Okay, it's 1 o'clock. Thank you, everybody, for coming. Welcome. This is going to be the session, Extrapulmonary and Extraordinary Infections, this oral podium presentations. We're going to have four speakers today, and we're going to invite Dr. Chang as our first presenter. Thank you very much. And you have eight minutes. Thank you, Dr. Tinkers, and everyone for attending this session. I am Dr. Siwon Chang from South Korea. I'm a clinical fellow, first year in Division of Pulmonary and Critical Care Medicine in Severance Hospital in Seoul, South Korea. I have nothing to disclose. So today I would like to open the session by describing a rare case of disseminated NTM infection complicated by exogenous lipo-pneumonia in an immunocompetent individual. And after that, I will briefly review the relevant literature to this case. So a 72-year-old male has presented to our clinic, referred from another institution with three months of recurrent fever, a productive cough, and shortness of breath. Before his referral, he was hospitalized for multiple times to treat for suspected bacterial pneumonia. But at his presentation, his first vital signs were stable without any fever or desaturation, and his physical exam findings were unremarkable. The patient was an ex-smoker with a medical history for hypertension and dyslipidemia and chronic rhinitis. He reported of regularly aspirating squalene nasally for the past five months as an alternative remedy for his rhinitis. He was admitted for further evaluation with the impression of lipo-pneumonia. Initial CT scans on the day of his admission showed multifocal ground glass capacities with crazy paving patterns in the dependent areas of both lungs. These consolidations also contained areas of fat density. So after that, endoscopic evaluation was performed, and transbronchial lung biopsy targeting the consolidation seen at the posterior basal segment of right lower lobe yielded fibrinous organizing pneumonia. Bronchoalveolar lavage performed also at the posterior segment of right upper lobe returned turbid whitish milky fluid. But the routine fluid analysis was inconclusive for any other specific etiology. So based on the chest CTs, the history and the endoscopic results, we diagnosed the patient with exogenous lipoid pneumonia. During also the first few days of his admission, the patient was started on broad-spectrum antibiotics for intermittent fever. But initially, evaluations for infections were negative, except for a positive acid-basalized smears. And subsequent cultures returned NTM, which was later identified as mycobacterium abscessus, subspecies abscessus. So for his initial NTM treatment, the patient was started on azithromycin, IV imipenem, IV amikacin, and nebulized amikacin. Subsequent cultures from sputum and BAL and lung tissues were persistently positive for M abscessus, as you can see throughout the follow-up. And on the day of the first administration for the NTM treatment, the blood cultures that were drawn were returned positive for NTM, which established the diagnosis of disseminated disease. The cultures remained, or blood cultures remained positive, and clofazamine and linezolid were added. But the first negative blood cultures were not seen until day 45 of treatment. Meanwhile, we also studied for immune deficiency in this patient, but there were no evidence of immune deficiency, including normal CD4 and CD8 counts, negative HIV studies, and also a negative NGS panel that we performed at our institution to check for immune deficiency. The patient was discharged on day 71 of treatment, with a maintenance dose of prednisolone for the lipo and pneumonia. Despite decreasing the dose of steroids, his shortness of breath did not get worse. But his follow-up CT scans gradually aggravated. And also, the respiratory tract specimens, including BAL and bronchial tissue, remained also positive for NTM, as I just mentioned, despite continued treatment. In addition, the patient also showed gradual decline in general condition and cognitive function, and was referred for rehabilitation. And these multiple hospitalizations were for intensive rehabilitation, but during these hospitalizations, he also had episodes of delirium. By 234, he was admitted for the fifth time. And on day 248 of NTM treatment, the patient was started on ICU care for drowsy mental status and aggravation of his pneumonia. At the suspicion of drug-induced encephalopathy, all drugs except for macrolide were discontinued. And brain MRI scans showed ventriculitis. So, with neuro consult, we performed cerebral spinal fluid study. And on day 268 of treatment, the CSF study returned positive PCR for NTM, but negative culture. Despite continued treatment, the patient expired by day 290. So, regarding the literature. Superinfection of various pathogens were reported in lipoid pneumonia, including NTM. Although very uncommon, most NTM cases were caused by rapid-growing NTM species, including M. abscesses. And in the review published earlier this year, cases of M. abscesses superinfection is rare. Only three cases out of 20 that was reported in this review. One mechanism for the increased pathogenicity seen in lipoid pneumonia patients is the impairment of phagocytic and bactericidal activities in lipid-laden macrophages. And also briefly touching on disseminated diseases. It is well-known that disseminated NTM occurs mainly in the immunocompromised. And rapid-growing NTM species mostly occur in patients with organ transplant or hematologic malignancy or chronic steroid use. Another review article published in 2020 summarized various mechanisms that explain the immune evasion of mycobacteria, even also in immunocompetent patients. And some studies described in this review documents defects in interferon gamma and also pathways in these patients. Another study, or another set of studies described the impairments of phagolysosome and autophagy in the removal of phagocytosed NTM pathogens. And these impairments are caused by, in conditions where it is lipid-rich. And several mechanisms describe this. So taking everything together, the increased pathogenicity seen in this case can be a result of macrophage dysfunction aggravated by lipoid pneumonia. And it may help explain the uncontrolled disease in this patient, even without any evidence of immunosuppression. So I think that it is prudent to screen for the presence of any typical pathogens, especially in patients who are refractory to treatment. Here are my references. And thank you for your attention. Thank you. Thank you, Dr. Chang. And any questions from the audience? Don't be shy. I do have a question, and thank you very much. Unfortunately, it's very difficult to treat NTM, especially mycobacterium abscesses. I noticed that at the beginning of the presentation, the patient was treated with steroids for lipoid pneumonia. Yes. For how long was that treatment established for? And do you think that contributes to the overall progression of disease and persistence of disease in this patient? Initially, the patient was started on steroids right from the bat after doing the CT scans. And he was maintained on one milligram per kg of ibuprofen for the first months. So that might have, I think, contributed to the disease. But looking at the, I didn't mention it in the presentation, but looking at the antimicrobial resistance patterns that was already seen at the initial culture specimen, I think the core of the difficulty was the set of resistance patterns. Because the patient was only susceptible to amikacin. Everything else was resistant. So I think that was the more difficult point in this case, rather than the steroids. Because we tapered steroids pretty rapidly after his shortness of breath subsided. So I think that's the main reason. You make an excellent point about mycobacterial infection and resistance, right? We do that routinely for mycobacteria and tuberculosis for MAC as well. But abscesses also we can test for some mutation that predict a good regimen to be successful. Well, thank you very much, Dr. Chang. Thank you. Pleurisy is associated with shallow breathing, nonproductive cough, tachypnea, and pleuritic chest pain. Common causes include chest or rib trauma, blood exacerbation, pulmonary embolism, and infection. Pennybacillus urinalis is a facultative anaerobic endospore-forming mesophilic bacteria, generally seen in the agricultural industry. Pennybacillus is a lethal disease for honeybees and major cause for dairy product spoilage. 20-year-old first-time pregnant female was suffering from pleuritic chest pain resulting in tachypnea, shallow breathing, dypsnea on exertion, and insomnia for five days. She had five separate emergency department visits prior to eventual admission to our hospital. She was able to be admitted after we contacted her OBGYN due to persistent pleuritic chest pain after being sent home from the ED multiple times. The case was then presented to the pulmonary service. She was noted to have elevated D-dimer and abnormal liver function tests. Computerized tomography pulmonary angiogram did not reveal any pulmonary embolism. Instead, it showed seven separate bilateral ground glass pleurally-based nodular densities. Pulmonary consultants suspected septic emboli based on clinical picture and chest CT scan. Fetal ultrasound found fetus in good condition. Chest X-ray did not reveal any abnormalities, as seen here. Chest CT scan showed the presence of multiple pleurally-based nodular densities, as noted by the blue arrows. both of these here, and here. Started with ampicillin sulbactam and vancomycin as initial empiric antibiotics, heparin drip and incentive spirometer were initiated. Vasculitis screening panel was unremarkable. Negative urinary streptococcal pneumonia and legionella pneumophilia antigens. Cryptococcal antigen and COX-C antibody were negative. Blood culture was notably positive for pennybacillus urinalis 48 hours after collection. Heparin drip was discontinued after negative finding of pulmonary embolism on CTPA. Infectious disease consultant was also made and did not believe to be an infection, but instead malignancy such as lymphoma. Due to his clinical assessment, he believes it is most likely suggestive of gestational trophoblastic disease or other alternative diagnosis. Pulmonary service, however, elected to continue with antibiotic therapy. Patient had remarkable improvement in 48 hours with decreased pleurisy, resolution of leukocytosis, and was discharged home with antibiotic. At the time of abstract submission, she had near complete resolution of her pleurisy and was able to take much deeper breaths. Repeat CT scan was pending until after delivery. Since abstract was completed, she now has complete resolution of pleurisy and repeat chest CT was done three months later. Here are the images before and after the antibiotic therapy treatment. Noted by the blue arrows on the left side are the septic emboli, indicated here, here, here, here, here, and here. Please note the resolution of the multiple septic emboli on the right side of the panels in comparison to the left. The right side indicates complete resolution due to there being no septic emboli. Inflammation of the pleura due to inflammatory mediators and cytokine activation can result in serious symptoms of chest pain, shortness of breath, unrelenting cough, and other devastating sequelae. Most septic emboli are commonly distributed in multiple bilateral and peripheral patterns. There has been no known report of pleurally based location of septic emboli. Pennybacillus urinalis is commonly seen in the agricultural arena, but has never been shown to be a pathogen in humans. Despite the delay in diagnosis, our PREEMI-PARIS patient with pennybacillus urinalis bacteremia and septic emboli was successfully treated with antibiotic and pain control. She did not require any supplemental oxygen, inhalers, or steroid. We are reporting the very first known case of PREEMI-PARIS pregnancy associated with pennybacillus urinalis pleurisy and bacteremia with a delay in diagnosis and unusual pleurally distribution of septic emboli. Heightened awareness of this organism will prevent delay in diagnosis and reduce incidence of mistreatment. Thank you. Thank you, Dr. Golden. Any questions from the audience? Have you heard about this bacteria before? Yeah, and that's actually a fascinating piece. I'm never actually, one thing that I learned when I come to this session to moderate is the new bacteria. And this bacteria you described as one of the first ones to be reported for bacteremia and septic emboli. So were you able to identify any particular risk factors in this pregnant woman before the onset of symptoms, such a cold, a UTI, a trouble, a wound, something that helps the clinician in this room consider this diagnosis. So let me just iterate what you're trying to ask. So you're just asking if we saw any signs or symptoms prior to her diagnosis? Thinking that may inoculate the patient, the port of entry, a risk factor that we should be aware of with this rare bacteria. So I do not believe that we noticed any factors, signs, or symptoms prior to admission. This was all done through our positive blood culture and her response to treatment. And from the literature review that you present and what you've been able to read, do you find a common source of infection that happened with this bacteria? No, however, I can look further into that and get back to you on that, but I personally did not find any. Any other question from the audience? Okay, well, another round of applause. Thank you. Thank you. Dr. Dyer. Okay, hi, everyone. My name is Chelsea. I'm a physician assistant at Memorial Sloan Kettering. Today, I'm gonna discuss a case about a patient with newly diagnosed AML and a rare fungal infection. I have no financial disclosures. The patient is a 24-year-old female. She presented to an outside hospital with fever and fatigue. Her workup was notable for labs that showed pancytopenia and myeloblasts, for which she underwent a bone marrow biopsy, and she was ultimately diagnosed with AML. She was started on induction therapy, and during this time, she complained of right chest wall pain as well as right shoulder pain, for which she had a CT chest, and CT chest showed a right upper lobe consolidation. It was concerning for infection, so she was started on broad-spectrum antibiotics as well as isobuconazole. During this time, she had a fine needle aspiration biopsy, the consolidation, and surgical pathology was consistent for angioinvasive fungal infection, and the fungal PCR later grew out, C. dysporium apiosperma. Unfortunately, the patient had failed induction therapy twice, and she was started on salvage therapy at this point, and she started to complain of new abdominal pain, for which she had a CT abdomen and pelvis, and this showed new spleen and liver lesions concerning for scattered abscesses. At this point, she was transitioned to Amphotericin B, giving concern for disseminated infection, and unfortunately, she failed salvage therapy and was transferred to MSK for a clinical trial. When she arrived at MSK, she had a repeat CT chest that showed enlargement of the right upper lobe consolidation. She also had a right upper extremity skin lesion that was concerning for dissemination, so it was biopsied by dermatology, and it confirmed the diagnosis, disseminated C. dysporium. At this point, we started her on voriconazole in addition to her Amphotericin B, and when she clinically improved and her neutrophil counts recovered, she was discharged on monotherapy with esavuconazole, given elevated LFTs on voriconazole, and she had interval follow-up with CT chest as an outpatient, and it showed an overall decrease in the size of the consolidation. At her initial presentation, her only past medical and surgical history consisted of her newly diagnosed AML. She lived in New York, and she worked as a certified nurse assistant. She had no negative PPDs, and she had no international travel or sick contacts. She was a non-smoker and had no illicit drug use. She had no known drug allergies, and her only medications included those from the outside hospital, which were allopurinol, pantoprazole, and Amphotericin B. Her physical exam was largely unremarkable, except for this right upper posterior arm subcutaneous nodule. It was one to one and a half centimeters in size, with some overlying hyperpigmentation and some minimal erythema. Her labs were notable for pancytopenia, and she had a beta-D glucan that was greater than 500. Her LDH and galactomanin were negative or within normal limits. So after being on maintenance esavuconazole for two years and her clinical trial medication, she was readmitted for an allostem cell transplant two years later. She remained on the esavuconazole, and we started her on broad spectrum antibiotics as prophylaxis for her transplant. And unfortunately, 16 days post her transplant and prior to engraftment, she had neutropenic fever. We did a repeat CT chest, and it showed an increase in the right upper lobe consolidation. And this time, we decided to do a robotic bronchoscopy to confirm the diagnosis and rule out any other concomitant infection. And the bronchoscopy did that. It confirmed C. dysphorium aviospermum, and there were no other organisms identified. She was then started on amphotericin B again, in addition to the esavuconazole, giving concern about recrudescence of her fungal infection. And a few weeks later, or a couple weeks later after she engrafted, she had a repeat CT chest that showed a decrease in the right upper lobe consolidation. And again, when she was stable for discharge and her neutrophil counts recovered, this time we sent her home on voriconazole, giving concern of breakthrough on her esavuconazole last, in her initial admission. On this slide on the left, this is a CT chest of her initial presentation. And at this point, she is only on amphotericin B. We then added voriconazole. And when she clinically improved, we ended up discharging her, like I said, on esavuconazole, given elevated LFTs. And the image on the right shows a CT chest at one of her interval follow-ups that shows a decrease in the size of the right upper lobe consolidation. And on this slide on the left, you can see an increase again in the size of the right upper lobe consolidation after her stem cell transplant. And at this point, she was only on esavuconazole. We then restarted her back on amphotericin B. And we had a repeat CT chest after she engrafted. Her neutrophil counts started to recover. And you can see the lesion has decreased in size. There's less GGOs and no intraceptal lobular thickening. On this slide, this is a picture of tissue from the robotic bronchoscopy. It's an H and E stain. And it shows fibrous tissue with chronic inflammation. And in the highlighted photo, you can see some faint purple crisscrossing. And those are fungal elements within necrotic tissue. And this slide here is a GMS stain or a silver stain. And it just highlights the fungal structures within necrotic tissue. And here you can see the fungal elements. They're branching hyphae in 45-degree angles. That's consistent for C. dysporium. However, you can also see this with other molds like Aspergillus. So to make the diagnosis, you need a culture in addition to histopathology. So what is C. dysporium? C. dysporium is a filamentous mold. It's found ubiquitously in the environment. It's in soil, sewage, and polluted water. It has a pretty wide global distribution, including Europe, Asia, Australia, South America, and North America. Infection results from inhalation of the spores from the environment or through direct inoculation of an open womb. And the most common sites are sinuses, lungs, skin, bones, soft tissue, and the central nervous system. So what did we learn? C. dysporium is a newly emerging fungal infection seen in immunocompromised patients. It has high intrinsic resistance to antifungals, and it carries a high mortality rate, especially in the absence of immune recovery. Voriconazole is currently the treatment of choice. And in this case, as well as several other case studies, we've seen improvement in the patient's infection when their neutrophil counts recover, suggesting that host immunity plays a very important role in controlling this infection. Thank you, guys. Thank you. Thank you. Any question from the audience? No question? I do have a question, and again, fungal infections in severely immunocompromised patient, right, and we're thinking about angioinvasive infections, such as Aspergillus. Any particular clinician aid that you can propose to help differentiate and start thinking about this fungal infection more often? Honestly, she didn't present any differently than someone with Aspergillus. I think it just should be on our radar more, because I think given the immuno, our population that are immunosuppressed is increasing, and we should just add this to our radar. And do you think maybe the dual antifungal coverage could have been thought of earlier in her progression of disease? Dual coverage? The dual antifungal coverage that you are implementing later? Sorry. With the Amphotericin and the Azole, if you think that combination could have been considered earlier? Oh, so it's interesting, actually, in my research, I found that Amphotericin B was not the best option, but we used it as dual therapy. I think that, I think if it was used sooner, I don't know if it would have made a difference. I think maybe if we tried Boriconazole earlier at the outside hospital, that might have made a difference. So more about thinking the etiology and the right is for the patient, rather than implementing a dual therapy. It's a good way to start thinking about it. I think, yeah, especially in the presence of Neutropenia, I think dual therapy is helpful. Thank you very much. Thank you. Kate Boylan? Kate Boylan? Okay. Hi, everyone. Today, I'll be presenting a case titled Endobronchial Actinomycosis associated with chicken bone aspiration. My name is Kate Boylan. I'm a PGY-2 at Summa Health Systems in Akron, Ohio. I have nothing to disclose. Today, I'll be reviewing a patient who aspirated a chicken bone, developed Endobronchial Actinomycosis, and I will be reviewing the relevant literature. Actinomyces is a gram-positive microarophilic bacterium normally colonizing the mouth, gastrointestinal tract, and vagina. There, it is usually harmless. Sulfur granules are the diagnostic hallmark. Pulmonary actinomycosis is exceptionally uncommon. Endobronchial actinomycosis, or EA, due to foreign body aspiration is even more unusual. EA is often misdiagnosed as a result. The patient is a 71-year-old male that was referred to the pulmonology office for evaluation of chronic cough of one-year duration. He had a past medical history of prior tobacco usage and hypertension. Should be noted that he had no history of immunodeficiency or recurrent infection. He was previously treated several times with antibiotics, steroids, inhalers, and antitussives without resolution. No sputum was cultured prior to presentation. Review of systems was positive for voice change, a choking event, and dyspnea. Further evaluation of the choking event revealed that it was with a chicken bone and it occurred 13 months previously. Physical exam was notable for right-sided ronchi and rails. Possible contributing factors to the patient's presentation of a chronic cough included that he was a previous 20-plus pack-year smoker, the aspiration event. He takes lisinopril for hypertension, which is known to cause a cough in several patients, and he works at a tire mold shop, to which he's exposed to aluminum. CT of the chest, here you can see in figure one a right upper lobe endobronchial calcified lesion. In figure two, you can also see the endobronchial calcified lesion as well. There we go. With subsequent level of post-obstructive atelectasis and possible pneumonia. In figure three, you can see right lower lobe, significant focal bronchiectasis with opacifications and infiltrates. Bronchoscopy was the next step. In the first and second picture of the right main stem bronchus, you can see significant purulent fluid. Brushings were sent for culture. In the remaining pictures, it shows the calcified lesion. It was semi-obstructive and calcified and pedunculated. The surrounding mucosa was friable and inflamed. Multiple attempts at suction were attempted, however, it had to be terminated due to significant bleeding. Cytology obtained from the right upper lung brushings was classic for actinomyces species. No malignant cells were found. The patient subsequently underwent interventional pulmonology, rigid bronchoscopy and foreign body removal. The object was identified as a chicken bone. He was treated with a prolonged course of oral amoxicillin and his symptoms resolved. He has not had to present back to the pulmonology office and he's been doing well since then. Endobronchial actinomycosis is an indolent, slowly progressive infection. It's thought to result from aspiration of oropharyngeal and gastrointestinal contents into the respiratory system. If left untreated, it may invade the pleura, chest wall, soft tissues and bony structures. Sinus tracts may form and spontaneously open and close. Given the rarity of this infection, the pathogenesis is not fully understood. It's thought to start as acute inflammation that goes into the chronic phase of fibrosis, necrosis and pulmonary cavities. EA due to foreign body aspiration is rare. However, in fact, EA due to chicken bone aspiration specifically is even more rare. Only nine other cases have been previously reported. Signs, symptoms, physical exam, basic, chest x-ray and lab tests are often nonspecific. As a result, EA can be misdiagnosed as lung cancer, unresolving pneumonia, bronchogenic carcinoma, endobronchial lipoma, pulmonary tuberculosis, among other things. Bronchoscopy with biopsy is needed for diagnosis. With early detection and proper treatment, prognosis is excellent. Treatment includes, one, you have to start by removing the foreign body, and then you would do prolonged course of antibiotics. There isn't a specific duration of time for antibiotics since this is so rare, but they recommend at least months of either penicillin, amoxicillin, tetracycline or clindamycin. In conclusion, endobronchial actinomycosis must be considered in the differential diagnosis of chronic cough, especially in patients who present with airspace consolidation or pulmonary masses. Even though it is rare, pulmonologists and radiologists must be aware of this, especially because an early diagnosis will prevent significant morbidity in patients. This case also raises the necessity of taking an excellent clinical history and maintaining a high index of suspicion in the management of endobronchial lesions. These are my sources. Thank you.

endobronchial actinomycosis

chronic cough

aspiration

chicken bone

bronchoscopy

foreign body removal

prolonged antibiotic therapy