From Covid to Bovid to Ovid: A Case of Disseminated Cryptococcus Neoformans

Case Report: Cryptococcosis is an opportunistic infection caused by the encapsulated yeast Cryptococcus, with C. neoformans and C. gattii being the most common species to cause human disease. Immunocompromised individuals are predisposed to infections with C. neoformans, which has known predilection to CNS and pulmonary lymph nodes. We present a unique case of disseminated cryptococcosis in the setting of end-stage renal disease (ESRD), cirrhosis, tumor necrosis factor inhibitor use and steroid use for COVID19. Method(s): A single-patient case report was conducted after IRB approval. Case Presentation: A 55-year-old woman with uncontrolled diabetes, lupus, rheumatoid arthritis on adalimumab, hepatitis C status post boceprevir, cirrhosis, former IV drug use, and ESRD on hemodialysis via bovine arterial-venous fistula graft presented with worsening dyspnea, cough, and altered mental status. Three months prior, patient was admitted to an outside hospital for COVID19, complicated by pulmonary embolism status post anticoagulation therapy. Patient was treated with an unknown steroid regimen, which was continued by a second outside facility when symptoms failed to improve. Patient then presented to our facility 24 hours after discharge due to continued symptoms. On admission, patient was noted to have altered mentation and hypoxia with pulmonary edema on chest x-ray and was urgently hemodialyzed. Further work-up was obtained due to non-resolving symptoms, including blood and sputum cultures, cocci serology and QuantiFERON gold. CT chest revealed bilateral consolidations. Patient was started on antibiotics for presumed hospital-acquired pneumonia. During the hospital stay, preliminarily blood cultures grew yeast and patient was started on Micafungin. However, Micafungin was changed to Liposomal Amphotericin B as ovoid structures seen on gram stain could not confirm nor rule out cryptococcus. Subsequent bronchial wash and bronchoalveolar lavage cultures, as well as final blood cultures resulted Cryptococcus neoformans. Serum cryptococcus antigen returned reactive, titer 1:512. Antibiotics were discontinued and Isavuconazonium was started with Liposomal Amphotericin B. Due to recurrent headaches, lumbar puncture was obtained and revealed lymphocytic pleocytosis without cryptococcal antigenicity. Patient completed 14 days of Liposomal Amphotericin B and Isavuconazole with continuation of Isavuconazole upon discharge. Conclusion(s): Disseminated cryptococcosis in non-HIV patients is rare in the modern HIV era. Clinicians should be aware and include it in their differential of any patient with multiple risk factors for opportunistic infection. In patients with cirrhosis and ESRD, treatment is limited given altered pharmacokinetics. Studies have shown improved survival with the addition of Isavuconazole in patients with disseminated cryptococcosis with CNS involvement in the setting of chronic liver disease and ESRD.

Maskne: Its relationship to skin microbiome and response to treatment

Mask-wearing during the ongoing COVID-19 pandemic has been associated with an increased occurrence of a form of acne mechanica, popularly termed 'maskne. However, our understanding of this entity is limited. Hence we aimed to study the role of changes in the skin microbiome in mask induced acne and its response to standard acne treatment regimens. This was a prospective observational study. Adult patients having new-onset of lesions suggestive of acne within 6 weeks of regularly wearing mask or exacerbation of pre-existing acne were recruited. Disease severity was assessed using the 'Global Acne Severity Grading System (GAGS). Sample collection was done from pustules or comedones. Treatment was given according to American Academy of Dermatology Guidelines and follow up was done till 12 weeks. Data was entered and analyzed using Statistical Package for Social Sciences (SPSS) v.25. Total 50 patients were recruited in the study. 56% patients were female and 44% were male. 60% patients had a history of similar lesions in the past. 56% patients used surgical mask, 34 % used N-95 mask and 18 % used cloth mask. The average duration of use for mask per day was 6.78 +/- 2.65. Cheeks were the most commonly involved site and 62% of patients had mild GAGS. The severity of acne was significantly higher in patients using N-95 mask ( p<0.05) but not associated with duration of mask use, history of mask re-use and use of moisturizers. 70% cases did not require systemic treatment. KOH was negative in all cases. Gram stain showed gram positive cocci and rods in 22% and 14 % cases respectively. Aerobic culture showed Staphylococcus aureus growth in 30% cases and Anaerobic culture showed Cutibacterum acnes growth in 20% cases. In our study we found that maskne presented with a milder variant of acne which in majority of cases responded well to topical treatment standardized for acne vulgaris and had a microbiome profile similar to acne vulgaris.Copyright © 2023

Streptococcus Pneumoniae Purulent Pericarditis

Background Bacterial pericarditis represents < 1 % of all cases of pericarditis in the United States. Most cases of bacterial pericarditis are from contiguous spread from underlying pneumonia or mediastinitis. We present a case of pneumococcal pericarditis in a patient with untreated pneumonia. Case A 54-year-old male with a past medical history of recent COVID-19 pneumonia presented with worsening dyspnea for the past 3 weeks. Vitals were T 99.3, BP 122/93, HR 159 BPM, O2 sat 94% on 3 L NC. ECG demonstrated atrial flutter with 2:1 block. CT scan demonstrated a pericardial effusion and bilateral pleural effusions. Decision-making In the ED, he became hypotensive and bedside echo demonstrated large pericardial effusion with RV collapse. Emergent pericardiocentesis produced 750 cc of purulent fluid. Streptococcus pneumoniae was isolated from the initial fluid aspirate. Right thoracostomy tube was placed with pleural fluid gram stain and culture without bacterial growth. Due to continued purulent drainage from the pericardial drain, repeat CT scan demonstrated persistent pericardial effusion and loculated right sided pleural effusion. He underwent video-assisted thoracoscopic surgery with pericardial wash out and window. He improved and was discharged with 6 weeks of Ceftriaxone. Conclusion Purulent pericarditis is typically a fulminant disease associated with high mortality and rapid progression. Prompt identification and management is critical for patient survival. [Formula presented]Copyright © 2023 American College of Cardiology Foundation

Bacterial Co-infections and Susceptibility patterns among admitted COVID 19 patients during 3rd wave of pandemic, in a Tertiary Care Hospital. Lahore

Objective: To check the Bacterial Co-infections and Susceptibility patterns among admitted COVID-19 patients during 3rd wave of pandemic. Study Design: Descriptive Cross Sectional study. Setting: Department of Microbiology, Combined Military Hospital Lahore Pakistan. Period: May 2021 to August 2021. Material & Methods: Six hundred and twelve COVID-19 positive patients having positive bacterial cultures were processed, Antibiotic susceptibility testing was done by Kirby-Bauer diffusion technique, all antibiotics were reported using breakpoints recommended in clinical and laboratory standards institute (CLSI 2021). Results: Out of 612 patients, 348 (56.9%) were male and 264 (43.2%) were female. Mean age of the patients was 57.2 ± 14.4 years with a range of 22 to 89 years. Bacterial coinfection was present in 70.4% of the patients. Gram negative bacteria (94.4%) were more prevalent in COVID-19 patients as compared to gram positive isolates (5.6%). Antibiotic sensitivity pattern of Staphylococcus aureus showed a high resistance against penicillin, ampicillin, tetracycline and doxycycline. Conclusion: Our study reported a high prevalence of bacterial coinfections in COVID-19 patients infected during the third wave of pandemic. A high percentage of gram negative species were identified in our study population, this could be due to the suppression in the immunity of individuals due to severity of COVID-19 infection and already present Antimicrobial resistance. [ FROM AUTHOR] Copyright of Professional Medical Journal is the property of Professional Medical Journal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

Rare case of post-COVID transverse myelitis

Case Report: Acute transverse myelitis (TM) is a rare inflammatory disease that typically presents asweakness, sensory alterations, and bowel or bladder dysfunction. Among the causes of TM are infections, paraneoplastic syndromes, or autoimmune conditions of CNS. Postinfectious TM can develop secondary to a viral or bacterial infection. SARS-CoV-2 is a recently discovered viral illness, and sequelae due to COVID-19 infection are still being studied. There is scarce literature relating the two conditions, and it is imperative to raise awareness. A 72-year-old man with hypertension and GERD, completely independent in ADL, was brought to the ED with sudden onset of bilateral lower extremity weakness. He reported symptoms started with difficulty climbing stairs that rapidly progressed to inability to ambulate independently and were associated with bilateral thigh soreness. Nine days prior, he developed fever and generalized malaise, and two days later, SARS-CoV-2 PCR and Ag tests were positive. He received azithromycin, Paxlovid, and dexamethasone as treatment. Upon evaluation, the patient was afebrile and hemodynamically stable. Neurological examination was remarkable for spasticity and hyperreflexia at bilateral lower limbs, clonus, preserved motor strength with adequate sensation to soft touch, and intact vibration and proprioception in all extremities. Cranial nerves were intact. These findings were consistent with an upper motor neuron lesion. On imaging, the Head CT scan was unremarkable. Thoracic/Lumbar Spine MRI was significant for distal thoracic and conus areas with central homogeneous brightness compatible with nonspecific myelitis. Laboratories showed leukocytosis without neutrophilia or bandemia, thrombocytosis, and elevated CRP. HIV and RPR tests were negative. A lumbar puncture for CSF analysiswas remarkable for mild monocytic pleocytosis (7 cell/muL), an increased level of total proteins (56 mg/dL), and normal glucose (57 mg/dL). CSF culture and gram stain were negative. CSF cytology yielded few lymphocytes and few monocytes and was negative for malignant cells. The meningoencephalitis panel was negative. Based on these findings, a clinical diagnosis of postinfectious myelitis secondary to COVID-19was made. The patient was treated with intravenous Methylprednisolone 1 g daily for five days. On follow-up, lower extremity weakness resolved completely, and he resumed his daily physical activities. Patients with COVID-19 infection can present with neurologic manifestations such as headache, myalgias, dizziness, dysgeusia, and anosmia. This case hopes to raise awareness of less commonly known neurological manifestations of SARS-CoV-2 infection and how the early recognition of symptoms can help expedite the diagnosis and treatment of the condition to avoid long-term sequelae. [Figure presented] Copyright © 2023 Southern Society for Clinical Investigation.

A Case of cryptococcal meningoencephalitis in an immunocompetent patient with Chiari I malformation

Case Report: Over 90% of cases of cryptococcal meningoencephalitis present in immunocompromised patients, with the majority of those being in patients with AIDS. However, this infection can also occur in patients with other immunocompromised states, such as steroid use, malignancy, rheumatologic diseases, and use of immunosuppressive medications. Delay in diagnosis can often lead to rapid neurological deterioration and mortality. Case: A young, otherwise immunocompetent patient, with a history of Chiari I malformation and recent COVID- 19 infection presented with syncope following two weeks of headaches, generalized body aches and weakness after COVID-19 diagnosis. Physical exam demonstrated an isolated CN VI palsy. Head imaging revealed new right caudate infarcts, and a cerebellar tonsillar descent compatible with history of Chiari I malformation. Initial lumbar puncture (LP) was deferred due to congenital brain herniation. Over the next few days, the patient continued to show increasing neurological deficits such as truncal ataxia and increased mood instability. The patient was transferred to the Intensive Care Unit, and LP was obtained under special neuro-critical care direction. Due to increased opening pressures and yeast on gram stain, cryptococcus was suspected and later confirmed. Although anti-fungal therapy was initiated, the patient continued to deteriorate, leading to cardiac arrest, intubation, and placement of lumbar drain. The patient unfortunately did not demonstrate neurologic recovery following arrest and progressed to brain death. Discussion(s): While cryptococcal meningoencephalitis is overwhelmingly a disease of immunocompromised patients, it can occur in immunocompetent hosts, and delay in diagnosis and treatment can lead to adverse and fatal outcomes. This patient had no known underlying conditions besides a recent mild COVID-19 infection and underlying Chiari I malformation, neither of which are known to be associated with cryptococcal meningoencephalitis. These factors may however have played a role in his disease and progression. Copyright © 2023 Southern Society for Clinical Investigation.

Granulomatous Pleuritis in a Previously Covid-19-Infected Patient

INTRODUCTION: The most common setting for granulomatous pleuritis is usually in the presence of Mycobacterium tuberculosis. This pathology draws interest due to its potential of long-term injury to lung pleura, as well as, the potential to harm the lung parenchyma by association. We present a rare presentation of granulomatous pleuritis following COVID19 infection. DESCRIPTION: The patient is a 28-year-old female who presents to the hospital with fever and malaise for one week. She reports having an outpatient CT which showed a large right pleural effusion so her pulmonologist instructed her to come in. She denies recent exposure to any sick contacts. She does note a history of COVID-19 a year ago which resulted in shortness of breath but did not require hospitalization. She has worked at a gun shooting range for the last two years, for which she assembles bullets. She notes that she is required to wear a particulate protection mask and has worn this consistently to limit exposure. Thoracic surgery was consulted and initially completed a thoracentesis with 500 mL of exudative fluid. Patient remained intermittently febrile with worsening right sided chest pain. Culture and gram stain were unremarkable. She subsequently underwent a bronchoscopy with bronchial washing, biopsy, and decortication. Pathology demonstrated non-necrotic granulomatous pleuritis with a small area of central fibrinoid necrosis. Repeat chest x-rays demonstrated a minimal pleural effusion, much improved from prior. Fevers had also subsided at this time. Patient was discharged home with instructions to follow-up with thoracic surgery regarding further management of steroids. DISCUSSION: The findings of non-tuberculosis-related granulomatous pleuritis are unique in that they frame the need to look for different perspectives and potentiators for pleural pathology. This case is also important given the unique presentation of the post-covid inflammatory response. Since COVID-19 is still so new, the field of post covid syndromes remains largely unknown.

Candidemia in a tertiary care hospital: Epidemiology, speciation and antifungal susceptibility pattern

Objective: The incidence of bloodstream fungal infection is on the rise and Candida species remains responsible for the majority of the cases. Candidemia is frequently associated with a high rate of mortality and morbidity. The purpose of this study was to characterize Candidemia, its epidemiology, species distribution, and antifungal susceptibility pattern in a tertiary care hospital. Methods and Material: Candida species isolated from the blood culture of 51 patients in a tertiary care hospital during the period from 2016 to 2021 were included in the study. The growth on SDA was confirmed by Gram staining and speciation and antifungal susceptibility were performed with Automated system VITEK 2.0. Result(s): Out of51 isolates, Candida auris wasthe most common speciesaccounting for about 37.2% followedby C.albicans 19.7%, C. tropicalis 17.6%, and C. famata 9.8%. Candida auris has emerged as the predominant species during severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) pandemic.The incidence has risen from 22% to 60% during the pandemi C. Candida specieswere foundto be96.08% sensitiveto flucytosine, 94.12% tovoricanazole, 90.19%to casp ofungin/micafungin, 60.78% to amphoterecin B, and 56.86% to fluconazole. Conclusion(s): Candida auris has emerged as the predominant species in ICU setup and during SARS-CoV-2 pandemi C. Empirical treatment with echinocandines would be appropriate in high-risk patients with suspected Candidemia.

Community-acquired Methicillin-resistant Staphylococcus aureus Pneumonia and Parapneumonic Effusion in a Male Patient with Diabetes: A Case Report

Methicillin-resistant Staphylococcus aureus (MRSA) infections are a primary health concern. They are commonly differentiated as hospital-acquired methicillin-resistant Staphylococcus aureus (HA-MRSA) and community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) infections, based on their epidemiology, susceptibility findings, and molecular typing patterns. Therefore, appropriate contact precautions and isolation measures should be implemented. CA-MRSA mostly causes skin and soft-tissue infections, but the probability and incidence of it causing sepsis and invasive infections have increased dramatically in recent years. In this study, we report a case of CA-MRSA pneumonia with pan-pneumonic effusion in a 59-year-old male diabetic patient with preexisting comorbidities such as diabetic ketoacidosis and non-ST elevated myocardial infarction. The early reporting of the organism's identity and its antimicrobial susceptibility, as well as timely initiation of antibiotic therapy, aided in the successful management and cure of the patient.

ATYPICAL PRESENTATION OF FAT EMBOLISM SYNDROME IN AN IMMUNOCOMPROMISED PATIENT

SESSION TITLE: Systemic Diseases with Deceptive Pulmonary Manifestations SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: Fat embolism is a syndrome that can occur during orthopedic procedures or fractures of the long bones, especially the femur and tibia. It can affect multiple organs, including the brain, skin, and lungs, causing the triad of altered mentation, petechiae, and hypoxemia. Here, we present a case of a 54-year-old woman at risk for graft versus host disease (GVHD) who presented with dyspnea a few weeks after an orthopedic procedure. Initial chest radiograph was notable for parenchymal infiltrates, and she was initially treated with antibiotics without improvement. CASE PRESENTATION: A 54-year-old woman with a history of leukemia, stem cell transplantation years ago, GVHD (skin liver, ocular, oral, joints (not lung), with clinical and cytogenetic remission underwent total hip arthroplasty. Two weeks later, she developed lethargy and dyspnea and presented to the emergency department. She was found to have an elevated WBC of x19.5 k/ul (normal 4.1-9.3k/uL) with a left upper lobe consolidation on the chest radiograph (Figure 1). She was treated empirically for pneumonia and discharged with a 7-day course of levofloxacin. Despite completing the course of antibiotics, her dyspnea worsened, and she presented to the emergency department two weeks later with worsening hypoxemia. Computed tomography (CT) of the chest showed bilateral diffuse ground-glass opacities (GGOs) with patchy consolidations in a broncho-vascular distribution (Figure 2). She was negative for COVID-19, Influenza A, B and Legionella urinary antigen. The differential diagnosis included infection and GVHD among others. She underwent bronchoalveolar lavage (BAL). The Gram stain and the culture did not suggest an infection. Pathology from BAL returned significant for reactive bronchial and squamous cells with lipid-laden macrophages. She was started on steroids. Her clinical status improved dramatically, and she was eventually discharged. At a 3-month follow-up her symptoms had improved. Her CT scan also showed significant improvement (Figure 3). DISCUSSION: Our case highlights the successful diagnosis of fat embolism in the lungs in a patient with complicated medical history. Fat embolism usually presents as ground glass opacities. However, the diagnosis was more challenging in this case due to a significant time lapse between her surgery and her presentation to the hospital. She also lacked the other common signs of fat embolism including altered mentation and skin changes. Therefore, other etiologies, such as GVHD, bacterial or viral infection were initially strongly considered. CONCLUSIONS: The diagnosis of fat embolism syndrome condition should still be suspected despite a delay from the initial surgery. Diagnosis in immunocompromised patients requires a detailed workup to rule out other etiologies. Reference #1: Johnson, M. J., & Lucas, G. L. (1996). Fat embolism syndrome. Orthopedics, 19(1), 41-49. Reference #2: Newbigin, K., Souza, C. A., Torres, C., Marchiori, E., Gupta, A., Inacio, J., … & Peña, E. (2016). Fat embolism syndrome: state-of-the-art review focused on pulmonary imaging findings. Respiratory medicine, 113, 93-100. Reference #3: Swiatek, K., Kordic, G., & Jordan, K. (2018). An Unlikely Presentation of Fat Embolism Syndrome. Chest, 154(4), 686A. DISCLOSURES: No relevant relationships by Raheel Anwar No relevant relationships by Boris Medarov

A TALE OF A DRUG THAT KILLED A BUG BUT CAUSED PNEUMONIA: A CASE REPORT OF DAPTOMYCIN-INDUCED ACUTE EOSINOPHILIC PNEUMONIA

SESSION TITLE: Critical Diffuse Lung Disease Cases 2 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Acute eosinophilic pneumonia (AEP) is dramatic in presentation mimicking infectious pneumonia or acute respiratory distress syndrome in previously healthy individuals. Medications are a commonly recognized cause of AEP. Daptomycin, has been strongly linked to AEP. Herein, we present a case of a patient with a septic joint treated with Daptomycin who went on to develop AEP. CASE PRESENTATION: Patient is an 80 year old man with history of hypertension, hypothyroidism, atrial flutter, complete heart block status post pacemaker, who had a hx of a mucinous cyst on his left index finger, requiring hospitalization. Blood cultures were positive for MRSA s/p debridement of the joint. He was discharged on 4 weeks of intravenous daptomycin. Two weeks after being discharged he presented back to the hospital with fevers, fatigue and worsening shortness of breath. His temperature was 103.8 and O2 saturation of 90% on 2L NC. Laboratory findings included WBC count of 8.6 with no eosinophilia on differential, ESR 110, negative blood cultures, sputum cultures with commensal flora, negative urine legionella, PCR for SARS COV-2 was negative. Chest radiograph showed mild interstitial airspace disease in the left mid and lower thorax, along with small bilateral pleural effusions. CT chest showed scattered bilateral consolidations and ground glass opacities and trace bilateral effusions. Daptomycin was switched to Vancomycin. Patients oxygen requirements had increased to 6l NC. Patient underwent airway exam with bronchoscopy and broncheoalveolar lavage in superior segment of the lingula, which showed inflamed bronchial mucosa with copious secretions. Cell count of the BAL showed increased eosinophil count with negative gram stain and culture. Patient was started on methylprednisolone 60 mg four times per day and then tapered. Vancomycin was switched to oral linezolid. Patient's hypoxia improved and was discharged home on 3l NC. At four week follow up, he no longer required oxygen on ambulation and chest radiograph showed complete resolution of infiltrates. DISCUSSION: Over 140 drugs have been recognized as a cause of drug induced eosinophilic pneumonia (DIEP). The diagnosis of DIEP requires febrile illness <5 days, diffuse bilateral infiltrates, hypoxemia and BAL showing 25% eosinophils or eosinophilic pneumonitis on lung biopsy. Additionally, a diagnosis of DIEP requires exposure to a candidate drug in the appropriate time frame, exclusion of infectious causes of eosinophilic pulmonary opacities. It also requires clinical improvement after cessation of medication. Daptomycin has been strongly linked to DIEP. In 2010 US FDA issued a warning about the risk of developing eosinophilic pneumonia during treatment with Daptomycin. CONCLUSIONS: Daptomycin is strongly linked with DIEP. Clinicians should maintain a high index of suspicion for DIEP in patient treated with daptomycin who develop respiratory distress. Reference #1: Uppal, P., LaPlante, K.L., Gaitanis, M.M. et al. Daptomycin-induced eosinophilic pneumonia - a systematic review. Antimicrob Resist Infect Control 5, 55 (2016). https://doi.org/10.1186/s13756-016-0158-8 Reference #2: Cottin V. Eosinophilic Lung Diseases. Clin Chest Med. 2016 Sep;37(3):535-56. doi: 10.1016/j.ccm.2016.04.015. Epub 2016 Jun 25. PMID: 27514599. Reference #3: Rosenberg CE, Khoury P. Approach to Eosinophilia Presenting With Pulmonary Symptoms. Chest. 2021 Feb;159(2):507-516. doi: 10.1016/j.chest.2020.09.247. Epub 2020 Sep 28. PMID: 33002503;PMCID: PMC8039005. DISCLOSURES: No relevant relationships by Kamelia Albujoq No relevant relationships by Rajaninder Sharma

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

LUNG CAVITY: A RARE FINDING IN COVID-19

SESSION TITLE: Post-COVID-19 Infection Complications SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Chest CT features in COVID-19 pneumonia include scattered ground-glass infiltrates in milder cases to confluent ground-glass change, dense consolidation, and crazy paving in the critically ill. However, cavitary lesions are uncommon in these patients. We present a case of lung cavity in a patient who had recent COVID-19 pneumonia. CASE PRESENTATION: A 33-year-old male diagnosed with COVID-19 four weeks ago presented with hemoptysis and exertional dyspnea. He had pleuritic chest pain without fever, night sweats, weight loss, skin rashes, hematemesis, or epistaxis. He had COVID-19 in Brazil, where he had received dexamethasone, hydroxychloroquine, ivermectin, colchicine, azithromycin, and rivaroxaban. The last dose of rivaroxaban was three days prior to the presentation. He had no history of travel to caves or exposure to birds or animals. His past medical history included hypertension, diabetes, and bariatric surgery. He had no history of smoking or IV drug use. He had moved from Brazil to the United States six years ago and worked as an interpreter. Physical examination was notable for stable vitals with O2 sat of 99%. Systemic examinations were unremarkable. Blood work including CBC, platelet count, PT/INR was within normal limits. COVID-19 testing (PCR) was negative. A chest CT revealed bilateral scattered ground-glass opacities with central cavitation in the left lower lobe concerning for septic pulmonary emboli. HIV 1/2, ANA, rheumatoid factor, and Quantiferon TB gold were negative. Blood cultures showed no growth. An echocardiogram was negative for any vegetations. Bronchoalveolar lavage from the left lower lobe was negative for AFB and gram staining. Sputum cultures, fungal cultures, and NAAT for Mycobacterium tuberculosis were negative, as was the cytology. He was started on amoxicillin-clavulanic acid during his hospital stay. He did not experience any recurrence of hemoptysis and was discharged home. The subsequent follow-up chest CT scans showed resolving cavitation at one month and a complete resolution of the cavity at 3 months. DISCUSSION: Cavitary lung lesions are usually related to fungal, mycobacterial, autoimmune, parasitic, thrombotic, or neoplastic etiologies. While not often seen in patients with viral pneumonia, lung cavitation can rarely occur in COVID-19. Mycobacterium tuberculosis and Nocardia were suspected given the history of being an immigrant and a recent trip to Brazil. As these tests were negative and the lung cavity resolved over a few months with conservative treatment, the etiology of the cavity was attributed to a late presentation of COVID-19 pneumonia. CONCLUSIONS: COVID-19 has variable complications which are still to be explored. The lung cavity in a COVID patient is an under-recognized entity. This case report highlights the need for further studies to determine the cause of cavitation, which could be related to COVID infection or its treatment. Reference #1: Selvaraj V, Dapaah-Afriyie K Lung cavitation due to COVID-19 pneumonia. BMJ Case Reports CP 2020;13:e237245. Reference #2: Chen Y, Chen W, Zhou J, Sun C, Lei Y. Large pulmonary cavity in COVID-19 cured patient case report. Ann Palliat Med 2021;10(5):5786-5791. doi: 10.21037/apm-20-452 Reference #3: Zoumot, Z., Bonilla, MF., Wahla, A.S. et al. Pulmonary cavitation: an under-recognized late complication of severe COVID-19 lung disease. BMC Pulm Med 21, 24 (2021). https://doi.org/10.1186/s12890-020-01379-1 DISCLOSURES: no disclosure on file for Raul Davaro;No relevant relationships by Susant Gurung No relevant relationships by Bijay Khanal No relevant relationships by Anil Phuyal No relevant relationships by Kamal Pokhrel No relevant relationships by REGINA SHRESTHA No relevant relationships by Mithil Gowda Suresh

TUBERCULOUS PLEURAL EFFUSION MASQUERADING AS DRUG-INDUCED LUPUS

SESSION TITLE: Critical Care Presentations of TB SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: TNFα plays a pivotal role in inflammation and maintenance of immune response against tuberculosis. The use of TNF inhibitors (TNFi) is associated with a significant increase in the incidence of tuberculosis (TB). TNFi may cause drug-induced lupus (ATIL) presenting as constitutional symptoms, rashes, pericardial and pleural effusions with positive autoantibodies. We present a case of pleural TB masquerading as drug-induced lupus. CASE PRESENTATION: A 68y/o woman with a history of ulcerative colitis (on infliximab, mesalamine), hypertension, T2DM, CAD, complained of low-grade fever, rashes, left-sided chest pain, dyspnea, and arthralgias for two weeks. Chest pain- worse with inspiration and cough. She emigrated from India to the USA 40 years ago. Six months before infliximab therapy, Quantiferon gold was negative. Exam: faint hyperpigmentation over shins, minimal swelling of MCPs and ankles, dullness to percussion over the left chest with decreased breath sounds. Labs: CRP 101 mg/dL, Hb 10.8 iron deficient, rheumatoid factor and anti-CCP negative, ANA 1:40, dsDNA 1:640, a reminder of ENA negative, anti-histone negative, C3/C4 normal, UA bland, protein/Cr 0.4 mg/gm, negative blood cultures, SPEP and LDH normal. CXR: opacification of the left lung up to midfield. CT chest: moderate left and small right pleural effusions, enlarged mediastinal lymph nodes. COVID and Quantiferon: negative. Thoracentesis: 850 ml of exudative fluid (2 out of 3 Light's criteria), lymphocytic predominance (76% of 4148 nucleated cells), adenosine deaminase (ADA) 42 U/L, gram stain, culture, acid-fast and MTB PCR negative, cytology negative. Thoracoscopy with biopsy of the parietal pleura: necrotizing granulomatous pleuritis with acid-fast bacilli. Sensitivity: pan-sensitive M. tuberculosis. Sputum: negative for TB. She was discharged on RIPE treatment for reactivation of TB. DISCUSSION: The incidence of infliximab-induced lupus is approximately 0.19% and confirming the diagnosis is challenging. The immunogenicity of infliximab is high, 66% of patients develop positive ANA. Anti-histone antibodies are less commonly associated with ATIL as opposed to classic drug-induced lupus and dsDNA is positive in up to 90% of cases of ATIL. Renal involvement is rare. The diagnostic usefulness of ADA (over 40 U/L) in lymphocytic pleural effusions for the diagnosis of tuberculosis in an immunosuppressed individual is demonstrated here. In countries with low TB burden, such as the USA, the positive predictive value of ADA in pleural fluid declines but the negative predictive value remains high. CONCLUSIONS: Tuberculous pleuritis is not always easily diagnosed since AFB smears and sputum may remain negative. When ADA level in lymphocytic pleural fluid is not low thorough search for TB with thoracoscopy and biopsy is justified. Reference #1: Shovman O, Tamar S, Amital H, Watad A, Shoenfeld Y. Diverse patterns of anti-TNF-α-induced lupus: case series and review of the literature. Clin Rheumatol. 2018 Feb;37(2):563-568. Reference #2: Benucci, M., Gobbi, F. L., Fossi, F., Manfredi, M. & Del Rosso, A. (2005). Drug-Induced Lupus After Treatment With Infliximab in Rheumatoid Arthritis. JCR: Journal of Clinical Rheumatology, 11 (1), 47-49. Reference #3: Valdés L, San José ME, Pose A, Gude F, González-Barcala FJ, Alvarez-Dobaño JM, Sahn SA. Diagnosing tuberculous pleural effusion using clinical data and pleural fluid analysis A study of patients less than 40 years-old in an area with a high incidence of tuberculosis. Respir Med. 2010 Aug;104(8):1211-7. DISCLOSURES: No relevant relationships by Adam Adam No relevant relationships by Moses Bachan No relevant relationships by Chen Chao No relevant relationships by Zinobia Khan No relevant relationships by Milena Vukelic

CARDIAC TAMPONADE SECONDARY TO COVID-19 INFECTION

SESSION TITLE: Infections In and Around the Heart Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Due to the novelty of COVID-19 virus, complications of this severe respiratory infection are continually emerging. The inflammatory response to the virus carries a high mortality rate and can lead to a variety of cardiothoracic complications such as acute coronary syndrome, thromboembolism, and heart failure [1]. Here, we present a case of a young female who suffered cardiac tamponade (CT) from a pericardial effusion (PEEF) attributed to COVID-19 infection, which has only been described a handful of times in the literature. CASE PRESENTATION: A 33-year-old female with a history of Down syndrome and morbid obesity presented with worsening dyspnea and fever for one week. Her initial oxygen saturation was 50% on room air, and bilevel noninvasive ventilatory support was initiated. Her viral PCR was positive for COVID-19. A computed tomography angiogram of the chest revealed small bilateral pulmonary emboli, diffuse ground-glass consolidations, and small bilateral pleural effusions. Her respiratory status continued to decompensate and she was placed on mechanical ventilation. She became hypotensive requiring vasopressor support. The following morning, an echocardiogram (TTE) revealed an ejection fraction of 40-45% and a new PEEF with early right ventricular diastolic collapse consistent with CT physiology. She underwent emergent pericardiocentesis, and 220 mL of bloody fluid was drained. PEEF studies revealed a glucose level of 186 mg/dL, LDH of 1380 U/L, and protein of 3.0 g/dL. Total nucleated count was 16,545/uL with 68% neutrophils. Gram stain showed a few white blood cells without organisms, and final bacterial, fungal, and acid-fast cultures were negative. A pericardial drain was left in place, but the procedure was complicated by a pneumothorax and a chest tube was placed. A follow-up TTE the next day revealed improvement of the PEEF without signs of CT. A repeat chest x-ray showed resolution of the pneumothorax. Unfortunately, the patient’s oxygenation and hemodynamic status continued to worsen. She eventually suffered cardiac arrest with pulseless electrical activity and succumbed to her illness. DISCUSSION: New knowledge regarding complications of COVID-19 infection is continually emerging. According to a February 2022 systematic review, only 30 cases of severe PEEFs with CT secondary to COVID-19 have been recorded. The mechanism by which PEEFs form is unclear. It is proposed that the entry of the virus into inflammatory cells causes a release of cytokines such as TNF-alpha, IL-1, IL-6, and IL-8. This resulting cytokine storm allows rapid inflammation and infiltration of fluid into the pericardial sac [1]. CONCLUSIONS: In a decompensated patient with COVID-19, a stat TTE should be obtained to rule out PEEF. Physicians must be cognizant of this uncommon yet highly fatal complication in unstable COVID-19 patients, as cardiac tamponade is a potentially reversible cause of cardiac arrest. Reference #1: Kermani-Alghoraishi, M., Pouramini, A., Kafi, F., & Khosravi, A. (2022). Coronavirus Disease 2019 (COVID-19) and Severe Pericardial Effusion: From Pathogenesis to Management: A Case Report Based Systematic Review. Current problems in cardiology, 47(2), 100933. https://doi.org/10.1016/j.cpcardiol.2021.100933 DISCLOSURES: No relevant relationships by Amanda Cecchini No relevant relationships by Arthur Cecchini No relevant relationships by Kevin Cornwell No relevant relationships by Krupa Solanki

A CASE OF MULTIFOCAL PNEUMONIA -A DIAGNOSTIC CHALLENGE

CASE: A 25 year old Vietnamese female initially presented to the emergency department (ED) with progressive dyspnea and cough for 2 weeks. Chest Xray (CXR) showed left lower lobe consolidation and was started on a 5-days of azithromycin. She returned to ED 3 days later with a worsening cough, yellowish sputum, dyspnea, pleuritic chest pain, chills, appetite loss, and a 6-pound weight loss. 7 years ago her pre-immigration screening was negative for tuberculosis. She worked in a nail salon and did gardening as a hobby. On exam, she was afebrile, appeared dyspneic with normal oxygen saturation, diminished breath sounds on left lower lobe with egophony. Labs showed leukocytosis of 22,300 with neutrophilia and negative COVID-19 test. Repeat CXR showed worsening left lower lobe opacity. On day 3, temperature peaked at 103.1F with worsening sputum production. Computed tomography (CT) chest showed complete consolidation of the left lower lobe with tree-in-bud opacities in bilateral upper lobes and right lower lobe. Antibiotics were switched from ceftriaxone and azithromycin to piperacillin-tazobactam and vancomycin. Bronchoalveolar lavage (BAL) gram stain, acid-fast bacilli stain and gomori stain, and blood cultures were negative. Follow-up CT chest was worse and repeat bronchoscopy with biopsy was done. On day 8, urinary blastomyces and histoplasma antigen tests were positive. BAL cytology showed budding yeast consistent with blastomycosis. IV voriconazole was added and her symptoms gradually improved. She was discharged on 6-month course of oral voriconazole. BAL and biopsy cultures came back positive for B. dermatitidis confirming the diagnosis. Outpatient follow-up with CXR after a month showed both clinical and radiological improvement. IMPACT/DISCUSSION: Blastomycosis is a fungal infection caused by thermally dimorphic fungi Blastomyces species, endemic in Ohio, Mississippi River Valleys, and the Great Lakes region in the United States. It commonly presents as a pulmonary infection following inhalation of spores. Severity varies from asymptomatic to life-threatening acute respiratory distress syndrome. Diagnosis delay is common with frequent misdiagnoses including bacterial pneumonia, malignancy, and tuberculosis. Pulmonary blastomycosis commonly presents as dense consolidation in the upper lobes but can have variable presentation. Serological tests, cultures and BAL studies can aid in diagnosis. Repeat bronchoscopies should be considered when the suspicion is high. Of note, blastomyces antigen can have cross-reactivity with histoplasma antigen which might be the case with our patient. CONCLUSION: This case highlights the resemblance of clinical and radiological presentation of blastomycosis with other respiratory conditions and the need for timely diagnosis, treatment, and antimicrobial stewardship. Practitioners need to keep a strong suspicion of this disease in patients with atypical presentation for pneumonia especially in endemic areas.

Rapidly Progressive Disseminated Aspergillosis in a Diabetic Patient

Invasive aspergillosis is a rapidly progressive, fatal infection that usually occurs in immunocompromised patients. The spectrum of clinical presentation ranges from non-invasive, invasive, destructive and allergic aspergillosis. It is rare to see overwhelming aspergillosis in an immunocompetent host. Nevertheless, certain risk factors such as underlying fibrotic lung disease, suppurative infection, long-term corticosteroid use and uncontrolled diabetes mellitus (DM) have been described. We hereby present a case of invasive pulmonary aspergillosis in a patient with uncontrolled DM. A 60-year-old man with a history of heavy smoking (50- pack-year), poorly controlled DM presented to the hospital with a large area of erythema with eschar over his left posterior thigh. Clinical examination and CT abdomen pelvis confirmed necrotizing fasciitis involving his perineum and left thigh. Admission CT abdomen showed a small left lower lobe infiltrate (Day 1, Panel A). He underwent urgent debridement and intraoperative tissue cultures grew coagulase-negative staphylococcus, Proteus Vulgaris and anaerobic gram-positive rods. He received piperacillintazobactam, vancomycin, and clindamycin for 16 days which was subsequently narrowed to ceftriaxone and metronidazole. He had worsening leukocytosis but all his blood cultures have been negative. Tracheal aspirate gram stain on day 5 showed moderate yeast, and cultures grew Candida albicans and Aspergillus fumigatus. CT scan of his chest showed bilateral reticulonodular opacities with a new loculated right pleural effusion (Day 16, Panel B). Trans-esophageal echocardiogram did not show any right-sided heart valve vegetation. He received intravenous voriconazole for disseminated aspergillosis. Despite of new prophylactic antifungal strategies, more sensitive and rapid diagnostic tests, as well as various efficacious treatments, survival of invasive disseminated aspergillosis remains poor. High clinical suspicion with a proactive investigation approach is the key to minimizing mortality. Various risk factors such as hematopoietic-cell transplantation, neutropenia, solid-organ transplantation, chemotherapy, prolonged ICU stay, structural lung disease, impaired mucociliary clearance after a recent pulmonary infection (including SARS-CoV-2) have been well described. Our case highlights the importance of recognizing uncontrolled DM as a crucial risk factor for disseminated aspergillosis. (Figure Presented).

A Case Report of Ribociclib-Induced Pneumonitis

Palbociclib, abemaciclib and ribociclib are cyclin-dependent kinase 4/6 (CDK 4/6) inhibitors used in the current treatment of HR-positive, HER2-negative metastatic breast cancer.1.2 As CDK 4/6 inhibitors are becoming more common it is important to be aware of some potentially fatal side effects. A 54-year-old woman with stage III breast cancer with prior mastectomy currently on hormonal and immunotherapy with anastrozole, ribociclib and goserelin presented with fever and shortness of breath. The patient became febrile with a negative COVID-19 test, and was treated for community acquired pneumonia. The fevers persisted despite antibiotics. CBC notable for leukopenia and uptrending absolute eosinophil count of 280 cells per microlitre. A chest CT scan revealed scattered, predominantly peripheral ground glass opacities in the bilateral upper, bilateral lower, and right middle lobes not present on prior imaging. A diagnostic bronchoscopy with BAL revealed 140 white-blood cells, 4 polys, 60 lymphocytes, 30 monocytes and 6 eosinophils. Flow cytometry yielded predominantly T-cells, abundant macrophages and inflammatory Infectious work up including PCP PCR, gram stain, fungal and AFB culture were negative. Ribociclib was discontinued and the patient improved symptomatically with return to baseline level of function. Reports of CDK 4/6 inhibitor drug-associated lung injury are limited There has been only one case report outside of clinical trials of Ribociclib pneumonitis.7 As these drugs become more commonly used, it is important for clinicians to be aware of this potentially fatal drug associated lung injury. Treatment with drug cessation has varying responses from recovery like in our patient to death.

Acute Eosinophilic Pneumonia Caused by Cigar Smoking

Introduction: Eosinophilic lung diseases (ELD) are a group of conditions that are characterized by pulmonary eosinophilia. Acute eosinophilic pneumonia (AEP) may be idiopathic in many patients, however, changes in smoking habits and drug use can trigger the disease. Case: A 24-year-old female presented to the emergency room with dyspnea for 1 week. She also had productive cough, fever of 38.7C (101.7F) and chest tightness. Although she had been vaping for the past year she switched to heavy cigar smoking 3 weeks prior to admission. Vital signs on presentation were blood pressure 127/72 mmHg, heart rate 122 beats/min, respiratory rate 28/min, oral temperature 37.4°C (99.4°F) and oxygen saturation 88% on room air. Lung exam revealed mild rhonchi. Blood work showed leukocytosis 29.13 x 103/mcL (N:4-12 x 103/mcL) with neutrophilia 26.6 x 103/mcL (N: 1.60-7.71 x 103/mcL), mild lymphopenia 1.07 x 103/mcL and a normal metabolic panel. SARS-CoV-2 PCR was negative 3 times. CT chest revealed consolidative opacities involving the right lung more than left and small bilateral pleural effusions. The patient was provided supplemental oxygen via nasal cannula and started on ceftriaxone and azithromycin for community acquired pneumonia. She rapidly declined requiring endotracheal intubation for invasive mechanical ventilation. Antibiotic coverage was broadened to vancomycin, piperacillin-tazobactam, doxycycline and levofloxacin. Further negative work up included viral pathogen panel, respiratory cultures, HIV screening, fungal antibodies, urine pneumococcal and legionella antigens, ANA and ANCA, and serum next-generation sequencing. She developed peripheral eosinophilia on hospital day 2 which peaked at 3.29 x 103/mcL (N: 0.0-0.40 x 103/mcL) on day 6. Bronchoscopy revealed no organisms on gram stain and there was no alveolar hemorrhage. Cell count from bronchoalveolar lavage (BAL) was not available. She was started on methylprednisone 60 mg every 6 hours IV for presumed AEP with marked improvement over the next 48 hours. She was discharged home shortly thereafter on an 8 week steroid taper. Discussion: AEP has been associated with new onset or resumption of cigarette smoking. Our patient had an acute onset febrile illness rapidly progressing to hypoxic respiratory failure, initial peripheral neutrophilic leukocytosis with subsequent peripheral eosinophilia, patchy bilateral ground glass and consolidative opacities with small pleural effusions, and immediate response to steroids. Prognosis is excellent if the disease is recognized and treated promptly. Conclusion: AEP is a rare cause of acute respiratory failure that can be confidently diagnosed with careful history, a constellation of symptoms and signs, and BAL eosinophilia (>20-25%).

CREUTZFELDT-JAKOB DISEASE: ACCELERATED BY COVID?

TYPE: Late Breaking TOPIC: Chest Infections INTRODUCTION: Creutzfeld Jakob Disease (CJD) is a collective group of rare neurodegenerative diseases characterized by rapidly progressing cognitive decline, deficits in cortical function (aphasia, apraxia, agnosia), myoclonic jerks and extrapyramidal symptoms with a mortality of 100%. CASE PRESENTATION: We present a 72-year-old female who initially presented with aphasia, dyscalculia, right hemiparesis and dysgraphia.Upon arrival, she was hemodynamically stable and labs were remarkable for a positive COVID PCR test. CT head and CT angiogram was within normal limits. MRI was nonspecific. EEG showed left temporal lateralized periodic discharges (PLDs) at 1 Hz with a triphasic morphology and Lumbar puncture disclosed a protein of 79 mg/dL, glucose 65 mg/dL, WBC 1, HSV 1 and 2 PCR, cryptococcus, gram stain/culture AFB, and cytology were all negative. With concern for autoimmune encephalitis she was empirically started on IVIG without improvement. Paraneoplastic and autoimmune evaluation resulted pan negative. 14-3-3 CSF protein assay reported positive and diagnosis CJD was made. After goals of care discussion with the family, she was discharged home with hospice. DISCUSSION: Sporadic type (sCJD) accounts for about 85% of cases and occurs after somatic mutation in the gene for PrP protein. Rapid neurocognitive decline and cortical function deficits with negative infectious, autoimmune, and paraneoplastic workups should prompt further evaluation for CJD. CSF protein 14-3-3 has a sensitivity of 92%–96% for sCJD. EEG showing of a 1/second periodic triphasic sharp wave complex is present in 1/3 cases. CONCLUSIONS: Most recently, there have been some case reports indicating that the systemic immune response in COVID-19 could accelerate the clinical course of sCJD, however, a potential causal link remains unclear. DISCLOSURE: No significant relationships. KEYWORD: CJD