Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The failure to eradicate group A beta-hemolytic streptococci from the pharynx is partly due to a low compliance, but above all, an alteration of the oropharyngeal microbiological flora: reduction of alpha-haemolytic streptococci which inhibit group A beta-hemolytic streptococci and increase of microorganisms such as Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis. These latter act indirectly destroying the beta-lactamic ring of penicillins. However, this obstacle is overcome by the use of antibiotics which do not contain beta-lactamic rings such as macrolides or associating amoxicillin with clavulanic acid or with new cephalosporins which are more resistant to beta lactamases. To restrict the diffusion of resistance to antibiotics, it is essential to limit their use diagnosing streptococcal tonsillopharyngitis more precisely, thanks to an improved use of micro-biological diagnostic tests and by a more extended use of tonsillectomy in recurrent tonsillitis (more than 6-7 in 1-2 years). Adenoiditis is closely related to the post nasal drip syndrome, to recurrent otitis media and to otitis media with effusion. All these situations could, therefore, represent an indication, although not well defined, for adenoidectomy. Nasopharyngeal obstruction due to adeno-tonsillar hypertrophy becomes critical during sleep when the hypotony of the upper airway muscles becomes additional to the anatomical obstruction. At this point the inspiratory effort required and the consequent decrease of intra airway pressure increase the pharyngeal obstruction suctioning the pharyngeal walls toward the median line. The resulting clinical picture is defined as sleep-disordered breathing (SDB) due to adenotonsillar hypertrophy (idiopathic), to be distinguished from SDB due to cranio-facial abnormalities or neuromuscular diseases. SDB includes both the more serious sleep apnea syndrome and the less severe upper airway respiratory resistance syndrome. A combination of symptoms and clinical data detectable both while awake or asleep, make the diagnosis simple. During sleep, both apnea and paradoxical inspiratory movements are highly specific while snoring is highly sensitive. To evaluate nasopharyngeal obstruction radiography and optic fibre endoscopy are both equally reliable. The gold standard test for non idiopathic SDB is the polysomnography, whereas for SDB, due to adenotonsillar hypertrophy, one is limited today to the recording during sleep of O2 saturation or of end tidal CO2. These investigations are, however, generally used up to 2 years of age, when the decision to carry out an adenoidectomy and especially a tonsillectomy is more difficult because of the greater risks which surgery involves at this age. The pharmacological therapy has a purely palliative function and is based on antibiotics, local vasoconstrictors, steroids and theophylline which acts more as an antiflogistic than as a breath stimulant. O2 therapy and nasal continuous positive airway pressure (CPAP) give better results, but are more difficult to carry out, in particular on a long term basis. Adenoidectomy especially if associated with tonsillectomy, leads to the resolution of the symptoms, but not always to a normalization of functional alterations (hypoxia and hypercapnia). For this reason, it is necessary to act on other factors which cause oedema of the nasopharyngeal mucosa contributing to the obstruction. In this area, the prevention of viral infections can be achieved by vaccination against influenza and by preventing the child from attending crowded day care centers. With regard to allergic inflammation, skin prick tests could be a first step in view of allergens avoidance measures. With regard to indoor air pollution, passive smoke must be stopped and the child kept out of the kitchen.
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PMID:[The tonsils and adenoids as a site of infection and the cause of obstruction]. 986 45

Adenotonsillar disease (adenoiditis and recurrent tonsillitis) is a prevalent otolaryngologic disorder aetiologically based on chronic inflammation triggered by a persistent bacterial infection. These bacteria, mostly Staphylococcus aureus, Haemophilus sp., and Streptococcus sp., persist predominantly intracellular and within mucosal biofilms. The recurrent or chronic inflammation of the adenoids and faucial tonsils leads to chronic activation of the cell-mediated and humoral immune response, resulting in hypertrophy of the lymphoid tonsillar tissue. This hypertrophic tissue is the cause for the prominent clinical symptoms: obstruction of the upper airways, snoring, and sleep apnea for adenoiditis or sore throat, dysphagia and halitosis for recurrent tonsillitis. Treatment strategies should target the persisting bacteria within their biofilm or intracellular shelter. Macrolide antibiotics like clarithromycin are able to modulate the immune system and to interfere in bacterial signaling within biofilms. Clindamycin, quinupristin-dalfopristin, and oritavancin are intracellular high active compounds. Surgical removal of the hypertrophic tissue by modern procedures like laser tonsil ablation, eliminates not only a mechanical obstacle of the airways, it removes also the basis for the aetiologic cause, the "biofilm carrier". This review summarizes the role of bacterial persistence in mucosal biofilms for the aetiology, diagnosis and treatment of adenotonsillar disease and relevant patents.
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PMID:Adenotonsillar disease. 2245 46