ER is a facultative, non-spore-forming, non-acid-fast, gram-positive bacillus. It is a ubiquitous commensal in wild and domestic animals, birds, and fish and has an enormous economic impact on animal husbandry and marine industry, causing animal erysipelas. Human infections are extremely rare, occupationally acquired zoonosis. Human infections are acquired through wounds, contact with sick animals, and carriers and commonly includes localized or generalized self-limited cutaneous erysipelas. Seldom, systemic infection and septicemia occur. We present here, a case of a 50-year-old immunocompetent retired shipyard welder who enjoyed fishing in his spare time and presented to the emergency room with fever, chest pain, significant weight loss, and dry cough lasting 2 to 3 months. He did not report any bites or injuries, intravenous drug abuse, or travel history. An echocardiogram showed mobile vegetation on aortic valve with severe regurgitation. Blood and tissue cultures grew E rhusiopathiae, identified by MALDI-TOF method. He was treated with empiric vancomycin followed by penicillin and aortic valve replacement with a mechanical valve. Cases of E rhusiopathiae–induced native valve endocarditis and septicemia are extremely infrequent in immunocompetent individuals, especially when occupation-related exposure is not noted. Even after surgery, it may entail fatality rates as high as 40%, higher than endocarditis caused by other bacteria. While some current reports suggest incidences of human infections are declining due to technological advances in animal industry, infection still occurs in specific environments. Additionally, it may be underdiagnosed due to its resemblance to other infections and problems encountered in isolation and identification. The natural resistance of E rhusiopathiae to glycopeptides underlines the importance of a prompt microbiological diagnosis of such an uncommon human infection, especially when presented in an unusual clinical presentation. Clinicians and microbiologists working with exposed population should be aware of this microbe and its manifestations.
Skeletal muscle involvement by noncaseating granulomata occurs in a variety of conditions, including sarcoidosis, infections, and rarely in association with primary inflammatory myopathies such as inclusion body myositis (IBM) and dermatomyositis (DM). Sarcoid myopathy is typically asymptomatic; however, a picture of acute myositis with proximal muscle weakness has been described. Immune-mediated necrotizing myopathy (IMNM) is a subgroup of inflammatory myopathies typically presenting with proximal muscle weakness and markedly elevated muscle enzymes, mostly occurring in the setting of statin treatment. IMNM is associated with positive autoantibodies, but a subset of cases is antibody negative. Here we describe a case of myopathy occurring in association with sarcoidosis with combined features of granulomatous and necrotizing myopathy. The patient was a 54-year-old African American male with medical history significant for statin use 3 years ago, which was discontinued due to myalgia and elevated muscle enzymes and biopsy-proven sarcoidosis diagnosed on a pulmonary lymph node biopsy. He presented with progressive worsening of bilateral proximal weakness involving the upper and lower extremities. Electromyogram showed features of active myopathy with no evidence of peripheral neuropathy. Myositis panel was negative for the following antibodies: anti-Jo1, Mi-2, anti-Ku, PL-7, PL-12, OJ, EJ, and SRP. However, there was elevation of aldolase, CRP, and CK-MB. Biopsy of thigh and deltoid muscle showed necrotic muscle fibers, myophagocytosis with associated minimal inflammation, and multiple well-formed nonnecrotizing granulomas with multinucleated giant cells. Myopathic features include increased internalized nuclei, round atrophic fibers, and scattered split fibers. Specific features of IBM or DM were not present. Conclusion Myopathies developing or worsening after discontinuation of statin are rare. The association of necrotizing myopathy with sarcoidosis is not well described in the literature. Additional studies are warranted to elucidate this association.
Introduction Variations in postnatal length of refrigerated, unfixed umbilical cords were studied over time to elucidate natural changes and times of stability. Methods Length was measured in 132 cords following severance, repeated at varying timed intervals and studied by analysis of variance and regression analysis. Results Data show immediate rapid initial phase shortening (mean 4.2+/-3.9 cm SD); an interval of lengthening; stable length at hours 3-4 following severance, a slower second phase shortening (mean 1.5+/-0.7 cm SD) beginning at 5 hours and peaking at 12 hours; and gradual lengthening to stable length after 23 hours. Overall, there was a significant net mean decrease of 3.49+/-2.29 cm SD. Shortening was greatest for intact long cord segments (p=0.0001), as much as 11 cm. Two highly significant models for predicting umbilical cord length at delivery (OL) were determined using the post-delivery lengths (Length) measured at different times following delivery (Hours), as follows: At ≤ 3 hours following delivery: OL=1.02xLength cm+1.11xHours At >3 hours following delivery: OL=1.07xLength+0.44xHours-0.01x(Hours)2 Conclusion Cord lengths stabilized between hours 3-4 and after 23 hours following severance. Phase one shortening resembles vasoconstriction; phase two resembles rigor mortis. The models allow prediction of the original umbilical cord length at delivery, regardless of the time of measurement.
Casestudy Hamartomas are benign, disordered, tumor-like growth of cellular constituents resembling the tissue of its origin. Hamartomas are usually seen in lung, heart, kidney and spleen. Pancreatic hamartomas (PH) are extremely rare, accounting for <1% of all hamartomas. PH occurs at any age (median: 50 years) without gender predilection. PH presents as single or multiple, solid and/or cystic mass composed of exocrine tissues. Admixed neuroendocrine cells may be seen, but well-formed islets are unusual. PH stroma is typically positive for CD34 by immunohistochemistry. We present a case of a PH resected for the clinical suspicion of malignancy, with the final diagnosis established postoperatively. The case is that of a 74-year-old male with an incidental 2.3 x 1.7 x 1.1 cm hyperenhancing solid mass of the pancreatic uncinate process, found during anemia workup. The radiologic appearance was suspicious for a neuroendocrine tumor. Biopsy of the mass showed benign-appearing pancreatic ductal and acinar tissue. Given the clinical suspicion of malignancy, the patient elected to undergo a pancreaticoduodenectomy. Macroscopically the mass was well-circumscribed with solid, tan-white, firm cut surface. Microscopic examination revealed well- circumscribed proliferation of disorderly-arranged, well-differentiated, bland exocrine pancreatic tissue. Chromogranin, synaptophysin and CD56 immunostains did not highlight significant neuroendocrine component. Ki-67 proliferation index was low (1%). CD34 and CD117 immunostains were negative in the stroma. The findings were consistent with PH. Conclusion PH may mimic a malignant process of the pancreas. The preoperative diagnosis of PH is extremely challenging due to the lack of characteristic clinical and radiological features, therefore, the diagnosis of PH is often made on resection specimen. CD34 immunostain is not always helpful for the diagnosis as it may be negative in PH stroma. Although extremely rare, pancreatic hamartoma should be considered in the differential diagnosis of a pancreatic tumor.
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