Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031350 (pharyngitis)
 2,405 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Streptococcus pyogenes, the Group A Streptococcus (GAS), is the most common cause of bacterial pharyngitis in children and adults. Innate and adaptive host immune responses are fundamental for defense against streptococcal pharyngitis and are central to the clinical manifestation of disease. Host immune responses also contribute to the severe poststreptococcal immune diseases that constitute the major disease burden for this organism. However, until recently, little was known about the host responses elicited during infection. Cellular mediators of innate immunity used during host defense against GAS include epithelial cells, neutrophils, macrophages, and dendritic cells (DCs), which are reported to secrete a number of soluble inflammatory mediators, such as antimicrobial peptides (AMPs); eicosanoids, including PGE2 and leukotriene B4 (LTB4 ); chemokines; and proinflammatory cytokines. Th1 and Th17 responses play significant roles in adaptive immunity in both murine models of GAS pharyngitis and in human tonsil tissue. A number of inflammatory complications are associated with GAS pharyngitis, which can lead to chronic disease in patients. These include scarlet fever, tonsillar hypertrophy, and sleep apnea, as well as postinfectious sequelae, such as acute rheumatic fever (ARF), poststreptococcal glomerulonephritis, and guttate psoriasis (GP). This review aims to present the current state of knowledge on innate and adaptive immune responses elicited during GAS pharyngitis, mechanisms by which GAS evades these responses, the emerging role of the pharyngeal microbiota, and how the interplay among these factors can influence the outcome of infection and inflammation-related complications.
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PMID:Group A streptococcal pharyngitis: Immune responses involved in bacterial clearance and GAS-associated immunopathologies. 2895 19

Contact dermatitis and psoriasis are common skin disorders which represent two distinct pathologies. Skin disorders heavily rely on corresponding history for diagnosis; this case demonstrates the challenges of relying on history alone for final identification. A patient presented to clinic for evaluation of a new rash on his abdomen. Past medical history was notable for recent initiation of a smoking cessation program utilizing nicotine patches as well as a pharyngitis treated with antibiotics 1 week prior. Despite use of topical steroid and cessation of the patches, the well-demarcated rash became more generalized. Patch testing for the nicotine patch and chemical sensitizers was negative and an eventual biopsy was consistent with guttate psoriasis. Contact dermatitis relies heavily on clinical history for diagnosis. This case demonstrates that history can be misleading. In retrospect, it is likely that a preceding presumed streptococcal infection was the primary inducer of guttate psoriasis.
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PMID:At First Glance: Psoriatic Response to Transdermal Nicotine Patch Application. 3208 60