Cavitary lesions of the lungs are a very frequent picture found in clinical practices resulting from a wide range of pathological processes with variable duration of formation depending on infectious pathogens. Common organisms causing cavitary lesions are Staphylococcus aureus , Klebsiella pneumoniae , Streptococcus pneumoniae , Haemophilus influenzae , typical and atypical Mycobacterium , and Aspergillus . Herein, we are presenting a case that developed cavitary lesions in both lungs colonizing Acinetobacter , a rare causative agent, within less than two months of a positive coronavirus disease 2019 (COVID-19) infection.

Background: Sodium-glucose cotransporter-2 inhibitors (SGLT2 inhibitors) are a relatively new class of medications used for the management of type II diabetes mellitus targeting the kidneys. Within the last decade, several warnings have been issued regarding the development of severe genitourinary infections, including necrotizing fasciitis, or Fournier's gangrene, in those with pre-existing type II diabetes and concomitant use of this drug class.Objective: The purpose of this review is to highlight and discuss the factors contributing to the development of Fournier's gangrene, its pathogenesis, and a review of existing literature describing patient outcomes, treatment, and future directions regarding early detection of this complication.Methods: Articles and studies addressing effective treatment adherence and key factors contributing to Fournier's gangrene with SGLT2 inhibitors were identified by effective keyword searches in PubMed Central, Google Scholar, and Cochrane, as well as the references found within these articles.Results: Using the keywords provided, 55 case reports, review articles, and meta-analysis reports written within the last 20 years were utilized as the source of the data presented in this systematic review article.

Osteoarthritis (OA) is one of the most prevalent degenerative joint diseases, which results in the inevitable destruction of joints leading to pain and joint immobility. Some studies have reported a potential link between diabetes mellitus (DM) and the worsening symptoms and severity of OA. Based on our literature review, the microcellular environment of patients with DM showed accelerated joint destruction and increased inflammation in every anatomical aspect of the joint including the bones, tendons, ligaments, cartilage, and synovium. Additionally, the biomechanical and biochemical properties of these tissues were more severely impacted in patients with DM and OA compared to those without DM, suggesting that DM plays an important role in the pathogenesis of OA. Specifically, we found that advanced glycation end products (AGEs) are the key to inducing the acceleration of joint destruction; however, their role in the pathogenesis has yet to be fully mapped out. In this narrative review, we aim to explore the role that DM plays in the acceleration of OA leading to increased reports of joint pain in those with both diseases. We believe this topic of discussion to be important due to the increased prevalence of both diseases over the last several decades, potentially leading to an increased medical burden on both patients and the community at large.

Rheumatoid arthritis is one of the most prevalent musculoskeletal disorders that, when insufficiently treated, results in detrimental sequelae including joint damage and reduced quality of life. Poor patient adherence to medication is a significant blockade to effective management. The purpose of this review is to highlight and discuss the factors responsible for defiance of antirheumatic medication and ways to overcome these barriers. Education level, health literacy, cohabitation status, multi-morbidities, complicated drug regimen, intermittent co-payments, prescribed regimen adverse effects, and cognitive impairment are a few among many common barrier factors leading to poorer outcomes in rheumatoid arthritis. While there is an abundance of inhibitory factors leading to worsening disease progression, they each can be easily dealt with an effective approach at the beginning or during the treatment course to ensure a better outcome.

Job syndrome or hyper-immunoglobulin E syndrome is one of the rare immunologic diseases with only about 300 cases described in the literature until now. Given their low prevalence, our understanding of both autosomal dominant and recessive Job syndromes is still evolving. No specific treatment options are available but early diagnosis may help in treating cases prophylactically with antibiotics and wound care to reduce the patient's burden. We recently encountered a patient diagnosed with Job syndrome with autism who presented with an abscess in the right axillary region. We report this case for its rarity and unique association with developmental neurologic disorder. It is crucial to review this rare syndrome to circumvent any diagnostic delay. Following the disease course and taking all the associations into account is also vital for the clinician's understanding as well as implementing the treatment plan.