A 50-year old woman, without any underlying disease, presented with pneumonia after experiencing flu-like symptoms. Streptococcus pneumoniae was identified on admission through blood culture and urine antigen tests. S...A 50-year old woman, without any underlying disease, presented with pneumonia after experiencing flu-like symptoms. Streptococcus pneumoniae was identified on admission through blood culture and urine antigen tests. Staphylococcus aureus and Streptococcus pneumoniae were present in the sputum culture. Computed tomography showed cavity development in the consolidation areas, typical of staphylococcal pneumonia. The patient was intubated and received mechanical ventilation as respiratory failure progressed. She exhibited improvement following antibiotic therapy. The change in type B influenza virus serum titer confirmed that this was a unique case of severe pneumonia caused by multiple bacterial organisms following type B influenza virus infection.展开更多
Streptococcus pneumoniae stimulated mouse peritoneal macrophagc to release tumor necrosis factor-α (TNFα) in vitro. When penicillin was added into the medium with bacteria, TNFα release was accelerated. Pentoxifyll...Streptococcus pneumoniae stimulated mouse peritoneal macrophagc to release tumor necrosis factor-α (TNFα) in vitro. When penicillin was added into the medium with bacteria, TNFα release was accelerated. Pentoxifylline (PTX), a phosphodiesterase inhibitor, significantly attenuated TNFα release caused either by Streptococcus pneumoniae or by its lysates. In this experiment, 150 Kunming mice were infected with Streptococcus peumoniae through inspiration. Dynamic changes of TNFα concentration in serum and bronchoalveolar lavage fluid were determined, and pulmonary pathological changes were also observed. It was found that PTX significantly attenuated TNFα activity in serum and bronchoalveolar lavage fluid, and inhibited white blood cell chemotaxis, emigration and infiltration. In conclusion, Streptococcus pneumoniae infection stimulates the release of TNFα which is probably the major mediater that causes tissue damage during Streptococcus pneumoniae infection. The mechanism is probably that Steptococcus pneumoniae and its lysates activate TNFα gene transcription. As penicillin accelerates TNFα release, treatment with penicillin alone may aggravate the tissue damage. Combined treatment with PTX may be more reasonable.展开更多
文摘A 50-year old woman, without any underlying disease, presented with pneumonia after experiencing flu-like symptoms. Streptococcus pneumoniae was identified on admission through blood culture and urine antigen tests. Staphylococcus aureus and Streptococcus pneumoniae were present in the sputum culture. Computed tomography showed cavity development in the consolidation areas, typical of staphylococcal pneumonia. The patient was intubated and received mechanical ventilation as respiratory failure progressed. She exhibited improvement following antibiotic therapy. The change in type B influenza virus serum titer confirmed that this was a unique case of severe pneumonia caused by multiple bacterial organisms following type B influenza virus infection.
文摘Streptococcus pneumoniae stimulated mouse peritoneal macrophagc to release tumor necrosis factor-α (TNFα) in vitro. When penicillin was added into the medium with bacteria, TNFα release was accelerated. Pentoxifylline (PTX), a phosphodiesterase inhibitor, significantly attenuated TNFα release caused either by Streptococcus pneumoniae or by its lysates. In this experiment, 150 Kunming mice were infected with Streptococcus peumoniae through inspiration. Dynamic changes of TNFα concentration in serum and bronchoalveolar lavage fluid were determined, and pulmonary pathological changes were also observed. It was found that PTX significantly attenuated TNFα activity in serum and bronchoalveolar lavage fluid, and inhibited white blood cell chemotaxis, emigration and infiltration. In conclusion, Streptococcus pneumoniae infection stimulates the release of TNFα which is probably the major mediater that causes tissue damage during Streptococcus pneumoniae infection. The mechanism is probably that Steptococcus pneumoniae and its lysates activate TNFα gene transcription. As penicillin accelerates TNFα release, treatment with penicillin alone may aggravate the tissue damage. Combined treatment with PTX may be more reasonable.
