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The guideline is intended for use by healthcare providers who care for adult and pediatric patients with group A streptococcal pharyngitis. The guideline updates the 2002 Infectious Diseases Society of America guideline and discusses diagnosis and management, and recommendations are provided regarding antibiotic choices and dosing. Penicillin or amoxicillin remain the treatments of choice, and recommendations are made for the penicillin-allergic patient, which now include clindamycin.

The guideline is intended for use by healthcare providers who care for adult and pediatric patients with group A streptococcal pharyngitis. The guideline updates the 2002 Infectious Diseases Society of America guideline and discusses diagnosis and management, and recommendations are provided regarding antibiotic choices and dosing. Penicillin or amoxicillin remain the treatments of choice, and recommendations are made for the penicillin-allergic patient, which now include clindamycin.

Kawasaki disease is recognized as the most common cause of acquired heart disease in children in the developed world. Clinical, epidemiologic, and pathologic evidence supports an infectious agent, likely entering through the lung. Pathologic studies proposing an acute coronary arteritis followed by healing fail to account for the complex vasculopathy and clinical course. Specimens from 32 autopsies, 8 cardiac transplants, and an excised coronary aneurysm were studied by light (n=41) and transmission electron microscopy (n=7). Three characteristic vasculopathic processes were identified in coronary (CA) and non-coronary arteries: acute self-limited necrotizing arteritis (NA), subacute/chronic (SA/C) vasculitis, and luminal myofibroblastic proliferation (LMP). NA is a synchronous neutrophilic process of the endothelium, beginning and ending within the first two weeks of fever onset, and progressively destroying the wall into the adventitia causing saccular aneurysms, which can thrombose or rupture. SA/C vasculitis is an asynchronous process that can commence within the first two weeks onward, starting in the adventitia/perivascular tissue and variably inflaming/damaging the wall during progression to the lumen. Besides fusiform and saccular aneurysms that can thrombose, SA/C vasculitis likely causes the transition of medial and adventitial smooth muscle cells (SMC) into classic myofibroblasts, which combined with their matrix products and inflammation create progressive stenosing luminal lesions (SA/C-LMP). Remote LMP apparently results from circulating factors. Veins, pulmonary arteries, and aorta can develop subclinical SA/C vasculitis and SA/C-LMP, but not NA. The earliest death (day 10) had both CA SA/C vasculitis and SA/C-LMP, and an \"eosinophilic-type\" myocarditis. NA is the only self-limiting process of the three, is responsible for the earliest morbidity/mortality, and is consistent with acute viral infection. SA/C vasculitis can begin as early as NA, but can occur/persist for months to years; LMP causes progressive arterial stenosis and thrombosis and is composed of unique SMC-derived pathologic myofibroblasts.

Background Kawasaki Disease (KD) can cause potentially life-threatening coronary arteritis in young children, and has a likely infectious etiology. Transcriptome profiling is a powerful approach to investigate gene expression in diseased tissues. RNA sequencing of KD coronary arteries could elucidate the etiology and the host response, with the potential to improve KD diagnosis and/or treatment. Methods Deep RNA sequencing was performed on KD ( n  = 8) and childhood control ( n  = 7) coronary artery tissues, revealing 1074 differentially expressed mRNAs. Non-human RNA sequences were subjected to a microbial discovery bioinformatics platform, and microbial sequences were analyzed by Metastats for association with KD. Results T lymphocyte activation, antigen presentation, immunoglobulin production, and type I interferon response were significantly upregulated in KD arteritis, while the tumor necrosis factor α pathway was not differentially expressed. Transcripts from known infectious agents were not specifically associated with KD coronary arteritis. Conclusions The immune transcriptional profile in KD coronary artery tissues has features of an antiviral immune response such as activated cytotoxic T lymphocyte and type I interferon-induced gene upregulation. These results provide new insights into the pathogenesis of KD arteritis that can guide selection of new immunomodulatory therapies for high-risk KD patients, and provide direction for future etiologic studies.

Although Kawasaki disease (KD) is the most common cause of acquired heart disease in children in the developed world, its aetiology remains unknown. In this Opinion, Anne Rowley and colleagues discuss evidence, including recently identified cytoplasmic inclusion bodies, which suggests that KD is caused by an infectious agent. Kawasaki disease (KD) has emerged as the most common cause of acquired heart disease in children in the developed world. The cause of KD remains unknown, although an as-yet unidentified infectious agent might be responsible. By determining the causative agent, we can improve diagnosis, therapy and prevention of KD. Recently, identification of an antigen-driven IgA response that was directed at cytoplasmic inclusion bodies in KD tissues has provided new insights that could unlock the mysteries of KD.

Background. Pharyngeal group A streptococcal (GAS) emm type surveillance enhances understanding of the epidemiology of pharyngitis and invasive GAS disease and formulation of multivalent type-specific vaccines. In addition, such surveillance provides pre-GAS vaccine baseline data. We assessed geographic and temporal trends in GAS emm -type distribution among pediatric pharyngeal isolates collected systematically in the United States and Canada from 2000 to 2007. Methods. We collected ∼100 acute GAS pharyngitis isolates from each of 13 widely scattered sites (10 in the United States and 3 in Canada) annually for 7 seasons (2000–2007) from 3- to 18-year-old children. We assessed emm type and subtype by DNA sequencing and analyzed temporal and geographic trends. Results. A total of 7040 US and 1434 Canadian GAS isolates were studied. The 6 most prevalent emm types (in descending order) were 1, 12, 28, 4, 3, and 2 in the United States and 12, 1, 28, 4, 3, 2, and 77 in Canada, constituting 70%-71% of isolates in each country; 10 emm types constituted 87%-89% total. Fifty-six emm types were identified in the United States, including 8 new types, and 33 types in Canada. Although a few types predominated nationally, marked variability among individual sites and at individual sites from year to year was observed. US-Canadian differences in type distribution were apparent. Twenty percent of isolates represented emm subtypes that differed slightly from reference types; 110 new subtypes were identified. An experimental 26-valent M protein vaccine covers 85% of pharyngitis isolates. Conclusions. Although overall US and Canadian emm type distribution was consistent and relatively few types dominated nationally, striking intersite and temporal variations within individual sites in prevalent emm types of GAS occurred. These results have important implications for the development and formulation of type-specific GAS vaccines.

order=\"0\" lang=\"eng\">When cases of severe acute respiratory syndrome coronavirus 2-associated multisystem inflammatory syndrome in children (MIS-C) were initially reported from Europe, the predominant clinical findings were persistent fever, marked abdominal symptoms, cytokine storm, myocardial dysfunction, and cardiogenic shock with left ventricular dysfunction in the setting of multisystem inflammation, reminiscent of toxic shock syndrome (TSS) or Kawasaki disease shock syndrome (KDSS) and requiring ICU care. Other clinical findings included those commonly observed in children with a variety of different infections and noninfectious illnesses, such as conjunctival injection, oral mucosal changes, and rash, features that are overlapping with TSS and incomplete Kawasaki disease. Because mucocutaneous findings are present in children with Kawasaki disease, and because patients with MIS-C sometimes developed mild coronary artery dilation, diagnostic confusion initially led some clinicians to conclude that the two conditions were the same. Here, Rowley et al discuss the importance of distinguishing MIS-C and Kawasaki disease.

The secreted cysteine proteinase SpeB is an important virulence factor of group A streptococci (GAS), whereby SpeB activity varies widely among strains. To establish the degree to which SpeB activity correlates with disease, GAS organisms were recovered from patients with pharyngitis, impetigo, invasive disease or acute rheumatic fever (ARF), and selected for analysis using rigorous sampling criteria; >300 GAS isolates were tested for SpeB activity by casein digestion assays, and each GAS isolate was scored as a SpeB-producer or non-producer. Highly significant statistical differences (p < 0.01) in SpeB production are observed between GAS recovered from patients with ARF (41.5% SpeB-non-producers) compared to pharyngitis (20.5%), invasive disease (16.7%), and impetigo (5.5%). SpeB activity differences between pharyngitis and impetigo isolates are also significant, whereas pharyngitis versus invasive isolates show no significant difference. The disproportionately greater number of SpeB-non-producers among ARF-associated isolates may indicate an altered transcriptional program for many rheumatogenic strains and/or a protective role for SpeB in GAS-triggered autoimmunity.

Key Points Epidemiologic data strongly suggest an infectious aetiology for Kawasaki disease, which is the leading cause of acquired heart disease among children in developed countries Necrotizing arteritis, subacute chronic vasculitis, and luminal myofibroblastic proliferation are three linked processes underlying the arteriopathy associated with Kawasaki disease Genetic susceptibility is indicated by the strikingly high rate of Kawasaki disease in children of Asian ethnicity and by its increased incidence in first-degree relatives of affected patients Timely diagnosis and treatment of Kawasaki disease with intravenous immunoglobulin (IVIg) and aspirin substantially decreases the risk of developing coronary artery abnormalities Adjunctive therapy with corticosteroids is of value in Japanese patients at particularly high risk of coronary complications, but identification of such high-risk patients is difficult in ethnically diverse populations Management of patients who do not respond to standard therapy is challenging; options include pulsed steroids, additional IVIg, and infliximab or other immunomodulatory agents Considerable progress has been made in understanding the pathologic processes and pathophysiology of Kawasaki disease. This article also discusses genetic susceptibility to Kawasaki disease and describes current approaches to treatment of the acute stage of the disease. This Review summarizes recent advances in understanding of the pathologic processes and pathophysiologic mechanisms leading to coronary arteritis in Kawasaki disease, and describes current approaches to its treatment. Kawasaki disease is the most common cause of acquired heart disease among children in developed countries, in whom the resulting coronary artery abnormalities can cause myocardial ischaemia, infarction and even death. Epidemiologic data strongly suggest an infectious aetiology, although the causative agent has yet to be identified. Genetic factors also increase susceptibility to Kawasaki disease, as indicated by its strikingly high incidence rate in children of Asian ethnicity and by an increased incidence in first-degree family members. The treatment of Kawasaki disease is based on timely administration of intravenous immunoglobulin and aspirin. However, the management of patients who do not respond to this standard therapy remains challenging; although several options are available, comparative data on which to base treatment decisions are scarce. The added value of adjunctive therapy with corticosteroids in patients at particularly high risk of coronary complications has been demonstrated in Japanese populations, but identification of high-risk patients has proven to be difficult in ethnically diverse populations.

Dr. Tom Farley, my one-time pediatric resident and mentee who is the former Commissioner of Health for New York City, is the author of a recent book Saving Gotham: A Billionaire Mayor, Activist Doctors, and the Fight for 8 Million Lives 1 as well as a recent op-ed piece in The New York Times called \"Fighting Obesity is not Just for Kids.\" 2 Dr. Farley points out that obesity rates in children age 6 to11 years have stabilized at 18% and among 2- to 5-year-olds have fallen below 10% for the first time since the 1980s. 2 However, adult obesity rates have continued to climb, now at 38%, with 70% of US adults considered overweight, and half diabetic or prediabetic. Most of those adults were not obese as children, supporting Dr. Farley's belief that the basic problem in the US is that normal people are overwhelmed by food marketing that is aided by more than $14 billion in ads annually. He argues that conquering the obesity epidemic will require fighting the marketing of junk foods everywhere, not only in schools but everywhere. 2