Cole P J
Infection. 1987;15 Suppl 3:S99-102. doi: 10.1007/BF01650650.
The host's respiratory defence mechanisms are transformed to chronic inflammatory reactions by the persistence of microorganisms and hence inflict damage on the host's own tissues. This change primarily reduces the capability of the mucociliary defence mechanisms. Such impairment can result from modifications to the mucus's physical chemical properties after an infection, or from damage to the ciliary epithelium. Haemophilus influenzae, Pseudomonas aeruginosa and Streptococcus pneumoniae cause ciliary dyskinesia and eventually lead to the destruction of the ciliary epithelium. Encapsulated type b H. influenzae strains appear to slow down the cilia most markedly. There is a fundamental difference between acute and chronic infections. In the case of acute infections the patient's normal defence mechanisms are usually intact. In chronic infections the chronic inflammatory response to the microorganisms causes the disease to progress. In such cases treatment must be considerably more aggressive since the host's "cleansing" capability is diminished. Thus, antibiotics must be applied which can effectively penetrate the bronchial tree and which also remain stable and bioactive in the presence of beta-lactamase producing microorganisms such as H. influenzae. It is conceivable that, in the future, antibiotic therapy will have to be combined with antiphlogistic agents.
由于微生物的持续存在,宿主的呼吸防御机制转变为慢性炎症反应,从而对宿主自身组织造成损害。这种变化主要降低了黏液纤毛防御机制的能力。这种损害可能源于感染后黏液物理化学性质的改变,或纤毛上皮的损伤。流感嗜血杆菌、铜绿假单胞菌和肺炎链球菌会导致纤毛运动障碍,并最终导致纤毛上皮的破坏。b型流感嗜血杆菌的包膜菌株似乎最明显地减缓纤毛运动。急性感染和慢性感染之间存在根本差异。在急性感染的情况下,患者的正常防御机制通常是完整的。在慢性感染中,对微生物的慢性炎症反应会使疾病进展。在这种情况下,治疗必须更积极,因为宿主的“清洁”能力减弱。因此,必须使用能够有效穿透支气管树并且在存在产β-内酰胺酶的微生物(如流感嗜血杆菌)时仍保持稳定和生物活性的抗生素。可以想象,未来抗生素治疗将不得不与抗炎药联合使用。