Cold Agglutinin Syndrome Associated with a 2009 Influenza A H1N1 Infection

Schoindre, Y.; Bollée, Guillaume; Dumont, M; Lesavre, Philippe

doi:10.1016/j.amjmed.2010.05.015

Cited by 16 publications

(16 citation statements)

References 3 publications

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“…Postinfectious cold agglutinins are seen with viral and bacterial pathogens, including mycoplasma, 19 Epstein-Barr virus, [20][21][22] and legionella. Case reports of cold agglutinin hemolysis induced by varicella, [23][24][25] Citrobacter, 26 and influenza 27,28 have been described. Polyclonal IgM antibodies are most commonly seen in children.…”

Section: History and Mechanismmentioning

confidence: 99%

Cold agglutinin disease

Swiecicki

Hegerova

Gertz

2013

Blood

265

298

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Cold agglutinin disease is a rare and poorly understood disorder affecting 15% of patients with autoimmune hemolytic anemia. We reviewed the clinical and pathologic features, prognosis, and management in the literature and describe our institutional experience to improve strategies for accurate diagnosis and treatment. Retrospective analysis identified 89 patients from our institution with cold agglutinin disease from 1970 through 2012. Median age at symptom onset was 65 years (range, 41 to 83 years), whereas the median age at diagnosis was 72 years (range, 43 to 91 years). Median survival of all patients was 10.6 years, and 68 patients (76%) were alive 5 years after the diagnosis. The most common symptom was acrocyanosis (n = 39 [44%]), and many had symptoms triggered by cold (n = 35 [39%]) or other factors (n = 20 [22%]). An underlying hematologic disorder was detected in 69 patients (78%). Thirty-six patients (40%) received transfusions during their disease course, and 82% received drug therapy. Rituximab was associated with the longest response duration (median, 24 months) and the lowest proportion of patients needing further treatment (55%). Our institution’s experience and review of the literature confirms that early diagnostic evaluation and treatment improves outcomes in cold agglutinin disease.

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Section: History and Mechanismmentioning

confidence: 99%

Cold agglutinin disease

Swiecicki

Hegerova

Gertz

2013

Blood

265

298

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“…Carbapenem‐resistant A. baumannii may also shelter carbapenem‐susceptible bacteria in a polymicrobial infection, exacerbating disease progression during carbapenem treatment (Liao et al ., ). Secondary bacterial infection with A. baumannii has also been seen in pandemic outbreaks of respiratory illness associated with the influenza A (H1N1) virus (Palacios et al ., ; Champunot et al ., ; Schoindre et al ., ).…”

Section: Polymicrobial Interactionsmentioning

confidence: 97%

Code blue: Acinetobacter baumannii, a nosocomial pathogen with a role in the oral cavity

Richards

Kwaik

Lamont

2014

Molecular Oral Microbiology

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SUMMARY Actinetobacter baumannii is an important nosocomial pathogen that can cause a wide range of serious conditions including pneumonia, meningitis, necrotizing fasciitis and sepsis. It is also a major cause of wound infections in military personnel injured during the conflicts in Afghanistan and Iraq, leading to its popular nickname of ‘Iraqibacter’. Contributing to its success in clinical settings is resistance to environmental stresses such as desiccation and disinfectants. Moreover, in recent years there has been a dramatic increase in the number of A. baumannii strains with resistance to multiple antibiotic classes. Acinetobacter baumannii is an inhabitant of oral biofilms, which can act as a reservoir for pneumonia and chronic obstructive pulmonary disease. Subgingival colonization by A. baumannii increases the risk of refractory periodontitis. Pathogenesis of the organism involves adherence, biofilm formation and iron acquisition. In addition, A. baumannii can induce apoptotic cell death in epithelial cells and kill hyphal forms of Candida albicans. Virulence factors that have been identified include pili, the outer membrane protein OmpA, phospholipases and extracellular polysaccharide. Acinetobacter baumannii can sense blue light through a blue-light sensing using flavin (BLUF) domain protein, BlsA. The resulting conformational change in BlsA leads to changes in gene expression, including virulence genes.

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“…Although secondary CHAD is a rare complication of mycoplasma infection, atypical or mycoplasma pneumonia accounted for 33% (23/70) of all CHAD patients in one series (Dacie & Worlledge, ). Influenza A has also been associated (Dacie, ; Schoindre et al , ) but a pathogen is not always identified. CHAD typically occurs 2‐3 weeks after onset of the illness.…”

Section: Infectionmentioning

confidence: 99%