were negative. Mycoplasma antibodies and Quantiferon test were also negative. HRCT chest showed the halo sign (Figure 1). Voriconazole IV was initiated. CT PE excluded pulmonary embolism.Diagnosis of CAPA was challenging because of absence of host factor, negative fungal culture, nonavailability of galactomanan test.Despite that she was managed as a possible CAPA with good response to voriconazole. The diagnosis depended on refractory fever, refractory hypoxia after a period of adequate antibiotics, negative procalcitonin, halo sign in HRCT, negative bacterial cultures, positive serum aspergillus antibodies and positive (1–3)-β-D-glucan. Prone positioning and (APRV) led to improved oxygenation. Intravenous 3 days pulse dose methylprednisolone started on the day of progressive HRCT chest.After (SPT) the patient was extubated. Voriconazole tab continued for 3 more weeks and prednisone tab 10 mg tab for 10 days. HRCT chest after 2 weeks showed improvment DISCUSSION: Patients may be moderately immunocompromised after COVID-19 infection hence, susceptible to CAPA. Early detection of radiologic finding in HRCT may warrant early initiation of antifungal if CAPA is clinically suspected. CONCLUSIONS: Serum Aspergillus IgG may be of clinical value indiagnosing IPA DISCLOSURE: Nothing to declare. KEYWORD: COVID, HYPOXIA, CAPA, IPA, HALO SIGN, SOLITARY LUNG CONSOLIDATION