Coronavirus disease 2019 (COVID-19) is a highly contagious viral illness caused by the RNA virus Coronaviridae subtype severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Rapid infection caused by this virus became overwhelming and resulted in millions of deaths worldwide. The effects of smoking have been heavily studied and lead to increased occurrence of COVID-19 viral infections and mortality. The phenomenon of cytokine storm has been shown as one of the leading factors of mortality. However, the question remains as to what factors, either genetic or environmental, ultimately lead to the increased incidence of cytokine storms compared to others. We present a case of two cohabitating, 57-year-old, male, identical twins (Twin A and Twin B) who contracted SARS-CoV-2 simultaneously. Both Twin A and Twin B had similar medical histories, except for Twin A being a former smoker while Twin B a current smoker. While both twins presented with cough and shortness of breath, Twin A also presented with hypoxia, leukocytosis, evidence of acute kidney injury, and transaminitis while Twin B presented normoxic with solely tachycardia. Due to his presentation and vital signs, Twin B received Bamlanivimab but developed hypoxia during the infusion. Both twins were subsequently initiated on Remdesivir, dexamethasone, and supplemental oxygen daily. After completion of treatment courses, both twins had improvement in their laboratory values and were subsequently discharged with supplemental oxygen to be further weaned in the outpatient setting. Due to the twins’ cohabitation, contracting SARS-CoV-2 simultaneously, and similar medical history, we highlight the potential mechanism of nicotine’s chemical ability to blunt the subsequent inflammatory process of COVID-19. Despite nicotine’s potential ability to dampen cytokine storms, smoking has well-documented adverse effects and we, like many experts, entirely discourage it. However, given the rare situation of identical twins contracting SARS-CoV-2, we can extrapolate information regarding the effects of the virus without obfuscation from genetic and environmental factors to identify areas of research for new therapies.

We present a 51-year-old male, with a past medical history of type 2 insulin-dependent diabetes mellitus (T2IDDM) without neuropathy, coronavirus disease 2019 in April 2020 without residual symptoms, Raynaud's, and recent occupational outdoor exposure to insects as a construction manager who came to the emergency room complaining of a three-week history of bilateral progressive numbness and weakness beginning in his lower extremities and ascending toward his pelvis. Notably, he received the second dose of his Moderna COVID-19 vaccine one week prior to symptom onset and four weeks prior to admission. He also reported a recent appearance of a maculopapular rash on his upper extremities and flanks. Physical exam was remarkable for bilateral distal motor weakness in the upper and lower extremities with associated paresthesia and decreased reflexes in the lower extremities. The patient had slight ataxia and difficulty with heel walk and toe walk. Notably, the cranial nerve exam was normal, and the patient was afebrile. Intravenous immune globulin (IVIG) was started empirically for the treatment of Guillain-Barre syndrome (GBS), and doxycycline 100mg intravenous twice a day and ceftriaxone 2g intravenous daily were started for possible tick-borne disease. Subsequently, rapid plasma reagin (RPR) returned reactive at 1:64, and cerebral spinal fluid (CSF) venereal disease research laboratory (VDRL) test was reactive at 1:2 with markedly elevated protein and pleocytosis. Human immunodeficiency virus (HIV) testing was negative. Lyme disease testing was negative. Nerve conduction studies (NCS) and electromyography (EMG) showed a sensorimotor polyneuropathy with mixed demyelinating and axonal features. IVIG was continued for a total of five days, and antibiotics were changed to penicillin G (PCN G) for a total of 14 days for definitive treatment of early neurosyphilis (NS). While both clinical and laboratory findings confirm a positive diagnosis of NS, the patient's CSF composition showed very elevated total protein levels and pleocytosis. Additionally, his early peripheral neuropathy and EMG findings are not characteristics of a single disease and, instead, suggested a mixed pathology. We postulate that this patient had confirmed secondary syphilis with early NS associated with, and possibly correlated with, a simultaneous episode of acute inflammatory demyelinating polyneuropathy (AIDP) and/or a vaccine-related phenomenon.

We present a 73-year-old male with a history of end-stage renal disease (ESRD) on dialysis, type 2 diabetes mellitus, coronary artery disease status post stents, prostate carcinoma status post radiation, and prostatectomy, with recurrent bladder neck contracture requiring suprapubic catheter, left urethral stricture with nephrostomy tube placement, penile implant, and recurrent urinary tract infections, who presented to the emergency room complaining of constant bilateral groin pain for one day. Physical exam was significant for suprapubic tenderness and a chronic suprapubic catheter and left-sided nephrostomy tube. An initial examination of the patient's urine revealed turbid, yellow-colored fluid, positive for white blood cells, leukocyte esterase, and bacteria. A urine culture was obtained, which returned positive for E. americana, with >100,000 colony-forming units (CFUs) as well as Enterococcus faecalis (E. faecalis) demonstrating low colony counts. The patient was treated with a seven-day course of meropenem 1 gm twice daily, which improved of his symptoms, and then completed a 10-day course of ertapenem 500 mg daily. The patient received a five-day course of vancomycin 1 gm on dialysis days for additional coverage of E. faecalis, despite low colony counts. This is the first documented case of a urinary tract infection caused by E. americana. The organism is primarily found in immunocompromised individuals, and a debate is still ongoing as to whether it is a true pathogen or exists primarily as an opportunistic infection. We suggest further inquiry and study of this resistant organism are paramount in establishing its role in both immunocompromised as well as immunocompetent individuals. E. americana is a multidrug-resistant organism, which to date has sparse documentation regarding its prevalence and potential for morbidity, especially in compromised individuals. In the era of increasing antibiotic resistance, we suggest that more research is needed to understand the pathogenicity of E. americana.

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We present a 62-year-old woman with a history of uterine cancer status post-total abdominal hysterectomy and bilateral salpingo-oophorectomy (TAH-BSO) on paclitaxel, who presented to the emergency department febrile at 101.7 Fahrenheit and complaining of fatigue and urinary incontinence. Laboratory testing revealed neutropenia and urinalysis showed elevated bacteria with minimal white blood cells, and negative leukocyte and negative nitrites. Urine cultures ultimately showed Staphylococcus lugdunensis with negative blood cultures.S. lugdunensis is a less frequently speciated Staphylococcus and has been increasingly found due to advances in identification using matrix-assisted laser desorption ionization time of flight mass spectrometry (MALDI-TOF MS). S. lugdunensis are Gram-positive cocci, nonsporulating, nonmotile, facultatively anaerobic, catalase-positive, coagulase-negative, oxidase-negative, delta-hemolytic organism. Traditionally, it is seen in skin and soft-tissue infections, as well as vascular infections, however, has minimal occurrences in urinary tract infections.The risk of infection is increased in immunocompromised states and empiric treatment is warranted while waiting for definitive results. Our patient was started on cefepime, valacyclovir, fluconazole, and a single dose of vancomycin while in the emergency department. Worsening thrombocytopenia during her antibiotic course necessitated the re-evaluation of antibiotic agents which can cause thrombocytopenia. Subsequently, due to the patient's improved clinical status, and low risk of severe outcome, fluconazole and valacyclovir were discontinued, and cefepime was changed to ceftriaxone.