This cross-sectional study estimated a one-time point seroprevalence rate of Chagas disease among people of Latin American descent in Suffolk County, Long Island, New York. Subjects who met the inclusion criteria were screened using the Chagas Detect Plus Rapid Test (InBios, Seattle, WA) with confirmation via Trypanosoma cruzi enzyme immunoassay and T. cruzi immunoblot assay. Administration of a questionnaire regarding demographics and risk factors followed. A seroprevalence rate of 10.74% was found. Identified risk factors included prior residence in a palm leaf house (odds ratio [OR], 10.42; P = 0.003; 95% CI, 2.18-49.76), residence in a house with triatomines (OR, 9.03; P = 0.006; 95% CI, 1.90-42.88), and history of triatomine bite (OR, 9.52; P = 0.009; 95% CI, 1.75-51.77). Our findings emphasize the importance of this frequently underdiagnosed disease and help highlight the importance of early screening among high-risk populations.

Chagas Disease (CD), a neglected tropical disease of Latin America (LA) is caused by the parasite Trypanosoma cruzi, transmitted by the triatomine insect (kissing bug), and known to cause cardiomyopathy (CMP), megacolon or achalasia. Despite the population of Latin Americans, by birth or descent, in Long Island (LI), New York (NY) approximating 20%, information regarding prevalence of CD in this region is scarce. This study aims to determine the seroprevalence and risk factors for T. cruzi infection among hispanics in LI. This is a cross-sectional study. Inclusion criteria included, birth or living in LA for > 3 years, mother born or lived in LA for ≥3 years, and residency in Suffolk County, LI. Patients were screened by Chagas Detect™ Plus Rapid Test (immunochromatographic strip assay for the qualitative detection of human IgG antibodies to T. cruzi; InBios Rapid test). Seropositivity was confirmed by enzyme immune assay and immunoblot. Participants answered a questionnaire regarding demographics and risk factors of CD. A total of 121 subjects (55.4% male) were tested from February 2018 to February 2020. Twelve were seropositive confirmed cases (9.9%; 66.7% male), with 9 cases from El Salvador (75%, p=0.06). Factors associated with infection were living in a palm house (OR=14.1, CI 2.7-74.7), history of triatomine bite (OR=9.5 CI=1.75–51.7), living in a house with triatomine (OR= 9.02, CI=1.9 – 42.8), and having relatives diagnosed with Chagas (OR= 7.6, CI=1.4 – 39.2). T. cruzi infected were most likely to have donated blood (OR=9.4, 95% CI=2.3–3.6). Two cases (16.6%) had CMP and did not qualify for treatment. One had gastrointestinal disease (8.3%). Eight started treatment with benznidazole. In conclusion, we found a prevalence of 9.9% of T. cruzi infection in this high-risk population of LI. Two cases were diagnosed with CMP during this screening study highlighting that there are unrecognized cases of CD in this region where 20% are Hispanics. Such high prevalence and unrecognized disease, highlights the importance of raising awareness among providers of early screening and to prevent potential deadly outcomes. All Authors: No reported disclosures

A 51-year-old man, resident of Long Island, New York, and an avid seaman (spends all the weekends on keeping his boat in a good sailing condition), presented to the emergency departmentwith a nonhealing swelling of the left fourth finger. He had sustained an injury due to a wood splinter on the same finger while working on his boat about 15 months before admission. After removing the splinter, a painless chronic mild swelling persisted for months. A month before admission, he received in the 4th finger a local steroid injection for possible gout, which resulted in worsening of the swelling to the point that hiswedding ring had to be cut off to alleviate the pressure. A well-demarcated swelling and redness was noted at the left 4th proximal interphalangeal (PIP) joint and dorsum of the finger (Figure 1A). A magnetic resonance imaging showed increased T2-weighted signal and enhancement involving only the soft tissues and small amount of fluid on the 4th PIP joint and extensor tendons (tenosynovitis), but no enhancement of the bone (Figure 1B). His white blood cell count was 9,710 ells/cm and C-reactive protein was 1.1 mg/L. There was no history of immunosuppression; he refused anHIV test. An incision and drainage (I&D) was performed, but no gross purulence was found, except for an extensive granulation tissue down to the tendon sheath. The histology depicted necrotic debris and granulation tissue with many acid-fast staining organisms, and Mycobacterium marinum was isolated in AFB culture incubated at 32 C at day 10 from I&D (Figure 2A andB). The final diagnosiswas tenosynovitis due to M. marinum. This is a fast-growing nontuberculous mycobacterium that is often acquired via traumatic injuries leading to infection by direct inoculation from fish fins, fish bites, or water from fish tanks. Clinical manifestations include papules, nodules, erythematous plaques, ulcerations, and sporotrichoid-like lesions mostly in the upper limbs. Cases of solitary nontender nodules on the hands of people working on boats have been reported. A failure to elicit the history of potential exposure and microbiologic features of this organism is responsible for the often-delayeddiagnosis. The incubationperiodofM.marinum can be from weeks to months after the inoculation. Invasive form of the infection involves deep structures such as tendon, synovium, and bone; these infections are often identified following corticosteroid therapy. Our patient did receive a corticosteroid injection locally followed by clinical worsening,

A 71-year-old Caucasian gentleman presented to our hospital with dyspnea and tachypnea of a day's duration. These symptoms started earlier on the day of presentation after eating lunch. He is a resident of a nursing home. Four months prior to presentation, he was diagnosed with glioblastoma multiforme of the left frontal lobe of the brain that was subsequently complicated by a stroke event. He was being treated with prolonged steroid and radiation therapy. In the emergency room, the patient was not febrile. He appeared lethargic but was able to answer simple questions. His pulse oximetry was 88% and supplemental oxygen was required. His respiratory rate ranged from 21 to 35 breaths per min, and arterial blood gas analysis on room air revealed a respiratory alkalosis with pH 7.52, pCO2 32 mm Hg, pO2 56.4 mm Hg and base excess 4.1 mmol/L. A computed tomography of the chest revealed multiple confluent airspace opacities in the left lower lobe and anterior segment of the right upper lobe with a cavitary lesion measuring 2.5 × 7.8 cm. The patient required admission to our intensive care unit and was treated with continuous positive airway pressure and empiric antibiotics for clinical suspicion for sepsis. He did not become hypotensive and did not require inotropes or pressor support. The white blood cell count was 5000 cells per mm3 with differential: 83% segmented neutrophils, 1% lymphocytes, 8% bands, and 3% monocytes. Few Döhle bodies and 2+ toxic granulations were appreciated in neutrophils but no cytoplasmic vacuoles. The alanine aminotransferase (ALT) was elevated to 107 IU/L, and the lactic acid dehydrogenase (LDH) was 314 IU/L. The lactic acid was 2.1 mmol/L. Blood cultures revealed Escherichia coli within 24 h of incubation. The acid-fast bacilli stain on sputa were negative thrice. Review of the peripheral smear showed sparse peculiar blue-green inclusions inside the granulocytes and monocytes (See 1A-E). As a result of worsening respiratory and mental status, the family requested comfort measures and the patient died on the third day of hospitalization. Smith first described in 1967, the case of an infant who died at 7 mo of age because of biliary cirrhosis caused by congenital atresia of the bile ducts and noted to have dull green, circular or oval inclusions in the cytoplasm of granulocytes and monocytes.1 It was not until Harris et al., in 2009 and Jazaerly et al., in 2014, who proposed the finding of these inclusions are likely related to liver failure and could serve as a prognostic indicator of impending death.2, 3 Hodgson et al. proposed the term “critical green inclusions” to be used and communicated by laboratory technicians.4 In their 20 case-report series where inclusions were identified, they reported five patients who survived. In addition, Hodgson et al. hypothesized the green inclusions to represent lipofuscin-like substance that was taken up by phagocytosis following ischemic injury to the liver. They based this hypothesis on the finding of prominent centrilobular hepatocellular lipofuscin on postmortem livers.4 Although the composition of these green neutrophilic inclusions remains largely unknown, they have variably been associated with laboratory findings such as leukocytosis, anemia, thrombocytopenia, hyperbilirubinemia, elevations in γ-glutamyl transferase, LDH and troponin; and clinical conditions such as malignancy, coagulopathy, lactic acidosis, chronic renal disease, infection, and sepsis.5 Jazaerly's et al. case involved a patient who died because of septic shock caused by E. coli bacteremia with the ALT being 116 U/L. Hodgson's et al. case series also included patients with septic shock. We hypothesize that in our case the green inclusions were the result of sepsis and liver injury. The authors would like to thank Dr. Timothy Pal for the peripheral smear images and Dr. Tesfa Asrat for her editorial assistance. None.

Abstract Background Carbapenem resistance (CR) in Enterobacteriaceae is a growing concern which the CDC has designated as an urgent threat. At our institution we have noted emergence of CR strains in clinical isolates including a growing number of Serratia marcescens. CR in Serratia marcescens in the United States is mostly reported to be encoded by the SME family of chromosomally encoded carbapenemases, while in Asia it has been described being mediated by transmissible plasmids such as KPC. Here we describe the emergence and characteristics of CR Serratia marcescens at an academic tertiary care hospital in New York. Methods Serratia marcescens isolates demonstrating in vitro carbapenem resistance were recovered over a 12-month period from six distinct patients. Antibiotic resistance was determined by standard methods. Real-time PCR for bla(KPC), mcr gene, bla(NDM-1), bla(VIM), and bla(OXA-48) was performed. Patient comorbidities, source of culture, location in the hospital, and co-infection with other CR organisms were investigated. Results Fourteen S. marcescens isolates demonstrating in vitro carbapenem resistance were recovered from six individual patients. All six patients had a history of chronic respiratory failure with tracheostomy and at least partial ventilator dependence. Five of the patients were located on the pulmonary intermediate care unit, and one in the pediatric intensive care unit. Twelve of the 14 isolates were tracheal or sputum cultures. Five of the sputum cultures from two patients were co-infected with CR Pseudomonas, and one sputum culture was simultaneously positive for CR Klebsiella pneumoniae and Enterobacter Cloacae. Nine out of 14 isolates were positive for blaKPC-3, two were blaKPC-2 positive, and three were blaKPC-negative, with no mechanism of carbapenem resistance determined yet. None of the other genes were detected. Conclusion Most carbapenem-resistant Serratia isolates were derived from respiratory tract and were found to be positive for blaKPC-3. This suggests that plasmid encoded carbapenemases are emerging among Serratia in the United States, which is already being reported in China. Genomic sequencing may establish whether this represents a clonal expansion and whether the blaKPC plasmid was transferred from Klebsiella or Enterobacter to Serratia in one of the patients. Disclosures All authors: No reported disclosures.