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Gram-negative bacteremia in hospitalized patients often leads to prolonged hospital stays, increased healthcare costs, and mortality rates. Simultaneously, the presence of comorbidities like chronic wounds increases the risk of severe infection and complicated hospital courses involving amputation, broad-spectrum antibiotic use, and repeat hospital admissions, after discharge. This case presents a 72-year-old male with a past medical history significant for chronic lower extremity cellulitis with multiple prior hospitalizations. On admission, the patient had a chief complaint of progressively worsening left lower extremity pain along with nausea, vomiting, and diarrhea. CT imaging of the left lower extremity suggested severe cellulitis without signs of osteomyelitis. Blood cultures initially suggested , but were sent to an outside facility due to ambiguity of results. The outside facility identified the pathogen as . After confirming the results, antibiotics were appropriately de-escalated to oral levofloxacin. The patient continued to show clinical improvement and was discharged with follow-up appointments scheduled for infectious disease and bi-weekly visits to wound care. Considering the increasing prevalence of chronic wounds in the United States, awareness and recognition of emerging pathogens are crucial for the timely diagnosis, treatment, and management of these complex patients. Our case adds to the growing body of reports on the management of bacteremia resulting from maggot-infested wounds.

is a pathogenic protozoan endemic to Asia, Africa, and Central and South America. However, with increased travel and emigration, it is becoming a common parasitic infection leading to many worldwide deaths. We present a case of a young Hispanic male immigrant with an amebic liver abscess. This case report highlights the complexities of diagnosing and treating infection.

Autoimmune encephalitis (AE) is a rare immune-mediated disorder comprised of non-infectious neuroinflammatory disease processes. Clinical presentation overlaps with a broad range of neurodegenerative disorders and infectious encephalitis; therefore, AE remains a diagnosis of exclusion. Patients may present with nonspecific symptoms such as psychiatric disturbances, cognitive deficits, seizures, movement disorders, and confusion. Prompt diagnosis and management are necessary for patients with AE to decrease mortality and improve quality of life. First-line therapy includes immunosuppression with corticosteroids, intravenous immunoglobulin, and plasmapheresis. We report the case of an 86-year-old female with a medical history of Parkinson's disease who presented with nonspecific seizure-like activity and was diagnosed with AE.

Acquired amegakaryocytic thrombocytopenia (AATP) is a rare disorder in which severely low platelet levels occur due to reduced or complete absence of megakaryocytes in the bone marrow. The pathophysiology of this disease is not fully understood, although anti-thyroid peroxidase antibodies (anti-TPO) binding to cellular-myeloproliferative leukemia (c-mpl) receptors is a proposed mechanism. Currently, no standard published guideline for treatment exists, but immunosuppressive therapies have been used based on the proposed mechanism and associated conditions. We present a case of a 57-year-old male who presented to the hospital with a 3-day history of progressive weakness and dysphagia. He had recently been discharged from an outside health system after evaluation for suspected gastrointestinal bleeding, although esophagogastroduodenoscopy and colonoscopy did not uncover a source of bleeding. Fifteen days later, he was admitted to our hospital for septic shock and acute renal failure with suspected lower gastrointestinal bleeding (melena on presentation). He was found to have a rapidly declining platelet count with a nadir of 0. Due to severe thrombocytopenia, filgrastim was administered. A bone marrow biopsy revealed findings consistent with amegakaryocytosis with otherwise preserved cell lines. Hematologic labs improved with the initiation of appropriate treatment for severe sepsis. After performing an extensive workup, the likely etiology of transient AATP in this case was severe sepsis-induced immune dysregulation and bone marrow suppression.

is a Gram-negative bacillus commonly seen in immunocompromised individuals and often misdiagnosed as . is an opportunistic pathogen found in aquatic environments. It is a nonfatal infection that has low virulence and endorses susceptibility to many common antibiotics. We report a case of a 53-year-old immunocompromised male who was managed for bacteremia.

Vanishing lung syndrome (VLS) also known as type I bullae disease or idiopathic bullous disease is characterized by giant emphysematous bullae that commonly develop in the upper lobes, occupying at least one-third of a hemithorax. It is a progressive and irreversible condition that involves pulmonary parenchymal destruction and alveolar dilation. It is commonly associated with middle-aged tobacco smokers, habitual marijuana users, and those with alpha-1-antitrypsin deficiency. This case involves an incarcerated male in his 30s with chronic marijuana smoking who presented with a three-month history of right-sided chest pain accompanied by cough, hemoptysis, fever, and weight loss. The patient reported month-long atypical chest discomfort associated with a cough productive of bloody sputum and was brought to the ED after developing acutely worsening right-sided chest pain. The patient underwent a chest X-ray that revealed a large pneumothorax on the left. Subsequently, CT chest imaging showed extensive bilateral bullous disease, left upper lobe consolidation, and enlarged mediastinal lymph nodes. This case illustrates a rare presentation of VLS in the setting of a young patient who other than reported regular marijuana use had no other risk factors and a negative workup for possible etiologies that could cause his severe bullous emphysema, including alpha-1 antitrypsin, HIV, Sjogren's syndrome, pulmonary Langerhans cell histiocytosis, two sputum Mycobacterium tuberculosis tests, and acid-fast bacteria sputum cultures, which were all negative. Identifying and assessing the degree of disease early in this progressive disease helps guide treatment while preventing further deterioration of lung parenchyma.

Severe, refractory asthma requires a combination of multiple maintenance inhalers and medications including high-dose inhaled corticosteroids and immunomodulators to achieve control of symptoms. The use of inhaled corticosteroids, however, increases the susceptibility of opportunistic bacterial infections, such as , resulting in pulmonary nocardiosis. This case describes a 46-year-old patient with a history of severe, refractory asthma who presented with progressively worsening asthma exacerbation symptoms. She was treated with immunomodulators, high-dose inhaled corticosteroids and oral steroids, and several courses of antibiotics. CT imaging revealed bibasilar peri-bronchial thickening and tree-in-bud nodularity in the right lower lobe. Pulmonary cultures collected from bronchoscopy grew complex. This was a rare case of persistent asthma exacerbation by complex bronchopulmonary infection. Broad differentials should be considered in patients with severe, refractory asthma who were previously controlled and were found to fail treatment therapies. Immunocompromised patients with chronic lung disease are at higher risk of severe infection with disseminated nocardiosis. These patients have a higher mortality and morbidity risk if early diagnosis of pulmonary nocardiosis does not occur.

Giant cell arteritis (GCA) is a medium-to-large vessel vasculitis most commonly affecting the aortic arch and carotid branches. Lingual necrosis is a rare complication of GCA caused by lingual artery vasculitis due to ischemia. A delay in diagnosis can result in irreversible complications such as tongue amputation. Our case involves an 83-year-old female patient whose hospital admission for evaluation of stroke-like symptoms was complicated by the development of tongue necrosis, requiring percutaneous endoscopic gastrostomy tube placement for severe odynophagia and dysphagia. The patient was treated with IV glucocorticoids; however, she required tongue amputation due to extensive necrosis as a result of delayed initiation of therapy. Treatment of GCA usually involves an initial high-dose steroid with prolonged steroid taper or immunomodulatory, as relapse is a common occurrence. Prompt diagnosis and appropriate therapy to treat GCA is crucial to prevent the progression of tongue necrosis.

BackgroundThe chronic inflammation associated with rheumatoid arthritis (RA) leads to focal and systemic bone erosion of the joints resulting in a crippling disability. Recent reports indicate an increase in the incidence of RA in the coming years, placing a significant burden on healthcare resources. The incidence of RA is observed to be increasing with age and a significant proportion of those new cases will be aggressively erosive.FindingsThe altered physiology, due to immune disturbances, contributes towards RA pathogenesis. The imbalance of inflammatory cytokines and non-cytokine immune modulators such as prostaglandin E2 (PGE2) and IL-23-induced pathogenic IL-17, plays a crucial role in persistent inflammation and bone degradation during RA. However, the molecular mechanism of IL-23, a key cytokine, and PGE2 in the development and perpetuation of IL-17 producing effector Th17 cells is poorly understood.ConclusionThis review focuses on research findings that provide insight into the contribution of PGE2 and IL-23 during the development of pathogenic Th17 cells. We also highlight the key transcriptional factors required for Th17 development and therapeutic strategies to disrupt the interaction between IL-23 and IL-17 to prevent the end-organ damage in RA.

Introduction: Infective endocarditis (IE) is an infection of the endocardium, which most commonly involves the mitral and aortic valve. The estimated incidence of IE in patients with heart defects is 1–2%. One of the predisposing factor is mitral valve leaflet prolapse accompanied by incompetence. The diagnosis of IE can prove difficult due to the possible occurrence of symptoms from multiple organs. A multidisciplinary approach, and taking into consideration possible numerous complications is essential during diagnostic procedures. The clinical picture of IE includes embolic complications. The presented study describes the case of a 58-year-old male patient with a mitral defect diagnosed due to multi-cause anaemia, which delayed the diagnosis of IE. Besides anaemia, the clinical picture was dominated by numerous embolic brain lesions, being complications of IE, which caused disorientation and confusion.