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1.
Ontario Veterinary Medical Association (OVMA) ; : 288-292, 2022.
Article in English | GIM | ID: covidwho-2291234

ABSTRACT

This paper describes the epidemiology, prevalence, transmission, prevention and control of some infectious diseases in companion animals, livestock, wild animals and humans in Ontario, Canada, in 2022, including SARS-CoV-2;Echinococcus multilocularis, Leishmania spp. and SARS-CoV-2;antimicrobial stewardship resources;2 cases of rabid dogs imported from Iran (July 2021 and January 2022);prevalence of extended-spectrum beta-lactamase (ESBL)-producing Enterobacteriacea, Dirofilaria immitis, Brucella canis, canine parainfluenza and adeno- and herpes viruses in dogs recently imported from Asia;Paragonimus kellicotti lung flukes and Streptococcus equi subsp. zooepidemicus in dogs;African swine fever in pet pigs, backyard pigs and wild pigs and blastomycosis in dogs and humans.

2.
Transcriptomics in Health and Disease, Second Edition ; : 395-435, 2022.
Article in English | Scopus | ID: covidwho-2301705

ABSTRACT

Mycoses are infectious diseases caused by fungi, which incidence has increased in recent decades due to the increasing number of immunocompromised patients and improved diagnostic tests. As eukaryotes, fungi share many similarities with human cells, making it difficult to design drugs without side effects. Commercially available drugs act on a limited number of targets and have been reported fungal resistance to commonly used antifungal drugs. Therefore, elucidating the pathogenesis of fungal infections, the fungal strategies to overcome the hostile environment of the host, and the action of antifungal drugs is essential for developing new therapeutic approaches and diagnostic tests. Large-scale transcriptional analyses using microarrays and RNA sequencing (RNA-seq), combined with improvements in molecular biology techniques, have improved the study of fungal pathogenicity. Such techniques have provided insights into the infective process by identifying molecular strategies used by the host and pathogen during the course of human mycoses. This chapter will explore the latest discoveries regarding the transcriptome of major human fungal pathogens. Further we will highlight genes essential for host–pathogen interactions, immune response, invasion, infection, antifungal drug response, and resistance. Finally, we will discuss their importance to the discovery of new molecular targets for antifungal drugs. © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2014, 2022.

3.
2023 OVMA (Ontario Veterinary Medical Association) Conference and Tradeshow ; : 284-288, 2023.
Article in English | CAB Abstracts | ID: covidwho-2286421

ABSTRACT

This paper describes the clinical signs and use of differential laboratory diagnostic techniques (computed tomography, cytology, histopathology, antigen/antibody detection and polymerase chain reaction) for infectious (viral, bacterial, fungal and parasitic) and non-infectious (inflammatory/immune mediated, neoplastic, cardiac, malformation, foreign body, smoke inhalation, aspiration of caustic material, non-cardiogenic, pulmonary oedema, traumativ, pneumothorax, pulmonary contusions and idiopathic) causes of respiratory diseases in cats and dogs in Ontario, Canada.

4.
Semin Immunol ; 66: 101728, 2023 03.
Article in English | MEDLINE | ID: covidwho-2262815

ABSTRACT

The respiratory tree maintains sterilizing immunity against human fungal pathogens. Humans inhale ubiquitous filamentous molds and geographically restricted dimorphic fungal pathogens that form small airborne conidia. In addition, pathogenic yeasts, exemplified by encapsulated Cryptococcus species, and Pneumocystis pose significant fungal threats to the lung. Classically, fungal pneumonia occurs in immune compromised individuals, specifically in patients with HIV/AIDS, in patients with hematologic malignancies, in organ transplant recipients, and in patients treated with corticosteroids and targeted biologics that impair fungal immune surveillance in the lung. The emergence of fungal co-infections during severe influenza and COVID-19 underscores the impairment of fungus-specific host defense pathways in the lung by respiratory viruses and by medical therapies to treat viral infections. Beyond life-threatening invasive syndromes, fungal antigen exposure can exacerbate allergenic disease in the lung. In this review, we discuss emerging principles of lung-specific antifungal immunity, integrate the contributions and cooperation of lung epithelial, innate immune, and adaptive immune cells to mucosal barrier immunity, and highlight the pathogenesis of fungal-associated allergenic disease. Improved understanding of fungus-specific immunity in the respiratory tree has paved the way to develop improved diagnostic, pre-emptive, therapeutic, and vaccine approaches for fungal diseases of the lung.


Subject(s)
COVID-19 , Mycoses , Humans , Lung , Fungi , Immunity, Innate
5.
Chest ; 162(4):A1578, 2022.
Article in English | EMBASE | ID: covidwho-2060843

ABSTRACT

SESSION TITLE: Rare Pulmonary Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: Pneumatoceles are air-filled cavitary lesions that are rarely seen in the lung after infection, trauma, or as part of a more diffuse cystic disease process. Several infectious agents have been associated with pneumatoceles, one of them being Pneumocystis Jirovecii, a potentially life-threatening fungus commonly seen as an opportunistic infection in immunocompromised patients. We present a case of bilateral extensive pneumatocele in a newly diagnosed HIV patient found to be positive for Pneumocystis pneumonia CASE PRESENTATION: A 52-year-old female presented to the emergency room for 2 months of shortness of breath, body aches, and chills. She was saturating at 86% on room air on arrival. Initial chest x-ray showed bilateral airspace disease. Had additional history of daily smoking, polysubstance abuse, and poor follow-up with doctors’ appointments due to social issues. She was started on oxygen support, steroids, antibiotics, and IV fluids. Labs were notable for normal overall WBC count but low lymphocyte count of 0.4. A CT Angiogram of the chest showed moderate to severe diffuse bilateral gas-filled cystic structures throughout the lungs, consistent with pneumatoceles. Infectious workup performed: COVID PCR, Influenza A/B antigen, legionella antigen, strep. pneumoniae antigen, B-D-glucan assay, histoplasma and blastomyces antigens, and HIV antibody. HIV antibody, strep pneumo antigen, and B-D-glucan assay came positive. She did not have a known diagnosis of HIV prior to this admission. Antibiotic regimen was changed to ceftriaxone, azithromycin, Bactrim, and fluconazole. Bronchoscopy with lavage was performed. Lavage samples were sent for cytology and found to be positive for Pneumocystis on GMS stain HIV viral load was checked and found to be at 1.4 million copies. CD4 count was less than 25 Patient was started on antiretroviral therapy in addition to prolonged course of Bactrim. She was ultimately discharged from the hospital in stable condition with pulmonary and infectious disease follow-up. At this time her pneumatoceles have improved on follow-up imaging. DISCUSSION: Pneumatoceles can rarely present as a complication of PCP pneumonia and can be a marker of more advanced disease. In our patient, pneumatoceles were identified first followed by diagnosis of HIV and PCP pneumonia. Overall incidence of post-infectious pneumatoceles is low at 2-8%. Prompt treatment and careful monitoring is needed due to risk of mortality from underlying infection and progression to pneumothorax. CONCLUSIONS: HIV with PCP infection complicated by pneumatocele formation is much less common due to improvements in HIV detection and screening for opportunistic infection, but should remain an important consideration in patients with unexplained cystic lung disease patterns, especially in patients without established outpatient follow-up or who don't see medical providers often. Reference #1: Thomas CF Jr, Limper AH: Pneumocystis pneumonia. N Engl J Med. 2004;350: pp. 2487-2498. Reference #2: Albitar, Hasan and Saleh, Omar M. Pneumocystis Pneumonia Complicated by Extensive Diffuse Pneumatoceles. Am J Med. 2019 May;132(5):e562-e563. Epub 2019 Jan 16. Reference #3: Ryu, Jay et al. Diffuse Cystic Lung Diseases. Frontiers of Medicine volume 7, pages 316–327 (2013) DISCLOSURES: No relevant relationships by Clifford Hecht

6.
Chest ; 162(4):A1120, 2022.
Article in English | EMBASE | ID: covidwho-2060774

ABSTRACT

SESSION TITLE: Critical Gastrointestinal Case Reports SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: Histoplasma capsulatum is a dimorphic fungus most commonly encountered as an opportunistic infection in immunosuppressed patients, particularly those with HIV/AIDS. However, patients immunosuppressed from other causes can also be at risk. Here is presented the case of a patient on multi-immunosuppressant therapy as treatment for Crohn's disease, who developed disseminated histoplasmosis. CASE PRESENTATION: A 44-year-old male with a past medical history of Crohn's disease (previously been on azathioprine, adalimumab and currently on Prednisone therapy), recently started on infliximab infusion for uncontrolled symptoms of IBD, diabetes mellitus, hypothyroidism, and COVID-19 infection (not requiring oxygen therapy) one month prior to the current admission initially presented to the hospital with chief complaints of exacerbated weakness, myalgias, fevers and diarrhea for 5 days;Symptoms of weakness, myalgias began after first infusion of infliximab and it got progressively worse after the 2nd infusion 2 weeks prior to the admission. White Blood Cell count was 1.1 K/uL, platelet count was 7 K/uL, hemoglobin was 7.9 g/dL. CRP was elevated to 142 mg/L, and ferritin was elevated to 39,000 ug/L. CT abdomen and pelvis demonstrated probable rectosigmoid colitis and splenomegaly. Subsequent chest x-ray demonstrated bilateral opacities with haziness over bilateral lung fields. Respiratory viral panel, stool panel, blastomyces antigen, cryptococcal antigen, toxoplasma antibodies, HIV antibody, CMV PCR, and blood cultures were unrevealing. Urinary histoplasma antigen was positive, and BD-glucan was elevated to over 500 ng/L. EBV panel was positive for reactivation, with EBV DNA 2.02 IU/mL. He was subsequently started on amphotericin B lipid complex, with itraconazole destination therapy. He was treated empirically for pneumocystis jiroveci pneumonia (PJP) with sulfamethoxazole-trimethoprim due to him being on chronic Prednisone therapy. Echocardiogram demonstrated left ventricular ejection fraction (LVEF) of 40%, with diffuse hypokinesis and wall motion abnormalities, posing some question of myocarditis. He was later discharged home in an improved state. DISCUSSION: Disseminated histoplasmosis in the setting of Crohn's disease on chronic immunosuppressive therapy has been very rarely reported,(1) with similar reports in patients on immunosuppressive therapy in the setting of rheumatologic disease being slightly more common.(2) The most commonly involved areas in gastrointestinal histoplasmosis are the terminal ileum and colon,(3) with this patient's rectosigmoid colitis and symptomatology being consistent with this pattern. The patient's myocarditis is also consistent with disseminated histoplasmosis infection. CONCLUSIONS: Clinicians should maintain suspicion for opportunistic infections in patients on immunosuppressive therapy in the setting of critical illness. Reference #1: Bhut, B., Kulkarni, A., Rai, V. et al. A rare case of disseminated histoplasmosis in a patient with Crohn's disease on immunosuppressive treatment. Indian J Gastroenterol 37, 472–474 (2018). https://doi.org/10.1007/s12664-018-0886-1 Reference #2: Wood KL, Hage CA, Knox KS, et al. Histoplasmosis after treatment with anti-tumor necrosis factor-alpha therapy. Am J Respir Crit Care Med. 2003;167(9):1279-1282. doi:10.1164/rccm.200206-563OC Reference #3: Galandiuk S, Davis BR. Infliximab-induced disseminated histoplasmosis in a patient with Crohn's disease. Nat Clin Pract Gastroenterol Hepatol. 2008;5(5):283-287. doi:10.1038/ncpgasthep1119 DISCLOSURES: no disclosure on file for Donald Dumford;No relevant relationships by Abhilash Bhat Marakini No relevant relationships by Palak Rath No relevant relationships by Sterling Shriber

7.
Chest ; 162(4):A877, 2022.
Article in English | EMBASE | ID: covidwho-2060716

ABSTRACT

SESSION TITLE: Critical Care Infections SESSION TYPE: Case Reports PRESENTED ON: 10/19/2022 09:15 am - 10:15 am INTRODUCTION: Francisella tularensis is a zoonotic disease by an aerobic, gram negative coccobacillus. It is transmitted by exposure to infected animal or vectors in individuals who landscape or camp. Common symptoms are fever, chills, anorexia, and headache. Abdominal tularemia can present with abdominal pain, emesis, diarrhea, and rarely intestinal ulceration and hemorrhage. It is treated with aminoglycosides, fluoroquinolones and tetracycline. CASE PRESENTATION: 38-year-old male presented with fever, cough, anorexia, and black stool for 5 days. Patient worked as a landscaper. He has no pets, travel history or sick contacts. He does not take any medications at home. Physical exam was significant for sinus tachycardia and rhonchi of right upper lobe. Significant labs include WBC of 9.8 with 41% bands, hemoglobin 15.5, sodium 125, procalcitonin 27.3, and lactic acid 1.8. COVID-19, MRSA, Legionella and Pneumococcal urine antigen were negative. CTA chest revealed mass-like opacity in right upper lobe with multiple bilateral pulmonary nodules. Lower respiratory culture showed Candida albicans. Patient was empirically started on ceftriaxone and azithromycin. He was transferred to intensive care for worsening respiratory status and was placed on non-invasive ventilation on hospital day 1. Antibiotics were broadened to ceftaroline and levofloxacin due to suspicion of tularemia. Amphotericin B was added. Labs for Histoplasma, Blastomyces, TB, Leptospira, and HIV were negative. Patient then suffered a cardiac arrest on hospital day 2 after having large brown secretions pouring from his mouth. Cardiopulmonary resuscitation was initiated and patient was intubated and started on vasopressors with return of spontaneous circulation. Massive blood transfusion protocol was initiated. Emergent bedside upper endoscopy showed large blood clot adherent to duodenal ulcer. Interventional radiology planned on performing gastric duodenal artery embolization. However, patient suffered two more cardiac arrest with resuscitation efforts terminated per family request. Karius Digital Culture later was positive for Francisella tularensis. Autopsy revealed diffuse alveolar hemorrhage, hilar lymphadenopathy, and perforated duodenal ulceration with large adherent clot. DISCUSSION: Gastrointestinal tularemia is rare and usually from drinking contaminated water or oral inoculation of bacteria. Intestinal tract involvement can present with mesenteric lymphadenopathy and ulcerative lesions resulting in gastrointestinal bleeding with case fatality rate of 50%. Even though this is noted in the literature, to our knowledge no case reports have been published. CONCLUSIONS: Careful history taking and early identification of risk factors are important when severe tularemia infection is suspected such as in individuals with extensive outdoor activities. Treatment should be empirically initiated in high risk patients. Reference #1: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4585636/ Reference #2: https://casereports.bmj.com/content/2017/bcr-2017-22125. Reference #3: Altman GB, Wachs JE. Tularemia: A pathogen in nature and a biological weapon. Aaohn Journal. 2002 Aug;50(8):373-9. DISCLOSURES: No relevant relationships by Maria Haider Baig

8.
Chest ; 162(4):A495, 2022.
Article in English | EMBASE | ID: covidwho-2060611

ABSTRACT

SESSION TITLE: Severe and Unusual Blastomycosis Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: The diagnosis of blastomycosis is often delayed due to its non-specific symptoms and imaging findings. Clinicians must have a high clinical index of suspicion to diagnose blastomycosis in a timely manner, especially in the setting of the current COVID-19 pandemic. CASE PRESENTATION: A healthy 44-year-old male presented to an urgent care center with complaints of cough, fevers, and malaise. CT scan of the chest revealed a left upper lobe mass concerning for rounded bacterial pneumonia versus malignancy. He was found to be COVID-19 positive. The patient was sent home with steroids and antibiotics. Three months later, a repeat CT scan of the chest was obtained which revealed progression of the consolidation and prompted further evaluation at the hospital. On presentation, he reported a persistent cough, weight loss, and the development of multiple painful nodules on his extremities and trunk within the past week. A skin lesion was biopsied. A bronchoscopy was also performed for biopsy and brushing. Biopsy of the skin lesion as well as specimens collected from the bronchoscopy resulted positive for Blastomyces. MRI of the brain demonstrated multiple enhancing lesions concerning for septic emboli. He was started on amphotericin B for treatment of disseminated blastomycosis with central nervous system (CNS) involvement. Repeat imaging of the brain and chest about 3 weeks after initiation of therapy showed interval decrease in the size of the lesions. He was then transitioned to oral itraconazole and discharged home. DISCUSSION: Blastomycosis is an endemic fungal infection that can affect immunocompetent and immunocompromised hosts. It tends to infect immunocompetent hosts more so than other invasive fungal infections. Symptoms can range from asymptomatic to rapidly progressive acute respiratory distress syndrome (ARDS). Disseminated blastomycosis has been reported in 20-50% of patients (1). In the above case, an immunocompetent patient developed pulmonary and dermatologic manifestations concerning for disseminated blastomycosis. Though he had no recent travel, occupational exposures, or contact with any construction work, the patient was living in an endemic area for Blastomyces. It is difficult to definitively ascertain if the patient already had pulmonary blastomycosis when he was diagnosed with COVID-19, but his extrapulmonary manifestations clearly developed after the diagnosis. Earlier detection and treatment of the pulmonary blastomycosis may have prevented the dissemination of the disease. CONCLUSIONS: This case serves as a reminder to consider other infectious etiologies, like endemic fungal infections, in the midst of the COVID-19 pandemic to prevent delays in treatment and progression of these diseases. Reference #1: McBride JA, Gauthier GM, Klein BS. Clinical Manifestations and Treatment of Blastomycosis. Clin Chest Med. 2017 Sep;38(3):435-449. doi: 10.1016/j.ccm.2017.04.006. Epub 2017 Jun 12. PMID: 28797487;PMCID: PMC5657236. Reference #2: Cafardi J, Haas D, Lamarre T, Feinberg J. Opportunistic Fungal Infection Associated With COVID-19. Open Forum Infect Dis. 2021 Jan 18;8(7):ofab016. doi: 10.1093/ofid/ofab016. PMID: 34621913;PMCID: PMC7928619. DISCLOSURES: No relevant relationships by Shannon Burke No relevant relationships by Abigail Go No relevant relationships by Jen Minoff No relevant relationships by David Stoeckel

9.
Pediatrics ; 149, 2022.
Article in English | EMBASE | ID: covidwho-2003076

ABSTRACT

Introduction: Blastomyces species are thermally dimorphic fungi endemic to North America, especially areas bordering the Mississippi, Ohio and St. Lawrence rivers, and the Great Lakes. Blastomycosis infections are estimated to occur in 3-13% in the pediatric population. Pediatric literature for blastomycosis has been mostly limited to small studies and case series. Recent literature suggests increasing rates of infections, less morbidity and mortality as compared to adults, with asthma as the most common comorbid condition. Although pulmonary disease is the most common presentation, it rarely progresses to acute respiratory distress syndrome (ARDS). Case Description: A 17- year-old female, living in the Chicago area, and with type 1 diabetes mellitus and childhood asthma, presented to the emergency room with acute hypoxemic respiratory failure after 14 days of cough, dyspnea, chest pain, and fevers as high as 105°F. Her initial radiographic imaging revealed bilateral infiltrates and consolidations in the right middle and lower lobes. She was admitted to the step down unit for further care. A respiratory viral panel, including COVID-19 evaluation, was negative. She was started on low-flow nasal cannula, ceftriaxone, azithromycin, albuterol, and maintenance IV fluids. On hospital day 2, she was transferred to the pediatric intensive care unit for worsening respiratory distress and escalated to high-flow nasal cannula. She was treated empirically for presumed bacterial pneumonia with ceftriaxone (7-day course), azithromycin (5-day course), cefepime (5-day course), clindamycin (2-day course), and vancomycin (14-day course). Despite this treatment, repeat chest imaging showed worsening disease and she required escalation to BiPAP for progression of her ARDS and impending respiratory failure. Karius testing results indicated Blastomyces dermatitidis at low levels typically not clinically relevant. Sputum and bronchoalveolar lavage cultures demonstrated no significant pathogenic bacteria. Pathology exam of the biopsy obtained from bronchoscopy was consistent with Blastomyces. Urine antigen test was positive for both Blastomyces and Histoplasma. She clinically improved after initiating Amphotericin B lipid complex (6-day course), with transition to oral itraconazole and adjunctive therapy with IV methylprednisolone. She was discharged home after a 30-day hospital stay. Discussion: Pulmonary blastomycosis presents with a broad variety of signs and symptoms. Timely diagnosis is challenging. Pulmonary blastomycosis has no pathognomonic radiographic patterns. Severe acute pulmonary infection that fails to respond to antibacterial treatment should prompt investigation for fungal infection, including urine antigen tests for Histoplasma and Blastomyces, serum galactomannan, beta-1,3-D-glucan, and next-generation sequencing of microbial cell-free DNA (eg, Karius test). Close respiratory monitoring should occur in a pediatric intensive care unit. Conclusion: Blastomycosis is not typically in the initial differential diagnosis unless the patient has other clinical findings, fails to improve on antibacterial therapy, or has identified risk factors for exposure. Failure of prompt recognition is associated with poor outcomes, increased morbidity and mortality, increased length of hospital stay, and cost.

10.
Journal of General Internal Medicine ; 37:S386, 2022.
Article in English | EMBASE | ID: covidwho-1995817

ABSTRACT

CASE: A 25 year old Vietnamese female initially presented to the emergency department (ED) with progressive dyspnea and cough for 2 weeks. Chest Xray (CXR) showed left lower lobe consolidation and was started on a 5-days of azithromycin. She returned to ED 3 days later with a worsening cough, yellowish sputum, dyspnea, pleuritic chest pain, chills, appetite loss, and a 6-pound weight loss. 7 years ago her pre-immigration screening was negative for tuberculosis. She worked in a nail salon and did gardening as a hobby. On exam, she was afebrile, appeared dyspneic with normal oxygen saturation, diminished breath sounds on left lower lobe with egophony. Labs showed leukocytosis of 22,300 with neutrophilia and negative COVID-19 test. Repeat CXR showed worsening left lower lobe opacity. On day 3, temperature peaked at 103.1F with worsening sputum production. Computed tomography (CT) chest showed complete consolidation of the left lower lobe with tree-in-bud opacities in bilateral upper lobes and right lower lobe. Antibiotics were switched from ceftriaxone and azithromycin to piperacillin-tazobactam and vancomycin. Bronchoalveolar lavage (BAL) gram stain, acid-fast bacilli stain and gomori stain, and blood cultures were negative. Follow-up CT chest was worse and repeat bronchoscopy with biopsy was done. On day 8, urinary blastomyces and histoplasma antigen tests were positive. BAL cytology showed budding yeast consistent with blastomycosis. IV voriconazole was added and her symptoms gradually improved. She was discharged on 6-month course of oral voriconazole. BAL and biopsy cultures came back positive for B. dermatitidis confirming the diagnosis. Outpatient follow-up with CXR after a month showed both clinical and radiological improvement. IMPACT/DISCUSSION: Blastomycosis is a fungal infection caused by thermally dimorphic fungi Blastomyces species, endemic in Ohio, Mississippi River Valleys, and the Great Lakes region in the United States. It commonly presents as a pulmonary infection following inhalation of spores. Severity varies from asymptomatic to life-threatening acute respiratory distress syndrome. Diagnosis delay is common with frequent misdiagnoses including bacterial pneumonia, malignancy, and tuberculosis. Pulmonary blastomycosis commonly presents as dense consolidation in the upper lobes but can have variable presentation. Serological tests, cultures and BAL studies can aid in diagnosis. Repeat bronchoscopies should be considered when the suspicion is high. Of note, blastomyces antigen can have cross-reactivity with histoplasma antigen which might be the case with our patient. CONCLUSION: This case highlights the resemblance of clinical and radiological presentation of blastomycosis with other respiratory conditions and the need for timely diagnosis, treatment, and antimicrobial stewardship. Practitioners need to keep a strong suspicion of this disease in patients with atypical presentation for pneumonia especially in endemic areas.

11.
Journal of General Internal Medicine ; 37:S486, 2022.
Article in English | EMBASE | ID: covidwho-1995592

ABSTRACT

CASE: A previously healthy, 27-year-old Caucasian male presented with erythema and edema in his extremities. He endorsed multiple years of injecting heroin into numerous areas from his chest to his toes, including both upper extremities. The patient was seen six months ago at local urgent care for swelling of both of his dorsal feet and a small abscess with surrounding cellulitis of the right hand. He was given a dose of Ceftriaxone and a 2-week course of Augmentin, which he completed with moderate improvement. A month prior to his presentation, he reported that this swelling started asymmetrically;it started in his legs, then in his right arm, and then in his left arm. He denied any discharge from any site on his skin. He last injected heroin the morning of his admission. He denied fever, shortness of breath, pleuritic chest pain, orthopnea, dyspnea on exertion, and any urinary symptoms. On presentation, he was afebrile and saturated 98% on room air. His extremities were warm, normal capillary refill, and distal pulses were strong and symmetric. There were also pitting edema in the right hand with associated volar erythema, pitting edema in the right foot, and left-hand edema with a punctate area around the mid-arch with associated tenderness to palpation without overlying redness, crepitus, or fluctuance. Blood cell count revealed mild leukocytosis to 12.0. CMP was unremarkable. While the infectious disease team was consulted for further evaluation, he was started on cefazolin 1g for 10 days. The urine drug screen was positive for benzodiazepines, THC, cocaine, and opiates. HIV negative, Covid negative, and blood cultures showed no growth. Histoplasma/ Blastomyces urine antigens were negative. Urinalysis without evidence of proteinuria, and transaminases were within the normal limit. Ultrasound showed occlusive cephalic vein thrombosis in the right upper extremities. Cefazolin was discontinued. Based on the presentation, the history, and the evaluation, it was concluded to be Puffy Hand Syndrome. IMPACT/DISCUSSION: Puffy hand syndrome is a form of lymphedema caused via the sclerosing nature of intravenously administered drugs, which our patient extensively utilized. Described by Abeles in 1965 as seen in New York prisoners, it affects between 7 to 16% of intravenous drug users. Its pathology is suspected to be caused due to a combination of lymphatic and venous insufficiency. Differential diagnosis of this syndrome involves identification of infection alongside cardiac or renal insufficiency, and edematous scleroderma. Treatment is mostly symptomatic. Patients are advised to stop IV drug use. Long-term use of low-stretch bandages and compression may be useful in decreasing the puffiness of the extremities. CONCLUSION: With the quality of care for drug addicts being a critical area of interest, this case displays a common drug abuse complication clinicians raise awareness for. This observation presents an opportunity to identify a possible drug abuser and intervene accordingly.

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