NEJM 200TH ANNIVERSARY
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Dialogues in Medicine: Physicians and Patients on 200 Years of Progress
Anthony Fauci, Paul Farmer, Eugene Braunwald and other prominent experts gathered in Boston on June 22 for a day-long symposium with four panel discussions on HIV/AIDS, maternal and fetal health, breast cancer, and cardiology. View the videos on the 200th anniversary site.
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This Week at NEJM.org | September 13, 2012
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Perspective
K. Outterson | September 12, 2012 | DOI: 10.1056/NEJMp1209249
L.H. Harris | N Engl J Med 2012;367:981-983
T.S. Jost and S. Rosenbaum | N Engl J Med 2012;367:983-985 | Published Online July 25, 2012
P. Hartzband and J. Groopman | N Engl J Med 2012;367:987-989
Original Articles
B. De Bruyne and Others | N Engl J Med 2012;367:991-1001 | Published Online August 28, 2012
N.P. Klein and Others | N Engl J Med 2012;367:1012-1019
B.S. Kennedy and Others | N Engl J Med 2012;367:1020-1024 | Published Online August 22, 2012
A. Pal and Others | N Engl J Med 2012;367:1002-1011
S. Girirajan and Others | September 12, 2012 | DOI: 10.1056/NEJMoa1200395
Special Article
B.D. Sommers, K. Baicker, and A.M. Epstein | N Engl J Med 2012;367:1025-1034 | Published Online July 25, 2012
Review Article
W.J. Wiersinga, B.J. Currie, and S.J. Peacock | N Engl J Med 2012;367:1035-1044
Images in Clinical Medicine
N. Goenka and A.H. Ropper | N Engl J Med 2012;367:1045-1045
J.E. Jesus and A. Landry | N Engl J Med 2012;367:e15
Case Records of the Massachusetts General Hospital
M.A. de Moya and Others | N Engl J Med 2012;367:1046-1057
Editorials
W.E. Boden | N Engl J Med 2012;367:1059-1061 | Published Online August 28, 2012
U. Smith | N Engl J Med 2012;367:1061-1063
H.G. Brunner | September 12, 2012 | DOI: 10.1056/NEJMe1209699
Correspondence
Corrections
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What is the diagnosis?
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Trends: Most Viewed (Last Week)
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September 6, 2012
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September 6, 2012
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FREE for a Limited-Time: Ten Most-Read Summaries in Clinical Research
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Chief of General Medicine and Primary Care. Tufts Medical Center. Lead an expanding General Medicine Division within a storied downtown Boston academic medical center. To learn more, contact Emerson Moses, MBA, FASPR, Senior Physician Recruitment Consultant: emoses@tuftsmedicalcenter.org
Looking for a new practice opportunity? View this job and other listings at NEJM CareerCenter. Search now for both permanent and locum tenens jobs in many specialties.
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TEACHING TOPICS from the New England Journal of Medicine
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Teaching Topics | September 13, 2012
Melioidosis: What are the clinical manifestations of melioidosis?
Abdominal-Wall Necrosis: What are the clinical manifestations of Sweet’s syndrome?
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NEJM 200th Anniversary
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Dialogues in Medicine: Physicians and Patients on 200 Years of Progress
Anthony Fauci, Paul Farmer, Eugene Braunwald and other prominent experts gathered in Boston on June 22 for a day-long symposium with four panel discussions on HIV/AIDS, maternal and fetal health, breast cancer, and cardiology. View the videos on the 200th anniversary site.
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Teaching Topic
Melioidosis
Review Article
W.J. Wiersinga, B.J. Currie, and S.J. Peacock
Melioidosis, caused by the environmental gram-negative bacillus Burkholderia pseudomallei, is classically characterized by pneumonia and multiple abscesses, with a mortality rate of up to 40%. It is an important cause of community-acquired sepsis in Southeast Asia and northern Australia.
Clinical Pearls
 Where is melioidosis endemic?
Among the major regions where melioidosis is endemic, the Top End of the Northern Territory in Australia and northeast Thailand represent hot spots, with annual incidence rates of up to 50 cases per 100,000 people. Melioidosis is the third most common cause of death from infectious disease in northeast Thailand, exceeded only by HIV infection and tuberculosis. Malaysia, Singapore, Vietnam, Cambodia, and Laos are also endemic regions. Reports have expanded the endemic zone to areas of the Indian subcontinent, southern China, Hong Kong, Taiwan, various Pacific and Indian Ocean islands, and parts of the Americas.
How is melioidosis transmitted and what are the risk factors for acquiring infection?
Melioidosis primarily affects persons who are in regular contact with soil and water. Infection results from percutaneous inoculation (e.g., by means of a penetrating injury or open wound), inhalation (e.g., during severe weather or as a result of deliberate release), or ingestion (e.g., through contaminated food or water). Melioidosis is predominantly seasonal; 75 to 81% of cases occur during the rainy season. Incidence peaks between 40 and 60 years of age, but melioidosis is well recognized in children. Melioidosis has been transmitted to infants through breast milk from mothers with mastitis. Since up to 80% of patients with melioidosis have one or more risk factors for the disease, it has been suggested that melioidosis should be considered an opportunistic infection that is unlikely to have a fatal outcome in a previously healthy person, provided that the infection is diagnosed early and appropriate antibiotic agents and intensive care resources are available.
Morning Report Questions
Q. What are the clinical manifestations of melioidosis?
A. In a descriptive study involving 540 patients in tropical Australia over a 20-year period, the primary presenting feature was pneumonia (in 51% of patients), followed by genitourinary infection (in 14%), skin infection (in 13%), bacteremia without evident focus (in 11%), septic arthritis or osteomyelitis (in 4%), and neurologic involvement (in 3%). Over half of patients have bacteremia on presentation, and septic shock develops in approximately one fifth. Internal-organ abscesses and secondary foci in the lungs, joints, or both are common.
Figure 3.Clinical Events after Infection with B. pseudomallei.
Q. How is melioidosis treated and what is the expected course?
A. Melioidosis has a notoriously protracted course; cure is difficult without a prolonged course of appropriate antibiotics. The treatment of melioidosis consists of an intensive phase of 10 to 14 days of ceftazidime, meropenem, or imipenem administered intravenously, followed by oral eradication therapy, usually with trimethoprim–sulfamethoxazole (TMP-SMX) for 3 to 6 months. B. pseudomallei is inherently resistant to penicillin, ampicillin, first-generation and second-generation cephalosporins, gentamicin, tobramycin, streptomycin, and polymyxin.
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Teaching Topic
Abdominal-Wall Necrosis
Case Records of the Massachusetts General Hospital
M.A. de Moya and Others
Necrotizing soft-tissue infection (also known as necrotizing fasciitis) is a rare but well-known postpartum complication. The four tenets of care for necrotizing infections are: early detection, aggressive débridement, adequate antibiotic therapy, and physiological support. CT can be useful when evaluating a necrotizing soft-tissue infection, with sensitivity and a negative predictive value of virtually 100%. Management with antibiotics alone is associated with mortality rates approaching almost 100%. Early surgical exploration is associated with lower mortality rates (20 to 50%).
Clinical Pearls
What is the typical presentation and course of postpartum necrotizing soft-tissue infection?
Signs and symptoms of necrotizing soft-tissue infection include fever, tachycardia, hypotension, erythema with induration that extends beyond the involved area, pain disproportionate to appearance, bullae, crepitus, subcutaneous gas, ecchymosis, and skin discoloration and necrosis. Postpartum necrotizing soft-tissue infection typically occurs within hours or a few days after delivery; typically organisms are identified by pathological examination, stains, or cultures. Most relapses of necrotizing soft-tissue infection occur hours or days after débridement, and late relapses are very rare.
What are the clinical manifestations of Sweet’s syndrome?
Sweet’s syndrome (acute febrile neutrophilic dermatosis) is characterized by the presence of two major findings: the abrupt onset of erythematous-to-violaceous, edematous cutaneous lesions and the histopathological finding of superficial dermal edema and a dense dermal neutrophilic infiltrate. Two of four minor criteria must also be present for the diagnosis: fever, leukocytosis, a rapid response to glucocorticoids, and an underlying condition or exposure.
Morning Report Questions
Q. How is Sweet’s syndrome distinguished from other neutrophilic dermatoses?
A. Sweet’s syndrome is distinguished from other neutrophilic dermatoses (Behçet’s disease, pyoderma gangrenosum, and bowel-associated dermatosis–arthritis syndrome) by the appearance of cutaneous lesions and the presence of systemic symptoms, as well as extracutaneous involvement, including arthritis, arthralgias, myalgias, aseptic meningitis, ocular involvement, and on rare occasions, neutrophilic infiltration of the lungs, bones, kidneys, muscles, or pancreas. Pathergy, which is a characteristic reaction involving a nonhealing lesion that occurs in the setting of even minor trauma (e.g., vascular puncture sites), is an important clinical finding in neutrophilic dermatoses.
Q. What underlying conditions are known to be associated with Sweet’s syndrome?
A. Associated conditions include cancer, especially hematologic cancers, which are the most common in adults; infections, particularly upper respiratory and gastrointestinal infections but also infection with human immunodeficiency virus; medications, especially granulocyte colony-stimulating factor and all-trans retinoic acid, although many others have been reported; inflammatory bowel diseases; and pregnancy.
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quote of the week
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“In the 2010 pertussis outbreak in California, a longer time since receipt of a fifth dose of DTaP was associated with an elevated risk of acquiring pertussis among children who had received all recommended acellular pertussis vaccines. In this study, the risk of pertussis increased by 42% each year after the fifth DTaP dose.”
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IMAGE CHALLENGE
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What is the diagnosis?
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images in clinical medicine
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images in clinical medicine
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videos in clinical medicine
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