ATYPICAL VARIANT OF GRANULOMATOSIS WITH POLYANGIITIS WITH EOSINOPHILIA

SESSION TITLE: Critical Systemic Disease Case Report Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Granulomatosis with polyangiitis (GPA) is a necrotizing granulomatous vasculitis affecting small-to-medium sized blood vessels. GPA is highly associated with antineutrophil cytoplasmic antibodies (ANCAs) and often triggered by environmental factors such as medications and infectious agents. Tracheobronchial stenosis and diffuse alveolar hemorrhage are serious complications of GPA. CASE PRESENTATION: A 35-year-old Caucasian male with a history of chronic sinusitis requiring balloon sinuplasty and recent tympanostomy had presented multiple times to the emergency room due to dyspnea and cough with pinkish sputum production. This was associated with sore throat and fever, which were attributed to his COVID-19 infection and treated with supportive care. Due to persistent drainage through his tympanostomy he was prescribed levofloxacin by his ENT specialist. After the second dose of levofloxacin, he developed Raynaud's phenomenon, diffuse purpuric lesions and swelling over his lower extremity, eyelids, and elbows. Four days later he developed worsening hemoptysis and dyspnea for which he was admitted for further evaluation. Laboratory findings were remarkable for peripheral eosinophilia, elevated ESR 19mm/hr, CRP 9.2mg/dl, c-ANCA 1:320 titer, positive proteinase-3 antibodies and normal p-ANCA titers. Urinalysis with microscopic hematuria. Chest CT scan showed ground glass opacity, consolidative infiltrate with subpleural sparing and minimal left bronchial stenosis. Bronchoscopy suggestive of diffuse alveolar hemorrhage. Limited lung biopsy showed ulcer and granulation tissue with abundant eosinophils, but no granulomatous inflammation noted. Pulse dose steroids and Rituximab were initiated, and rapid clinical improvement was noted. Patient was discharged on prednisone taper and Pneumocystis jiroveci prophylaxis. DISCUSSION: We believe that GPA may have been triggered by recent COVID-19 infection and levofloxacin use. Mild peripheral blood and tissue eosinophilia (<12%) has been described in GPA, however it is a rare finding. GPA and eosinophilic granulomatosis with polyangiitis (EGPA) are both ANCA vasculitis that involve lungs and kidneys. GPA presents with sinusitis, alveolar hemorrhage and high titers of PR-3 antibodies. EGPA presents with a history of atopic, asthma and high titers of myeloperoxidase-ANCA along with abundant peripheral eosinophils. Our patient best fits the diagnostic criteria for GPA with eosinophilia variant rather than EGPA. Our patient had no history of asthma or atopic disease and p-ANCA was normal, which also points away from EGPA. CONCLUSIONS: Clinicians should recognize the differential diagnosis for eosinophils in ANCA vasculitis. Early diagnosis of ANCA vasculitis and initiation of appropriate treatment is important to decrease morbidity and mortality. Reference #1: Potter MB, Fincher RK, Finger DR. Eosinophilia in Wegener's Granulomatosis. Chest 116: 1480-1483, 1999 Reference #2: Krupsky, Meir et al. Wegener's Granulomatosis With Peripheral Eosinophilia. CHEST, Volume 104, Issue 4, 1290 - 1292 Reference #3: Kitching AR, Anders HJ, et al. ANCA-associated vasculitis. Nat Rev Dis Primers. 2020 Aug 27;6(1):71. doi: 10.1038/s41572-020-0204-y. PMID: 32855422. DISCLOSURES: No relevant relationships by Afoma King No relevant relationships by Joshuam Ruiz Vega No relevant relationships by Krishna Shah no disclosure on file for Milos Tucakovic;

COVID-19 VACCINE-RELATED PNEUMONITIS

SESSION TITLE: Issues After COVID-19 Vaccination Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Since 2020, SARS-CoV-2 virus has spread rapidly and endlessly throughout the world, being one of the worst pandemics that the world has ever seen. The BNT162b2 mRNA COVID-19 has an efficacy rate around 95% and ability to reduce disease severity, but also associated with numerous adverse reactions. Here we present a case of a Vaccine Induced Pneumonitis following a booster of the BNT162b2 vaccine. CASE PRESENTATION: A 72-year-old female presented to the ED with 3-day history of cough and dyspnea after receiving the booster (3rd dose) Pfizer COVID-19 mRNA vaccine. On the second day following vaccination started to develop a non-productive cough, difficulty breathing, and later in the afternoon had several episodes of nausea, vomiting, and fever. Initial presentation to hospital concerning for community acquired pneumonia, and patient was started on IV fluids and empiric antibiotics. However, after initial treatment respiratory condition worsened drastically concerning for iatrogenic pulmonary edema. Patient received diuretics but still failed to improve respiratory condition. CT chest revealed bil ground-glass opacities. Microbiologic and serologic testing negative, except for positive ANA. As the patient's condition failed to improve still on heated high flow O2, the patient underwent bronchoscopy which revealed diffuse erythematous with copious, thick, whitish mucus plugging airways. BAL cell count showed WBC 204 /cumm with lymphocytic predominance. BAL cultures were only positive for candida albicans in 1/2 pooled samples. Silver stain negative for P. jirovecii. After a negative infectious workup, the patient was started on systemic steroid therapy and her symptoms improved in two days. After five days of treatment, the patient was able to be discharged home with oxygen therapy on 1 L/min along with a steroid taper. DISCUSSION: Although there was likely a component of iatrogenic fluid overload from IV hydration, the patient's clinical condition did not improve even after vigorous diuresis. Patient does not have any significant underlying pulmonary disease, or CT/PFTs in past. Extensive infectious and autoimmune workup has been negative. Based on the GGO distribution, clinical course including symptoms after exposure to COVID-19 booster, and improvement after steroids, BAL cell count with lymphocytic predominance, we consider vaccine-induced interstitial lung disease as the most probable diagnosis. CONCLUSIONS: Our case highlights challenges in managing patients with airspace disease in the era of COVID-19 and vaccination. We would like to share a possible case of vaccination-induced interstitial lung disease. Our conclusion was made after ruling out the most common infectious and noninfectious causes and after having a favorable response to steroids. Reference #1: Influenza vaccine-induced interstitial lung disease. Watanabe et al. European Respiratory Journal Feb 2013, 41 (2) 474-477;DOI: 10.1183/09031936.00146912 Reference #2: COVID-19 vaccine induced interstitial lung disease, Yoshifuji et al, Journal of Infection and Chemotherapy, 2021 Reference #3: COVID-19 mRNA Vaccine-induced Pneumonitis: A Case Report. Internal Medicine, Japanese Society of Internal Medicine. Matsuzaki S et al., Released October 26, 2021 DISCLOSURES: No relevant relationships by Harold Cedeno No relevant relationships by Chengtin Tseng

SIMILAR, YET SO DIFFERENT: A TALE OF TWO DISEASES

SESSION TITLE: COVID-19 Case Report Posters 3 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Pneumocystis Pneumonia (PCP) is an opportunistic infection caused by a yeast-like fungus pneumocystis jirovecii. It is characterized by hypoxemia and increased inflammatory markers with elevated lactate dehydrogenase (LDH) often used as a clinical indicator of possible infection. COVID-19 is a viral infection caused by severe acute respiratory syndrome coronavirus and presents with a variety of symptoms, pneumonia being the most frequent and serious manifestation. Common laboratory markers include lymphopenia, elevated LDH and inflammatory markers. CASE PRESENTATION: Our patient is a 54 yo African American male with an unremarkable history who presented to our facility from an outside hospital (OH) for worsening respiratory failure in the setting of a large left pulmonary artery thrombosis. He was infected with COVID-19, four months prior and had experienced worsening weakness, SOB and anorexia two months before admission. Work up at OH revealed the large pulmonary emboli as well as extensive multifocal opacities consistent with prior COVID infection and described as post- COVID fibrosis. His sputum also tested positive for pseudomonas aeruginosa and mycoplasma pneumoniae for which he was treated. Unfortunately his hypoxemia worsened and he required intubation;prompting transfer to our facility for hopes of thrombectomy. He continued with hypoxemic, hypercarbic respiratory failure and underwent a bronchoscopy which was grossly normal. As serology indicated lymphopenia and paraprotein gap > 4, we decided to order HIV RNA PCR, which came back positive (CD4 count 11cells/ mm3). One week later, pneumocystis jirovecii was identified from an immunohistochemical stain from bronchial alveolar lavage (BAL). DISCUSSION: PCP is a common opportunistic infection in patients with human immunodeficiency virus, generally presenting when CD4 counts decrease below 200 cells/ mm3. Along with similar symptoms and elevated inflammatory markers, COVID-19 and PCP share common radiographic findings of ground glass opacities. In addition to his compromised lung (from COVID-19) and prolonged hospitalization, the positive cultures of m. pneumoniae and p.aeruginosa were originally misleading. Although cases of co-infection of PJP and COVID-19 exist, our case demonstrates that having a broad differential after recovery from COVID-19 continues to be necessary. CONCLUSIONS: PCP and COVID-19 pneumonia share similarities in radiographic and laboratory findings proving difficult to differentiate from each other. This case highlights the importance of assessing the immunological status of patients with unknown HIV history especially in a time where considering different etiologies of pneumonia have taken the backseat in the height of the COVID-19 pandemic Reference #1: Anggraeni AT, Soedarsono S, Soeprijanto B. Concurrent COVID-19 and Pneumocystis jirovecii pneumonia: The importance of radiological diagnostic and HIV testing. Radiol Case Rep. 2021;16(12):3685-3689. Published 2021 Oct 2. doi:10.1016/j.radcr.2021.09.002 Reference #2: Analysis of underlying diseases and prognosis factors associated with Pneumocystis carinii pneumonia in immunocompromised HIV-negative patients. Roblot F, Godet C, Le Moal G, Garo B, Faouzi Souala M, Dary M, De Gentile L, Gandji JA, Guimard Y, Lacroix C, Roblot P, Becq-Giraudon B. Eur J Clin Microbiol Infect Dis. 2002;21(7):523. DISCLOSURES: No relevant relationships by Cynthia Espinosa No relevant relationships by Jason Kovacevic No relevant relationships by Laura Mendez Morente No relevant relationships by Zuleikha Muzaffarr

A RARE CASE OF PNEUMONIA BY CONCURRENT PNEUMOCYSTIS JIROVECI AND CYTOMEGALOVIRUS INFECTIONS

SESSION TITLE: Unusual Pneumonias SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Cytomegalovirus (CMV) is an important infectious organism in the morbidity and mortality of immunocompromised patients. CMV is a known cause of pneumoina in transplant patients, such as lung transplant recepients. Pneumocytis Jiroveci Pneumonia (PCP) is also a known risk factor for potentially life-threatening infections in immunocompromised patients. In this , we are presenting a rare case of an immunocompromised patient who had penumonia caused by a concurrent CMV and PCP infections. CASE PRESENTATION: A 53 year-old female patient with history of Rheumatoid Arthritis treated with immunomodulating medications admitted for Shortness of breath, fatigue and tiredness but no fever. COVID-19 and influenza infections (PCR) tests were both negative. At presentation, her WBC was 9900. CT with contrast of her chest showed no embolism, but multi-focal widespread groundglass opacities. Blood culture was negative, MRSA screen was negativetoo, but Fungitell test was positive (with a value of more than 500) and serum LDH test was elevated to 382. CMV quantitaive PCR was elevated to 10,000 copies. A bronchoscopy was done and CMV PCR Bronchoalveolar lavage (BAL) is detected at 650 copies/ ml. A BAL EBV PCR tests was negative. Pneumocystis Jiroveci pneumonia was detected on BAL Direct fluorescent antibody test (DFA). CMV retinitis has been ruled out by an ophthalmology exam. Patient was diagnosed with concurrent CMV and PCP pneumonia infection and her respiratory status worsened mandating a brief ICU stay. Treatment was started with Bactrim, Valganciclovir and Ganciclovir with progressive improvement. In a follow up appointment at the infectious diease clinic two months later, the patient condition improved but was still in need for supplemental oxygen through nasal canula. DISCUSSION: A concurrent CMV and PCP microorganisms lung infection is rare, but patient with underlying immunocompromise constitue a major risk factor for that. CONCLUSIONS: Patients with underlying immuncompromise conditions are at risk of many infections with grave morbidity and mortality risks. Though it is a rare to have a concurrent CMV and PCP lung infection, a patient treated with immunomodulating medications including methotrexate, prednisone and rituximab was a culprit for severe infection. Reference #1: Peghin, M., Hirsch, H. H., Len, Ó., Codina, G., Berastegui, C., Sáez, B., Solé, J., Cabral, E., Solé, A., Zurbano, F., López-Medrano, F., Román, A., & Gavaldá, J. (2016). Epidemiology and immediate indirect effects of respiratory viruses in lung transplant recipients: A 5-year prospective study. American Journal of Transplantation, 17(5), 1304–1312. https://doi.org/10.1111/ajt.14042 DISCLOSURES: No relevant relationships by MohD Ibrahim

THE ERA OF HIV-NEGATIVE PNEUMOCYSTIS PNEUMONIA

SESSION TITLE: Chest Infections in Immunocompromised Patients Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Pneumocystis pneumonia (PCP) is a life-threatening opportunistic infection caused by Pneumocystis jirovecii. HIV-negative patients with PCP are primarily individuals receiving immunosuppressive therapy for other disease processes. In rare instances, PCP could be an initial manifestation of underlying defected or suppressed cell-mediated immunity that needs to be diagnosed to prevent morbidity and mortality. CASE PRESENTATION: 75-year-old female with a history of hypertension and hypothyroidism presented to the emergency department for evaluation of cough, fever, and shortness of breath gradually worsening over the last few weeks. She received outpatient treatment with no improvement. She was vaccinated against covid-19. On presentation, the temperature was 103F, heart rate was 108 bpm, blood pressure was 163/93 mm Hg, and oxygen saturation was 86% on room air. Hemogram showed leukocytosis with left shift with elevated inflammatory markers. Chest X-ray revealed bilateral ground glass opacities. She was started on broad-spectrum antibiotics, but symptoms worsened over the next few days. CT chest showed diffuse bilateral ground glass opacities with prominent interstitial markings. BAL obtained from bilateral upper lobes was lymphocyte predominant with pneumocystis jirovecii diagnosed on Gomori methenamine silver (GMS) staining. She was started on PCP-directed antibiotics with intravenous glucocorticoids, and workup for an underlying immunodeficiency was started. Subsequent BATS biopsy revealed diffuse organizing alveolar damage, with possible associated acute interstitial pneumonia pattern. This could be a rare manifestation of PCP or a primary presentation in the appropriate clinical setting. Autoimmune panel, leukemia, and lymphoma panel came back negative. AFB smear, HIV, EBV, CMV, HTLV I/II also returned negative. The lymphocyte subset panel revealed a CD4 count of 205 and a subsequent count a few days later of 64 with decreased total IgG. The patient was treated with high dose steroids for an extended period along with treatment for PCP however continued to decline clinically. The patient and family eventually decided to pursue comfort care. DISCUSSION: The predisposition to PCP in patients is primarily due to a decrease in cell-mediated immunity regardless of HIV infection. In our patient, the etiology of idiopathic CD4+ T cell lymphocytopenia cannot be determined due to the lack of serial laboratory data measurement. One of the proposed etiologies of ICL is systemic persistent immune activation in the setting of exogenous mRNA, the current technology that is being widely used for vaccine development. CONCLUSIONS: In this era of biotechnology, with advancements in immunosuppressive therapy and mRNA-based vaccines, increased awareness around the potential immune system activation and potential downstream complications needs to be further highlighted to raise awareness among physicians. Reference #1: Li, Y., Ghannoum, M., Deng, C., Gao, Y., Zhu, H., Yu, X., & Lavergne, V. (2017). Pneumocystis pneumonia in patients with inflammatory or autoimmune diseases: usefulness of lymphocyte subtyping. International Journal of Infectious Diseases, 57, 108-115. Reference #2: Pardi, N., Hogan, M. J., Porter, F. W., & Weissman, D. (2018). mRNA vaccines - a new era in vaccinology. Nature reviews. Drug discovery, 17(4), 261–279. https://doi.org/10.1038/nrd.2017.243 Reference #3: Vijayakumar, S., Viswanathan, S., & Aghoram, R. (2020). Idiopathic CD4 Lymphocytopenia: Current Insights. ImmunoTargets and therapy, 9, 79–93. https://doi.org/10.2147/ITT.S214139 DISCLOSURES: No relevant relationships by Santhosh Gheevarghese John No relevant relationships by Konstantin Golubykh No relevant relationships by Iuliia Kovalenko No relevant relationships by Maidah Malik No relevant relationships by Hafiz Muhammad Siddique Qurashi No relevant relationships by Taj Rahman No rel vant relationships by Tabinda Saleem

AN UNEXPECTED RECURRENCE: A CASE OF PNEUMOCYSTIS JIROVECI AND SARS-COV-2 IN AN IMMUNOCOMPROMISED PATIENT

SESSION TITLE: COVID-19 Co-Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Pneumocystis jirovecii pneumonia (PJP) remains a significant cause of morbidity and mortality in the immunocompromised population. It can be difficult to discern the radiographic imaging of COVID-19 from PJP. This case describes a noncompliant HIV positive male with remote history of PCP pneumonia and COVID-19 pneumonia who presents with simultaneous recurrence of both disease processes. CASE PRESENTATION: A 45-year-old male with PMH of HIV/AIDS noncompliant on ART (CD4+ 10) presented for evaluation of exertional dyspnea and productive cough for the past 2 weeks. Of note, patient had a history of covid-19 pneumonia about 15 months ago when he was treated with remdesivir and steroids and required supplemental oxygen support. He was also admitted about 8 months prior for PJP pneumonia and underwent treatment with steroids and TMP-SMX for 21 days also requiring supplemental oxygen support. During this presentation, initial vital signs showed: T 36.5 C HR 98 BP 112/63 RR 20 saturating 95% breathing ambient air. ABG on presentation showed PaO2 65 while breathing room air. Physical exam suggested bilateral crackles diffusely with chest radiography significant for increased interstitial markings bilaterally. CT chest showed bilateral groundglass changes suggestive of inflammatory process. He was initially started on antibiotic coverage with azithromycin, ceftriaxone, and TMP-SMX as the initial differential included PJP recurrence since he was noncompliant on secondary prophylaxis after recent infection. He was also started on steroids due to low PaO2. SARS-CoV-2 PCR returned positive however, the low CD4+ count, and a positive serum B-D-glucan assay prompted us to schedule a bronchoscopy to evaluate for PJP pneumonia. BAL showed positive silver stain along with bronchial wash was elevated PCR for PJP (5.6 million copies/mL). A diagnosis of concurrent COVID-19 pneumonia and PJP pneumonia was made. Patient did not receive remdesivir during this admission since his oxygenation began to improve during the hospitalization. Patient was discharged on appropriate regiment for PJP pneumonia and continued steroid taper. He was seen as a follow-up in outpatient clinic about 2 months later compliant on his ART regimen and secondary PJP prophylaxis (CD4 120). DISCUSSION: If it wasn't for the serum B-D-glucan, we likely would not have pursued further causes for hypoxia in an otherwise COVID-19 positive patient with characteristic radiographic findings. The sheer co-incidence and concurrent nature of presentation of these two disease processes make our case extremely unique. Going forward, it is reasonable to keep PJP in the differential when treating a hypoxic immunocompromised patient even if an alternative cause for hypoxia is present. CONCLUSIONS: Herein we present a case of a patient with remote history of COVID-19 pneumonia and PJP pneumonia now presenting with a simultaneous co-infection. Reference #1: Mouren, D., Goyard, C., Catherinot, E., Givel, C., Chabrol, A., Tcherakian, C., Longchampt, E., Vargaftig, J., Farfour, E., Legal, A., Couderc, L. J., & Salvator, H. (2021). COVID-19 and Pneumocystis jirovecii pneumonia: Back to the basics. Respiratory medicine and research, 79, 100814. https://doi.org/10.1016/j.resmer.2021.100814 Reference #2: Huang, L., Cattamanchi, A., Davis, J. L., Boon, S. d., Kovacs, J., Meshnick, S., Miller, R. F., Walzer, P. D., Worodria, W., & Masur, H. (2011). HIV-associated Pneumocystis pneumonia. Proceedings of the American Thoracic Society, 8(3), 294–300. https://doi.org/10.1513/pats.201009-062wr Reference #3: Tasaka, S. (2015). pneumocystis pneumonia in human immunodeficiency virus–infected adults and adolescents: Current concepts and Future Directions. Clinical Medicine Insights: Circulatory, Respiratory and Pulmonary Medicine, 9s1. https://doi.org/10.4137/ccrpm.s23324 Group, T. R. C. (2020). Dexamethasone in hospitalized patients with covid-19. (2021). New England Journal of Medicine, 384(8), 693–704. https://doi.org/10.1056/nejmoa2021436 KOLDITZ, M., HALANK, M., BANDT, D., SPORNRAFT-RAGALLER, P., & HÖFFKEN, G. (2009). Early recurrence ofPneumocystis jirovecipneumonia in two HIV-infected patients: Linking infection relapse and immune reconstitution syndrome. Respirology, 14(6), 910–912. doi:10.1111/j.1440-1843.2009.01583.x Mussini C, Pezzotti P, Antinori A, Borghi V, Monforte Ad, Govoni A, De Luca A, Ammassari A, Mongiardo N, Cerri MC, Bedini A, Beltrami C, Ursitti MA, Bini T, Cossarizza A, Esposito R;Changes in Opportunistic Prophylaxis (CIOP) Study Group. Discontinuation of secondary prophylaxis for Pneumocystis carinii pneumonia in human immunodeficiency virus-infected patients: a randomized trial by the CIOP Study Group. Clin Infect Dis. 2003 Mar 1;36(5):645-51. doi: 10.1086/367659. Epub 2003 Feb 12. PMID: 12594647. DISCLOSURES: No relevant relationships by Mourad Ismail No relevant relationships by Carlos Palacios No relevant relationships by Rutwik Patel

A CASE OF PNEUMOCYSTIS JIROVECI PNEUMONIA MIMICKING METHOTREXATE-INDUCED PNEUMONITIS

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

A CHALLENGING CASE OF MYCOBACTERIUM TB-INDUCED HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS

SESSION TITLE: Challenging Cases of Hemophagocytic Lymphohistiocytosis SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Hemophagocytic lymphohistiocytosis (HLH) is a syndrome of excessive immune activation in response to a variety of insults including malignant, autoimmune and infectious processes. The most common infectious trigger is a viral infection, but other pathogens have also been implicated including Mycobacterium tuberculosis (MTB) CASE PRESENTATION: 62-year-old male from Bangladesh presented due to lethargy, weakness, and anorexia for several weeks. He also reported fevers, diarrhea, and unintentional weight loss. On examination, he appeared acutely ill with diffuse bibasilar crackles on lung exam. Labs showed platelets of 132, ESR 45 mm/hr, CRP 9.6mg/dL, ferritin 1,765ng/mL and transaminitis. A viral panel was positive for Rhinovirus. Computed tomography (CT) of the chest showed diffuse bilateral ground-glass opacities and he was started on antibiotics for pneumonia. On day 3, his respiratory status worsened and he was emergently intubated. He underwent bronchoscopy and bronchoalveolar lavage (BAL) and started on high-dose steroids for possible hypersensitivity pneumonitis. On day 5, he was extubated to nasal cannula, however, his condition worsened despite treatment. Extensive infectious workup, including HIV, Covid and P jirovecii PCR, sputum, and blood cultures, and preliminary AFB smear were negative. Subsequent labs noted rising ferritin levels (4,164 ng/mL), high triglycerides, pancytopenia and transaminitis. Calculated H score was 211 which gave a 93-96% probability of HLH. Initiation of Etoposide was discussed but family deferred. He was later transferred to another facility. On follow-up, IL-2 receptor antibodies were elevated, bone marrow biopsy showed hemophagocytosis and necrotizing granulomas. He was intubated for worsening hypoxemia. Repeat bronchoscopy and BAL analysis showed many acid-fast bacilli. Anti TB treatment (ATT) was deferred due to his critical state. He further declined and eventually expired. DISCUSSION: The exact mechanism for which MTB triggers HLH is unclear, however, it is thought that MTB serves as an obligate intracellular pathogen after phagocytosis by phagocytic cells to induce TH1-mediated cytotoxicity, activating macrophages and NK cells, further releasing a large quantity of cytokines and chemokines. The lack of specific clinical signs, low sensitivity for acid-fast staining, and time-consuming culture make the diagnosis of TB-HLH difficult. However, the use of NAATs has improved the yield of sputum testing. Exceedingly high ferritin levels should serve as a red flag in cases of undetermined diagnosis. Moreso, Cytopenias, elevated LFTs, and coagulation dysfunction are other clues that a diagnosis of HLH should be on the differential. It is believed that early and effective ATT is the key to preventing HLH in TB patients. CONCLUSIONS: It is paramount to both recognize the features of TB as well as HLH as early diagnosis and treatment favor better outcomes. Reference #1: Padhi S, Ravichandran K, Sahoo J, Varghese RG, Basheer A. Hemophagocytic Lymphohistiocytosis: An Unusual Complication in Disseminated Mycobacterium Tuberculosis. Lung India (2015) 32(6):593–601. doi: 10.4103/0970-2113.168100 Reference #2: Dalugama, C., Gawarammana, I.B. Fever with pancytopenia: unusual presentation of extrapulmonary tuberculosis: a case report. J Med Case Reports 12, 58 (2018). https://doi.org/10.1186/s13256-018-1596-0 Reference #3: O M P Jolobe, Timely recognition of hematophagocytosis attributable to coexistence of lymphoma and tuberculosis, QJM: An International Journal of Medicine, Volume 112, Issue 4, April 2019, Page 315, https://doi.org/10.1093/qjmed/hcy198 DISCLOSURES: No relevant relationships by Katherine Acosta No relevant relationships by Chika Winifred Akabusi No relevant relationships by Uma Medapati No relevant relationships by Hector Ojeda-Martinez No relevant relationships by Busala Oke No relevant relationships by Mar o Torres

A CASE OF BORDETELLA BRONCHISEPTICA AND PNEUMOCYSTIS JIROVECI PNEUMONIA IN A YOUNG PATIENT

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: Pneumonia is a common condition that is seen in hospitals. Pneumocystis Jirovecii is an opportunist fungal pathogen. Bordetella bronchiseptica is a gram negative bacteria that causes infectious bronchitis in dogs and other animals, but rarely infects humans. CASE PRESENTATION: Patient is a 34 year old African American female with history of sickle cell trait, reported Lupus (not on treatment), asthma, COVID pneumonia who was admitted for worsening shortness of breath & productive cough with yellow sputum. She was previously hospitalized and discharged after being treated for Community-Acquired Pneumonia. In the ER, she was febrile, tachycardic, tachypneic, & hypoxic requiring BiPAP. CXR obtained showed findings concerning for multifocal pneumonia. Chest CT Angiogram was negative for PE. Patient was started on Vancomycin & Meropenem for treatment of her pneumonia. Blood cultures, Legionella, Strep pneumoniae, Aspergillus, Beta-D-glucan, Sputum culture, & MRSA screen were ordered for further evaluation of her infection. ANA screen reflex panel, lupus anticoagulant, anticardiolipin antibodies, beta-2 glycoprotein antibodies were also ordered given patient's reported history of SLE and the concern for SLE pneumonitis: ANA & Sjogren's Anti-SSA were positive;otherwise, autoimmune workup was unremarkable. During hospitalization, patient was eventually weaned down to nasal cannula and antibiotic was de-escalated to levaquin. However, sputum culture eventually grew Bordetella Bronchiseptica that was resistant to Levaquin so antibiotic regimen was switched to Doxycycline. In addition, Beta-D-glucan was noted to be elevated. Bronchoscopy was done for further evaluation;multiple transbronchial biopsies were positive Pneumocystis Jirovecii. Patient was then initiated on Bactrim for treatment of PJP Pneumonia along with a steroid taper. Patient was tested for HIV and it was negative. DISCUSSION: In this case, patient was found to have two rare pathogens, that are more common in immunocompromised patients such as those with HIV/AIDS, on high-dose corticosteroids or malignancy. This patient had a unconfirmed diagnosis of SLE and past COVID Pneumonia. Patient had Bordetella bronchiseptica pneumonia that is frequently isolated in the respiratory tract of animals but can cause severe respiratory infection in humans. This microorganism can cause upper respiratory tract infections, pneumonitis, endocarditis, peritonitis, meningitis, sepsis and recurrent bacteremia. Upon further discussion with the patient, she was found to have a recent pet dog. CONCLUSIONS: High level of clinical suspicious is needed in patient presenting with recurrent pneumonia with chest imaging findings suggestive of multifocal pneumonia. The mainstay of treatment for PJP is TMP-SMX and steroid. We recommend Fluoroquinolones or tetracycline for Bordetella bronchiseptica pneumonia. Reference #1: Benfield T, Atzori C, Miller RF, Helweg-Larsen J. Second-line salvage treatment of AIDS-associated Pneumocystis jirovecii pneumonia: a case series and systematic review. J Acquir Immune Defic Syndr. 2008 May 1;48(1):63-7. Reference #2: de la Fuente J, Albo C, Rodríguez A, Sopeña B, Martínez C. Bordetella bronchiseptica pneumonia in a patient with AIDS. Thorax. 1994 Jul;49(7):719-20. doi: 10.1136/thx.49.7.719. PMID: 8066571;PMCID: PMC475067. DISCLOSURES: No relevant relationships by Priya George No relevant relationships by ELINA MOMIN No relevant relationships by Mohammedumer Nagori

SYSTEMATIC LITERATURE REVIEW on the SCREENING and PROPHYLAXIS of CHRONIC and OPPORTUNISTIC INFECTIONS

Background: Opportunistic and chronic infections can arise in the context of treatment used for Autoimmune Rheumatic Diseases (ARDs). Although it is recognized that screening procedures and prophylactic measures must be followed, clinical practice is largely heterogeneous, with relevant recommendations not currently developed or disparately located across the literature. Objectives: To conduct a systematic literature review (SLR) focusing on the screening and prophylaxis of opportunistic and chronic infections in ARDs. This is preparatory work done by members of the respective EULAR task force (TF). Methods: Following the EULAR standardised operating procedures, we conducted an SLR with the following 5 search domains;1) Infection: infectious agents identifed by a scoping review and expert opinion (TF members), 2) Rheumatic Diseases: all ARDs, 3) Immunosuppression: all immunosuppressives/immunomodulators used in rheumatology, 4) Screening: general and specifc (e.g mantoux test) terms, 5) Prophylaxis: general and specifc (e.g trimethop-rim) terms. Articles were retrieved having the terms from domains 1 AND 2 AND 3, plus terms from domains 4 OR 5. Databases searched: Pubmed, Embase, Cochrane. Exclusion criteria: post-operative infections, pediatric ARDs, not ARDs (e.g septic arthritis), not concerning screening or prophylaxis, Covid-19 studies, articles concerning vaccinations and non-Εnglish literature. Quality of studies included was assessed as follows: Newcastle Ottawa scale for non-randomized controlled trials (RCTs), RoB-Cochrane tool for RCTs, AMSTAR2 for SLRs. Results: 5641 studies were initially retrieved (Figure 1). After title and screening and removal of duplicates, 568 full-text articles were assessed for eligibility. Finally, 293 articles were included in the SLR. Most studies were of medium quality. Reasons for exclusion are shown in Figure 1. Results categorized as per type of microbe, are as follows: For Tuberculosis;evidence suggests that tuberculin skin test (TST) is affected by treatment with glucocorticoids and conventional synthetic DMARDs (csDMARDs) and its performance is inferior to interferon gamma release assay (IGRA). Agreement between TST and IGRA is moderate to low. Conversion of TST/IGRA occurs in about 10-15% of patients treated with biologic DMARDs (bDMARDs). Various prophylactic schemes have been used for latent TB, including isoniazide for 9 months, rifampicin for 4 months, isoniazide/rifampicin for 3-4 months. For hepatitis B (HBV): there is evidence that risk of reactivation is increased in patients positive for hepatitis B surface antigen. These patients should be referred for HBV treatment. Patients who are positive for anti-HBcore antibodies, are at low risk for reactivation when treated with glucocorticoids, cDMARDs and bDMARDs but should be monitored periodically with liver function tests and HBV-viral load. Patients treated with rituximab display higher risk for HBV reactivation especially when anti-HBs titers are low. Risk for reactivation in hepatitis C RNA positive patients, treated with bDMARDs is low. However, all patients should be referred for antiviral treatment and monitored periodically. For pneumocystis jirovecii: prophylaxis with trimeth-oprim/sulfamethoxazole (alternatively with atovaquone or pentamidine) should be considered in patients treated with prednisolone: 15-30mg/day for more than 4 weeks. Few data exist for screening and prophylaxis from viruses like E B V, CMV and Varicella Zoster Virus. Expert opinion supports the screening of rare bugs like histoplasma and trypanosoma in patients considered to be at high risk (e.g living in endemic areas). Conclusion: The risk of chronic and opportunistic infections should be considered in all patients prior to treatment with immunosuppressives/immunomod-ulators. Different screening and prophylaxis approaches are described in the literature, partly determined by individual patient and disease characteristics. Collaboration between different disciplines is important.

SPONTANEOUS PNEUMOTHORAX IN AN HIV/AIDS PATIENT WITH CONCURRENT COVID-19 AND PNEUMOCYSTIS PNEUMONITIS

CASE: A 25-year-old homeless male with nonadherent HIV presented with dyspnea on exertion for 4 days, productive cough for 1 week, fevers, chills and night sweats. He arrived hypoxic to 74% requiring 2L O2 and was cachectic on exam. WBC, lactate and procalcitonin were normal. C-reactive protein was 26.7 mg/L, LDH was 686 units/L and COVID-19 was positive. An arterial blood gas showed a primary respiratory alkalosis with a secondary metabolic alkalosis. Computed tomography of the chest, abdomen and pelvis with contrast showed multifocal large thin-walled cavitary lesions throughout the bilateral lungs with subpleural large cystic disease. Dexamethasone, remdesivir and empiric antibiotics were initiated. Absolute CD4 count was 7 cells/uL with HIV-1 RNA load of 139,000 copies/mL. Sputum was positive for Pneumocystis jirovecii (PCP) by DFA and PCR, but no evidence of mycobacterium. Trimethoprim-sulfamethoxazole (TMP-SMX) was added. On hospital day 13, he developed severe right-sided chest pain, dyspnea and required up to 15L O2. A chest x-ray revealed a large right-sided pneumothorax (PTX) and a chest tube was placed. Cardiothoracic Surgery was consulted for consideration of bullectomy with pleurodesis;this was not recommended as the cystic lesions were extensive with some intraparenchymal. His oxygen requirements improved and his chest tube was removed in 6 days. He was discharged on hospital day 21 to begin prophylactic dosing of TMP-SMX until his CD4 count was over 200 cells/uL and to attend his first appointment at an outpatient HIV clinic the following day. IMPACT/DISCUSSION: Secondary spontaneous pneumothorax (SSP) can be a complication of necrotizing pneumonia due to PCP. In one study, in a cohort of 599 patients with HIV infection, only 1.2% developed a PTX. Bilateral PTX is more common with PCP, unlike in our patient. In HIV, the degree of immunosuppression can influence the cause of PTX. Our patient had a PTX with a CD4 count under 200, which is more common with PCP. In addition, SSP as a complication of SARS-CoV-2 is more rare. There are case series that describe COVID-19 patients who develop PTX in the absence of barotrauma secondary to mechanical ventilation. However, this is uncommon as one retrospective study reports PTX occurring in 1% of patients with COVID-19 requiring hospital admission. In this case, it is unclear to what extent the patient's concomitant COVID-19 contributed to the development of a PTX. Our patient was ineligible for definitive intervention to prevent recurrence, thus underwent tube thoracostomy placement which is consistent with the majority of treated patients. While the prognosis of PTX secondary to COVID-19 is generally good, prognosis of cominant co-infection with PCP is an area of further research as the overall mortality of PCP-induced PTX alone can be 23%. CONCLUSION: This case represents a rare occurrence of spontaneous pneumothorax secondary to both PCP and COVID-19. We suggest the incidence to increase as the pandemic continues.

PNEUMOCYSTIS JIROVECI PNEUMONIA IN A PATIENT WITH SARCOIDOSIS ON CHRONIC STEROIDS

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.

An etiology of ground - glass images during COVID-19: Pneumocystis jiroveci pneumonia.

Pneumocystis jiroveci pneumonia is a common pathology in HIV-infected but also in uninfected immunocompromised individuals. The pandemic coronavirus disease 2019 (COVID-2019) is a new type of coronavirus disease caused by SARS-COV-2, and the chest imaging is often used as complementary tool in patients' evaluation. The imaging finding is similar with many pulmonary pathologies. Chest computed tomography scan is gold standard imaging and shows a central and diffuse distribution, ground- glass pattern with septal thickening with "crazy paving pattern." We reported a case of 57-year-old man patient, followed in oncology for laryngeal cancer who presented of Pneumocystis jiroveci pneumonia during his follow-up. The diagnosis is confirmed by polymerase chain reaction with bronchoalveolar lavage fluid. Other immunochemical tests can be performed but are less specific. Both curative and preventive treatment in subjects at risk remains trimethoprim-sulfamethoxazole. Corticosteroid therapy may be associated depending on the case.

A Case of Suspected COVID-19 Identified with AIDS, PCP and Tuberculosis

HIV (Human Immunodeficiency Virus) is the virus that causes AIDS (Acquired Immune Deficiency Syndrome), while PCP (Pneumocystis jiroveci pneumonia), tuberculosis, CMV (Cytomegalovirus) and candidiasis are the OIs (opportunistic infections) occurring due to immune deficiency. OIs, and bacterial pneumonias in particular, are the most common causes of mortality, which makes the screening and prophylactic therapy for OIs necessary. The synergy between tuberculosis and HIV has long been known, and worsens the prognosis. PCP is an OI that is caused by a fungus named P. jiroveci. COVID-19 has emerged as a new cause of death among AIDS patients. Screening and prophylactic therapy for Ols is vital for patients with AIDS, however, mortality may be high due to delays in screening and prophylaxis in those whose HIV positivity is detected coincidentally. We report here on a patient who applied to our hospital with suspected COVID-19 pneumonia who was found during followup to be HIV positive with PCP and pulmonary tuberculosis.

Hypoxic Respiratory Failure Due to Pneumocystis Jiroveci and Cytomegalovirus Co-Infection in a Severely Immunocompromised Patient

Introduction:Immunocompromised individuals, such as those with HIV and low CD4 counts, are at increased risk for opportunistic infections. Although uncommon, these patients can be infected with multiple organisms, making diagnosis and management challenging for clinicians. Mortality remains high, as the data on initiating and adjusting antimicrobials when there is concern for co-infection is lacking. We present a case of Pneumocystis jiroveci (PCP) and cytomegalovirus (CMV) coinfection resulting in severe hypoxic respiratory failure and death. Case Report:A 38-year-old male with no past medical history presented with fever, dyspnea, and nonproductive cough. Vital signs were notable for a fever of 102.3°F, respiratory rate of 24, and oxygen saturation of 77% on room air. Physical examination revealed an ill-appearing male with bilateral rhonchi who became dyspneic with minimal conversation. Laboratory studies were significant for an elevated c-reactive protein, erythrocyte sedimentation rate, ferritin and lactate dehydrogenase. CT chest demonstrated bilateral ground glass opacities with multifocal consolidations. The patient was admitted for hypoxic respiratory failure secondary to suspected COVID pneumonia, despite negative testing. By hospital day 4, the patient had shown little improvement. Further work-up revealed that he was HIV positive with a CD4 count of 5, so he was empirically started on oral trimethoprim-sulfamethoxazole (TMPSMX) for presumed PCP pneumonia. On hospital day 9, the patient underwent endotracheal intubation for worsening hypoxia and subsequent bronchoscopy for further evaluation. PCP PCR confirmed the diagnosis, and the patient was transitioned to intravenous TMP-SMX. Still with minimal improvement, micafungin was added as potential salvage therapy. After 12 days of TMPSMX, treatment was changed to clindamycin/primaquine. CMV PCR from the bronchoalveolar lavage fluid came back positive at this time, so ganciclovir was added to the regimen. Despite multiple antimicrobials, the patient continued to decline. He was deemed not to be a candidate for ECMO given his profoundly immunocompromised status and ultimately died. Discussion:This case highlights the difficulties clinicians have in managing severely immunocompromised patients who worsen despite appropriate care. Little data exists providing guidelines on when to change to second and/or third-line agents in treating PCP pneumonia. Additionally, further studies need to be completed to delineate in whom empiric antimicrobials should be initiated early when co-infection is a possibility. ECMO may serve a purpose in this patient population given that lung rest is necessary to allow healing, but only a few cases of its use exist at this time.

A Rare Case of Eltrombopag-Induced Pneumonitis

Introduction Immune thrombocytopenia (ITP) is an acquired thrombocytopenia due to autoantibodies. Eltrombopag is a thrombopoietin receptor agonist (TPO-RA) used as a second-line agent in the setting of persistent or chronic ITP. Potential severe adverse effects include hepatotoxicity, thromboembolism, and increased risk of myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML). Upper respiratory infections and pharyngitis have also been described, but to our knowledge, no known cases of eltrombopag-induced pneumonitis have been reported to date. Case Presentation We present a 68-year-old male with a history of recent onset ITP, stage IV mantle cell lymphoma (in remission), and Pneumocystis pneumonia who was initiated on eltrombopag 11 days prior to admission for ITP refractory to corticosteroid therapy. Three weeks prior to admission, the patient underwent a bone marrow biopsy without evidence of monoclonal B cells or immunophenotypically abnormal T cell populations. Following initiation of eltrombopag, the patient had progressive dyspnea on exertion associated with subjective fevers and chills requiring hospitalization. Oxygen saturation was 88% on room air with exam notable for coarse crackles to the bilateral lung bases. CT angiogram of the chest revealed bilateral pulmonary emphysema, ground glass opacities, and bilateral bronchiectasis most pronounced in the lower lobes (Figure 1). No pulmonary embolism or mediastinal adenopathy was identified. Cytomegalovirus DNA, aspergillus antigen, and COVID-19 NAAT testing were negative. A respiratory viral panel was positive for Rhinovirus. Bronchoalveolar lavage (BAL) and right middle lobe lung parenchymal biopsy were subsequently performed. Pathology demonstrated focal intra-alveolar organization and fibroblast plugs, interstitial fibrosis, pneumocyte hyperplasia, and mixed (predominantly chronic) inflammatory infiltrate (Figure 2a & 2b). BAL was negative for malignant cells. Pneumocystis jirovecii DNA was detected, but < 250 copies/mL were identified and thus was thought to be less likely contributing to the disease process.Given the suspicion for eltrombopag-induced pneumonitis, the patient was initiated on high-dose corticosteroid therapy with a slow taper over the span of several weeks. Following initiation of corticosteroids, the patient was noted to have gradual improvement in his respiratory status. The patient was ultimately discharged on room air 1 month later due to other hematologic complications necessitating a prolonged hospital stay. Discussion The exact mechanism of eltrombopag-induced pneumonitis is unclear, although we postulate that it is related to an exaggerated immune response involving T-cell homeostasis resulting in alveolarcapillary permeability, inflammation, and fibrosis. Suspicion for eltrombopag-induced pneumonitis should prompt initiation of early corticosteroid therapy to prevent acute and chronic complications of pneumonitis. (Figure Presented).

SVILUPPO DI SINDROME DA IMMUNODEFICIENZA ACQUISITA DOPO SOMMINISTRAZIONE DI VASCCINO ANTI-SARAS-COV2

Il SARS-CoV2 è trasmesso tra gli umani attraverso particelle respiratorie e l'infezione può determinare un largo spettro di manifestazioni cliniche. Precedenti studi hanno dimostrato il ruolo centrale dell'immunità cellulo-mediata nel limitare la gravità delle infezioni da virus respiratori. I linfociti T-helper CD4+ sono coinvolti in funzioni di coordinazione e regolazione dell'immunità anti-virale: determinano lo sviluppo di anticorpi neutralizzanti ad alta affinità e la differenziazione dei centri germinali a cellule B in cellule della memoria secernenti anticorpi con lunga vita. Nessun dubbio sul ruolo cruciale della risposta a cellule T durante l'infezione da SARS-CoV2 o dopo la vaccinazione. Descriviamo il caso di un paziente di 39 anni, vaccinato con ChAdOx1-S. Dopo due settimane il paziente accusava dispnea e febbricola. Il test molecolare per SARS-CoV2 era negativo;agli esami ematici la PCR era aumentata. La TC del torace escludeva embolia polmonare e rivelava pattern a vetro smerigliato bilaterale, come da flogisi. All'ecocardiogramma i parametri erano nella norma. L'ECG mostrava tachicardia sinusale. Il paziente veniva dimesso dal PS con terapia cortisonica. Una settimana dopo i sintomi peggiooravano. Una nuova TC torace mostrava difetti di opacizzazione di rami secondari dell'arteria polmonare ed aspetto bilaterale a vetro smerigliato. Si iniziava terapia con EBPM ed antibiotici a largo spettro. Il test molecolare e la sierologia per SARS-CoV2 erano negativi. Negativi i test per Mycoplasma, Chlamydia, Legionella e CMV DNA. L'emocromo mostrava ridotti linfociti (6,8%) con neutrofilia relativa (90,4%), ma normale valore dei bianchi. La TC-HR mostrava aspetto “crazy paving” bilaterale suggestivo per infezione virale o micotica (pattern come da infezione da Pneumocystis Jiroveci). Il test per HIV aveva esito positivo;alla tipizzazione linfocitaria ridotti i livelli di linfociti T-Helper (CD3+/CD4+) e rapporto CD3+/CD4+ 0%. Per il rapido deterioramento del quadro clinico il paziente veniva trasferito in terapia intensiva. Dopo 30 giorni dalla diagnosi di AIDS il paziente giungeva ad exitus. Il ruolo dei linfociti T nello sviluppo di anticorpi neutralizzanti e di cellule della memoria durante l'infezione da SARS-CoV2 è la chiave nella strategia di vaccinazione per ridurre il dilagare della pandemia, tuttavia nel nostro paziente questo meccanismo non ha funzionato rivelando il deficit del suo sistema immunitario da una latente infezione da HIV. (Figure Presented).

Acute Pneumocystis jirovecii Pneumonia Due to Absolute Lymphopenia.

Pneumocystis pneumonia (PCP) is an opportunistic fungal infection associated with human immunodeficiency virus (HIV) infection as an acquired immunodeficiency syndrome (AIDS)-defining illness. The PCP incidence in patients with HIV has declined over the last few decades due to effective antiretroviral therapy and prophylaxis. The PCP incidence in HIV-negative patients has increased due to the increasing use of a wide array of immunosuppressants in cancer and autoimmune disease. PCP clinical course varies from patients with HIV in their clinical features, the severity of clinical presentation, and mortality. PCP in autoimmune diseases is rare, especially in rheumatoid arthritis (RA) in the United States of America (USA). Here, we describe an elderly Caucasian female with rheumatoid arthritis and left lung mucinous adenocarcinoma status post recent resection with no chemotherapy on a low dose of methotrexate (MTX) and prednisone presenting with acute hypoxic respiratory failure due to PCP from absolute lymphopenia.

Cough and Dyspnea in 2021: A Case of Asthma, COVID-19, or.?

Background: COVID-19 has changed the perspective through which medical staff look at dyspnea and hypoxemia cases. Epidemiological links are frequently missing, and clinical and imagological findings are often unspecific, overlapping substantially with other respiratory infections. Case summary: We report the case of an 11-year-old girl with a known history of asthma who had recently moved from Guinea-Bissau with her mother. Although the mother reported being Ag HBs positive, no serologic studies had ever been performed on the child. The patient was admitted to the Emergency Room after 4 days of cough and the feeling of thoracic oppression, without fever. No contact with suspected or confirmed individuals infected with SARS-CoV-2 or other respiratory viruses was reported. She presented with peripheral oxygen saturation of 90%, costal retractions and a prolonged expiratory phase. After an unsuccessful course of bronchodilators and prednisolone, she was admitted to the Pediatric Intermediate Care Unit because of a sustained need for oxygen therapy. Polymerase chain reaction analysis for SARS CoV-2 came back negative. A chest radiograph displayed a bilateral reticular infiltrate, and therapy with azithromycin was started. Due to a deterioration of the dyspnea, a chest tomography was eventually performed, revealing an exuberant and bilateral ground glass-like densification suggestive of alveolar injury. Echocardiogram and e electrocardiogram were both normal. After a positive serologic result for HIV, the patient was transferred to a Level III hospital, and Pneumocystis jirovecii was identified in bronchoalveolar lavage. T cell count was 12/mm3. Highly active antiretroviral therapy and cotrimoxazole were started, prompting clinical and analytical recovery. Discussion: Pneumocystis jirovecii can cause fatal pneumonia in immunocompromised children. Even though an asthma exacerbation and atypical bacterial or viral infections, namely COVID-19, present as more usual causes of dyspnea, a low suspicion index is warranted in children coming from HIV-endemic countries, particularly those who are unresponsive to conventional bronchodilator and antibiotic therapy.