United States

Background: Amiodarone is a class III antiarrhythmic agent used for the management of certain cardiac arrhythmias. Although effective and relatively safe, amiodarone is associated with a spectrum of adverse effects including neurotoxicity. There have been sparse reports of drug-induced parkinsonism (DIP) as a consequence of amiodarone use; however, the mechanism and clinical implications remain an area of limited understanding and documentation. Parksinon’s disease (PD) is associated with degeneration of dopaminergic pathways in the basal ganglia, manifesting in the classic constellation of symptoms, including “pill-rolling” tremors. These dopaminergic pathways can also be disrupted by certain medications, notably antipsychotics, antiemetics, and antiepileptics, which may mimic the symptoms of PD.

Case Presentation: 92 year-old female with a past medical history of atrial fibrillation, hypothyroidism, heart failure, COPD, and dementia presented with resting tremors of the bilateral hands for 2 months. Pt endorsed no new bradykinesia, loss of balance, or muscle stiffness. Denied any fever, chills, myalgia, cough, dysuria, nausea, vomiting, diarrhea, or weight gain or loss. Physical exam demonstrated isolated bilateral resting tremors, with an otherwise unremarkable neurologic exam. There was no muscle rigidity, cerebellar dysfunction, motor/sensory deficits, or bradykinesia compared to baseline. Vital signs were normal and labwork including TSH, RPR, and vitamins B12 and B9 were unremarkable. Following review of the patient’s medication regimen, we reduced amiodarone dosing from 200mg to 100mg due to concern for neurotoxicity rather than late-onset PD. On follow up at 2 weeks and 1 month, resting tremors resolved completely and the patient had no further concerns.

Discussion: Despite the established neurotoxicity of amiodarone, reports of amiodarone-induced Parkinsonism remain sparse. Here, we present a case of Parkinsonism occurring in a patient receiving long-term amiodarone therapy. Through this case report, we aim to broaden understanding of potential neurotoxic effects of amiodarone and emphasize the importance of recognizing drug-induced parkinsonism (DIP). DIP is a reversible form of Parkinsonism caused by the blockade of dopamine receptors or interference with dopamine transmission in the basal ganglia, mimicking the dopaminergic deficiency seen in PD. Misdiagnosing DIP as Parkinson&#39;s disease could lead to inappropriate treatment, potentially causing harm. Hence, clinical vigilance is warranted in patients receiving long-term therapy with amiodarone. 


AMA Research Challenge 2024 

Amiodarone-Induced Parkinsonism: A Case Report Highlighting Neurotoxicity and Clinical Vigilance in Long-Term Therapy

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AMA Research Challenge 2022

Welcome to the largest national, multi-specialty research event featuring research from 750 medical students, residents and fellows, and international medical graduates.


Background: Amiodarone is a class III antiarrhythmic agent used for the management of certain cardiac arrhythmias. Although effective and relatively safe, amiodarone is associated with a spectrum of adverse effects including neurotoxicity. There have been sparse reports of drug-induced parkinsonism (DIP) as a consequence of amiodarone use; however, the mechanism and clinical implications remain an area of limited understanding and documentation. Parksinon’s disease (PD) is associated with degeneration of dopaminergic pathways in the basal ganglia, manifesting in the classic constellation of symptoms, including “pill-rolling” tremors. These dopaminergic pathways can also be disrupted by certain medications, notably antipsychotics, antiemetics, and antiepileptics, which may mimic the symptoms of PD.

Case Presentation: 92 year-old female with a past medical history of atrial fibrillation, hypothyroidism, heart failure, COPD, and dementia presented with resting tremors of the bilateral hands for 2 months. Pt endorsed no new bradykinesia, loss of balance, or muscle stiffness. Denied any fever, chills, myalgia, cough, dysuria, nausea, vomiting, diarrhea, or weight gain or loss. Physical exam demonstrated isolated bilateral resting tremors, with an otherwise unremarkable neurologic exam. There was no muscle rigidity, cerebellar dysfunction, motor/sensory deficits, or bradykinesia compared to baseline. Vital signs were normal and labwork including TSH, RPR, and vitamins B12 and B9 were unremarkable. Following review of the patient’s medication regimen, we reduced amiodarone dosing from 200mg to 100mg due to concern for neurotoxicity rather than late-onset PD. On follow up at 2 weeks and 1 month, resting tremors resolved completely and the patient had no further concerns.

Discussion: Despite the established neurotoxicity of amiodarone, reports of amiodarone-induced Parkinsonism remain sparse. Here, we present a case of Parkinsonism occurring in a patient receiving long-term amiodarone therapy. Through this case report, we aim to broaden understanding of potential neurotoxic effects of amiodarone and emphasize the importance of recognizing drug-induced parkinsonism (DIP). DIP is a reversible form of Parkinsonism caused by the blockade of dopamine receptors or interference with dopamine transmission in the basal ganglia, mimicking the dopaminergic deficiency seen in PD. Misdiagnosing DIP as Parkinson's disease could lead to inappropriate treatment, potentially causing harm. Hence, clinical vigilance is warranted in patients receiving long-term therapy with amiodarone. 


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Abstract Title
Atrial Fibrillation Presenting as Renal Infarction
Background
Renal infarction is caused by occlusion of renal artery or its branches, due to emboli from cardiac sources or in situ thrombosis. It presents as sudden flank or abdominal pain, with labs showing elevated LDH, hematuria, proteinuria. Prompt diagnosis is crucial to initiate timely revascularization therapies.

Case Presentation
A 78-year-old male with past medical history of hypertension, diabetes mellitus, hyperlipidemia, COPD, meningioma presented to the emergency department with complaints of pain in the left flank and umbilical region which started gradually over the past few days and was described as dull and non-radiating. Physical evaluation revealed stable vital signs with hypertension, chronic normocytic anemia, irregularly irregular pulse, Left costovertebral angle (CVA) tenderness, bilateral chronic hand tremors. No focal neurological deficits. Denies fever, nausea, vomiting, diarrhea, constipation, anorexia, alcohol use, changes with meal, similar pain, incontinence, dysuria, hematuria, changes with urine output, urinary frequency, chest pains, palpitations, syncope, orthopnea, PND, edema. Initial Diagnostic workup included negative troponin, COVID-19/flu/RSV tests, and a chest X-ray showing mediastinal widening. Further investigations with a CT angiography chest ruled out aortic aneurysm or dissection but noted a region of low density in the left kidney parenchyma suggestive of multiple cortical infarcts. Urinalysis was positive for microscopic blood and 1 RBC. An EKG demonstrated new-onset atrial fibrillation (Afib). Cardiology consulted recommended to start anticoagulation therapy for atrial fibrillation and electrophysiology with no immediate plan for cardioversion. Later, CTAP with and without contrast show findings consistent with multiple acute renal infarcts (ARI) in the left kidney. Urology was consulted and determined no surgical intervention was indicated, recommending anticoagulation to prevent further complications from kidney infarcts. The patient was educated about his condition and discharged with appropriate outpatient follow-up.

Discussion
ARI is potentially serious medical condition but its clinical presentation of is often
nonspecific, leading to delays in diagnosis and treatment. Autopsy studies suggest the incidence of renal infarction is 14 per 1000, or 1.4%. Other retrospective studies of ER admissions found an incidence of 0.004% to 0.007%. In our case, the patient's abdominal pain with no previous history of arrhythmias prompted further evaluation, revealing new-onset AFib on EKG and subsequent diagnosis of renal infarction on imaging. Afib can cause thrombotic complication to any body part, most commonly being ischemic stroke. Clinicians should suspect other systemic embolization phenomena in patients with Afib.


Atrial Fibrillation Presenting as Renal Infarction: A Case Report

Introduction. Variegate Porphyria (VP) is a rare autosomal dominant disorder characterized by mutations in the protoporphyrinogen oxidase (PPOX) gene, leading to diminished enzymatic activity, critical for heme biosynthesis. The clinical manifestations of VP are highly variable, with some patients exhibiting significant neurovisceral symptoms and others presenting with cutaneous photosensitivity, many with a combination of both. This variability reflects the disease's ability to often go undiagnosed, especially in pediatric populations, where the disease is not frequently seen in clinical practice.

Methods. This case study focuses on a 12-year-old male who presented with persistent photosensitivity, painful blistering, severe abdominal pain, and dark-colored urine. Despite normal renal and liver serology testing, elevated porphyrin levels in both urine and stool samples supported the presumptive diagnosis of VP, though the diagnosis was significantly delayed resulting in multiple unnecessary hospitalizations secondary to recurrent acute attacks.

Discussion. The complexity of VP, particularly in pediatric patients, often results in diagnostic delays due to the vague symptoms that oftentimes represent other medical conditions. Our case emphasizes the importance of a thorough clinical evaluation, family history, and awareness of this rare disorder. Management strategies, including sun protection and beta-carotene supplementation, were implemented to mitigate the risk of acute attacks.

Conclusion. This study emphasizes the need for increased awareness and understanding of VP, aiming to promote earlier diagnoses and improve patient outcomes through timely and appropriate interventions.

Case Study: Navigating the Complexities of Variegate Porphyria

Anti-TNF therapy has revolutionized the treatment of various autoimmune conditions. However, it has also been associated with an increased risk of bacterial infections. To our knowledge, no case of Acinetobacter baumannii bacteremia has been reported with adalimumab treatment.

A 63-year-old female with generalized pustular psoriasis (GPP) was referred to the ED by her dermatologist for worsening rash, severe weakness, and fatigue. Symptoms began a week prior and acutely worsened after adalimumab infusion a day before hospital presentation. This was her second infusion, the first had been two weeks earlier. In the ED, her vital signs and labs were unremarkable. However, she had chills, prompting the collection of two blood cultures at different sites, which were both positive for A. baumannii. She had no clear infection source. Infectious disease (ID) was consulted, and she was started on ampicillin-sulbactam. Her weakness and fatigue improved shortly after starting antibiotics. A transthoracic echocardiogram showed no vegetations, and repeat blood cultures were negative. Dermatology attributed her worsening rash to a GPP flare, and spesolimab was recommended. Her medical records showed a positive Quantiferon-TB Gold, with a low mitogen-nil value and a chest X-ray showing no evidence of past or current tuberculosis infection. ID suggested the result was a false positive, but a subsequent positive T-spot confirmed latent tuberculosis. Biologic treatment was suspended until completing one month of latent tuberculosis treatment. Outpatient ID planned to initiate once-weekly isoniazid plus rifapentine. Meanwhile, acitretin was started, with dermatology follow-up scheduled for one month later to begin spesolimab after latent tuberculosis treatment. She was discharged on ciprofloxacin to complete her antibiotic course.

Acinetobacter baumannii, part of the ESKAPE organisms, is predominantly associated with healthcare-related infections and known for developing antibiotic-resistant strains. In the US, community-acquired A. baumannii cases are rare, with most being hospital-acquired infections. Moreover, shaking chills is an independent predictor of bloodstream infection. Given that blood is generally sterile, there is a low likelihood it was a contaminant. This case highlights the importance of clinical exam findings to maintain a high index of suspicion for severe infections such as bacteremia in immunocompromised individuals, and the necessity for physicians to broaden differentials to include rare organisms even in the absence of recent clinical exposure. Fortunately, the isolate was pan-sensitive, as multidrug-resistant A. baumannii infections can be life-threatening. Additionally, we are not suggesting that the patient's symptoms were solely due to bacteremia; reactivation of latent tuberculosis may have contributed.



Community Acquired Acinetobacter baumannii Bacteremia After Receiving an Infusion of Adalimumab

Title: Delayed Diagnosis of Disseminated Coccidioidomycosis Due to Misdiagnosis
of Lymphoma: A Case Report.

Background:
Coccidioidomycosis, or valley fever, is a fungal infection caused by inhaling Coccidioides imitis/posadasii. These fungi are endemic to the southwestern USA, Mexico, and Central and South America. Incidence has been rising, likely due to population growth, climatechange, and increased awareness. The infection presents diversely, with most cases being asymptomatic. About one-third develop pulmonary illness, and a small percentage experience dissemination to other body areas, commonly to skin, bone, and CNS, particularly in immunocompromised individuals and certain ethnic groups.

Case presentation:
A 39-year-old Hispanic female with a history of non-Hodgkin's lymphoma and treated tuberculosis presented with painful ulcerative skin lesions. Initial labs showed mild leukocytosis, microcytic anemia, hypokalemia, and hypoalbuminemia. Imaging revealed bilateral pulmonary infiltrates, mediastinal adenopathy, and extensive lymphadenopathy. A skin biopsy report from Mexico indicated non-Hodgkin lymphoma, but no treatment was initiated at the time of diagnosis. A neck lymph node biopsy revealed fungal spherules and hyphae, consistent with coccidioidomycosis. Serology confirmed high titer IgG for Coccidioidomycosis. Further testing ruled out other conditions, including lymphoma. The patient started high-dose fluconazole. A lumbar puncture showed positive IgG for Coccidiomycosis in CSF, indicating CNS involvement. A repeated skin biopsy was negative for lymphoma, confirming disseminated coccidioidomycosis and ruling out
lymphoma diagnosis. The patient was discharged on oral fluconazole and prophylactic TMP-SMX. Two months later, she was readmitted with worsening weakness and altered mentation. Despite adequate treatment, the imaging showed new lytic lesions in the left scapula and T2 body. Repeated lumbar puncture confirmed CNS involvement. Her condition improved with continued antifungal. Not candidate for amphotericin B.

Discussion:
This case highlights the difficulty in diagnosing coccidioidomycosis, which is often
mistaken for other conditions. The patient's initial misdiagnosis of lymphoma while
undergoing care in Mexico led to a delay in appropriate treatment. Initially, treatment focused on a superimposed skin infection, assuming the underlying cause was NHL. However, even after diagnosing pulmonary coccidioidomycosis, the misdiagnosis of NHL persisted until a repeat skin biopsy ruled it out. This case highlights the challenge of differentiating reactive inflammatory changes from malignancy, which can delay a definitive diagnosis. The diagnosis was eventually confirmed through lymph node biopsy and subsequent serology testing, the most appropriate diagnostic methods. The initial treatment with fluconazole was appropriate as azoles remain the gold standard for therapy. The case underscores the need for timely and accurate diagnosis to initiate appropriate antifungal therapy and prevent complications.

Delayed Diagnosis of Disseminated Coccidioidomycosis Due to Misdiagnosis of Lymphoma: A Case Report

Background: 
Infectious myositis, a rare but significant inflammatory muscle disease, involves infection of skeletal muscle tissue, typically caused by bacteria, viruses, fungi, and parasites. Staphylococcus aureus is the most common bacterial pathogen. Symptoms range from localized pain and swelling to systemic manifestations like fever and malaise. Early recognition and management are crucial to prevent complications like abscess formation, sepsis, and chronic disability 1. Here, we detail the case of a 21-year-old female with right lower extremity (RLE) pain and swelling who developed infectious myositis and an abscess in the anterior leg compartment despite having no skin defects.

Case Presentation:
A 21-year-old female with systemic lupus erythematosus (SLE) presented to the ED after a mechanical fall with RLE pain, swelling, and fevers for two days. Physical examination revealed RLE swelling and tenderness without overlying skin findings. Lab results showed creatine phosphokinase (CPK) 125, C-reactive protein (CRP) 12.3, erythrocyte sedimentation rate (ESR) 72, and D-dimer 4.19 FEU. Initial CT of the RLE indicated subcutaneous edema, muscle atrophy, and fascial plane blurring, suggesting myositis. A RLE Doppler ultrasound was negative for thromboembolic processes. Given symptom worsening despite a negative workup, repeat CT of the RLE with contrast was obtained five days later which revealed a complex, multiloculated fluid collection indicative of an abscess within the anterior compartment. She was treated with IV vancomycin and underwent incision and drainage of the RLE. Intraoperative cultures grew methicillin-resistant S. aureus. Despite persistent fevers, extensive workup was unrevealing, and blood cultures were negative. At discharge, she was afebrile with improved RLE symptoms and uneventful wound healing.

Discussion:
This case highlights an atypical presentation of infectious myositis in an immunosuppressed patient following a mechanical fall without any obvious historical or exam findings of skin lacerations. Differential diagnosis included myositis, pyomyositis, deep vein thrombosis, hematoma, and compartment syndrome. Despite high suspicion for myositis, normal CPK levels, lack of leukocytosis, and unrevealing CT imaging complicated diagnosis and management. Elevated ESR and CRP levels were ambiguous due to her SLE history. CT imaging, although useful, has limitations in detecting early or subtle inflammatory changes in soft tissue and persistence of symptoms necessitated further investigation. This case underscores the importance of maintaining a high index of clinical suspicion for infectious myositis and the need for repeat imaging or alternative diagnostic modalities 2 when initial tests are inconclusive, given the risk of serious complications like sepsis, osteomyelitis, and necrotizing fasciitis with delayed treatment.

Diagnostic Dilemma: Atypical Presentation of Infectious Myositis in a Young Immunocompromised Female Following a Mechanical Fall

Abstract Title
Drug Induced ANCA Vasculitis with Long-standing Tolerance to Hydralazine.
Background
Anti-neutrophil cytoplasmic antibodies (ANCA) associated vasculitis has a varied presentation and positive ANCA antibodies are commonly found in granulomatosis with polyangiitis, microscopic polyangiitis (MPA), renal-limited vasculitis, and drug-induced vasculitis. Specific ANCA antibodies, anti-protease 3 (PR3) and myeloperoxidase (MPO), can help differentiate between the various vasculitides with MPO-ANCA most closely associated with MPA, renal limited, and drug induced. Kidney biopsies most frequently demonstrate necrotizing crescentic glomerulonephritis. Symptoms vary depending on the organ system involved but consistently involve signs of systemic inflammation and end organ damage.
Case Presentation
This case presents a 67-year-old male with history of chronic obstructive pulmonary disease (COPD), chronic kidney disease stage IV (CKD IV), and hypertension presenting with newfound hematuria, acute respiratory failure, and altered mentation. He was found to be hypertensive and ultimately required intubation for airway protection. On review of home medications, antihypertensive regimen includes hydralazine, carvedilol, and nifedipine.
Urinalysis was significant for significant hematuria and proteinuria. Lab work was significant for elevated creatinine, blood urea nitrogen, and respiratory acidosis. Rheumatologic work up revealed positive titers for antinuclear antibodies 1:640, ANCA, myeloperoxidase antibodies at 35 U/mL, and weakly positive anti-histone antibodies at 1.3 units. Work up negative for C3 abnormalities, anti-glomerular basement membrane antibodies, and anti-PR3 titers. Renal biopsy showed pauci-immune necrotizing crescentic glomerulonephritis. 
A presumptive diagnosis of drug-induced ANCA-associated MPA was made and methylprednisolone was started for 3 days. The patient was transitioned to high dose prednisone with appropriate taper until outpatient follow up for reevaluation. The patient also started on a two part rituximab infusion occurring 14 days apart. The patient’s renal and pulmonary function responded well to the steroid and rituximab treatment. The patient was successfully stabilized and discharged with appropriate prophylaxis and scheduled appointments for the outpatient Rituximab infusion and nephrology follow up.
Discussion
ANCA-associated vasculitis has a wide spectrum of symptom presentations. Thorough medication reconciliation and work up for any new acute kidney injury should include investigation into autoimmune pathologies when occurring with widespread organ involvement. Drug -induced ANCA vasculitis can present in a patient even after years of taking high risk medications, and as such previous tolerance should not exclude a new drug reaction. Furthermore, the proper coordination of inpatient services with outpatient therapy is required to promote optimum patient outcomes.


Drug Induced Anca Vasculitis with Long-Standing Tolerance to Hydralazine

Introduction:
Essential thrombocythemia (ET) is a BCR-ABL1 negative myeloproliferative neoplasm with an incidence of 1-2.5/100,000 population per year. It is caused by mutations in the JAK2, CALR, or MPL genes. ET is considered benign, with a low risk of leukemic transformation, a good prognosis, and long-term survival. However, severe complications such as myelofibrosis (MF) and acute myeloid leukemia (AML) can occur. Recent studies indicate ET progresses to MF in 4.8% of cases and to AML in 3.3% of cases. Additionally, leukemia cutis occurs in 3% of AML patients. Here, we report an extremely rare case of ET that progressed to MF and subsequently transformed into leukemia cutis.

Case presentation:
We present a unique case report highlighting the clinical progression of a 75-year-old female diagnosed with JAK2-positive Essential Thrombocythemia (ET) in 1990. Initially, she presented in 2014 for thrombocytosis evaluation, and a bone marrow biopsy revealed a hypercellular marrow with megakaryocytic hyperplasia, confirming ET. Treatment with hydroxyurea yielded variable responses. In 2021, abnormal WBC results prompted further investigation. Flow cytometry revealed myeloid left shift, increased myeloblasts, and teardrop-shaped red blood cells, confirming Post-ET myelofibrosis. Trisomy 8 and a 1:21 translocation were detected with FISH. Her condition was stabilized with Ruxolitinib (Jakafi) therapy. In July 2023, she presented with hepatosplenomegaly and multiple skin nodules on her upper abdomen, back, and face. A bone marrow biopsy in January 2024 revealed a hypocellular marrow, severe reticulin fibrosis (MF-3), and >20% blasts, indicating progression to acute myeloid leukemia. Flow cytometry revealed an aberrant CD34-positive blast population expressing several monocytic markers. Subsequent histopathological examination of the nodules demonstrated perivascular infiltration of immature mononuclear cells resembling blasts immunoreactive to MPO, CD117, CD163, and C68 surface markers, confirming leukemia cutis. In February 2024, the patient began treatment with venetoclax and completed one cycle of Azacitidine. Due to an inadequate response, Azacitidine was switched to Decitabine combined with Cedazuridine (Inqovi) and low-dose Jakafi. Despite undergoing six cycles of Inqovi, the patient remains unresponsive to treatment.

Conclusion:
This case report illustrates the rare clinical progression of essential thrombocythemia (ET) into acute myeloid leukemia (AML), manifesting as leukemia cutis. The transition from ET to AML, while uncommon, is frequently associated with unfavorable cytogenetics and a poor prognosis. This emphasizes that close monitoring, early identification, and appropriate intervention are critical in the management of leukemic transformation.

Essential Thrombocythemia to Leukemia Cutis: A Blood-to-Skin Transformation

Background
Malaria is a parasitic infection transmitted by the Anopheles mosquito, with Plasmodium falciparum being the most severe species. Initial symptoms include fever, headaches, and nausea, often leading to a robust immune response. Diagnostic challenges arise in non-endemic regions, and cross-reactivity with other tests may occur.
Case Presentation
A 49-year-old woman traveling from Yemen via Djibouti presented in the Midwest with irregular fluctuating fevers, cough, headache with behavioral changes, and abdominal pain with emesis. Initial workup showed pancytopenia, hemolysis, and significant splenomegaly on CT scan. Blood smear confirmed Plasmodium falciparum malaria, classified as severe due to cerebral involvement and hyperparasitemia. Despite a positive fourth-generation HIV test, confirmatory HIV differentiation test and HIV nucleic acid amplification were negative, indicating a false positive likely due to severe malaria. The patient was successfully treated with three days of artemether-lumefantrine, and symptoms subsided.

Discussion
This case highlights the potential for false positive fourth-generation HIV tests in the context of severe malaria. The high sensitivity (99.8%) and specificity (99.5%) of these tests are generally reliable, but cross-reactivity can occur, necessitating confirmatory testing to avoid misdiagnosis. Previous cases have reported similar findings. For instance, a 2019 case report described a tourist returning from West Africa with severe P. falciparum malaria who tested false positive on the fourth-generation HIV test, but confirmatory testing was negative. Another case in 2023 documented a woman with P. malariae presenting a false positive HIV test, which was subsequently negated by differentiation testing. These false positives are thought to occur due to the immune system's response to malaria, which can produce antibodies or immune complexes that cross-react with HIV test antigens. Studies have shown that younger patients with malaria might produce more nonspecific antibodies, leading to higher rates of false positives. Historical enzyme immunoassay tests also reported similar issues, with significant rates of false positives in malaria patients. The unique presentation of our patient shows the necessity of considering false positives in regions where malaria is rare but HIV testing is common. This case reinforces the need for thorough diagnostic evaluations and the importance of reflexive confirmatory testing to prevent misdiagnosis and unnecessary treatment.


False Positive Fourth Generation HIV Test in a Woman with Severe Malaria

Abstract

Background: Actinomyces neuii is a gram-positive, non-branching rod-shaped bacteria, It rarely causes infection in humans. We report potentially the first case of primary actinomycosis of both breasts with Actinomyces neuii in an immunocompetent male.
Case description: A 40-year-old man reported chronic green bilateral nipple discharge. The patient underwent incision and drainage of the left breast abscess in the outpatient setting as well as a course of Clindamycin, Trimethoprim / Sulfamethoxazole (TMP-SMX), and short-term Penicillin. The patient continued to have drainage while on antibiotics. A culture of exudate in blood agar media was positive for Actinomyces neuii. A thorough history revealed nipples were pierced years earlier. A breast mammogram confirmed an abscess. Then the patient received an extended course of penicillin. When the prolonged course of penicillin was administered without improvement, the patient was put on oral linezolid; the induration continued even after the bilateral breast drainage stopped.
Conclusion: Actinomycosis is an invasive, progressive, and occasionally recurrent granulomatous infection caused by this genus. Actinomyces (A.) israelii is the common cause of actinomycosis whereas A. neuii relatively rarely causes it. This case of primary actinomycosis involving both breasts with Actinomyces neuii in a healthy male patient highlights the potential for this organism to cause significant pathology, particularly in the context of compromised barriers such as previous nipple piercings. This unusual presentation prompts considerations regarding the etiology, diagnosis, and management of A. neuii infections, which typically require prolonged antibiotic therapy and may necessitate surgical intervention in refractory cases. 



First Case Of Bilateral Breast Abscess By Actinomyces neuii In An Immunocompetent Male

Background
Ovarian cancer is the fifth-leading cause of cancer related deaths for women worldwide, and women have a lifetime risk of 1.3%. Factors known to increase your risk are familial genetic syndromes such as BRCA1/BRCA 2 tumor suppressor gene mutations, increasing age, obesity, and post-menopausal hormone therapy. Women present with abdominal pain/pressure, fatigue, and early satiety (1). Ovarian cysts have an unknown prevalence since most women are asymptomatic and they tend to be found incidentally while performing imaging for another cause. However, if causing symptoms, the patient may complain of pelvic pain/pressure, vaginal bleeding, and early satiety with or without nausea. Cancer antigen 125 (CA125) is a glycoprotein antigen present on various tissues including those lining the ovaries, fallopian tubes, and non-gynecological organs such as stomach and colon. It can be present in healthy tissue and malignant tissue. The normal range is between 5–35 IU/mL and values > 35 IU/mL are present in 6% of ovarian cysts (3). 

Case Presentation
Our patient was a 43-year-old female who presented with a chief complaint of abdominal fullness and dyspnea. She had been having ongoing increasing abdominal girth and pressure for the past nine months with new onset dyspnea at rest. On physical exam she was cachectic, abdomen was firm/distended, and she had 3+ bilateral lower extremity edema up to the knees bilaterally. The CT abdomen was significant for a left sided adnexal mass 20x20x30cm with severe abdominal distention and ascites. She underwent paracentesis on three consecutive days (day 1: 2.3L, day 2: 15L, and day 3: 2L) for a total removal of 19.3L. The ascitic fluid studies showed bloody fluid with >400,000 red blood cells without malignant cells present. Blood tests were unremarkable and subsequent cancer antigens were obtained. The results were: cancer antigen 125 (CA125) 114, carcinoembryonic antigen (CEA) 4.2, and cancer antigen 19-9 (CA19-9) 93. Patient underwent total abdominal hysterectomy (TAH) and bilateral salpingo-oophorectomy (BSO). After excision of the mass, the final histopathology showed a benign epithelial cyst measuring 27cm.

Discussion
Rapid onset worsening abdominal pressure accompanied with diffuse ascites and elevated CA125 leads one to the differential diagnosis of gynecological malignancy, mainly ovarian in origin. However, giant ovarian cysts defined as >10cm have a similar presentation. CA125 is associated with malignant ovarian cancer, but the specificity of this marker is low and can be falsely elevated in benign conditions and premenopausal women (4).

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