RESUMO
BACKGROUND: Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is increasing in incidence and manifests as skin and soft tissue infections including furuncles. The majority of studies have focused on the epidemiology of single furuncles and not recurrent disease. There is a lack of data concerning the incidence of furunculosis outside the U.S.A. OBJECTIVES: This report reviews the literature of recurrent furunculosis and the impact of CA-MRSA on the disease. METHODS: Article citations were searched within PubMed. Search terms used were 'furunculosis', 'recurrent furunculosis', 'skin abscess' and 'recurrent boils'. Articles were discarded if they did not refer to furunculosis secondary to S. aureus. RESULTS: A total of 1515 articles were initially retrieved with the term 'furunculosis', 77 with the term 'recurrent furunculosis', 2778 with the term 'skin abscess', and 1526 with the term 'recurrent boils'. After excluding articles not referring to S. aureus furunculosis, 86 articles were included for this review. CONCLUSIONS: Furunculosis is increasing within the U.S.A. secondary to the CA-MRSA epidemic and the resistant organism's close association with the Panton-Valentine leucocidin (PVL) virulence factor. PVL is associated with follicular infections in general, having its strongest association with furunculosis and its recurrence. The majority of furuncles in the U.S.A. are caused by CA-MRSA, while elsewhere in the world they are caused by methicillin-sensitive S. aureus. Nasal carriage of S. aureus is the primary risk factor for recurrent furunculosis and occurs in 60% of individuals.
Assuntos
Furunculose/microbiologia , Staphylococcus aureus Resistente à Meticilina/isolamento & purificação , Infecções Estafilocócicas/microbiologia , Toxinas Bacterianas , Farmacorresistência Bacteriana , Exotoxinas , Furunculose/diagnóstico , Humanos , Leucocidinas , Staphylococcus aureus Resistente à Meticilina/efeitos dos fármacos , Recidiva , Fatores de Risco , Infecções Estafilocócicas/diagnóstico , Fatores de VirulênciaRESUMO
The role of protein-tyrosine phosphorylation in the signal transduction of platelet activating factor (PAF) was investigated in rabbit platelets with a range of synthetic compounds that inhibit protein-tyrosine kinases. In particular, erbstatin (IC50 approximately 20 micrograms/ml) abrogated a wide range of platelet responses to PAF, including tyrosine phosphorylation of cellular proteins, polyphosphoinositide turnover, activation of membranous protein kinase C, platelet aggregation, and serotonin secretion. With about a third of the potency of erbstatin, compound RG50864 also inhibited many of these responses, whereas at 100 micrograms/ml, genistein, 670C88 and ST271 were without effect. Finally, the ability of thrombin to cause platelet aggregation and serotonin secretion was also compromised by erbstatin.
Assuntos
Plaquetas/fisiologia , Hidroquinonas/farmacologia , Fosfatidilinositóis/sangue , Fator de Ativação de Plaquetas/farmacologia , Inibidores da Agregação Plaquetária/farmacologia , Proteína Quinase C/sangue , Proteínas Tirosina Quinases/sangue , Serotonina/sangue , Animais , Anticorpos , Plaquetas/efeitos dos fármacos , Ativação Enzimática , Hidrólise , Técnicas In Vitro , Cinética , Fosfatos de Fosfatidilinositol , Fosforilação , Fosfotirosina , Agregação Plaquetária , Proteína Quinase C/antagonistas & inibidores , Proteínas Tirosina Quinases/antagonistas & inibidores , Coelhos , Tirosina/análogos & derivados , Tirosina/análiseAssuntos
Doenças Musculares/etiologia , Esforço Físico , Adulto , Aspartato Aminotransferases/sangue , Nitrogênio da Ureia Sanguínea , Creatina Quinase/sangue , Creatinina/sangue , Seguimentos , Ginástica , Humanos , Masculino , Medicina Militar , Militares , Tono Muscular , Doenças Musculares/enzimologia , Estados UnidosAssuntos
Medicina Militar , Mioglobina/sangue , Mioglobinúria/etiologia , Esforço Físico , Adolescente , Adulto , Animais , Aspartato Aminotransferases/sangue , Testes de Fixação de Complemento , Creatina Quinase/sangue , Humanos , Soros Imunes , Imunoensaio , L-Lactato Desidrogenase/sangue , Masculino , Mioglobinúria/enzimologia , Aptidão Física , Estudos Prospectivos , Coelhos/imunologia , South CarolinaAssuntos
Mioglobina/sangue , Mioglobinúria/etiologia , Esforço Físico , Doença Aguda , Adolescente , Adulto , Humanos , Masculino , Medicina Militar , Estados UnidosRESUMO
Reasons are enumerated why the medical malpractice crisis has abated. Further advice is given on how to avoid a complaint from the Florida Department of Professional Regulation and an explanation is presented of how the DPR functions. An understanding is essential to prevent an investigation and possible disciplinary action by the Board of Medicine.
Assuntos
Jurisprudência , Médicos , Contabilidade , Prescrições de Medicamentos , Controle de Medicamentos e Entorpecentes , Florida , Humanos , Imperícia/legislação & jurisprudência , Prontuários Médicos , Relações Médico-Paciente , Garantia da Qualidade dos Cuidados de Saúde/legislação & jurisprudênciaRESUMO
We have compared the cardiovascular effect of endotoxin with platelet-activating factor (PAF) in rats. Endotoxin injected into perfusate of isolated rat heart did not induce significant changes in heart function, whereas PAF induced elevation of coronary perfusion pressure (CPP), decrease in ventricular pressure (VP), decrease in coronary flow (CF), but no significant changes in heart rate (HR). Neither endotoxin nor PAF caused contraction or relaxation of isolated rat arteries. However, endotoxin in the presence of macrophages caused contractions of rat aortic strips. These contractions were potentiated when platelets were present in the macrophage preparation. PAF in the presence of platelets caused profound contraction of the aortic strips, and this action of PAF was entirely blocked by either PAF antagonists or thromboxane antagonists. Injection of endotoxin into rats (i.v.) caused a decrease in blood pressure (BP) without significantly affecting the HR. At higher concentrations (greater than or equal to 10 mg/kg), endotoxin caused ventricular tachycardia (VT) associated with ventricular fibrillation (VF). PAF in vivo caused a rapid and sustained decrease in BP, with an ED50 of 3 micrograms/kg. PAF antagonists significantly prevented overall mortality induced by PAF and short-term endotoxin-induced mortality, but not the long-term (week) mortality. Endotoxin (10 mg/kg) injected into rats caused the release of PAF into the circulation, reaching a maximum after 2-5 min. Tritiated PAF injected into rats i.v. was metabolized over 60 min into lyso-PAF (approximately 30%), acyl-PAF (approximately 10%), and some degraded products (approximately 10%), and the remainder was found in the form of PAF. The results of the present study suggest that PAF may play a significant role in the pathogenesis of endotoxin shock. The action of PAF requires the participation of cells such as platelets, macrophages, neutrophils, and monocytes and involvement of arachidonic acid metabolites.
Assuntos
Fenômenos Fisiológicos Cardiovasculares , Endotoxinas/farmacologia , Hemodinâmica , Fator de Ativação de Plaquetas/farmacologia , Animais , Aorta , Plaquetas/metabolismo , Pressão Sanguínea , Células Cultivadas , Circulação Coronária , Endotoxinas/antagonistas & inibidores , Coração/fisiologia , Frequência Cardíaca , Macrófagos/metabolismo , Monócitos/metabolismo , Contração Muscular , Músculo Liso Vascular/fisiologia , Neutrófilos/metabolismo , Fator de Ativação de Plaquetas/antagonistas & inibidores , Fator de Ativação de Plaquetas/biossíntese , Ratos , Ratos EndogâmicosRESUMO
The relationship between polyphosphoinositide hydrolysis and protein kinase C (PKC) activation was explored in rabbit platelets treated with the agonists platelet-activating factor (PAF), thrombin and 12-O-tetradecanoylphorbol 13-acetate (TPA), and with the anti-aggregant prostacyclin (PGI2). Measurement of the hydrolysis of radiolabelled inositol-containing phospholipids relied upon the separation of the products [3H]inositol mono-, bis- and tris-phosphates by Dowex-1 chromatography. PKC activity, measured in platelet cytosolic and Nonidet-P40-solubilized particulate extracts that were fractionated by MonoQ chromatography, was based upon the ability of the enzyme to phosphorylate either histone H1 in the presence of the activators Ca2+, diacylglycerol and phosphatidylserine, or protamine in the absence of Ca2+ and lipid. Treatment of platelets for 1 min with PAF (2 nM) or thrombin (2 units/ml) led to the rapid hydrolysis of inositol-containing phospholipids, a 2-3-fold stimulation of both cytosolic and particulate-derived PKC activity, and platelet aggregation. Exposure to TPA (200 nM) for 5 min did not stimulate formation of phosphoinositides, but translocated more than 95% of cytosolic PKC into the particulate fraction, and induced a slower rate of aggregation. PGI2 (1 microgram/ml) did not enhance phosphoinositide production, and at higher concentrations (50 micrograms/ml) it antagonized the ability of PAF, but not that of thrombin, to induce inositol phospholipid turnover, even though platelet aggregation in response to both agonists was blocked by PGI2. On the other hand, PGI2 alone also appeared to activate (by 3-5-fold) cytosolic and particulate PKC by a translocation-independent mechanism. The activation of PKC by PGI2 was probably mediated via cyclic AMP (cAMP), as this effect was mimicked by the cAMP analogue 8-chlorophenylthio-cAMP. It is concluded that this novel mechanism of PKC regulation by platelet agonists may operate independently of polyphosphoinositide turnover, and that activation of cAMP-dependent protein kinase represents another route leading to PKC activation.