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Sơ lược về các cầu khuẩn gây bệnh -Bao gồm các vi khuẩn hình cầu, đòi hỏi điều kiện hiếu khí hoặc kỵ khí tuỳ tiện (các cầu khuẩn kỵ khí tuyệt đối không trình bày trong phần này). -Tổn thương do các cầu khuẩn thường có mủ, nên còn được gọi là cầu khuẩn sinh mủ. -Dựa vào nhuộm Gram, chia các cầu khuẩn thành: | CẦU KHUẨN GÂY BỆNH ThS.BS. Huỳnh Minh Tuấn huynhtuan@yds.edu.vn GRAM (+) GRAM (–) ☺ Tụ cầu (staphylococci) ☺ Liên cầu (streptococci) Phế cầu (Streptococcus pneumoniae) ☺ Lậu cầu (Neisseria gonorrhoeae) ☺ Màng não cầu (Neisseria meningitidis) STAPHYLOCOCCI HÌNH DẠNG NUÔI CẤY TĂNG TRƯỞNG ĐỘC TỐ Ngoại độc tố Leucocidin Exfoliative toxin Toxic shock syndrome toxin Độc tố ruột (Enterotoxin) Damage to the Host S aureus can express several different types of protein toxins which are probably responsible for symptoms during infections. Some damage the membranes of erythrocytes, causing hemolysis; but it is unlikely that hemolysis is relevant in vivo. The leukocidin causes membrane damage to leukocytes and is not hemolytic. Systemic release of α-toxin causes septic shock, while enterotoxins and TSST-1 cause toxic shock. Membrane Damaging Toxins (a) α-toxin The best characterized and most potent membrane-damaging toxin of S aureus is α-toxin. It is expressed as a monomer that binds to the membrane of susceptible cells. Subunits then oligomerize to form hexameric rings with a central pore through which cellular contents leak. Susceptible cells have a specific receptor for α-toxin which allows low concentrations of toxin to bind, causing small pores through which monovalent cations can pass. At higher concentrations, the toxin reacts non-specifically with membrane lipids, causing larger pores through which divalent cations and small molecules can pass. However, it is doubtful if this is relevant under normal physiological conditions. In humans, platelets and monocytes are particularly sensitive to α-toxin. They carry high affinity sites which allow toxin to bind at concentrations that are physiologically relevant. A complex series of secondary reactions ensue, causing release of eicosanoids and cytokines which trigger production of inflammatory mediators. These events cause the symptoms of septic shock that occur during severe infections caused by S aureus. The notion that | CẦU KHUẨN GÂY BỆNH ThS.BS. Huỳnh Minh Tuấn huynhtuan@yds.edu.vn GRAM (+) GRAM (–) ☺ Tụ cầu (staphylococci) ☺ Liên cầu (streptococci) Phế cầu (Streptococcus pneumoniae) ☺ Lậu cầu (Neisseria gonorrhoeae) ☺ Màng não cầu (Neisseria meningitidis) STAPHYLOCOCCI HÌNH DẠNG NUÔI CẤY TĂNG TRƯỞNG ĐỘC TỐ Ngoại độc tố Leucocidin Exfoliative toxin Toxic shock syndrome toxin Độc tố ruột (Enterotoxin) Damage to the Host S aureus can express several different types of protein toxins which are probably responsible for symptoms during infections. Some damage the membranes of erythrocytes, causing hemolysis; but it is unlikely that hemolysis is relevant in vivo. The leukocidin causes membrane damage to leukocytes and is not hemolytic. Systemic release of α-toxin causes septic shock, while enterotoxins and TSST-1 cause toxic shock. Membrane Damaging Toxins (a) α-toxin The best characterized and most potent membrane-damaging toxin of S aureus is α-toxin. It is expressed as a monomer that binds to the .
